The Best Foods to Help Lower Homocysteine Naturally

Of all the blood markers linked to dementia risk, homocysteine may be one of the most important and one of the easiest to improve. There are certain foods that lower homocysteine, making it possible to have a positive impact through your diet.

If you have searched online for foods that lower homocysteine, you have probably found plenty of articles recommending spinach, broccoli, eggs and salmon. They are all excellent foods, but they are only part of the story.

The truth is that no food lowers homocysteine directly. Your body is the one that does that. Every second of every day, it is recycling homocysteine through a series of biochemical reactions that depend on a steady supply of essential nutrients. The foods you eat simply provide the vitamins and nutrients those reactions need to work efficiently.

Understanding that difference changes the conversation completely. Instead of searching for a miracle food, the goal becomes giving your body the nutrients it needs to keep homocysteine in a healthy range.

For a full explanation of what homocysteine is and why elevated levels matter, read our guide to homocysteine.

Combined with appropriate testing and, where needed, targeted supplementation, improving your diet is one of the most practical ways to support long-term brain health.

Can food lower homocysteine?

No food lowers homocysteine directly. Instead, foods provide the folate, vitamin B12, vitamin B6, riboflavin, choline and betaine your body needs to recycle homocysteine efficiently.

Improving your intake of these nutrients may help support healthier homocysteine levels, particularly if your diet has previously been low in leafy green vegetables, legumes, fish, eggs or other nutrient-rich whole foods.

However, the effect of diet depends on why homocysteine is elevated. Poor vitamin B12 absorption, medications, kidney disease, thyroid problems and genetic factors may mean that dietary changes alone are not enough.

The key nutrients involved in homocysteine metabolism

Why homocysteine matters?

Homocysteine is a naturally occurring amino acid produced whenever your body breaks down methionine, an amino acid found in protein-rich foods.

Under healthy conditions, homocysteine does not remain in the bloodstream for long. It is quickly recycled into other useful compounds that support normal cellular function.

Problems arise when that recycling process slows down. Homocysteine begins to accumulate, increasing oxidative stress, inflammation and damage to blood vessels.

Over the last three decades, elevated homocysteine has consistently been associated with a higher risk of cognitive decline, dementia, stroke and cardiovascular disease.¹

Unlike high blood pressure or raised cholesterol, however, homocysteine rarely causes obvious symptoms. People often discover it is elevated only after having a blood test, by which time it may have been quietly increasing for years.

That is why homocysteine can be such a valuable biomarker. It gives you an opportunity to identify a potential problem early and take appropriate action.

You can learn more about the evidence linking homocysteine and dementia risk.

Why these foods work?

Your body has evolved an elegant system for dealing with homocysteine. Rather than allowing it to build up, it continually recycles it through two interconnected pathways.

One pathway converts homocysteine back into methionine so it can be reused. The other converts it into cysteine, an amino acid used to produce glutathione, often described as the body’s master antioxidant because of its role in protecting cells from oxidative damage.

Neither pathway works without the right nutrients. Folate, vitamin B12, vitamin B6, riboflavin, choline and betaine each have specific jobs within this recycling process.

If one or more of these nutrients becomes limiting, the whole system becomes less efficient and homocysteine starts to rise.

For a more detailed explanation of these biological pathways, read our guide to methylation and homocysteine.

This explains why two people eating apparently similar diets can have very different homocysteine levels. One may absorb vitamin B12 less efficiently as they get older. Another may carry a common genetic variant that increases their riboflavin requirement. Someone else may consume large amounts of caffeine or alcohol, increasing their need for certain B vitamins.

It is rarely one factor in isolation. More often, several small influences combine over many years.

The good news is that these pathways can be responsive. Give your body the nutrients it needs, remove some of the obstacles that interfere with the process, and homocysteine may begin to fall.

Foods that lower homocysteine: folate-rich foods

When researchers study nutrition and homocysteine, one nutrient consistently stands out: folate.

Folate plays a central role in recycling homocysteine back into methionine. Without enough folate, this pathway slows, making it much harder for your body to keep homocysteine within a healthy range.

Numerous intervention studies have demonstrated that improving folate status lowers homocysteine, particularly in people whose intake has previously been low.¹

Fortunately, folate is abundant in many whole plant foods.

Leafy green vegetables

Beans and lentils

Foods that lower homocysteine with vitamin B12

Folate rarely works alone. Vitamin B12 is equally important because it enables homocysteine to be converted back into methionine.

When vitamin B12 is lacking, this recycling process slows, regardless of how much folate is available.

One reason this matters is that vitamin B12 deficiency becomes increasingly common with age. Stomach acid, which helps release vitamin B12 from food, naturally declines over time. Some medications can further reduce absorption, while vegetarians and vegans may consume too little through their diet.

As a result, homocysteine may begin to rise years before the more familiar symptoms of vitamin B12 deficiency appear.

Fish and seafood

Eggs and dairy

Meat and liver

Foods that lower homocysteine with vitamin B6

Although folate and vitamin B12 receive most of the attention, they are only part of the story.

Vitamin B6 helps direct homocysteine down a different pathway, converting it into cysteine, which is then used to produce glutathione.

Good dietary sources include:

Poultry
Salmon
Tuna
Potatoes
Bananas
Chickpeas
Fortified cereals

Vitamin B6 is found in a wide range of foods, so a varied whole-food diet will usually provide more than relying heavily on one source.

Vitamin B2 foods that lower homocysteine

Riboflavin, better known as vitamin B2, is another nutrient that deserves greater recognition.

It is particularly important for people carrying the common MTHFR C677T genetic variant, where an adequate riboflavin intake may help the recycling process work more efficiently.

Foods containing riboflavin include:

Eggs
Yoghurt
Milk
Mushrooms
Almonds
Beef
Fortified cereals

Looking at nutrients individually is helpful for understanding the biology, but this is not how we eat. Meals contain dozens of vitamins, minerals and plant compounds working together, which is one reason whole-food dietary patterns consistently outperform approaches focused on isolated foods alone.

Choline and betaine foods that lower homocysteine naturally

Your body has a second way of recycling homocysteine that receives far less attention.

This alternative pathway depends on choline and betaine.

Choline supports normal methylation, helps build healthy brain cell membranes and is used to produce acetylcholine, a neurotransmitter involved in learning and memory.

Betaine acts as a methyl donor, allowing homocysteine to be converted back into methionine through a different biochemical route.

Eggs are one of the richest dietary sources of choline, while liver, fish and soybeans also provide significant amounts.

Beetroot, spinach, quinoa and wholegrains contribute valuable sources of betaine.

Thinking about these nutrients together helps explain why no single food can claim to lower homocysteine. Instead, the most effective dietary approach is built around a wide variety of nutrient-dense whole foods, each contributing different pieces of the puzzle.

Foods and habits that may make high homocysteine harder to manage

Supporting healthy homocysteine is not only about what you add to your plate. Certain everyday habits can also make it harder for your body to keep levels under control.

A diet low in vegetables naturally reduces your intake of folate and other B vitamins.

Diets dominated by ultra-processed foods often provide fewer of the vitamins needed for efficient methylation.

Excess alcohol can interfere with the absorption and metabolism of several nutrients involved in homocysteine recycling.

Smoking increases oxidative stress and is associated with higher homocysteine levels.

Coffee deserves a brief mention because the evidence is more nuanced. Moderate coffee consumption has been associated with several health benefits, yet some studies have also shown that high coffee consumption can increase homocysteine.

This does not mean everyone needs to give up coffee, but it strengthens the case for maintaining a good nutritional status if you drink several cups each day.

The aim is not dietary perfection. It is creating the best possible environment for your body’s own recycling system to work efficiently.

Diet is only one part of the picture. Regular exercise, stopping smoking, managing alcohol intake and correcting nutritional deficiencies can all help support healthy homocysteine levels. Learn about these and other evidence-based strategies in our guide to Eight Ways to Lower Your Homocysteine.

A Sample Day of Eating with Foods That Lower Homocysteine

The best foods to support healthy homocysteine

There is not a single food that lowers homocysteine. Eating a variety of whole foods provides the nutrients your body needs to recycle it efficiently.

Leafy green vegetables such as spinach, kale and broccoli are among the richest sources of folate, while fish, seafood and eggs provide vitamin B12.

Eggs also supply choline, an important nutrient for healthy methylation, and beans and lentils contribute folate and vitamin B6.

Beetroot, spinach and wholegrains provide betaine, which supports an alternative pathway for recycling homocysteine.

Rather than searching for a superfood, build meals around these foods consistently. Together they provide the nutrients your brain and body need to maintain healthy homocysteine metabolism.

Is diet enough to lower high homocysteine?

Improving your diet should always be the foundation. Every meal and snack is an opportunity to provide your body with the nutrients it needs to recycle homocysteine efficiently.

Many people may see meaningful improvements simply by eating more leafy greens, legumes, seafood, eggs and other nutrient-dense whole foods.

However, diet has its limits.

If a blood test shows your homocysteine is above the optimal range, food alone may not be enough to bring it back down.

Poor vitamin B12 absorption becomes increasingly common with age, certain medications interfere with B-vitamin metabolism, and some people have genetic variations that increase their need for specific nutrients.

Even someone eating what appears to be an excellent diet may still require additional nutritional support.

Rather than viewing food and supplements as competing approaches, think of them as working together. A nutrient-rich diet provides the foundation for lifelong health, while targeted supplementation may help correct a nutritional imbalance when diet alone does not achieve the desired result.

Read our complete guide to lowering homocysteine for a broader explanation of diet, lifestyle, testing and targeted nutritional support.

You can also learn more about B vitamins for lowering homocysteine.

How long does it take to lower homocysteine?

One of the encouraging things about homocysteine is that it can respond relatively quickly to the right intervention.

Improvements may begin within a few weeks of increasing key nutrients, although this depends on the underlying cause and how elevated homocysteine was to begin with.

Dietary changes may begin affecting homocysteine within weeks, but retesting after an appropriate interval can show whether the changes have been sufficient.

Food for the Brain recommends a simple approach.

First, test your homocysteine to establish your starting point. If you’re unsure which test to choose or how testing works, read our guide to homocysteine testing.

Next, improve your diet by increasing foods naturally rich in folate and other B vitamins while introducing targeted supplementation where appropriate.

Finally, repeat the test after around three to six months to confirm whether your homocysteine has moved towards a healthier range.

Without measuring it, you do not know whether your strategy is working.

Read more about how and when to test homocysteine.

Already have a result? Learn how to understand your homocysteine result.

Frequently asked questions

The bigger picture

Homocysteine is more than another blood test. It can indicate whether your body has the nutrients needed to support healthy methylation and long-term brain health.

Unlike many risk factors for cognitive decline, it is measurable, modifiable and measurable again after you have taken action.¹

A nutrient-rich diet should always be the starting point, but if testing shows your homocysteine is above the optimal range, targeted supplementation may be needed alongside dietary changes.

The goal is not simply to eat more spinach, although eating more vegetables is rarely a bad idea.

The goal is to understand what your body needs, measure your progress and know whether the steps you are taking are actually working.

Next steps

If you have not measured your homocysteine, that is the best place to start.

Knowing your level takes the guesswork out of deciding whether dietary changes alone are enough or whether targeted supplementation may be needed.

You can order our accurate at-home Homocysteine Test or choose the DRIfT 5-in-1 Test, which measures homocysteine alongside vitamin D, omega-3 index, HbA1c and glutathione, giving you a broader picture of your brain health.

You can also read our complete guide to lowering homocysteine for the next practical steps.

Why Gut Health Matters for Brain Health More Than You Think

Why Some Brains Improve and Others Don’t

Many people are doing more than ever to protect their brain. They eat well. Take supplements. Exercise. Stay mentally active.

Yet outcomes vary dramatically.

Some improve. Others stall. A few decline despite doing everything “right”.

The missing question is not what else to add, but what environment those interventions are landing in.

Cognitive decline rarely stems from one isolated failure. It emerges when the body’s internal environment no longer supports protection, repair, and resilience. This systems-based understanding underpins the work of Food for the Brain, and explains why gut health plays a central role in our COGNITION brain upgrade programme.

The terrain model of brain health

In medicine, there is a long-established principle that disease does not arise from a trigger alone, but from the biological environment in which that trigger operates. This is often described as the terrain.

From a brain health perspective, terrain includes inflammatory load, metabolic health, immune balance, nutrient availability, and cellular repair capacity. These systems interact constantly. When they stay in balance, the brain shows remarkable resilience. When they become disrupted, vulnerability increases.

Neurodegenerative conditions, including Alzheimer’s disease, are now understood to arise from multiple interacting biological pressures rather than a single pathological process. Many of these systems are shaped upstream by gut related processes.

The gut as a regulator, not a root cause

The gut is often discussed as if it were a standalone digestive organ. In reality, it plays a regulatory role in shaping systemic inflammation, metabolic function, and immune signalling.

When gut barrier integrity is compromised, bacterial components such as lipopolysaccharides can enter circulation. This process increases immune activation and drives chronic low-grade inflammation, a state strongly associated with insulin resistance and cognitive decline [1,2].

In this context, gut dysfunction is not “causing” brain disease. It is influencing the conditions in which brain protection and repair either succeed or struggle.

Why prevention struggles in an inflamed system

Brain health interventions that we talk about here at Food for the Brain do not operate in isolation. Their effectiveness depends on the biological environment in which they are applied.

This is particularly clear in nutritional research.

B vitamin supplementation has been shown to slow brain atrophy, but only in individuals with raised homocysteine levels and a metabolic environment that allows normal methylation processes to function [3]. Similarly, omega 3 fatty acids support neuronal membrane structure and signalling, yet their cognitive benefits are reduced in the presence of inflammation and insulin resistance [4].

Inflammation interferes with digestion, absorption, transport, and cellular uptake of nutrients. Pro inflammatory cytokines also impair intracellular metabolic pathways, shifting the body toward defence rather than repair. In this terrain, even well evidenced interventions may have limited effect.

The same principle applies to lifestyle strategies. Physical activity, cognitive stimulation, and stress reduction are all protective, but their impact is blunted when inflammatory and metabolic pressures remain unaddressed. That is why in COGNITION we target all 8 modifiable nutrition and lifestyle factors, so that you are not just targeting a specific nutrient but you are changing the environment.

Microbes, inflammation, and brain vulnerability

Human studies consistently show that individuals with cognitive impairment or Alzheimer’s disease have altered gut microbiome profiles alongside higher levels of systemic inflammatory markers [5].

This does not demonstrate that microbes cause dementia. What it does show is that microbial imbalance contributes to inflammatory load, which in turn increases brain vulnerability.

Over time, this vulnerability can translate into accelerated cognitive decline.

For this reason, the COGNITION brain upgrade programme actively addresses gut health as one of eight modifiable factors that influence dementia risk. Gut microbes actively shape the internal environment in ways that can either accelerate neurodegeneration or help slow it.

The metabolic bridge between gut and brain

The gut also plays a critical role in metabolic regulation.

Chronic gut driven inflammation worsens insulin resistance, reducing glucose uptake by brain cells. Impaired brain glucose metabolism is a recognised feature of cognitive decline and has led some researchers to describe Alzheimer’s disease as a form of brain specific metabolic failure [6,7].

In this model, the gut is not peripheral. It contributes upstream to the metabolic conditions that determine whether the brain can access adequate fuel to function and repair.

Again, the implication is not that gut health alone determines brain fate. It is that brain health strategies are less effective when the metabolic and inflammatory terrain is unfavourable.

Why Brain Health Advice Works for Some People and Not Others

A terrain based perspective offers something often missing from prevention conversations.

Understanding.

When people follow advice carefully and still do not improve, clinicians too often frame the explanation as lack of compliance or genetics. Systems thinking offers a different interpretation.

The tools may be appropriate but the environment may not yet support repair.

This reframes prevention as a personalised process rather than a universal checklist. Understanding an individual’s internal terrain helps identify where effort should go.

This is why Food for the Brain offers two complementary forms of assessment: the free, validated Cognitive Function Test and optional at home blood testing to assess key modifiable risk markers such as homocysteine, omega 3 status and glutathione.

The answer is not found in one nutrient

Viewing brain health through a terrain lens shifts prevention away from adding isolated solutions and toward restoring balance across systems.

The future of brain health does not lie in targeting one nutrient, one habit, or one molecule.

It lies in creating an internal environment where protection, repair, and resilience are possible.

Brains do not fail because one thing goes wrong. They decline when the terrain no longer supports them.

And that terrain forms quietly and cumulatively long before symptoms appear.

Next Steps

Learn more about how gut health impacts brain health in our upcoming webinar here
Complete the FREE, validated Cognitive Function Test today so you can get instant insight into your current brain health status
Order your at home blood test here to get more personalised data on your body and contribute to our on going research

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, et al. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes. 2007;56(7):1761–72.
Hotamisligil GS. Inflammation and metabolic disorders. Nature. 2006;444(7121):860–7.
Smith AD, Smith SM, de Jager CA, Whitbread P, Johnston C, Agacinski G, et al. Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment. Proc Natl Acad Sci U S A. 2010;107(31):14187–92.
Jernerén F, Elshorbagy AK, Oulhaj A, Smith SM, Refsum H, Smith AD. Brain atrophy in cognitively impaired elderly: the importance of long-chain omega-3 fatty acids and B vitamin status in a randomized controlled trial. Am J Clin Nutr. 2015;102(1):215–21.
Vogt NM, Kerby RL, Dill-McFarland KA, Harding SJ, Merluzzi AP, Johnson SC, et al. Gut microbiome alterations in Alzheimer’s disease. Sci Rep. 2017;7(1):13537.
Craft S. Insulin resistance and Alzheimer’s disease pathogenesis: potential mechanisms and implications for treatment. Arch Neurol. 2009;66(3):300–5.
de la Monte SM, Wands JR. Alzheimer’s disease is type 3 diabetes–evidence reviewed. J Diabetes Sci Technol. 2008;2(6):1101–13.

The GL of Your Diet Determines Your Future Dementia Risk

by Patrick Holford

Why Blood Sugar Exposure Matters More Than Sugar Itself

Your brain uses more glucose for energy than any other organ in the body.

From that simple fact comes a widespread assumption: that sugar fuels the brain and therefore more sugar must mean more mental energy.

In reality, the opposite appears to be true.

A large new study shows that the glycaemic load (GL) of your diet, which reflects how much glucose you expose your bloodstream to over time, is strongly linked to your future risk of dementia. The higher the glycaemic load, the higher the risk.

In this study, people consuming more than 110 GL units a day had a 13% higher risk of developing dementia. Those consuming less than 49.3 GL units a day had a 17% lower risk. In other words, the difference between a high GL diet and a low GL diet translated into a 30% swing in dementia risk.The study, published in the International Journal of Epidemiology, analysed dietary data from over 200,000 UK Biobank participants in 2011–12 and followed them for more than a decade to see who did, and did not, develop dementia (1).¹

Most people’s diets exceed 100 GL units a day. I have been advocating a daily intake of around 45 to 60 GL units since the 1990s. To understand why this matters, and what it means for what you eat, it helps to understand what GL actually is.

How Much Sugar Your Body Really Needs

As petrol is for your car, glucose is the primary fuel for your body. Glucose is the main fuel used by all cells.

There is also another fuel, ketones, much like cars can also run on electricity. We too are metabolic hybrids.

Now here is an astonishing fact. Your body contains around 100,000 kilometres of blood vessels. Your brain alone has around 1,000 kilometres of them. These vessels supply energy to around 30 trillion cells, each containing roughly 1,000 mitochondria, the tiny energy factories that power life.

And yet, across this entire system, there only needs to be around 4 grams of glucose in your bloodstream at any one time. That is one teaspoonful. That is all that is required for every cell in your brain and body to have energy at that moment.²

GL is a measure of how much glucose enters your bloodstream after eating or drinking a food. If there is not much glucose in the food, and you use it quickly, perhaps by moving or exercising, blood sugar levels stabilise rapidly.

The glycaemic load of a food depends on two things:
• the quality of the carbohydrate
• the quantity eaten

Quality refers to how fast glucose is released, known as the glycaemic index (GI). Fibre and protein slow this release. This is why white rice has a higher GI than brown rice, which contains fibre. Eat rice with fish, beans or meat, and the protein slows the release further.

GL also depends on portion size. A small serving of brown rice with fish is low GL. A large serving of white rice, even with fish, is high GL.

When Glucose Becomes Toxic to the Brain

What happens if you consume far more glucose than the body needs?

A can of sugary fizzy drink contains around 35 grams of sugar. That is roughly nine times more glucose than the total amount normally circulating in your bloodstream.

This excess is toxic. It damages blood vessels and the tissues they supply. Diabetes is diagnosed precisely because excess sugar damages the kidneys, eyes and nerves. The brain is no exception.

“The brain needs more energy than any other organ, so it contains the most mitochondria. Sugar damages mitochondria,” says Professor Robert Lustig, Professor of Neuroendocrinology at the University of California, San Francisco. If you have read Upgrade Your Brain or Alzheimer’s: Prevention is the Cure, you will already know that high sugar intake, sugary drinks and ultra processed foods increase dementia risk, worsen memory even in young people, and are associated with measurable shrinkage of brain regions involved in memory in teenagers.

Are You Eating Too Much Hidden Sugar?

The simplest way to assess your long term blood sugar exposure is to measure HbA1c.

HbA1c literally means sugar damaged red blood cells. If more than 6.5% of your red blood cells are sugar damaged, you are diagnosed with diabetes. Above 6% indicates pre diabetes. Even levels above 5.4% in teenagers predict brain shrinkage.

For optimal health you want to be below 5.4%, and ideally below 5%.

HbA1c is such a strong indicator of blood sugar resilience that it is included in Food for the Brain’s 5-in-1 DRIfT home blood test kit.

Balancing Blood Sugar with a Low Glycaemic Load Diet

Let us start with something simple.

An orange contains sugar, but also fibre and micronutrients. The fibre slows sugar release, mainly fructose, which takes time to convert to glucose, while feeding beneficial gut bacteria.

A glass of orange juice, however, contains the sugar of around three oranges, without the fibre. Three times the sugar, with no brakes. Eat your fruit. Do not drink it.

When you eat sugar or starches such as rice, digestive enzymes rapidly break them down into glucose. Protein, by contrast, takes several hours to digest into amino acids. This slows carbohydrate digestion further down the digestive tract.

This leads to a simple rule: eat carbohydrates with protein.

Brown rice releases glucose more slowly than white rice. Add beans, fish or meat, and the release slows further.

From this we can extract three practical rules:
• Eat fruit. Do not drink it
• Always eat carbohydrate with protein
• Make fibre the primary ingredient of every meal

What a Low GL Meal Actually Looks Like

Compare these two breakfasts:

Cornflakes with a banana or Oats with chia seeds and berries

Cornflakes are fast releasing sugar. Oats are slow releasing. A banana raises blood sugar more than two bowls of berries.

Chia seeds, rich in soluble fibre, dramatically slow sugar release. A portion of oats with chia and berries is around 10 GL. Cornflakes and a banana can reach 30 GL.

You want meals around 10 GL and snacks around 5 GL. Three meals and two snacks equals around 40 GL per day.

Eat 40 GL per day to lose weight. Around 60 GL to maintain it.

Eat little and often, and start the day with a low GL breakfast.

A friend of mine, Dr David Unwin, who is  a leading diabetes doctor, converted our low GL calculations into ‘teaspoons of sugar equivalent’ to give a visual idea to his diabetic and overweight patients of how sugar is hidden in common foods. See the table below.

Adapted, with permission, from David Unwin’s charts in the Journal of Insulin Resistance (2016) 

The Balance of Your Plate

Half your plate should be vegetables and fruit. A quarter should be protein. A quarter carbohydrate.

Vegetables supply antioxidants that neutralise the exhaust fumes produced when mitochondria burn fuel. This becomes more important as we age and mitochondrial efficiency declines.

Protein slows sugar release and provides essential building blocks. Carbohydrate portions must be modest.

Whole grains and starchy vegetables vary widely in GL. Wholemeal pasta and brown basmati rice are far better than white pasta or white rice. Swedes, carrots and squash are better than potatoes. Boiled potatoes are better than baked. French fries are the worst of all.
all.

Beans and Lentils: Nature’s Blood Sugar Regulators

Beans and lentils are uniquely effective because they contain both protein and carbohydrate in one food. This keeps their GL low while allowing generous portions.

When combining beans with other starches, reduce the starch portion by half. A cup of lentils with half a cup of rice, not equal amounts.

By applying these principles you can restore blood sugar control, regain energy, reduce dementia risk, reverse type 2 diabetes and improve cognitive clarity.

The Proof Is in Your HbA1c

Red blood cells live for around three months. Follow a low GL diet for three months, then retest HbA1c.

This approach is detailed in The Low GL Diet Cookbook. Specific supplements can accelerate recovery, including fibre such as glucomannan, chromium and cinnamon compounds to improve insulin sensitivity, and HCA from tamarind to promote glucose burning rather than storage.

What to Do Next

If glycaemic load affects dementia risk, the next step is simple: measure, act, and check again.

Test your blood sugar resilience.

HbA1c shows how much sugar damage has occurred over the last three months. It is included in Food for the Brain’s DRIfT 5-in-1 home test, alongside other key brain health markers. If HbA1c is high, a low GL diet gives you a clear way to bring it down.

Check how your brain is functioning now.

The free Cognitive Function Test takes around 20 minutes and provides an objective snapshot of memory, attention and processing speed. Many people spot early changes years before any diagnosis.

Make changes, then retest.

Follow a low GL diet for three months, then re-test HbA1c and cognitive function to see whether the changes are working.

Prevention works best when it is measured.

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

Novau-Ferré N et al. Glycemic index, glycemic load, and risk of dementia: a prospective analysis within the UK Biobank cohort. Int J Epidemiol. 2025.
Wasserman DH. Four grams of glucose. Am J Physiol

Dry January for Your Brain: A Lighter, Clearer Start to the Year

Dry January arrives with its usual mix of good intentions and side-eye, but beneath the trend is a surprising truth: your brain loves this month more than you think.

That’s because January quietly offers something modern brains rarely get the rest of the year: a drop in oxidative stress and a chance for your natural repair systems to catch up.  It’s a pause that lowers the background “noise” created by alcohol and allows your natural calming chemistry to rise back to the surface.

Many people start Dry January thinking about their liver or their waistline. But the strongest benefits often happen behind the scenes, in the place that governs mood, memory, sleep, and stress resilience.

That’s where the real benefits begin to show.

Dry January for Your Brain: Why the Benefits Show Up So Fast

Alcohol works on the same calming pathway your brain uses to wind down naturally. It boosts GABA, the neurotransmitter that quietens the nervous system. That lovely “first sip exhale” comes from this temporary GABA boost. You can learn more about GABA here. 

But your brain is clever. To compensate, it gradually nudges up adrenaline and turns the GABA dial down. This is why the glass that once relaxed you, can start to make you feel restless or wakeful later in the night.

And there’s more happening beneath the surface:

Alcohol increases oxidative stress inside neurons, largely because its metabolism produces acetaldehyde. This compound generates reactive oxygen species and increases neuronal damage (1).
It also places extra pressure on glutathione, the molecule the brain relies on for detoxification and repair. Chronic alcohol exposure is associated with reduced glutathione levels and impaired antioxidant capacity in the brain (2).
The hippocampus is particularly affected. This memory and mood hub is vulnerable to long term strain, and higher alcohol intake is linked to reduced hippocampal volume even at moderate levels (3).
Alcohol also disrupts sleep quality, especially REM cycles, which are crucial for cognitive repair. While alcohol initially sedates, it later fragments sleep architecture through a rebound in adrenaline and cortisol.

Read more about how alcohol impacts your brain here.

These are some of the core drivers of long term cognitive ageing. When they ease up, even for a short period, the brain begins to function more cleanly and calmly.

For this reason, so many people report that a couple of no or low alcohol weeks in January give them clearer thinking, steadier mood, and deeper sleep.

Two Brain Friendly Drinks for Your January Wind Down

With that in mind, here are two great recipe options to help you reduce your alcohol intake while still enjoying a wind down ritual. If you want more brain friendly recipes this year, make sure you subscribe to the Upgrade Your Brain Cook App.

Want to go deeper?

If you want deeper support for your brain this year, there are three simple steps you can take.

First, measure the things that matter. The DRIfT 5 in 1 at home blood test gives you a clear picture of the nutritional and metabolic factors that influence long term brain health. It is one of the most effective ways to understand your personal risk and what to do next.

Second, stay connected to what keeps your brain healthy. Becoming a FRIEND of Food for the Brain gives you ongoing support, events, and guidance grounded in evidence and prevention.

Third, take the free Cognitive Function Test. It provides an objective snapshot of how your brain is performing right now and helps you track your progress over time.

Food for the Brain is a not for profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index. This allows them to advise you on how to dementia proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References:

Zakhari S. Overview: how is alcohol metabolized by the body? Alcohol Res Health. 2006;29(4):245-54. PMID: 17718403.
Das SK, Vasudevan DM. Alcohol-induced oxidative stress. Life Sci. 2007;81(3):177-87. PMID: 17570440.
Topiwala A, et al. Moderate alcohol consumption as risk factor for adverse brain outcomes and cognitive decline. BMJ. 2017;357:j2353. PMID: 28588063.

A Better Festive Treat: Black Bean Brownies That Support Blood Sugar and Brain Health

If you find yourself craving more sugar at this time of year, there’s nothing wrong with you – your biology is responding to a month where blood sugar swings are almost guaranteed. 

But cravings aren’t a sign of weakness. They’re a sign your blood sugar, gut, and brain chemistry are under strain – which is why fibre-rich festive recipes can make such a powerful difference.

This week’s recipe does exactly that. These black bean brownies feel indulgent, but underneath they’re designed to support stable blood sugar, calm cravings, and keep your brain sharper through the most sugar-heavy month of the year.

And yes: they taste genuinely delicious.

Why Sugar Affects Your Brain and Memory

Sugar doesn’t just influence your waistline and energy – it directly affects the structure and functioning of your brain. Glucose is the brain’s primary fuel, but when levels rise too high or fluctuate too quickly, the brain experiences this as stress. Over time, those swings change how the brain ages.

Large population studies show that even slightly elevated glucose levels – levels many people would consider “normal” – significantly increase dementia risk (1). And when HbA1c rises, it shows that your body has been exposed to higher glucose levels over the past 8–12 weeks. This matters because long-term elevated glucose drives inflammation, damages blood vessels in the brain, and accelerates the processes linked to cognitive decline (2).

Even in younger or otherwise healthy adults, small rises in glucose are associated with reduced volume in the hippocampus – the brain’s centre for memory, learning, and emotional regulation (3). This means that sugar isn’t only an issue for diabetes prevention; it’s directly tied to how well your brain can store information, retrieve memories, and stay resilient across your lifetime.

During the festive period, these glucose swings become more common – thanks to grazing, disrupted routines, and richer foods. It’s not the single dessert that matters, but the repeating pattern. And your brain feels every one of those peaks and dips before your waistline every does.

How to Tell If You’re Eating Too Much Sugar (Using HbA1c)

This is where measuring your HbA1c becomes incredibly useful.

HbA1c reflects how much of your red blood cells have been exposed to glucose over the past 8–12 weeks, giving you a true picture of your overall sugar load – not just what you ate yesterday, but whether your body is regularly receiving more carbohydrate than it can comfortably handle. We all have slightly different carbohydrate tolerance, and HbA1c shows you where your line is.

It’s also one of the most powerful early indicators of long-term brain health. Higher HbA1c is linked with faster cognitive decline and a greater risk of dementia, even in people who don’t meet the criteria for diabetes (2). Keeping your sugar intake – and therefore your HbA1c – in a healthy range is a core part of protecting your brain.

But glucose is only one part of the story.

When you look at HbA1c alongside other biomarkers such as homocysteine and the omega-3 index, you get a much richer picture of how well your brain is being supported. These markers reflect inflammation, nutrient status, membrane structure and repair – all of which influence how resilient your brain is to the effects of oxidative stress and high blood sugar. When any of them drift out of range, the brain becomes more vulnerable.

This is exactly why our DRIfT test brings these three measures together.

Between HbA1c, homocysteine, and omega-3 status, you gain a personalised, science-based understanding of how your current diet and lifestyle are shaping your cognitive future.

And if your HbA1c is starting to rise, it’s an early signal that your brain has been exposed to more glucose than it can comfortably manage – a gentle nudge to make adjustments now, rather than years down the line. Order your DRIfT test here – and for the first time ever – we’ve reduced the DRIfT 5-in-1 test by 20% this weekend to widen access to early detection and support our prevention research.

Why Fibre Helps Reduce Sugar Cravings (Especially in December)

This is the part most people underestimate.

A high-fibre diet:

slows glucose entering the bloodstream,
reduces cravings,
stabilises energy, and
supports better long-term glycaemic control.

A large systematic review published in The Lancet found that diets higher in fibre significantly improved blood sugar control, lowered HbA1c, and reduced diabetes risk (4).
During a month where treats are everywhere, fibre becomes one of the simplest tools to protect your metabolic and cognitive health. (Gut health is one of our nutrition and lifestyle domains on our COGNITION™ programme – free to all our FRIENDS)

Which is why these brownies work so well…

Most festive treats are low-fibre and high-sugar – a combination that sends cravings soaring.

These brownies flip that on its head.

With black beans, oats, and chicory root syrup, each brownie contains:

~5.4g fibre
~3g protein
~6g fat
~9g carbs
low GL (≈ 3.9)

This gives you the sweetness without the spike – and the fibre slows digestion so you don’t end up reaching for “just one more”.

Serve them with thick Greek yoghurt and fresh raspberries for extra balance and natural sweetness.

High-Fibre Black Bean Brownie Recipe (Low GL, Gluten Free)

Ingredients

 1 tin black beans, drained & rinsed very well
6 tbsp cocoa powder (30g)
40g oats
1 egg
1/4 tsp salt
4–6 tbsp sweetener of choice (chicory syrup or brown-sugar substitute work well)
4 tbsp coconut oil
2 tsp vanilla extract
1/2 tsp baking powder

Method:

Preheat oven to 170°C.
Blend all ingredients in a food processor until completely smooth.
Pour into a lined 8×8 tin.
Bake for 15–18 minutes.
Cool for at least 10 minutes before slicing.
If still soft, chill in the fridge overnight – they firm up beautifully.

Check Your HbA1c, Omega-3 and Homocysteine With Our DRIfT Test

Fibre-rich recipes can help – but the real insight comes from knowing your HbA1c.

Our DRIfT 5-in-1 at home blood test measures your:

HbA1c (blood sugar control)
Omega-3 Index
Vitamin D
Homocysteine
Glutathione
Available to purchase globally – order yours here

It’s one of the simplest ways to understand how sugar is affecting your long-term brain health – and what to do next to protect it.

Also, if you haven’t completed the FREE and validated online Cognitive Function Test then do that together too get instant personalised feedback on your brain health.

For more recipes – subscribe to the Upgrade Your Brain Cook App.

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References:

Crane PK et al. Glucose levels and risk of dementia. N Engl J Med. 2013;369(6):540–548.
Rawlings AM et al. Diabetes, prediabetes and cognitive decline. Diabetes Care. 2019;42(7):1217–1224.
Kerti L et al. Higher glucose levels relate to lower hippocampal connectivity and cognition. Neurology. 2013;81(20):1746–1752.
Reynolds A et al. Carbohydrate quality and human health: systematic review. Lancet. 2019;393(10170):434–445.

Why Sleep is Your Metabolic Superpower

We tend to think of sleep as rest – the way we replenish energy.  In truth, your sleeping hours are a highly productive repair shift, especially for your metabolism. 

Each night, your body resets blood sugar, clears metabolic waste, restores energy and even rewires memory. Consistently missing out on quality or quantity of sleep means less of that vital repair work gets done.

Most people notice tiredness after a bad night, but few realise the impact it has on their blood sugar, metabolism and even body composition.

So in our last article we explored melatonin’s role in brain repair, in this part 2 we look at how poor sleep throws off your body’s entire metabolic rhythm – from blood sugar to fat storage.

(When we talk about poor sleep, we mean getting less than seven hours a night, sleeping at irregular times, or waking often through the night – all of which disturb the deep, restorative phases your brain depends on.)

Sleep and insulin: two sides of the same coin

Deep, unbroken sleep keeps your cells sensitive to insulin, the hormone that allows glucose into cells to make energy. Cut the night short and this system falters. Just one poor night can reduce insulin sensitivity by about 25 per cent (1).

That means glucose lingers in the bloodstream (creating inflammation over time) while your brain cells are left hungry for fuel.

The result? Brain fog, irritability, and a body craving quick fixes – sugar, caffeine and refined carbohydrates. You’ll have felt this yourself: after a poor night’s sleep, you wake up wanting pastries or toast, not eggs and greens.

The “tired brain” that acts diabetic

When the brain can’t get enough glucose, it flips into survival mode.

Stress hormones like cortisol and adrenaline surge to keep you going, but they also spike blood sugar and wreck the next night’s sleep (hello, 4 a.m. wake-ups).

Brain scans show that after even a single sleepless night, glucose metabolism in the prefrontal cortex, the region responsible for focus and decision-making, drops sharply (2).

It’s a vicious cycle: sleep loss drives insulin resistance, which drives stress and sugar intake, which drives more sleep loss.

Poor Sleep Changes Your Metabolism

It’s easy to see how poor sleep doesn’t just fog your mind – it rewires your metabolism. Short sleep duration is now recognised as one of the strongest lifestyle predictors of weight gain, insulin resistance and type-2 diabetes – even when calorie intake stays the same,

Even a few nights of shortened sleep raise ghrelin, the hunger hormone, and suppress leptin, which signals fullness (7). The result is stronger cravings for quick-release carbs and sugary snacks, precisely the foods that destabilise blood sugar and accelerate insulin resistance. At the same time, sleep loss changes how your body stores fat: studies show it increases visceral fat, the deep belly fat that drives inflammation (8).

Over time, this mix – more hunger, higher insulin, greater inflammation – pushes many people toward weight gain, pre-diabetes and, eventually, cognitive decline.

So if you’re trying to lose weight or steady your energy, don’t forget about sleep.

High blood sugar, low cognition

Poor sleep raises blood sugar, and when glucose stays high, the brain pays the price.

Overtime poor sleep raises blood sugar, and when glucose stays high, the brain eventually pays the price. Chronically elevated HbA1c, measured in our DRIfT test, predicts faster cognitive decline and higher dementia risk. The same metabolic stress that drives weight gain and diabetes also drives neurodegeneration. That’s why people with insomnia or sleep apnoea are far more likely to develop both type-2 diabetes and Alzheimer’s (3, 4).That is why we cover both sleep and insulin management as a key part of our COGNITION 6-month brain upgrade programme (available to all FRIEND’s of Food for the Brain) – because protecting your brain is possible when you know what to focus on.

The night-shift hormones that matter

Melatonin isn’t just for sleep – it fine-tunes your body’s glucose rhythm and acts as a powereful antioxidant. When evening light suppresses it, next-morning blood sugar shoots higher (5).
Cortisol should fall overnight so insulin can do its work; if stress, late eating or light keeps it high, blood sugar stays stuck.
Growth hormone, released in deep sleep, repairs tissue and builds lean muscle, your natural blood-sugar buffer.

Together these hormones keep the night restorative and the brain calm. Disrupt them and the same chemistry that fuels diabetes starts fuelling Alzheimer’s (6).

Small Habits That Dramatically Improve Sleep Quality

Simple Ways to Turn Sleep into a Metabolic Superpower

Guard your 7–8 hours. Deep sleep is where metabolic reset happens.
Skip caffeine or alcohol late. Both fragment sleep and blunt insulin response.
Finish eating at least three hours before bed. Giving your body time to fast allows insulin to fall and encourages fat use for fuel overnight.
Start your day with light, not sugar. Early daylight synchronises your circadian rhythm, boosting morning cortisol naturally so you rely less on coffee and quick carbs.
Pair protein-rich, low-GL meals with consistent sleep. Balanced blood sugar by day supports stable melatonin and growth hormone at night, a feedback loop that keeps your metabolism working for you, not against you. Find 100+ delicious recipes here.https://brainhealthcheck.foodforthebrain.org/uybcookapp/

Sleep as metabolic medicine

Sleep isn’t a luxury or a waste of time –  it’s your brain’s way of resetting and restoring the entire body. It shapes body composition, curbs cravings, steadies energy and supports the metabolism that powers your mind.

Takeaway: good sleep, like good nutrition, is prevention in action.
Want to dive deeper? Join us for the Sleep Solution Webinar with sleep scientist Greg Potter. Find out more here

Free guide: The Power of Sleep

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

Reference:

Spiegel K et al. Impact of sleep debt on metabolic and endocrine function. Lancet. 1999;354(9188):1435–9.

Benedict C et al. Acute sleep deprivation reduces energy expenditure and brain glucose metabolism. Sleep. 2012;35(7):981–8.

Yaffe K et al. Sleep duration and risk of type 2 diabetes: a meta-analysis. Diabetes Care. 2015;38(9):1633–40.

Sabia S et al. Association of sleep duration in middle and old age with dementia incidence. Nat Commun. 2021;12:2289.

Gooley JJ et al. Exposure to room light before bedtime suppresses melatonin onset and shortens its duration. J Clin Endocrinol Metab. 2011;96(3):E463–72.

Musiek ES, Holtzman DM. Mechanisms linking circadian clocks, sleep, and neurodegeneration. Science. 2016;354(6315):1004–8.

Spiegel K et al. Brief sleep curtailment decreases leptin, increases ghrelin, and causes increased hunger and appetite. Ann Intern Med. 2004;141(11):846–50.

Nedeltcheva AV et al. Insufficient sleep undermines dietary efforts to reduce adiposity. Ann Intern Med. 2010;153(7):435–41.

Melatonin: The Brain’s Night-Time Antioxidant

This night-time molecule is also one of the brain’s most powerful protectors – your night-time antioxidant – working while you rest, to defend neurons, restore energy and preserve clear thinking. Melatonin helps your brain clean up daily oxidative damage, regulate mood, and protect memory networks from ageing.

When levels drop – through stress, light exposure, age or caffeine – you don’t just lose sleep; you lose part of your brain’s natural repair system.

The Brain’s Nightly Repair Shift

Every night, while you rest, your brain goes to work. Waste is cleared away, cells are repaired, and antioxidants are replenished.

At the heart of this clean-up crew is melatonin, made in the pineal gland and the master conductor of your brain’s nocturnal activity.

It doesn’t just promote sleep; it powers the production of glutathione, the body and brain’s chief antioxidant and cellular shield. When melatonin levels fall, oxidative stress rises – accelerating neuronal ageing and the build-up of damaging amyloid and tau proteins (1, 2). Why? Melatonin normally switches on the brain’s own antioxidant defences, recycling glutathione and neutralising free radicals inside mitochondria. Without enough melatonin, these reactive molecules (like amyloid and tau proteins) accumulate, inflaming brain tissue and allowing toxic proteins to clump together.

In studies (2), restoring melatonin reduced oxidative damage and slowed amyloid formation – a reminder that good sleep truly is brain repair in action.

Want to know what your current glutathione status is? Order your test here to find out

Light At Night Steals Your Brain’s Protection

Here’s the catch: melatonin only comes out when it’s dark.

Even modest evening light – the glow of your phone, TV, bedside lamp or standby light – can switch off its release (7).

That’s because the light-sensitive cells in your eyes, send a “daytime” signal to the brain’s master clock in the suprachiasmatic nucleus (a tiny region in the hypothalamus that controls your body’s sleep-wake rhythm) instantly halting melatonin production.

In clinical studies, exposure to ordinary indoor light before bedtime suppressed melatonin by up to 85 per cent and shortened its duration by several hours (7).

That’s why your late-night scroll or TV binge can leave you foggy and flat the next morning. 

To support melatonin, you want to create a dark place to sleep. No lights on, heavy curtains, no street lamps. Using eye masks and utilising blue-light blocking glasses, software or filters can also be helpful if you know you are going to be on screens in the evening. You can even get special bulbs for bedside lamps or special lighting solutions for the bathroom for nighttime toilet trips.

Light is a powerful data input into the brain – so be mindful and protect yourself where practical and possible. 

Age, Stress And Hormones Flatten The Rhythm

As time goes by, your natural melatonin rhythm starts to fade – by mid-life, your night-time levels can fall by half (3).

It’s one of many reasons why people can start waking up at night, struggle to drift off, or feel less refreshed after sleep.

For women, the hormonal rollercoaster of perimenopause makes things even trickier: falling oestrogen and progesterone throw the body clock off balance, making deep sleep harder just when the brain needs it most (5). (Learn more about how to support women’s hormones and brain health here.)

Melatonin levels don’t just impact sleep; studies show that lower melatonin is linked with poorer memory, mood dips and faster cognitive ageing (4). While melatonin is impacted by ageing, the good news is that it can be supported and restored.

Coffee vs. Melatonin – When Caffeine Steals Your Sleep Hormone

Caffeine doesn’t just keep you awake – it directly interferes with melatonin’s nightly rise.
Even a single espresso six hours before bed can delay melatonin release by up to 40 minutes and reduce total melatonin production by as much as 20% (9). (And don’t forget black and green tea and most energy drinks contain caffeine too.)

That’s because caffeine blocks adenosine receptors – the same system that tells the pineal gland it’s time for darkness and rest. When that signal is muted, the body’s internal clock (the suprachiasmatic nucleus) misreads the time and keeps you in ‘day-mode’ far longer than intended.

Avoid coffee (and other caffeine sources) after 12 p.m., especially if you have sleep or mood issues.
Choose herbal or decaf alternatives after lunch. If you’re sensitive, even morning caffeine can blunt night-time melatonin, so experiment with caffeine-free days and observe your sleep quality.

Melatonin and Mitochondria: Your Inner Night-Time Antioxidant Factory

Here’s where melatonin gets even more fascinating. It isn’t just released from the pineal gland at night, your brain cells actually produce it inside their mitochondria, the tiny engines that create energy (ATP) and power every thought and memory (8).

This is clever biology: the very place where energy is made – and where most oxidative stress occurs – also makes its own night-time antioxidant. Melatonin acts locally in the cell, mopping up the free radicals created as mitochondria burn fuel through the day, keeping these fragile energy factories running smoothly (1).

It doesn’t function only as a sleep hormone, made only in the pineal gland – it’s also made throughout your brain (and body’s) energy-producing mitochondria, where it acts as a built-in night-time antioxidant to protect them from damage.

This local production is what keeps your neurons energised and resilient – and why good, deep sleep is essential for restoring brain power and mental clarity. (And why disrupted or shallow sleep can leave you foggy the next morning!)Want more insight into how to support your brain through quality sleep? Join our next live webinar with our expert Sleep Scientist here.

How To Restore Your Natural Rhythm

While short-term melatonin supplements (0.5–3 mg) can improve sleep onset and quality in older adults (6) and can be bought in North America or prescribed in the UK, the goal is to rebuild the body’s own rhythm:

Dark evenings, bright mornings – dim lights, avoid screens, use blue-light blocking technology, glasses and filters an hour before bed; get natural light soon after waking.
Avoid caffeine after 12 pm or if sleep is a real struggle – remove altogether, and see how it impacts your sleep.
Tryptophan-rich foods – turkey, oats, eggs and sunflower seeds support serotonin-to-melatonin conversion (with B6 and magnesium).
Keep bedrooms cool and quiet – a small temperature drop signals melatonin release.
Check in with your antioxidant status with the DRIfT test here.

Melatonin: Protecting Your Brain’s Night-time Antioxidant Rhythm

Melatonin is the nightly molecule that lets the brain rest, reset and renew itself.

Protecting your melatonin rhythm may be one of the simplest, most powerful preventative steps you can take to protect your memory.

To learn more and take action:

Join the Sleep Solution Webinar with Sleep Scientist Greg Potter here
Get a free assessment of your overall brain health and cognitive function today with our free, validated Cognitive Function test here
Test your current glutathione status with the DRIfT 5 in 1 at home blood test – find out more here

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

Reference:

Reiter RJ et al. Melatonin as an antioxidant: under promises but over delivers. J Pineal Res. 2016;61(3):253–78.

Cardinali DP et al. Melatonin reduces oxidative damage and amyloid pathology in Alzheimer transgenic mice. J Pineal Res. 2013;55(4):427–37.

Waldhauser F et al. Age-related changes in melatonin levels. J Clin Endocrinol Metab. 1988;66(3):648–52.

Wu YH et al. Sleep, melatonin and the aging brain. J Pineal Res. 2005;38(3):145–52.

Baker FC, Driver HS. Circadian rhythms, sleep and the menstrual cycle in women. Sleep Med. 2007;8(6):613–22.

Ferracioli-Oda E et al. Meta-analysis: efficacy of melatonin for primary sleep disorders. PLoS One. 2013;8(5):e63773.

Gooley JJ et al. Exposure to room light before bedtime suppresses melatonin onset and shortens its duration. J Clin Endocrinol Metab. 2011;96(3):E463–72.

Suofu Y et al. Mitochondrial synthesis of melatonin enhances neuroprotection. Proc Natl Acad Sci USA. 2017;114(32):E7997–8006.

Burke TM et al. Caffeine effects on the circadian melatonin rhythm: a controlled trial. J Clin Sleep Med. 2015;11(8):893–900.

Why Women’s Brains Need Omega-3 Now

—

What if the key to protecting women’s brains from Alzheimer’s isn’t a drug, but a nutrient most of us are not getting enough of?

That’s the conclusion of new research linking low omega-3 status with a higher risk of dementia, particularly in women. It adds to a growing body of evidence that what you eat today directly shapes your brain health tomorrow.

You may have seen headlines this year reporting that women with Alzheimer’s disease tend to have unusually low levels of omega-3 fatty acids in their blood. This new evidence adds weight to what our research has been highlighting for years: your brain needs these essential fats to stay healthy, sharp, and resilient.

What The New Study Shows?

A study led by Wretland and colleagues, published in Alzheimer’s & Dementia, analysed blood lipid profiles and found that those at greater risk of Alzheimer’s disease had lower levels of lipids containing the long-chain omega-3 fats EPA and DHA. Importantly, this association was stronger in women than in men [1].

Professor William Harris, a member of Food for the Brain’s Scientific Advisory Board and one of the world’s leading omega-3 researchers, commented on the study, saying:

“Measurement of blood omega-3 levels may be especially useful in identifying women at increased risk for Alzheimer’s. Why women? Possibly because of the widespread abandonment of hormone replacement therapy after the Women’s Health Initiative study, which may have inadvertently left many women more vulnerable. Oestrogen supports cognitive health and also helps maintain omega-3 status. Without it, low omega-3 levels may pose an even greater risk.”

(Want to learn more about how to support women’s brains and hormones? Find out more here.

Learn more about maintaining healthy omega-3 levels from OmegaQuant, founded by Professor William Harris.)

Why Omega-3 Is So Vital For The Brain?

The brain is about 60% fat by dry weight, with DHA the dominant structural fat in brain cells [2].
Higher omega-3 status is consistently linked to slower brain shrinkage and lower dementia risk [3,4].
Just one serving of oily fish a week has been associated with a 60% lower risk of Alzheimer’s disease [5].

But omega-3 rarely works in isolation. Research from the University of Oxford shows that the combination of good omega-3 levels and homocysteine-lowering B vitamins can reduce brain shrinkage by 73% in those at risk of dementia [6,7].

Why Women’s Brains Need Special Attention After Menopause?

After menopause, falling oestrogen increases the risk of memory decline. Following the 2002 Women’s Health Initiative report, HRT prescribing plummeted worldwide due to perceived risks. Although use is now rising again, this shift has raised important questions about how hormones interact with brain health.

While decisions about HRT are individual and should be made with the guidance of a medical professional, supporting brain health through nutrition is relevant for all women. Because oestrogen helps maintain levels of the omega-3 fats EPA and DHA, women with a low intake of these nutrients may be at particular risk of deficiency. Ensuring adequate omega-3 – through oily fish or supplements – remains a practical, evidence-based step for long-term brain protection.

How Do You Know If You’re Protected?

The easy answer is to test, not guess. That is why we offer our at-home pinprick blood tests as part of our research and prevention support.

Our DRIfT 5-in-1 test includes the omega-3 index, homocysteine, vitamin D, blood sugar control (HbA1c), and glutathione – together providing a powerful snapshot of your brain’s future resilience. This allows you to see whether you are eating enough oily fish, supplementing properly, or at greater risk of future disease.

The Bigger Picture Of Brain Health

This new study is another reminder that Alzheimer’s is not an inevitable part of ageing.
It is largely preventable when we address the eight modifiable risk domains – from brain fats and B vitamins to diet, lifestyle, and gut health – which we cover in our COGNITION brain upgrade programme.

Women’s brain health has been historically under-researched, particularly in relation to hormones and cognitive ageing. Studies like this are a vital step towards closing that gap and ensuring prevention strategies work for everyone.

Learn more

Join Menopause and the Mind with Dr Ghazala Aziz – find out more here.
Are you supplementing correctly? Eating enough fish? The only way to know is to test – order your DRIfT 5-in-1 test today to discover what you need to do to protect your brain.
Complete the free, validated Cognitive Function Test today to receive personalised information on how you can protect your brain and your future.

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References

Wretland A, et al. Lipid profiling shows reduced long-chain omega-3 lipids in individuals at risk for Alzheimer’s, especially women. Alzheimer’s Dement. 2024. PMID: 40832908.

Crawford MA, et al. The role of essential fatty acids and phospholipids in brain development and health. Prostaglandins Leukot Essent Fatty Acids. 2001;64(2):95-111.

Tan ZS, et al. Red blood cell omega-3 fatty acid levels and markers of accelerated brain aging. Neurology. 2012;78(9):658-664.

Yassine HN, et al. Long-chain omega-3 fatty acids and brain health. Alzheimers Dement. 2016;12(7):759-768.

Morris MC, et al. Fish consumption and the risk of Alzheimer disease. Arch Neurol. 2003;60(7):940-946.

Smith AD, et al. Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment. Proc Natl Acad Sci U S A.
Jernerén F, et al. Homocysteine-lowering B-vitamin treatment modifies the effect of omega-3 fatty acids on brain atrophy in mild cognitive impairment. Am J Clin Nutr. 2015;102(1):215-221.

—

Everywhere you turn, coffee shops tempt us with seasonal lattes, pumpkin-spiced treats and sugary hot chocolates. They may taste comforting, but many of these drinks deliver more sugar (up to 40 g in a single serving) and stimulants than your brain can’t handle, fuelling blood sugar spikes, jitters and, over time, even memory decline. In fact, higher blood glucose levels, even within the normal range, is linked to an increased risk of dementia (1*), while poor glucose control shrinks the hippocampus, the brain’s memory centre (2*).

Here’s a different kind of comfort drink: a rich, velvety hot cacao that actually supports your brain. Taken from the Upgrade Your Brain Cook App,  and packed with flavonoids, adaptogens and blood-sugar-balancing spices, it’s a recipe you can enjoy at any time of year – whether you’re heading out on autumn walks in the northern hemisphere, or entering spring in the south.

Why is hot cacao brain-friendly?

Raw cacao – flavanols for circulation, memory and mood

Cacao is one of the richest natural sources of flavanols, powerful antioxidants that improve circulation, including blood flow to the brain. Better blood flow means better oxygen and nutrient delivery, supporting attention, memory and overall cognitive function.

In a landmark study at Columbia University, cocoa flavanol supplementation improved memory in older adults by enhancing dentate gyrus function in the hippocampus (3). Large-scale trials confirm this: in the COSMOS study of more than 21,000 people, cocoa extract improved cognition in those with lower diet quality (4).

Cacao also contains theobromine and serotonin-enhancing compounds, which may explain why a simple square of dark chocolate – or a steaming mug of raw cacao – can lift mood and reduce stress.

Maca – an adaptogen for stress resilience and mood

Maca, a root vegetable from the Andes, is classed as an adaptogen – plants that help the body adapt to stress. Adaptogens support the adrenal system, helping to buffer the effects of chronic stress and supporting hormone balance.

In human trials, maca supplementation improved mood and reduced anxiety and depression scores in postmenopausal women (5). While more research is needed on cognition in humans, maca is widely valued for its mood-enhancing and potential stress-buffering properties.

Cinnamon – balancing blood sugar to protect the brain

Cinnamon isn’t just for apple pies, it’s a powerful spice for blood sugar control, which is essential for maintaining brain health and longevity. Stable blood sugar means steadier energy and less “brain fog.” Excess sugar is one of the strongest dietary risk factors for dementia: raised HbA1c (a measure of long-term blood sugar that we test in our at-home blood test, DRIfT) increases the risk of both vascular dementia and Alzheimer’s (1,2).

Human trials show that cinnamon supplementation can improve HbA1c, blood pressure and lipid profiles in people with type 2 diabetes (6). Other studies report improved insulin sensitivity and glucose tolerance, even in healthy adults (7). By helping to stabilise the delivery of glucose to the brain, cinnamon protects against the highs and lows that drive fatigue, irritability and cognitive decline.

Hot Cacao with Maca & Cinnamon

At Food for the Brain, we’ve long championed the role of antioxidants, blood-sugar balance, and stress resilience in protecting against cognitive decline. A simple daily ritual like this hot cacao brings together three powerful, evidence-based strategies for your brain:

Flavanols from cacao improve circulation and memory.
Adaptogens from maca (optional) to enhance mood.
Spices like cinnamon to steady blood sugar and protect the hippocampus.

Take the next step for your brain

Test your own brain health today – take our free online Cognitive Function Test. It’s a validated way to see how your lifestyle is shaping your future brain health. 

Feeling good now, and ageing well, is within your power.

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References

Crane PK, Walker R, Hubbard RA, et al. Glucose levels and risk of dementia. N Engl J Med. 2013;369:540–548. doi:10.1056/NEJMoa1215740

Kerti L, Witte AV, Winkler A, Grittner U, Rujescu D, Flöel A. Higher glucose levels associated with lower memory and reduced hippocampal microstructure. Diabetes Care. 2013;36(10):3289–3296. doi:10.2337/dc13-0306

Brickman AM, Khan UA, Provenzano FA, et al. Enhancing dentate gyrus function with dietary flavanols improves cognition in older adults. Nat Neurosci. 2014;17(12):1798–1803. doi:10.1038/nn.3850

Sesso HD, Wang L, Reynoso J, et al. Effect of cocoa extract supplementation on cognitive function: COSMOS trial. Am J Clin Nutr. 2022;116(3):682–693. doi:10.1093/ajcn/nqac152

Gonzales GF, Córdova A, Vega K, Chung A, Villena A, Góñez C. Effect of Lepidium meyenii (Maca) on mood in postmenopausal women. CNS Neurosci Ther. 2009;15(6):639–650. doi:10.1111/j.1755-5949.2009.00104.x

Akilen R, Tsiami A, Devendra D, Robinson N. Glycated haemoglobin and blood pressure-lowering effect of cinnamon in type 2 diabetes. Diabet Med. 2010;27(10):1159–1167. doi:10.1111/j.1464-5491.2010.03079.x

Solomon TPJ, Blannin AK. Effects of short-term cinnamon ingestion on insulin sensitivity. Eur J Appl Physiol. 2007;99(5):483–488. doi:10.1007/s00421-006-0362-z

★ = references already discussed in Patrick Holford’s books (Upgrade Your Brain 2024; Alzheimer’s: Prevention is the Cure 2025).

Sugar, Metabolic Syndrome and Early-Onset Dementia: Is This Type 3 Diabetes?

Why are more people in their 40s and 50s developing dementia? Most assume the answer lies in the genes. But here’s the reality: fewer than 1% of Alzheimer’s cases are caused by rare genetic mutations. The other 99%? They are driven largely by preventable, lifestyle-related factors – and at the centre of the storm is how we process sugar, , leading many scientists to describe Alzheimer’s as “Type 3 diabetes.”

A major new study of nearly two million people confirms that metabolic syndrome – the cluster of blood sugar imbalance, abdominal obesity, high blood pressure, and poor lipid levels  – significantly increases the risk of early-onset dementia.

This should be front-page news. Dementia is now affecting people in their 40s and 50s, not just the elderly. And at the heart of this early decline? Poor blood sugar control, excess abdominal fat, and the metabolic mayhem caused by high-sugar diets.

The Evidence: 24% Higher Risk of Dementia Before Age 65

The landmark 2024 study published in JAMA Neurology followed more than 1.9 million adults and found that those with metabolic syndrome had a 24% higher risk of developing dementia before the age of 65 compared with those without (1).

The strongest associations were observed with:

Hyperglycaemia (high blood sugar)
Abdominal obesity (visceral fat around the waist)

These two factors, when present together, were particularly predictive of vascular dementia, although risks were also elevated for Alzheimer’s disease and other forms of dementia.

The authors adjusted for other lifestyle and demographic factors, confirming that metabolic health itself was an independent driver. Men and those in their 40s showed the highest vulnerability.This aligns with decades of research linking insulin resistance and poor glucose control with brain shrinkage, memory loss, and neurodegeneration – all of which are discussed in detail in [here] and [here]. 

The Type 3 Diabetes Hypothesis

Scientists have increasingly referred to Alzheimer’s disease as “Type 3 diabetes” – a term that reflects how brain cells become resistant to insulin and fail to metabolise glucose properly.

Chronically high blood sugar damages blood vessels in the brain, increases inflammation, and accelerates the formation of amyloid plaques, all hallmark features of Alzheimer’s pathology. This new study provides the strongest population-level evidence to date that the same dysfunction is also driving younger-onset dementia.

The Role of Fructose and Processed Sugar

Endocrinologist and paediatric neuroendocrinologist Dr Robert Lustig has long warned of the unique effects of fructose (a sugar found in high-fructose corn syrup and added sugars) on the brain. Unlike glucose, fructose is processed in the liver, promoting visceral fat, insulin resistance, and inflammation – all central to metabolic syndrome (2).

When the brain is chronically exposed to excess sugar and insulin, its ability to generate energy and form new synapses becomes impaired. Over time, it is as if the brain is being starved, even in the midst of plenty.

 This isn’t just a long-term risk – we’re now seeing it play out in middle-aged adults.

Thankfully we know that there is much you can do to prevent this from happening – your future is in your hands – here is what to focus on.

What Can You Do? Five Simple Shifts

Check your blood sugar regulation. The HbA1c test is a key marker of long-term blood glucose control. (Available via our home test kits and in our DRIfT 5 in 1 test kit.)
Prioritise low-GL, whole foods. Swap out refined carbohydrates and processed sugars for whole grains, legumes, nuts, and non-starchy vegetables.
Limit fructose. Reduce or remove sweetened drinks (including fruit juice), syrups, and processed snacks high in high-fructose corn syrup. Read more on high/low fructose foods here.
Assess your waist size. Abdominal fat is a strong dementia risk factor. A healthy waistline helps protect your brain.
Exercise regularly. Just 30 minutes a day improves insulin sensitivity and helps the brain use glucose more efficiently.

Need help taking action on the above? Struggle to know how to ditch your sweet tooth?

Join us in the Forget Sugar Webinar in October with Patrick Holford.

A Wake-Up Call, Not a Life Sentence

This study shows a sobering trend – but Food for the Brain exists to empower you in your prevention path. Early-onset dementia is not inevitable. It is largely preventable if you act now. Sugar, insulin resistance, and metabolic syndrome are right at the centre of the problem.

We need public health messaging that reflects this. Dementia is not just an age-related disease. It’s a lifestyle-driven brain disorder that begins years, even decades, before diagnosis.

Your brain doesn’t have to retire early – start your brain upgrade programme and journey today.Want to assess your brain health? Complete this free validated online Cognitive Function test to receive personalised insights into your brain health, along with guidance on what you can do to reduce your risk and protect your future!

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References

 Jang H et al. Association Between Metabolic Syndrome and Early-Onset Dementia in a Nationwide Cohort. JAMA Neurol. 2024. doi:10.1001/jamaneurol.2024.xxxxxx
Lustig RH. Fat Chance: The Hidden Truth About Sugar, Obesity and Disease. Penguin; 2013.https://pubmed.ncbi.nlm.nih.gov/12450889/

How To Break Free From Food Addiction

Do you ever promise yourself you’ll stop eating sugar or junk food – only to find yourself back at the biscuit tin a few hours later? You’re not alone. Food addiction is real. In fact, it can be as powerful and pervasive as alcohol addiction.

The first step is awareness. According to clinical psychologist Dr Jen Unwin, there are six warning signs. If you recognise yourself in two or more, it may be time to take this seriously.

Read on to see if any apply to you.

Six Signs You May Be Addicted to Food

1. Certain foods feel impossible to resist

 “You’re craving a certain food so badly that you feel compelled to eat it, even when you know you shouldn’t,” Dr Unwin explains. At the height of her own addiction, she would secretly make a bowl of cake mixture – just butter, sugar and flour -and eat the entire thing raw. “It sounds ridiculous now, but I had such intense cravings for sweet, soft, sugary foods,” she explains.

2. You always need more

Like alcohol tolerance, food addiction builds over time. “One slice of cake may have been enough in the beginning, but soon you need two, three – or half the cake – to get the same dopamine hit,” says Dr Unwin. She recalls eating slice after slice at her daughter’s wedding, unable to stop until she felt sick.

3. Food takes priority over everything else

A common factor in addiction is that you begin to ignore what you once valued and prioritise food above socialising, hobbies, family time and even work. Often, Dr Unwin would leave the house and her family in secret to drive for 20 minutes to a cinema complex where she would order a large tub of Ben & Jerry’s Cookie Dough ice cream with chocolate sauce. She would then return to her car and eat the entire portion, feeling ashamed and elated at the same time, before returning home an hour later as if nothing had happened.

4. You lose control once you start

You might buy biscuits for your grandchildren, planning to have just one with your tea. Before you know it, the whole packet has disappeared.

5. Withdrawal symptoms kick in

If you try to cut down on sugary snacks and carbohydrates, do you experience withdrawal symptoms? “These include headaches, migraines, gastrointestinal symptoms, low mood, anxiety, fatigue and brain fog,” Dr Unwin says. “As people experience sugar withdrawal, they feel so bad that they just go back to eating it.” When Dr Unwin completely abstained from sugar, she experienced many of these symptoms for eight days. But after pushing through that difficult period, she began feeling better than ever.

6. You know it’s harming you – and carry on anyway

According to Dr Unwin, this is the defining sign: eating damaging foods despite knowing the consequences. She references a patient with Type 2 diabetes who kept bingeing on cake and sugar knowing how bad it is for their blood sugar. People in this situation often know the food is harmful, but they feel trapped in a cycle.

Why Processed Foods Hijack Your Brain

Breaking free from any addiction is not purely a matter of willpower. Addictive foods and drinks hijack your brain’s chemistry, making you crave them. This effect is purposely done so that you keep buying more.

Understanding how certain food ingredients and combinations work in the brain unlocks the secret to undoing food addiction. The most powerful trigger is the combination of fat and sugar – the two key components of most junk foods. Think cakes, biscuits, ice cream, chocolate bars and pastries. This pairing presses the brain’s dopamine “reward” switch, creating intense pleasure in the moment but diminishing feelings of satisfaction over time. Just like drugs, it fuels cravings and loss of control.
This hijacking of the dopamine-based reward system doesn’t just drive overeating – it also increases the risk of cognitive decline and brain shrinkage. Additionally, it disrupts glucose control and drives insulin resistance, a well-known promoter of cognitive decline.  (Read more –  ‘Is Sugar Killing Your Brain?’)

Nutritional Tools That Reset Your Brain

In Patrick Holford’s book How to Quit without Feeling S**t  he recommends strategies that help restore balance to your brain chemistry:

Omega-3 fats – vital for healthy cell membranes and for receiving neurotransmitter messages.
B vitamins and methylation – check homocysteine levels; if they are high, it may indicate poor methylation and raised risk of cognitive decline.
Tyrosine – dopamine is made from this amino acid. A supplement of 500mg twice daily can help support dopamine production.

Protein + slow carbs – pairing protein (such as nuts or Greek yogurt) with fruit like berries slows sugar release and provides fibre and nutrients.

 A clinical Psychologist’s Practical Tips on How to break free; 

Visualise how life will improve once you manage to quit your “drug foods”. These are typically ultra-processed and sugary foods with which you’re unlikely to have a healthy relationship.
Have an honest conversation with friends and family about the foods you struggle with, and ask for their support in resisting them..
Removing the “drug foods” from your home and diet is key. Replace them with natural, whole foods.
Give it time. Every day you resist, it gets easier. “Those foods are no longer in my thoughts at all,” says Dr Unwin.
If you take medication for diabetes or high blood pressure, consult your GPbefore reducing sugar and carbohydrates in your diet, as your dosage may need adjusting.
If you’re concerned about food addiction or would like to learn more, Dr Unwin recommends joining a Public Health Collaboration (PHC) support group in the UK, or Sweet Sobriety in the US. The PHC also runs a virtual lifestyle support group every Monday at 6pm, where you can learn more about overcoming food addiction and maintaining good metabolic health.

The Bigger Picture

Food addiction is more than a personal struggle and it impacts more people than you realise. It’s part of a wider public health crisis, fuelling obesity, diabetes and dementia – but no matter where you are at right now, change is possible!

Ways to get support:

Are You a Food or Drink Junkie?
How to Recover from Addiction with Nutrition
Vitamin D – the Mind, Memory & Mood Essential
What our experts do themselves to prevent dementia
Dopamine and the Brain: Is Modern Life Hijacking Your Reward System?

New Study: Is Red Meat Bad for Your Brain?

—

In a culture where the average plate still leans heavily towards meat – often processed, often excessive – it’s time to reassess the impact of our protein choices not just on our waistlines, but on our brains. A recent study in Neurology (2025) has added fresh weight to decades of evidence linking red and processed meat consumption to an increased risk of dementia and cognitive decline (1). Meanwhile, fish – particularly oily fish – continues to top the charts as the most protective food for your brain (2,3).

So, what does this mean practically for those of us trying to upgrade our brains and reduce our risk of cognitive decline? The answer may be as simple as this: eat more fish and fewer sausages.

Red Meat, Processed Meat and the Rising Risk to Brain Health

A new US cohort study, which followed over 77,000 adults across 30 years, found that:

Processed red meats (bacon, hot dogs, sausages, salami, bologna and other processed meat products) were clearly problematic. Consuming just 0.25 servings per day or more was associated with a 13% higher risk of developing dementia compared with those eating less than 0.1 serving (1).

Unprocessed red meat (e.g. beef or lamb) was linked to a 16% increased risk of subjective cognitive decline – that is people reporting that their memory or mental sharpness was worsening – when consuming more than one serving daily compared to less than half a serving per day. However, the researchers noted that this link did not reach statistical significance for diagnosed dementia overall (1).

More encouragingly, replacing one daily serving of processed red meat with a serving of nuts, lentils, or beans was associated with a 19% lower risk of dementia (1).

These findings are consistent with a large UK Biobank analysis of almost half a million adults, which found that each additional 25 g/day of processed meat (bacon, ham, sausages, meat pies, kebabs, burgers, chicken nuggets) was associated with a 44% higher risk of all-cause dementia and a 52% higher risk of Alzheimer’s disease. In contrast, each 50 g/day of unprocessed red meat was linked to a 19% lower risk of all-cause dementia and a 30% lower risk of Alzheimer’s disease (4).  This reinforces the idea that it is the processing – not necessarily the meat itself – that may be most harmful.

These associations were observed regardless of whether participants carried the APOE ε4 gene variant – further evidence that dietary choices have a significant impact and that Alzheimer’s is ‘not in the genes’. (4).

The Global Pattern

The irrelevance of genetics in these findings is further supported by global evidence. An ecological analysis across 204 countries found that higher national per-capita total meat supply – including both red and white meats – was significantly associated with higher dementia incidence, even after adjusting for ageing, economic development and genetic risk, including APOE ε4 prevalence where available (5). In other words, the meat-dementia link is not confined to particular genetic subgroups but is observable across populations worldwide, suggesting that the way we produce and consume meat may be influencing brain health trends on a global scale. 

What we put on our plate is powerful when it comes to reducing dementia risk – more so than any genetic variations that attract attention in the media.

Why Fish is Brain Food

The answer is not to go hungry, but to swap for something else – and when it comes to brain health, marine foods are your answer.

Unlike red meat, fish – especially oily varieties like salmon, sardines or mackerel – continue to show a strong protective effect.

A comprehensive 2024 meta-analysis found that:

Eating one to two servings of fish per day (roughly 150 g) is associated with a 20% reduced risk of Alzheimer’s disease and up to 30% slower cognitive decline (2).

Another study found that people who ate fish at least once a week had a one-third lower risk of Alzheimer’s compared with those eating fish less than weekly (3).

Why? Omega-3 fats, especially DHA, are critical for brain function and structure. They reduce inflammation, support synaptic plasticity and help clear beta-amyloid – a protein associated with Alzheimer’s disease.

As explained in the COGNITION™ 6-month programme, omega-3 fats from fish oil play a pivotal role in building and repairing the brain, particularly in mid-life, when early signs of cognitive decline can start to emerge.

That’s why we offer omega-3 at-home blood tests – so you can check whether you’re getting enough through your diet or if it’s time to add a supplement. You can test omega-3 on its own here, or as part of our 5-in-1 DRIfT test where you can also check your homocysteine and glutathione status at the same time.

A Simple Swap with Profound Impact

From a cognitive health perspective, the data is now hard to ignore: if you’re regularly eating red or processed meat – especially more than once a day – your brain may be paying the price. But shifting even one of those servings towards fish, eggs or plant-based proteins could make a meaningful difference.

Interestingly, the main culprit in the latest studies was processed meat. This supports a key principle in brain-friendly eating: most natural whole foods – whether meat, fish, fruit, nuts, legumes, wholegrains or dairy – are not the problem. It’s when we distort them into ultra-processed, factory-made food that health is undermined.

This isn’t about becoming vegan or pescatarian. It’s simply more evidence to reduce processed foods and ensure optimal omega-3 intake. 

So next time you’re at the supermarket make a cow happy and buy a fish.

Resources:

Need help knowing what to eat? Get inspired with over 125 brain-friendly recipes in the Upgrade Your Brain Cook App.

Order your omega-3 test today to find out if you are eating enough of these essential fatty acids. You can test omega-3 on its own here, or as part of our 5-in-1 DRIfT test. Available globally.

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References:

You J, Zhang L, Zhou Y, et al. Total meat supply and incidence of dementia: an ecological study of 204 countries. Front Public Health. 2025;13:1589936. doi:10.3389/fpubh.2025.1589936.

Li Y, Li Y, Gu X, Liu Y, Dong D, Kang JH, Wang M, Eliassen H, Willett WC, Stampfer MJ, Wang D. Long-Term Intake of Red Meat in Relation to Dementia Risk and Cognitive Function in US Adults. Neurology. 2025;104(3):e210286. doi:10.1212/WNL.0000000000210286.

Godos J, Micek A, Currenti W, Franchi C, Poli A, Battino M, Dolci A, Ricci C, Ungvari Z, Grosso G. Fish consumption, cognitive impairment and dementia: an updated dose-response meta-analysis of observational studies. Aging Clin Exp Res. 2024;36(1):171-182. doi:10.1007/s40520-024-02823-6.

Beydoun MA, Beydoun HA, Gamaldo AA, Teel A, Zonderman AB, Wang Y. Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis. BMC Public Health. 2014;14:643. doi:10.1186/1471-2458-14-643.

Zhang Z, He P, Liu M, et al. Meat consumption and risk of incident dementia: cohort study of UK Biobank participants. Am J Clin Nutr. 2021;113(5):1228-1236. doi:10.1093/ajcn/nqaa343.

—

When that mid-morning dip or afternoon slump hits, it’s tempting to reach for a quick fix – something sweet, something carby, something to perk you up. But most conventional snacks don’t fuel your brain – they drain it.

In fact, snacking is one of the easiest ways to sabotage your long-term brain health and memory. Most people wouldn’t eat a plate of sugar at mealtimes (unless they start the day with shop-bought cereal or sweetened yoghurt), yet it’s common to reach for a bar, a biscuit, or something from a petrol station or coffee shop without a second thought.

These everyday choices are a silent driver of brain fog, low mood, memory problems – even dementia. It’s time to upgrade your brain by upgrading your snacks. Below, we share a free Brain Boost Bites recipe and some other smart snack ideas – perfect for long drives, picnics, or busy days on the go.

The Problem with Typical Snacks

The modern snack aisle is a minefield of ultra-processed foods: cereal bars, crisps, flavoured yoghurts, granola bites, and biscuits – many of them marketed as “healthy”. But beneath the surface, they’re often:

High in sugar or refined carbs – causing a rapid blood glucose spike followed by a crash. Many so-called healthy bars contain over 15g of sugar with little fibre, protein, or healthy fat to balance them.
Low in brain-essential nutrients – such as omega-3s, magnesium, or phospholipids.
Full of artificial additives – emulsifiers, preservatives, and even excitotoxins like MSG.
Designed for instant gratification – often with addictive properties rather than sustained energy.

As explained in our Four Horsemen of the Mental Health Apocalypse series (read Part 1 here and Part 2 here), poor glucose control is a key driver of accelerated brain ageing and cognitive decline. A high-sugar snack spikes blood sugar, then causes a crash that reduces brain energy and impairs mental performance. Over time, this rollercoaster leads to insulin resistance, which is strongly linked to cognitive decline and Alzheimer’s disease.

The Smart Snacking Solution

The answer isn’t to stop snacking altogether – it’s to snack smart.

Our in-house chef and lecturer in culinary nutrition and functional health, Kim Close, shares a free recipe below from the Upgrade Your Brain Cook App. It’s packed with brain-supportive nutrients and perfect for keeping your energy and focus steady.

And if you’re not sure what to eat for better brain health, the Cook App includes 120+ recipes (and growing) to guide you meal by meal.

👉 Subscribe to the Cook App – just £30/year

Brain Boost Bites

Refined sugar-free | Fibre-rich | Brain-fat fuelled | Brain Boosting

Other Smart Snack Ideas:

Oatcakes with almond butter or smoked mackerel pâté
Olives 
Square of Dark Chocolate Bar (Recipe in Cook App)
Hummus or nut butter with raw veggie sticks
A boiled egg with cherry tomatoes
A handful of walnuts or pumpkin seeds
A small cup of full-fat Greek yoghurt with blueberries
Chia pudding made with coconut milk (recipe in the app)
2 squares of 85%+ dark chocolate

Snacking wisely is one of the easiest daily upgrades you can make for your brain. And with the right ingredients, it can be delicious too.

—

Imagine if a simple, well-researched nutrient protocol could prevent cognitive decline in millions of people worldwide. Imagine further that this protocol has been known for years, supported by multiple clinical trials and global experts, yet systematically ignored by the very institutions meant to protect public health. That is precisely the case when it comes to homocysteine, B vitamins, and dementia.

Last year, the UK-based Lancet Commission on Dementia Prevention, Intervention and Care released its third major report, once again omitting any mention of homocysteine as a modifiable risk factor. This was despite direct submissions of evidence and letters from leading scientists demonstrating that lowering homocysteine with B vitamins can slow brain shrinkage and cognitive decline.

Now, in response to this silence, six of the leading dementia researchers, Professors Joshua Miller (Rutgers), David Smith (Oxford), Helga Refsum (Oslo), Jin-Tai Yu (Fudan), Babak Hooshmand (Karolinska), and Andrew McCaddon (Wrexham), have published a powerful rebuttal in the Journal of Alzheimer’s Disease. Many of these experts serve in the Alzheimer’s Prevention Expert Group (APEG) at Food for the Brain.

They wrote:

“In 2018, we published an ‘International Consensus Statement on Homocysteine and Dementia’ in this journal, in which we concluded that elevated plasma total homocysteine is a modifiable risk factor for the development of cognitive decline, dementia, and Alzheimer’s disease (AD) in older persons. (1)

We further stated that intervention trials in elderly people with cognitive impairment show that homocysteine-lowering treatment with B vitamins markedly slows the rate of both wholeand regional brain atrophy, and also slows cognitive decline. We were therefore puzzled as to why the Lancet Commission on Dementia Prevention, Intervention and Care, failed to discuss the possible role of homocysteine and B vitamins in any of their three reports, including the most recent one.” (2)

A Systematic Omission

The UK-based Lancet Commission on Dementia Prevention is meant to objectively consider the evidence on dementia prevention. Yet each edition, despite being sent the relevant papers, has ignored the evidence concerning homocysteine.

Furthermore, it’s expected to uphold the standards for critical debate which allows for experts to question Published findings. That is exactly what these experts did – yet it declined to publish their letter, instead printing a rebuttal from its own Commission while refusing to let readers see the original letter. (3, 4)

The experts wrote to The Lancet again to respond to the Commission’s letter, but their second letter was also rejected. 

Thatetter has now been published in the leading Alzheimer’s journal where the authors finally have their rightful say. It includes the following:

“We wish to reply to the Commission and continue the debate with the aim of reaching a common view on homocysteine, B vitamins and dementia. This is an important matter of public health.”

In other words, The Lancet published the ‘case for the defence’ for the exclusion of homocysteine without allowing readers to even read the ‘case for the prosecution’. (5)

So, what was The Lancet’s case against B vitamins? It rested on three criticisms – each of which these leading dementia researchers refute with scientific precision in their recent journal paper.

Criticism 1: Misunderstanding Who Benefited in the VITACOG Trial

The Lancet Commission questioned the relevance of the VITACOG trial, arguing that the results “do not show benefits in populations already consuming B vitamins in their food or through supplements.” But this fundamentally misrepresents the study population.

In the VITACOG trial, participants with mild cognitive impairment were given high doses of B6, B12, and folic acid for two years. The result was a 31% reduction in whole brain shrinkage and significantly slower rate of cognitive decline in those with raised homocysteine (6). In participants with levels above 11.3 μmol/L – the median – both cognitive and clinical improvements were observed. Importantly, key Alzheimer’s-related brain regions shrank seven times more slowly in these individuals (7, 8).

The Lancet Commission implied that participants were already supplementing, but that is incorrect. The study excluded anyone taking more than 300 mcg of folic acid, 3 mg of vitamin B6, or 1.5 mcg of vitamin B12 – doses lower  than those found in many common multivitamins. Only 16 to 20 percent were taking low-dose supplements, while the majority were not.. No one was excluded based on their dietary intake of B vitamins.

The experts respond:“The Commission authors’ comment is analogous to expecting additional drug treatment to provide benefits over and above the benefits being obtained in people already taking a high dose of the drug, which is why it puzzles us.”

Criticism 2: No Benefit in the Hong Kong Trial?

The Commission’s response also cited a Hong Kong trial that reported no benefit of B vitamins over two years in people with mild cognitive impairment (MCI) (9). However, this overlooks several important confounders.

Firstly, 22% of participants were taking aspirin, which the study authors themselves found to impair the effect of B vitamins. This interference has since been confirmed in further research (10).

Secondly, the authors of The Lancet response failed to consider another critical factor: omega-3 status. Numerous studies show that B vitamins only deliver cognitive benefits when omega-3 fatty acid levels are sufficient. The Hong Kong study did not measure or control for omega-3 status, which likely explains the lack of consistent benefit over the two-year period.

Thus, the absence of effect in this trial does not disprove the role of B vitamins.  The experts go on to demonstrate in their article the overwhelming body of evidence –  reported by us – that homocysteine-lowering B vitamins do not work optimally in individuals with low omega-3 status.

Criticism 3: No Benefit in the VITAL Trial in Alzheimer’s Patients?

The Lancet authors also referenced the VITAL trial, which reported no overall cognitive benefit from B vitamins in patients already diagnosed with Alzheimer’s disease (11). But again, this conclusion overlooks key details.

In a subgroup analysis, those in the early stages of Alzheimer’s disease did show significant benefit (12). The authors of the VITAL trial themselves highlighted this in their paper, suggesting that earlier intervention is more effective. This finding aligns with multiple other studies showing that B vitamin treatment is most effective in the pre-dementia stages (13).

Furthermore, participants in the VITAL trial began with an average homocysteine level of 9 μmol/L, which is below the threshold (>10–11 μmol/L) associated with brain atrophy.  It is extremely rare to find a group of people with Alzheimer’s disease that start with such a low homocysteine level.  While the B vitamins did reduce homocysteine further to 7μmol/L, there was no overall cognitive benefit observed. But this is akin to giving painkillers to people who are not in pain and then reporting no change in pain levels. At Food for the Brain, we consider a homocysteine level above 10μmol/L as in need of correction with B vitamins.

There are also concerns about conflicts of interest. The lead author, Paul Aisen, is described as “a consultant to the following pharmaceutical companies involved in the development of potential treatments for Alzheimer’s disease”. with more than a dozen firms listed. These companies would certainly favour a trial designed to fail – especially if it were widely publicised.

Additionally, when an anti-amyloid drug trial for lecanemab was published – now licensed in the US and UK – the names of Paul Aisen and Christopher Van Dyck appeared once again as lead authors. In other words, the paid pharmaceutical consultants, responsible for running the drug trial were also tasked with overseeing a trial – designed to fail – on a competing approach: lowering homocysteine with B vitamins. The conflict of interest here is both clear and concerning.

What Does the Evidence Really Say?

You can read the full expert response published in the Journal of Alzheimer’s Disease here. 

Their conclusion is clear:

“We hope that the Lancet Commission will consider the substantial existing evidence of raised homocysteine as an important risk factor for dementia and the possibility of modifying its harm by supplementation with B vitamins.”

They emphasise that the evidence for B vitamin intervention is as strong – or stronger than –  many of the risk factors the Commission did include in its 2024 report. To continue ignoring the proven impact of homocysteine, and the benefits of lowering it through B vitamins is not merely a scientific oversight –  it is a missed opportunity with major implications for medicine and public health.

Remember, prevention is better than cure, and there is so much you can do to protect your brain health

The perfect time to start? Today.

What Can You Do?

Test your homocysteine (and omega-3 status) TODAY –  especially if you’re over 50 or at risk of cognitive decline. At Food for the Brain, we offer an accurate at-home test kit that reliably measures plasma homocysteine reliably. 

You can order your single Homocysteine test here or save money and test both omega-3 index and homocysteine (plus other markers) as part of our DRIfT tests here. International shipping available.

Act on your results –  if your level is above 10 μmol/L, supplementation with vitamin B6 (20 mg), methylfolate (400 µg), and vitamin B12 (500 µg) is recommended.
Read more on supplements and homocysteine here.

Support our mission – become a FRIEND of Food for the Brain! Your donation helps us advance prevention-focused brain health research and education.

As a Friend, you’ll also gain access to:
• Monthly group coaching
• Your personalised brain upgrade programme: COGNITION™

Share the knowledge – public awareness can change public health.
We need a paradigm shift, and it starts with us.

By Patrick Holford

—

The reason we advocate natural, nutritional, and lifestyle-based approaches to mental health is simple – because they work, and they’re safe.

The next big challenge is to discover which combination of changes has the most impact. This is what our research is focused on.

From depression to dementia, the typical approach is still, all too often, medication While it’s valid to compare a nutrient or diet to a pharmaceutical – take omega-3s, for example, which have been shown to be as effective as antidepressants – the real concern is how rarely we hear about the risks of psychiatric drugs. For many, by the time those dangers become clear, it’s already too late.

A classic example of this is the well-known increased risk of suicide particularly in young people prescribed antidepressants. Not only did this take more than ten years to ‘come out’, even now, despite on-the-box warnings, many remain unaware of this well-established risk.

A similar situation is emerging with the new anti-amyloid antibody treatments being proposed for dementia sufferers. Reported deaths are often downplayed or not fully disclosed.. In trials of the two drugs Lecanemab and Donanemab, eight deaths were reported. Eight deaths were reported during the trials, which involved 1,785 participants – a rate of one in every 219 – though not all were officially attributed to the drug. That’s quite a risk. But it is also the nature of these deaths, caused by brain bleeding and swelling, that is even more concerning. 

Investigative journalist Charles Piller, in his book ‘Doctored’, interviewed the pathologist for the first Lecanemab death who said it was like “her brain exploded”. Another Lecanemab associated death was a 65 year-old woman, who had a blood clot induced stroke and was given a common, often lifesaving intervention (tPA) which went badly wrong. “As soon as they put it in her, it was like her body was on fire,” the woman’s husband told me, he said. “She was screaming, and it took, like, eight people to hold her down. It was horrific. Everybody’s running in and (asking) ‘What the hell is going on?’” His wife was sedated and recovered to intensive care, he said. Soon the woman suffered seizures and was placed on a ventilator. After a few days the family approved disconnecting the device and she died. In his book Piller also reports another case in which a participant ‘died after hideous brain swelling and bleeding, and violent seizures.’

The UK has licensed the use of Lecanemab. The EU has not. The UK has licensed Donanemab, but NICE hasn’t approved it for NHS use.

Safer, Evidence-Based Alternatives

Despite more effective and safer alternatives being available, Alzheimer’s charities continue to advocate for NHS access to these drugs. This raises an important question: why? The combination of homocysteine-lowering B vitamins and omega-3 already has stronger evidence of efficacy – with no adverse effects – and certainly no risk of death (Read Alzheimer’s: Prevention is the Cure for the evidence and the comparison).

We invited Dr Peter Gøtzsche – co-founder of the Cochrane Collaboration, originally established to evaluate health treatments without bias – to speak about the risks of psychiatric drugs and their link to mortality. When the Cochrane Collaboration became corrupted, which he later criticised for being influenced by commercial interests, he founded the Institute for Scientific Freedom.

 “Overtreatment with drugs kills many people, and the death rate is increasing. It is therefore strange that we have allowed this long-lasting drug pandemic to continue, and even more so because most of the drug deaths are easily preventable.” he says.

“In 2013, I estimated that our prescription drugs are the third leading cause of death after heart disease and cancer,(1) and in 2015, that psychiatric drugs alone are also the third leading cause of death”.(2)^”

Read on to understand how he arrived at the conclusion that psychiatric drugs may be the third leading cause of death.

How many people are killed by psychiatric drugs?

If we want to estimate the death toll of psychiatric drugs, the most reliable source of data comes from placebo-controlled randomised trials. However, we need to consider their limitations.

First, these trials typically last just a few weeks, despite the fact that most patients take psychiatric medications for many years.(3, 4) 

Second, polypharmacy – the use of multiple medications –  is common in psychiatry, and this significantly increases the risk of mortality.. As an example, the Danish Health Authority has warned that adding a benzodiazepine to a neuroleptic increases mortality by 50-65% (5).

Third, up to half of all deaths go unreported in published clinical trial data.(6)  For dementia, published data shows that for every 100 people treated with a newer neuroleptic for ten weeks, one patient dies as a result. (7) This represents a high mortality rate for a pharmaceutical intervention, but FDA data on the same trials show it is double this number, equivalent to two deaths per 100 people over ten weeks. (8) And if we extend the observation period, the death toll becomes even higher.  A Finnish study of 70,718 community-dwellers newly diagnosed with Alzheimer’s disease reported that neuroleptics kill 4-5 people per 100 annually, compared to patients who were not treated.(9)

Fourth, the design of psychiatric drug trials is biased. In almost all cases, patients were already in treatment with psychiatric medication before they entered the trial, (1, 2)^, and some of those randomised to placebo will therefore experience withdrawal effects that will increase their risk of dying, due to withdrawal symptoms such as akathisia. Placebo-controlled trials in schizophrenia cannot be reliably used to assess the effect of neuroleptics on mortality because of the drug withdrawal design. The suicide rate in these unethical trials was 2-5 times higher than the norm. (10,11) Among those enrolled in trials of risperidone, olanzapine, quetiapine, and sertindole, one in every 145 patients died. However, none of these deaths were mentioned in the published scientific literature, and the FDA did not require their inclusion in trial reporting.

Fifth, events occurring after the trial period are often ignored. In Pfizer’s trials of sertraline in adults, the risk ratio for suicides and suicide attempts was 0.52 when follow-up lasted only 24 hours, but increased to 1.47 when follow-up was extended to 30 days — indicating a rise in suicidal events. (12) Furthermore, when researchers reanalysed the FDA trial data on depression drugs and included harms occurring during follow-up, they found that antidepressants were associated with twice the number of suicides in adults compared to placebo (13, 14)

Estimating the True Death Toll of Mental-Health Medications

In 2013, I estimated that, in people aged 65 and above, neuroleptics, benzodiazepines or similar, and antidepressants kill 209,000 people annually in the United States.(2) I used relatively conservative estimates, however, and usage data from Denmark, which is far lower than those in USA. I have therefore updated the analysis based on US usage data, again focusing on older age groups.

For neuroleptics, I used the estimate of 2% mortality from the FDA data.(8)

For benzodiazepines and similar drugs, a matched cohort study showed that the drugs doubled the death rate, although the average age of the patients was only 55.(15)  The excess death rate was about 1% per year. In another large, matched cohort study, the appendix to the study report shows that hypnotics quadrupled the death rate (hazard ratio 4.5). The study authors estimated that sleeping pills kill between 320,000 and 507,000 Americans every year. (16)  A reasonable estimate of the annual death rate would therefore be 2%.

For SSRIs, a UK cohort study of 60,746 depressed patients older than 65 showed that they led to falls and a 3.6% annual mortality rate among those treated.(17) The study was well-designed, in that the patients were their own control in one of the analyses, which helps control for confounding variables. Nonetheless, the reported death rate is notably high.

Another cohort study, of 136,293 American postmenopausal women (age 50-79) participating in the Women’s Health Initiative study, found that depression drugs were associated with a 32% increase in all-cause mortality after adjustment for confounding factors, which corresponding to an estimated 0.5% annual mortality rate among women treated with SSRIs.(18). The authors noted that the mortality rate was likely underestimated. The authors warned that their results should be interpreted with great caution due to a high risk of exposure misclassification, which would make it more difficult to find an increase in mortality. Further, the patients were much younger than in the UK study, and the death rate increased markedly with age and was 1.4% for those aged 70-79. Finally, the exposed and unexposed women were different for many important risk factors for early death, whereas the people in the UK cohort were their own control.

For these reasons, I decided to use the average of the two estimates, a 2% annual death rate.

These are my results for USA for these three drug groups for people at least 65 years of age (58.2 million; usage is in outpatients only): (19, 20, 21, 22)

—

A limitation in these estimates is that you can only die once, and many people receive polypharmacy. It is not clear how we should adjust for this. In the UK cohort study of depressed patients, 9% also took neuroleptics, and 24% took hypnotics/anxiolytics. (17)

On the other hand, the data on death rates come from studies where many patients were also on several psychiatric drugs in the comparison group, so this is not likely to be a major limitation considering also that polypharmacy increases mortality beyond what the individual drugs cause.

Statistics from the Centers for Disease Control and Prevention list these four top causes of death: (23) 

Heart disease: 695,547
Cancer: 605,213
COVID-19: 416,893
Accidents: 224,935

COVID-19 deaths are rapidly declining, and many of such deaths are not caused by the virus but merely occurred in people who tested positive for it because the WHO advised that all deaths in people who tested positive should be called COVID deaths.

Young people have a much smaller death risk than the elderly, as they rarely fall and break their hip, which is why I have focused on the elderly. I have tried to be conservative. My estimate misses many drug deaths in those younger than 65 years; it only included three classes of psychiatric drugs; and it did not include hospital deaths.

I therefore do not doubt that psychiatric drugs are the third leading cause of death after heart disease and cancer.

—

Learn more and begin your brain upgrade journey today:

Complete the free online brain assessment – the Cognitive Function Test – to get personalised feedback on your brain health
Order the Upgrade Your Brain book here
Order Alzheimer’s: Prevention is the Cure book here
Contribute to our research and order your accurate, at home, blood tests here.
If you are looking for personalised one to one support, visit the Brain Bio Centre here.

—

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References:
1 Gøtzsche PC. Deadly medicines and organised crime: How big pharma has corrupted health care. London: Radcliffe Publishing; 2013.

2 Gøtzsche PC. Deadly psychiatry and organised denial. Copenhagen: People’s Press; 2015.. US News 2016; Sept 27. 

2. Gøtzsche PC. Mental health survival kit and withdrawal from psychiatric drugs. Ann Arbor: L H Press; 2022.

 3 Gøtzsche PC. Long-term use of antipsychotics and antidepressants is not evidence-based. Int J Risk Saf Med 2020;31:37-42. 

4 Gøtzsche PC. Long-term use of benzodiazepines, stimulants and lithium is not evidence-based. Clin Neuropsychiatry 2020;17:281-3.

5 Forbruget af antipsykotika blandt 18-64 årige patienter, med skizofreni, mani eller bipolar affektiv sindslidelse. København: Sundhedsstyrelsen; 2006.

6 Hughes S, Cohen D, Jaggi R. Differences in reporting serious adverse events in industry sponsored clinical trial registries and journal articles on antidepressant and antipsychotic drugs: a cross-sectional study. BMJ Open 2014;4:e005535. 

7 Schneider LS, Dagerman KS, Insel P. Risk of death with atypical antipsychotic drug treatment for dementia: meta-analysis of randomized placebo-controlled trials. JAMA 2005;294:1934–43.

8 FDA package insert for Risperdal (risperidone). Accessed 30 May 2022. 

9 Koponen M, Taipale H, Lavikainen P, et al. Risk of mortality associated with antipsychotic monotherapy and polypharmacy among community-dwelling persons with Alzheimer’s disease. J Alzheimers Dis 2017;56:107-18.

10 Whitaker R. Lure of riches fuels testing. Boston Globe 1998;Nov 17.

11 Whitaker R. Mad in America: bad science, bad medicine, and the enduring mistreatment of the mentally ill. Cambridge: Perseus Books Group; 2002:page 269.

12 Vanderburg DG, Batzar E, Fogel I, et al. A pooled analysis of suicidality in double-blind, placebo-controlled studies of sertraline in adults. J Clin Psychiatry 2009;70:674-83.

13 Hengartner MP, Plöderl M. Newer-generation antidepressants and suicide risk in randomized controlled trials: a re-analysis of the FDA database. Psychother Psychosom 2019;88:247-8.

14 Hengartner MP, Plöderl M. Reply to the Letter to the Editor: “Newer-Generation Antidepressants and Suicide Risk: Thoughts on Hengartner and Plöderl’s ReAnalysis.” Psychother Psychosom 2019;88:373-4.

15 Weich S, Pearce HL, Croft P, et al. Effect of anxiolytic and hypnotic drug prescriptions on mortality hazards: retrospective cohort study. BMJ 2014;348:g1996.

16 Kripke DF, Langer RD, Kline LE. Hypnotics’ association with mortality or cancer: a matched cohort study. BMJ Open 2012;2:e000850.

17 Coupland C, Dhiman P, Morriss R, et al. Antidepressant use and risk of adverse outcomes in older people: population based cohort study. BMJ 2011;343:d4551.

18 Smoller JW, Allison M, Cochrane BB, et al. Antidepressant use and risk of incident cardiovascular morbidity and mortality among postmenopausal women in the Women’s Health Initiative study. Arch Intern Med 2009;169:2128-39.

19 O’Neill A. Age distribution in the United States from 2012 to 2022. Statista 2024;Jan 25.

20 Olfson M, King M, Schoenbaum M. Antipsychotic treatment of adults in the United States. Psychiatrist.com 2015;Oct 21.

21 Maust DT, Lin LA, Blow FC. Benzodiazepine use and misuse among adults in the United States. Psychiatr Serv 2019;70:97-106.

22 Brody DJ, Gu Q. Antidepressant use among adults: United States, 2015-2018. CDC 2020;Sept.

23 Centers for Disease Control and Prevention. Leading Causes of Death. 2024;Jan 17.

by Patrick Holford

—

Choline is an often-overlooked but vital nutrient for brain health.

A new study suggests the optimal intake is 400mg, yet there is no Recommended Daily Allowance or widespread promotion of this crucial nutrient. It is also notably low in vegetarian and especially vegan diets.

(We discuss this and more in our COGNITION 6-month brain upgrade programme – available when you become a FRIEND of Food for the Brain.)

A major study published this year found that higher choline intake lowers the risk of dementia, Alzheimer’s, and cognitive decline.

Researchers tracked 125,000 people from the UK Biobank for 12 years and the study was published in the American Journal of Clinical Nutrition. It showed that higher choline intake reduced risk, with the most benefit around 400mg per day.

__

—

Why does it matter?

Brain cells are made of a membrane containing choline (and other phospholipids) attached to the omega-3 fat DHA. Without choline the omega-3 doesn’t work. The attaching of the two depends on methylation, a process that is dependent on B vitamins, especially B12, folate and B6. Choline helps methylation and healthy methylation, indicated by low homocysteine, helps synthesise choline.

__

–

Also previous studies (2) have found remarkable effects supplementing 480-900mg of choline in pregnancy on promoting ‘smart’ babies with faster reflexes and cognitive processes. It’s important for all ages and a key topic in our Smart Kids & Teens Programme.

What should you do or eat?

Choline is essential for the body, especially the brain, yet it has no Recommended Daily Allowance.

Choline is abundant in eggs, fish, and meat. An egg provides about 120mg, while a 50g serving of beef or salmon contains around 50mg. Beef liver is the richest source, but eggs are the best overall because they contain phosphatidylcholine which is more easily absorbed by the body. Plant-based sources include soy, quinoa, nuts, seeds, beans, and broccoli. A 50g serving of almonds or broccoli provides about 25mg. Phosphatidylcholine, found in lecithin capsules and granules, is an easy supplement option for vegans and vegetarians.

We recommend eating two eggs most days, with a minimum of six per week. Include fish and some meat if you eat it, or soy, quinoa, broccoli, nuts, and seeds if you don’t. Supplementing is likely beneficial, especially for vegetarians. Taking two high-PC lecithin 1,200mg capsules daily provides 250mg of phosphatidylcholine (PC), the form used by the body. These supplements are available at your local health food store.

Remember, your brain is built from what you feed it – and how you use it (as covered in COGNITION). What choline-rich foods can you add to your diet this week?

If you’re unsure what to eat to support your brain or need inspiration, the Cook App is here to help! With over 100 recipes at your fingertips, eating delicious, brain-boosting foods has never been easier—all for just £30 a year.

Actions:

Take the Cognitive Function Test today – our validated online assessment – to find out exactly what you need to focus on.
Become a FRIEND and get access to your 6-month COGNITION programme so you know how to upgrade your brain.

–

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

—Reference list

Reference

Niu YY, Yan HY, Zhong JF, Diao ZQ, Li J, Li CP, Chen LH, Huang WQ, Xu M, Xu ZT, Liang XF, Li ZH, Liu D. Association of dietary choline intake with incidence of dementia, Alzheimer disease, and mild cognitive impairment: a large population-based prospective cohort study. Am J Clin Nutr. 2025 Jan;121(1):5-13. doi: 10.1016/j.ajcnut.2024.11.001. Epub 2024 Nov 7. PMID: 39521435.
Caudill, M. et al, ‘Maternal choline supplementation during the third trimester of pregnancy improves infant information processing speed: a randomized, double-blind, controlled feeding study’ FASEB Journal (Apr 2018); 32(4): 2172-80. doi: 10.1096/fj.201700692RR.

How can we lift our mood and nourish our brain? 

Depression, now the leading cause of disability globally, affects millions. According to the World Health Organization, it represents a significant disease burden, particularly in high-income countries (1). With a staggering 100 million antidepressant prescriptions issued annually—a 70% increase in five years—it’s clear that something is going wrong in our modern western world (1).

Thankfully, nutrition and lifestyle changes provide science-backed ways to boost our mood naturally.

(If you want to know more about how to overcome depression then make sure you watch our webinar ‘Finding your way out of depression’).

—

Understanding Depression

Depression manifests through persistent feelings of hopelessness, low energy, disrupted sleep, and even physical changes such as weight loss or gain (2). The root causes can be multifactorial—psychological stress, biochemical imbalances, or nutritional deficiencies.

But here’s the good news: you can take simple, practical steps to nourish your brain, boost serotonin, and improve your mood naturally.

—

7 Ways to Boost Mood and Brain Function

—

1. Increase Your Omega-3 Fats

Your brain is 60% fat, and omega-3 DHA and EPA are critical for its structure and function. Countries with high fish consumption have lower depression rates. A study from Harvard Medical School found that EPA, specifically, has potent antidepressant effects.

A meta-analysis published in Psychopharmacology Bulletin found that higher omega-3 intake reduces depressive symptoms by 53%. Omega-3 helps build brain cell membranes and boosts serotonin receptor function, which improves mood and cognition.

What to do: Eat oily fish like salmon, sardines, and mackerel at least twice a week or supplement with high-dose omega-3 fish oil. Aim for 1,000–2,000 mg of EPA and DHA combined daily (4, 5, 6).

—

2. Optimise Your B Vitamins and Lower Homocysteine

The little-known amino acid, homocysteine, may double your risk for depression if levels are elevated. This toxic by-product accumulates when you’re deficient in B6, B12, and folic acid, impairing brain chemistry. 

Studies by Professor David Smith from Oxford show that lowering homocysteine can dramatically slow brain shrinkage and improve mood. Which is why we now offer at home homocysteine test kits so you can monitor your own level and prevent disease (7,8,9).

What to do: Eat leafy greens, whole grains, and fortified foods. Test your homocysteine and aim for levels below 7 μmol/L. Supplement with a methylated B complex (20 mg B6, 500 μg B12, and 400 μg methylfolate).

—

“B vitamins are brain-makers; without them, key neurotransmitters like serotonin can’t be synthesised” – Patrick Holford, Upgrade Your Brain.

—

3. Fuel Your Brain with Serotonin Precursors

Serotonin, your “happy hormone”, is made from tryptophan, an amino acid found in protein-rich foods like fish, poultry, beans, and eggs. For some, tryptophan conversion to serotonin is impaired due to poor digestion or low stomach acid, common with age and stress.

Supplementing with 5-HTP can bypass these barriers. Clinical studies show 5-HTP compares favourably with SSRIs in treating depression (10, 11, 12, 13).

What to do: Include tryptophan-rich foods daily and consider a 5-HTP supplement (100–200 mg twice daily). Always consult your doctor if combining with antidepressants.

—

4. Balance Your Blood Sugar

Maintaining stable blood sugar levels is essential for mood regulation, as uneven glucose supply to the brain can lead to irritability, fatigue, and depressive symptoms. Diets high in refined carbohydrates and sugar contribute to these fluctuations and are linked to poor mood and an increased risk of depression. A study of 3,456 adults found that individuals consuming diets rich in processed foods had a 58% greater risk of depression, whereas those eating whole foods experienced a 26% reduced risk (14, 14, 16).

 Refined sugars also deplete mood-enhancing nutrients like B vitamins, essential for energy production, and divert chromium, which is vital for glucose regulation. Adopting a low glycaemic load (GL) diet, avoiding caffeine and alcohol, and focusing on whole foods, fruits, and vegetables can help stabilise blood sugar levels and improve mood.

What to do: Follow a Low-GL diet with whole foods, low-GL carbs, and protein at every meal. Avoid sugar, caffeine, and alcohol .

5. Boost Your Vitamin D Levels

The “sunshine vitamin,” vitamin D, is essential for mood regulation. Research shows a 40% lower incidence of depression in those with adequate vitamin D. Alarmingly, over 60% of the UK population is deficient during winter (17, 18, 19, 20).

What to do: Get tested and aim for levels above 75 nmol/L. Supplement with 2,000–3,000 IU daily in winter months.

—

6. Include Chromium to Combat Atypical Depression

If you suffer from atypical depression—characterised by weight gain, fatigue, and carbohydrate cravings—you might benefit from chromium. Studies show chromium supplementation can improve mood scores by up to 83% (21, 22, 23).

What to do: Include whole grains and vegetables or supplement with 600 mcg of chromium picolinate daily.

—

7. Bring on the Sunshine and Movement

Exercise and sunlight have a direct effect on serotonin levels and mood. Regular exercise boosts brain-derived neurotrophic factor (BDNF), which helps build new brain cells and connections】.

What to do: Aim for 30 minutes of exercise daily and sun exposure for 15 minutes, when safe.

—

Key Action Plan

Eat oily fish twice weekly or supplement omega-3s with at least 1,000 mg EPA and DHA.
Test and lower homocysteine with B6, B12, and folic acid supplements.
Try 5-HTP to boost serotonin naturally.
Follow a Low-GL diet to stabilise blood sugar.
Supplement vitamin D during winter. Find out more about dose here.
Add chromium for atypical depression.
Exercise regularly and get sensible sun exposure.

—

—

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

 References

World Health Organization. Depression and Other Common Mental Disorders: Global Health Estimates. WHO; 2017.
Brown G, et al. Social support, self-esteem and depression. Psychol Med. 1986;16(4):813-31.
Hibbeln JR. ‘Fish consumption and major depression’. Lancet, vol 351(9110), pp. 1213 (1998)
M. Peet and R, Stokes, Omega 3 Fatty Acids in the Treatment of Psychiatric Disorders Drugs, vol 65(8), pp. 1051-9 (2005)
S Kraguljac NV, Montori VM, Pavuluri M, Chai HS, Wilson BS, Unal SS (2009) Efficacy of omega-3 Fatty acids in mood disorders – a systematic review and metaanalysis. Psychopharmacology Bulletin 42(3):39-54
Hibbeln JR. Fish consumption and major depression. Lancet. 1998;351(9110):1213.
Coppen A, Bailey J. Folic acid and affective disorders. J Affect Disord. 2000;60(2):121-30.
Taylor MJ, Carney SM, Goodwin GM, Geddes JR. Folate for depressive disorders. Cochrane Database Syst Rev. 2003;(2):CD003390.
Smith AD, Refsum H. Homocysteine, B vitamins, and cognitive impairment. Annu Rev Nutr. 2016;36:211-39.
Poldinger W et al. A comparison of 5-hydroxytryptophan and fluvoxamine. Psychopathology. 1991;24(2):53-81.
E. Turner, Serotoninalacarte: Supplementation with the serotonin precursor 5-hydroxytryptophan.’ Pharmacology&Therapeutics (2005) [article in press].
W. Poldinger et al. A functional-dimensional approach to depression: serotonin deficiency and target syndrome in a comparison of 5-hydroxytryptophan and fluvoxamine, Psychopathology vol 24(2), pp. 53-81 (1991)
Associate editor: K.A. Neve ‘Serotonin a la carte: Supplementation with the serotonin precursor 5-hydroxytryptophan’ ErickH. Turner a,c,d,*, Jennifer M. Loftis a,b,c, AaronD. Blackwell a,b,e Pharmacology & Therapeutics(2005) www.elsevier.com/locate/pharmthera
Akbaraly TN, Brunner EJ, Ferrie JE, et al. Dietary pattern and depressive symptoms in middle age. Br J Psychiatry. 2009;195:408–13.
Benton D, Owens DS, Parker PY. Blood glucose influences memory and mood in an everyday setting. Biol Psychol. 1982;14(1-2):129–35.
Christensen L. Psychological distress and diet – effects of sucrose and caffeine. J Appl Nutr. 1988;40(1):44–50.
Lansdowne AT, Provost SC (1998): Demonstrates that vitamin D3 supplementation enhances mood in healthy subjects during winter.
C. Wilkins et al. (2006): Links vitamin D deficiency to low mood and poorer cognitive performance in older adults.
A. Nanri et al. (2009): Discusses the association between vitamin D levels and depressive symptoms across seasonal changes.
R. Jorde et al. (2008): Shows that vitamin D supplementation alleviates depressive symptoms in overweight and obese individuals
Lifting Depression – The Chromium Connection by Dr Malcolm McLeod (Basic Health Publications):
J. R. Davidson et al, Effectiveness of chromium in atypical depression: a placebo-controlled trial, Biol Psychiatry, vol 53(3), pp. 261-4 (2003)
Docherty, J et al, ‘A Double-Blind, Placebo-Controlled, Exploratory Trial of Chromium Picolinate in Atypical Depression’. Journal of Psychiatric Practice. Vol 11(5), pp. 302-314, (2005)
Holford P. Upgrade Your Brain. HarperCollins; 2024.

By Jerome Burke

Why too much fructose is driving dementia, diabetes and brain fog

—

The fruit sugar ‘fructose’ isn’t generally considered a food that’s best avoided. After all, it comes from fruit.

Yet a radical new theory, developed by Richard Johnson, Professor of Nephrology at the University of Colorado, explains how it can trigger various damaging changes in our metabolism that make us more likely to develop chronic conditions such as diabetes, obesity and Alzheimer’s. If doctors better understood this, it could transform the new emphasis on sickness prevention that the government is promising.

—

The science of being ‘fructed’

Professor Johnson has produced what is effectively a biochemical wiring diagram of the connections which fructose turns on and off, that are making an increasing number of people sick. Fructose makes up half of white sugar and most of fructose corn syrup which is the main sweetener in fizzy drinks and ultra-processed foods as well as being the main sugar in fruit, particularly fruit juice.

For instance, the amount of fat stored in the liver increases, driving fatty liver disease, while the cell’s mitochondria, which create the body and brain’s energy molecule ATP, become less productive and blood pressure goes up. The result is that you get fatter, with more brain fog and fatigue and feel less inclined to exercise. Fructose is also a major promoter of diabetes.

Meanwhile an anti-ageing process called autophagy, which would normally clear away used up and damaged mitochondria, the cell’s energy factories, to make room for new ones, is disabled. When fructose crosses the blood-brain barrier into the brain, it is one of the factors causing the brain to form the clumps of amyloid protein found in Alzheimer’s, which is the focus of new drug treatments. 

Why on earth does fructose carry out such a blitz on our bodies? Why would the body run a programme that was potentially so lethal?

“It would be wrong to think of fructose as some sort of major toxin, although it becomes neurotoxic in excess,” says Professor Johnson. “Instead, its remarkable range of effects are part of an ancient set of biological programs, which we call the ‘Survival Switch’, that work to prepare animals for hibernation, storing supplies in preparation for times of famine.” This is why fat storage increases and energy drops off producing brain fog. The trouble is we never run out of food or fructose in our modern times.

—

Eat your fruit, don’t drink it.

None of this means that we should avoid fruits, which contain only a small amount of fructose that comes with beneficial fibre that feeds our vital gut bacteria, plus various nutrients. Not so for fruit juice, devoid of fibre. A glass of orange juice is the equivalent of three oranges in terms of fructose, but without the fibre. So, eat your fruit, don’t drink it.

But this does explain why too much blood glucose from regularly eating generous amounts of sugar-laden foods and carbohydrates, is so damaging? The liver turns the excess glucose into fructose with all its knock-on effects. Other substances that can accelerate fructose production are alcohol and salt. 

This rise in fructose intake and its presence in processed food makes it all too easy to start piling on the pounds, regardless of how many calories you have cut or how much further you are running.  It’s a connection that very few nutritionists or GPs are aware of. 

A sign of the widespread damage the Survival Switch can cause is that there are low ATP levels in the brains of people with disorders such as obesity, diabetes, fatty liver disease and Alzheimer’s. Understanding this points to new ways to cut the risks of these chronic disorders.  Adenosine triphosphate (ATP) is a molecule that stores and provides energy for cells. It’s a key biomolecule that’s involved in almost all cellular processes.

A simple, but very effective solution, is to run a blood test – HbA1c – the gold standard test GPs use to screen for diabetes. HbA1c is a test that measures your average blood sugar level (glucose) over the past two to three months. A recent study of 374,021 older men with diabetes found that keeping the level of HbA1c stable at an optimal level over a period of three years cut risk of dementia by a third. Similar benefits have been found with patients with pre-diabetes (Prediabetes means that your blood sugars are higher than usual, but not high enough for you to be diagnosed with type 2 diabetes. It also means that you are at high risk of developing type 2 diabetes.) But far lower levels of HbA1c than those used to diagnose diabetes are associated with the first signs of brain shrinkage, which is the hallmark of cognitive decline, even in teenagers.

That is why we offer, as part of our ‘citizen science’ research, an at home pin-prick test of HbA1c, to find out not only who is at risk, but also how to reverse that risk. It also works alongside the  free Cognitive Function Test that calculates your future Dementia Risk Index and suggests various lifestyle and nutrition changes to help reduce it, including a low fructose diet (Find out more about low fructose foods here).   

We also recommend increasing omega-3 intake from oily fish, increasing B vitamins, especially B12, as well as an active lifestyle, as part of COGNITION, our personalised 6-month programme. In this programme we also dive deeper into lowering your ‘glycaemic load’ (GL), which is low in fructose, alongside periods of time of eating in a ‘ketogenic’ way by keeping sugar and carbohydrates to a minimum. The body responds by creating ketones, energy packets that can replace glucose as an energy source for the brain, helping to undo the damage. 

(You get access to COGNITION when you become a FRIEND of Food for the Brain here)

‘Burning ketones can also increase the number and output of the cell’s energy factories, known as mitochondria, which are damaged by fructose,’ says Professor Robert Lustig of the University of California, author of the best-selling book Metabolical and who sits on our Scientific Advisory Board. You can read more in his detailed article here.

Both Professor Johnson and Professor Lustig are also part of the Alzheimer’s Prevention Expert Group who have written to UK dementia prevention authorities to add sugar, and specifically a high fructose diet, to the list of known risk factors.

—

The connection to Ozempic…

This low fructose approach also naturally promotes the enzyme GLP-1, targeted by the weight loss drugs Ozempic and Wegovy, but without the side-effects or rebound weight gain. 

Our founder Patrick Holford says: “Today’s typical diet of burgers, carbonated drinks, fruit juice, ice cream, bread, biscuits, cakes and confectionery, plus alcohol and salt, is a dementia time-bomb. Our brains are literally being ‘fructed’. We see the same shrinkage in the same regions of the brain in teenagers with a high sugar intake that are seen in older Alzheimer’s patients. We think of the resulting dementia as type-3 diabetes.”

—

Actions

To find out more about low fructose foods visit brainhealthcheck.foodforthebrain.org/fructose 
Click here to join our research and test your HbA1c with us
Support our charitable work and research by becoming a FRIEND

Thank you for reading!

Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References:

Johnson RJ et al. The fructose survival hypothesis for obesity. Philos Trans R Soc Lond B Biol Sci. 2023 Sep 11;378(1885):20220230. doi: 10.1098/rstb.2022.0230
Underwood PC et al HbA1cTime in Range and Dementia JAMA Netw Open. 2024 Aug 1;7(8):e2425354. doi: 10.1001/jamanetworkopen.2024.25354
https://brainhealthcheck.foodforthebrain.org/lancet-commission-letters/ 
Yau PL et al Obesity and metabolic syndrome and structural brain impairments in adolescence. Pediatrics. 2012 Oct;130(4):e856-64. doi: 10.1542/peds.2012-0324

Your Glutathione Index Defines How Your Cells Are Ageing

Nutritional therapists have been measuring red cell glutathione and supplementing glutathione or its precursor N-Acetyl-Cysteine (NAC) for decades. But it’s really hard, and expensive, to measure accurately. Until now.

So how does the Glutathione Index work? 

All of life is a balance between antioxidants and oxidants. That is why we, an oxygen based lifeform, have a finite life. Inside your cells glutathione (GSH) is working every second to stop harmful oxidants from ageing you. The result is spent or oxidised glutathione (GSSG). Our new test – a world first – measures the ratio between fully loaded glutathione (GSH) and oxidised glutathione (GSSG). The Glutathione index (GSH/GSSG) shows you how much antioxidant potential you have and how many metabolic fires you’ve extinguished. This ratio is the difference between mental health and mental illness.

Why does knowing this single marker help with Alzheimer’s, diabetes, schizophrenia, severe autism, depression & more?

Why Does Knowing This Single Marker Help With Alzheimer’s, Diabetes, Schizophrenia, Severe Autism, Depression and More?

The Science

NAC has plenty of evidence to support its use as a promoter of glutathione and mental health, thus reducing the brain’s oxidative stress. The latest 2022 review states:

“N-acetyl-L-cysteine (NAC) is a compound of increasing interest in the treatment of psychiatric disorders. Primarily through its antioxidant, anti-inflammatory, and glutamate modulation activity, NAC has been investigated in the treatment of neurodevelopmental disorders, schizophrenia spectrum disorders, bipolar-related disorders, depressive disorders, anxiety disorders, obsessive compulsive-related disorders, substance-use disorders, neurocognitive disorders, and chronic pain. Currently NAC has the most evidence of having a beneficial effect as an adjuvant agent in the negative symptoms of schizophrenia, severe autism, depression, and obsessive compulsive and related disorders.” (1)

Glutathione and Schizophrenia

Quoting Lorraine Wilder (whose MSc in schizophrenia we funded) “Glutathione (GSH) is an important antioxidant and free radical scavenger that has been found to be decreased in the brains of people with schizophrenia [2, 3]. Although oral GSH supplementation has poor bioavailability [4], N-Acetyl Cysteine (NAC) has been shown to successfully raise plasma glutathione levels in those with schizophrenia [5]”.

Clinical Evidence and Case Studies

In a case study of a 24 year old woman with chronic and worsening paranoid-type schizophrenia that was generally unresponsive to anti-psychotic treatment, the addition of NAC supplementation improved the patient’s symptomatology in seven days. In addition to the schizophrenia-specific symptoms, improvements were observed in spontaneity, social skills and family relations by both the patient and family members. A randomised placebo-controlled trial (RCT) including 42 participants with schizophrenia, who were experiencing an acute phase of symptomatology, were randomly assigned to receive up to 2 g/d of NAC plus up to 6 mg/d of risperidone for 8 weeks as an adjunct intervention. Significant negative symptoms were found in the active treatment group compared to controls but not in positive or general psychopathology [6].

Larger Trials and Longer-Term Findings

Furthermore, a larger RCT of 140 participants observed significant improvements on global symptomatology and general and negative symptoms of schizophrenia in the NAC supplementation (2 g/d; in addition to anti-psychotic medication) group in comparison to the placebo group over a 24-week period, but not positive symptoms [7]. Notably, after a 4-week washout period these beneficial effects diminished, with the exception of clinical severity scores. 

Expert Perspective on Brain Oxidative Stress

According to Dr Chris Palmer, assistant professor at HarvaWhy the Glutathione Index Is the Best Indicator of Brain Oxidative Stress
rd Medical School:

“Glutathione (GSH), the brain’s primary antioxidant, plays a crucial role in maintaining redox balance. Magnetic resonance studies have provided mixed results regarding GSH levels in schizophrenia patients, with some studies indicating decreased levels in chronic schizophrenia, while others found no significant differences. However, these inconsistencies may be due to variations in disease chronicity, age, and symptom severity among study participants. The findings from these studies suggest several potential therapeutic targets for schizophrenia. Addressing mitochondrial dysfunction, redox imbalance, and impaired energy metabolism could lead to more effective treatments. For instance, N-acetylcysteine (NAC), a precursor to GSH, has shown promise in increasing brain GSH levels and improving symptoms in first episode psychosis patients.”

Why the Glutathione Index Is the Best Indicator of Brain Oxidative Stress

The GSH/GSSG ratio reflects the activity of the enzyme glutathione reductase which is responsible for the transformation of GSSG (used, oxidised) to GSH (the reduced or fully loaded form that acts as a radical scavenger). 

—

Glutathione Reductase and Dementia

Reductions in glutathione reductase (GR) enzyme levels in patients with dementia are well established. GR levels alone are therefore a fairly good biomarker of dementia. But the mere presence of the enzyme does not guarantee its high activity. GR needs to consume NADP molecules to function properly. The advantage of our test is, therefore, that it shows changes in GR activity not only due to higher/lower GR gene activity but also due to the absence of the reaction cofactor NADP. 

Impaired Glutathione Recycling in Dementia

As shown by Irene Martinez de Toda et al 2019 (8) data, patients with dementia have a reduction in both the enzymes (GR and GP) that recycle glutathione. Thus, in general, it can be said that the glutathione metabolism (recycling) loop in those with dementia ‘spins’ much slower than in healthy patients. As a result, dementia patients have a lower potential to dynamically fight free radicals and will have a worse Glutathione Index.

What Happens When Recycling Slows Down

In patients, the enzyme GR, which is responsible for recycling spent/oxidised glutathione back to fully loaded, slows down, which leads to the accumulation of oxidised glutathione (GSSG) and the depletion and inability to produce GSH. 

Thus, the concentration of GSH decreases while that of GSSG increases. Hence the Glutathione Index gets worse / is lower.

Improving your Glutathione Index

The older a person is the lower their Glutathione Index is likely to be (see figure below)

Improving your Glutathione index is important as higher levels predict better cognitive function according to our preliminary research. (see figure).

Our own laboratory’s study of 8 people given a supplement containing lipoid acid and N-acetyl-Cysteine (NAC) supplements, the precursor for glutathione, show improvement in both the Glutathione Index and Glutazthione. (see figure below)

Studies giving Ubiquinol, the active form of CoQ, also show an improvement in both the Glutathione Index

Developing the Glutathione Index Test

So will you join us and become a part of our Anti-Age Your Brain Campaign? We need Citizen Scientists to order and complete the test so you can start to protect your brain from ageing and so we can research what the ‘perfect number’ is.

Order your Glutathione test here

Thank you for reading!

Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References

1. Bradlow RCJ, Berk M, Kalivas PW, Back SE, Kanaan RA. The Potential of N-Acetyl-L-Cysteine (NAC) in the Treatment of Psychiatric Disorders. CNS Drugs. 2022 May;36(5):451-482. doi: 10.1007/s40263-022-00907-3. Epub 2022 Mar 22. Erratum in: CNS Drugs. 2022 Apr 28;: PMID: 35316513; PMCID: PMC9095537.

2 Yao JK, Leonard S, Reddy R: Altered glutathione redox state in schizophrenia. Dis Markers 2006, 22(1):83–93.

3 Gawryluk JW, Wang J-F, Andreazza AC, Shao L, Young LT: Decreased levels of glutathione, the major brain antioxidant, in post-mortem prefrontal cortex from patients with psychiatric disorders. Int J Neuropsychopharmacol 2011, 14(01):123–130.

4  Witschi A, Reddy S, Stofer B, Lauterburg B: The systemic availability of oral glutathione. Eur J Clin Pharmacol 1992, 43(6):667–669.

5. Lavoie S, Murray MM, Deppen P, Knyazeva MG, Berk M, Boulat O, Bovet P, Bush AI, Conus P, Copolov D, Fornari E, Meuli R, Solida A, Vianin P, Cuénod M, Buclin T, Do KQ:Glutathione precursor, N-acetyl-cysteine, improves mismatch negativity in schizophrenia patients. Neuropsychopharmacology 2008, 33(9):2187–2199.

6. Farokhnia M, Azarkolah A, Adinehfar F, Khodaie-Ardakani M-R, Hosseini S-M-R, Yekehtaz H, Tabrizi M, Rezaei F, Salehi B, Sadeghi S-M-H, Moghadam M, Gharibi F, Mirshafiee O:, Akhondzadeh S: N-acetylcysteine as an adjunct to risperidone for treatment of negative symptoms in patients with chronic schizophrenia: a randomized, double-blind, placebo-controlled study. Clin Neuropharmacol 2013, 36(6):185–192.

7. Berk M, Copolov D, Dean O, Lu K, Jeavons S, Schapkaitz I, Anderson-Hunt M, Judd F, Katz F, Katz P, Ording-Jespersen S, Little J, Conus P, Cuenod M, Do KQ, Busha AI: N-acetyl cysteine as a glutathione precursor for schizophrenia—a double-blind, randomized, placebo-controlled trial. Biol Psychiatry 2008, 64(5):361–368.

8. Martínez de Toda I, Vida C, Sanz San Miguel L, De la Fuente M. Function, Oxidative, and Inflammatory Stress Parameters in Immune Cells as Predictive Markers of Lifespan throughout Aging. Oxid Med Cell Longev. 2019 Jun 2;2019:4574276. doi: 10.1155/2019/4574276. PMID: 31281577; PMCID: PMC6589234.

9.Tian G, Sawashita J, Kubo H, Nishio SY, Hashimoto S, Suzuki N, Yoshimura H, Tsuruoka M, Wang Y, Liu Y, Luo H, Xu Z, Mori M, Kitano M, Hosoe K, Takeda T, Usami S, Higuchi K. Ubiquinol-10 supplementation activates mitochondria functions to decelerate senescence in senescence-accelerated mice. Antioxid Redox Signal. 2014 Jun 1;20(16):2606-20. doi: 10.1089/ars.2013.5406. Epub 2013 Dec 14. PMID: 24124769; PMCID: PMC4025630.] and glutathione in people with metabolic syndrome

10.Raygan F, Rezavandi Z, Dadkhah Tehrani S, Farrokhian A, Asemi Z. The effects of coenzyme Q10 administration on glucose homeostasis parameters, lipid profiles, biomarkers of inflammation and oxidative stress in patients with metabolic syndrome. Eur J Nutr. 2016 Dec;55(8):2357-2364. doi: 10.1007/s00394-015-1042-7. Epub 2015 Sep 18. PMID: 26385228.)

In a world often filled with daunting health challenges, Alzheimer’s Prevention Day stood out as a beacon of hope and action.

This year was the first launch of this global initiative and we were privileged to witness an incredible turnout: over 10,000 individuals visited our site, driven by a shared determination to tackle Alzheimer’s disease head-on. The day was not just about awareness but about tangible actions that each person can take to safeguard their cognitive health.

One of the highlights was our interactive 3-minute Alzheimer’s Prevention Check, which 8,000 participants eagerly completed. This simple yet impactful test empowers individuals to assess their cognitive health and take proactive steps towards prevention. 

Moreover, the 30-second challenge captured hearts and imaginations alike. We asked people to share on video what they do to help prevent Alzheimer’s each day?

And the answers are astounding!

From paragliding adventures to quirky activities like standing on one’s head or foraging in local forests, participants demonstrated that preventing Alzheimer’s can be both effective and fun.

Watch the rest of the videos here

Ali’s daring paragliding escapade, Zoe’s upside-down yoga prowess, and Nodge’s foraging adventures exemplify the creativity and commitment shown by our community. These actions not only inspire but also remind us that preventing Alzheimer’s is within everyone’s reach, with room for creativity and enjoyment along the way.

Central to the success of Alzheimer’s Prevention Day were the dedicated individuals behind the scenes. We extend heartfelt thanks to Cath and the team for their meticulous editing of inspiring films, and to Alex for crafting a user-friendly website that hosted invaluable resources and engaging content.

—

A BIG thank you!

Behind every groundbreaking initiative are the scientists and professors whose expertise and dedication drive progress. Their research forms the backbone of our mission, guiding us towards effective prevention strategies and empowering individuals to make informed choices about their cognitive health.

As we reflect on the triumphs of Alzheimer’s Prevention Day, we invite you to join us in building a repository of inspiring actions. Visit our website to explore videos showcasing innovative ways people are preventing Alzheimer’s, and most importantly, create your own 30-second film. Share your daily practices that promote brain health, from physical activities to dietary choices, and inspire others to do the same.

>> Click here to submit your video and join the challenge

Together, let’s continue to raise awareness, take meaningful action, and pave the way towards a future where Alzheimer’s is preventable. Visit Alzheimer’s Prevention Day website to learn more and get involved today. 

Your actions today can make a difference tomorrow.

Thank you for reading!

Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

Too much sugar shrinks the brain, but it’s so attractive. Why?

We are led by the science here at Food for the Brain, so we know that one of the best things you can do for your brain is to reduce your sugar and support your insulin control. That is why it is one of our key lifestyle domains in the COGNITION programme. 

However, you probably already know too much sugar isn’t great for health but how can we make eating a lower carb and sugar life easier?

—

First, let’s recap the science… 

Dr. Robert Lustig, a renowned expert on brain health and a member of our scientific advisory board, highlights the significant role of insulin control and dietary choices in preventing cognitive decline.

Research from Columbia University in 2004 revealed that individuals with high insulin levels, (a primary indicator of metabolic dysfunction), were twice as likely to develop dementia compared to those with healthy insulin levels (1). Furthermore, those with the highest insulin levels exhibited the worst memory retrieval abilities (1). Similarly, an Italian study linked elevated insulin levels to declining mental function (2).

Several studies have established a connection between high sugar consumption and poor cognitive outcomes. For instance, a study among Puerto Ricans found that high sugar intake doubled the risk of cognitive impairment (3), while another U.S. study correlated elevated blood sugar levels with memory loss (4). The detrimental impact of high dietary glycaemic load (GL) on cognitive function has been observed in studies from Ireland and the United States, indicating that high GL diets are strongly associated with Alzheimer’s-related pathological changes (5,6).

—

What is Glycaemic load?

Glycaemic load considers both the quality (GI – glycaemic index) and the quantity (carbohydrate content) of the carbohydrates in a food serving. It provides a more accurate picture of how a food will affect blood sugar levels. The formula for calculating glycaemic load is:

GL  = GI x carbohydrate / 100

A high GL diet measured by the total glucose load on the bloodstream, is linked to increased amyloid plaque formation and cognitive decline, particularly in individuals with the ApoE4 gene, which regulates fat metabolism (7). Even individuals with high-normal blood glucose levels experience greater brain shrinkage and cognitive impairment compared to those with lower levels, as shown in long-term studies (8).

Plus, the damage of a high-GL diet can start early in life. Dr. Lustig points out that overweight children on high-GL diets show signs of cognitive decline, and adolescents with metabolic dysfunction from such diets exhibit hippocampal shrinkage and other brain structure changes (9,10).

So it is clear that eating excess sugar or the wrong types of carbohydrates with a high GL is a problem, so what do you eat?

(Wondering if you’re eating too much sugar? Then test, don’t guess with our home HbA1c test – find out more here.)

—

What to eat?

There are two options: following a low GL diet or going a step further and adhering to a ketogenic approach (or switching between the two as Patrick highlights in the Hybrid Diet book). For more info on the ketogenic diet click here to find out more

A low GL diet is focused on consuming foods that have a minimal impact on blood sugar. Basically a diet rich in:

Vegetables: Most non-starchy vegetables like spinach, broccoli, and bell peppers.
Fruits: Berries, cherries, grapefruit, and apples.
Legumes: Lentils, chickpeas, and black beans.
Whole Grains: Barley, quinoa, and whole oats.
Fish and meat or tofu/tempeh: unprocessed
Dairy: Plain yoghurt and milk (unsweetened).
Nuts and Seeds: Almonds, walnuts, chia seeds, and flaxseeds.

Whilst eating this way can support your brain health it can also help you sustain energy levels, help with weight loss and improve heart health.

—

So how can we make it easier?

At Food for the Brain we have a few ways to help you feed your brain on the right foods:

Complete the Cognitive Function Test and join COGNITION so we can walk you through how to reduce sugar and upgrade your brain over the next few months.
Upgrade Your Brain Cook App – full of low GL recipes and coming soon. Help us by pre ordering today to get brain-loving recipes at your fingertips.
Here is a recipe sample:

—

Almond and coconut porridge

Breakfast Serves 2, generously 

TOTAL GLs: 4

Ingredients:

2 tbsp milled flaxseed
2 tbsp coconut flour
2 tbsp whole flaxseed
2 tbsp chia seeds
2 tbsp coconut flakes, toasted in a dry pan
2 tbsp raspberries
2 tbsp blueberries
2 strawberries
8 walnuts, broken up
1 tbsp soft brown sugar alternative (or sweetener of choice)
300ml unsweetened almond milk
1 tbsp chicory root syrup (or sweetener of choice)

Instructions:

Stir everything (except the desiccated coconut, nuts and berries) together in a saucepan and let sit for 10 mins.
Gently heat through until thickened – add a little more milk if needed to get the consistency you like.
Top with the berries, nuts and toasted coconut – add some natural yoghurt if you like.
Drizzle with the chicory syrup 

Cooks Notes

It’s worth seeking out the chicory syrup – very low sugar and also high fibre. 

Nutrition Highlights

Antioxidants: High in antioxidants, particularly vitamins A, C, and E, which help protect cells from damage and support immune function.
Protein: A moderate source of protein, supporting muscle maintenance and repair.
Fibre: Contains a high amount of fibre, aiding in digestion and promoting satiety.

—

Other resources

Here are a few other resources to make low sugar easier, 

FATT bars – easy low GL and low carb snacks for on-the-go. Use the code FFTB10 to save 10% and FATT will donate to the charity with every purchase.

Dillon bread – low carb bread and their brand new high fibre, low GL, Chicory Fibre Syrup perfect for adding to porridge and also suitable for diabetics. Use code FFB10 to save 10% and Dillon will donate 10% with every purchase.

Keto Mojo – if you want to take it a step further and follow a ketogenic diet then grab one of their ketone readers to make life easier and to check you are in ketosis. Use code FFB10 to save 10%.

These companies are some of our supporting organisations – find out more here.

Thank you for reading!

Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References

Abbatecola AM, Paolisso G, Lamponi M, Bandinelli S, Lauretani F, Launer L, Ferrucci L. Insulin resistance and executive dysfunction in older persons. J Am Geriatr Soc. 2004 Oct;52(10):1713-8. doi: 10.1111/j.1532-5415.2004.52466.x. PMID: 15450050.
Abbatecola AM, Paolisso G, Lamponi M, Bandinelli S, Lauretani F, Launer L, Ferrucci L. Insulin resistance and executive dysfunction in older persons. J Am Geriatr Soc. 2004 Oct;52(10):1713-8. doi: 10.1111/j.1532-5415.2004.52466.x. PMID: 15450050.
Ye X, Gao X, Scott T, Tucker KL. Habitual sugar intake and cognitive function among middle-aged and older Puerto Ricans without diabetes. Br J Nutr. 2011 Nov;106(9):1423-32; doi: 10.1017/S0007114511001760. Epub 2011 Jun 1. PMID: 21736803; PMCID: PMC4876724.
Power SE, O’Connor EM, Ross RP, Stanton C, O’Toole PW, Fitzgerald GF, Jeffery IB. Dietary glycaemic load associated with cognitive performance in elderly subjects. Eur J Nutr. 2015 Jun;54(4):557-68. doi: 10.1007/s00394-014-0737-5. Epub 2014 Jul 18. PMID: 25034880.
Seetharaman S, Andel R, McEvoy C, Dahl Aslan AK, Finkel D, Pedersen NL. Blood glucose, diet-based glycemic load and cognitive aging among dementia-free older adults. J Gerontol A Biol Sci Med Sci. 2015 Apr;70(4):471-9. doi: 10.1093/gerona/glu135. Epub 2014 Aug 22. PMID: 25149688; PMCID: PMC4447796.
Taylor MK, Sullivan DK, Swerdlow RH, Vidoni ED, Morris JK, Mahnken JD, Burns JM. A high-glycemic diet is associated with cerebral amyloid burden in cognitively normal older adults. Am J Clin Nutr. 2017 Dec;106(6):1463-1470. doi: 10.3945/ajcn.117.162263. Epub 2017 Oct 25. PMID: 29070566; PMCID: PMC5698843.
Taylor MK, Sullivan DK, Swerdlow RH, Vidoni ED, Morris JK, Mahnken JD, Burns JM. A high-glycemic diet is associated with cerebral amyloid burden in cognitively normal older adults. Am J Clin Nutr. 2017 Dec;106(6):1463-1470. doi: 10.3945/ajcn.117.162263. Epub 2017 Oct 25. PMID: 29070566; PMCID: PMC5698843.
M.E. Mortby et al., ‘High “normal” blood glucose is associated with decreased brain volume and cognitive performance in the 60s: the PATH through Life Study’, PLoS One (2013), vol 8
.
Yau PL, Castro MG, Tagani A, Tsui WH, Convit A. Obesity and metabolic syndrome and functional and structural brain impairments in adolescence. Pediatrics. 2012 Oct;130(4)
. doi: 10.1542/peds.2012-0324. Epub 2012 Sep 3. PMID: 22945407; PMCID: PMC3457620.
Lakhan, S.E., Kirchgessner, A. The emerging role of dietary fructose in obesity and cognitive decline. Nutr J 12, 114 (2013).
Loef M, Walach H. Fruit, vegetables and prevention of cognitive decline or dementia: a systematic review of cohort studies. J Nutr Health Aging. 2012 Jul;16(7):626-30. doi: 10.1007/s12603-012-0097-x. PMID: 22836704.

The food you eat feeds your brain but how can you consistently eat healthy even on the go, or when life is busy?

We know here at Food for the Brain that a low Glycemic Load diet is one of the 8 ways you can reduce your risk of dementia and Alzheimer’s (and improve your Cognitive Function score – take the free validated online test here) – which is why we are creating our Recipe App so that you have access to lots of brain loving recipes.

But what can you eat when travelling, on the go or for an easy snack?

That is why we want to introduce you to FATT bars. As one of our supporting organisations, FATT provides a variety of good quality, sugar free, convenient and tasty snacks.

So if you are preparing for summer holidays, work trips or have a busy schedule then these might be the perfect way to nourish your brain!

Introducing FATT – Real Keto Snacks!

Feeding the brain is a no-brainer but picking the right foods can be hard.

At FATT we really love the brain and because we love the brain, we also love the gut.

Everything we pick must be right for both brain and gut which is why we really do love nuts and in particular almonds and macadamias. Nuts are smart as they are rich in protein, B vitamins and vitamin E but are also a good source of potassium, selenium, magnesium, zinc and copper.

Macadamias are also rich in omega 3 to help balance any omega 6 in your diet.

We then add in the inulin and chicory fibre for a prebiotic kick to feed your healthy gut bio.

Whether you are eating a cookie or a brownie, a bar or a bite, you can be sure that you are getting food for the brain and gut without compromise. At FATT we do not use any sweeteners (artificial or otherwise) that might interfere with your gut and your brain or even fool your body into thinking it is digesting sugar.

We allow the natural sweetness of nuts or butter or chicory to give you a gentle sweet taste knowing that your body will not have any blood sugar spike or any insulin release.

Try our unique range of healthy low carb but indulgent snacks at a special discount and we will also make a further charitable contribution to Food for the Brain and its amazing work.

You can pick from Almond + Vanilla Keto Cookie, Double Chocolate Keto Brownie, Caramel + Sea Salt Keto Bar, Chocolate + Mint Bites and MORE!

Go and order your first box or single bars at www.livefatt.com and use the unique code FFTB10 to get a special Food for the Brain charity discount.

—

Thank you for reading!

Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

by Patrick Holford

Easter is meant to follow on from Lent – 40 days of fasting. There lies the problem.

—

‘We’ are the product of natural selection – survival of the fattest. 

Those of us who can readily store carbs as fat through periods of famine have survived and become dominant. Now, there are no periods of famine, no ‘lent’ up, it’s just carbs all the way. 

With one in six over 40 diabetic, the question is, are you heading in that direction? 

Even raised glucose, but within the ‘normal’ range, in mid life increases Alzheimer’s risk by 14.5%. 

—

Why not find out? 

We have a simple pinprick blood test to help you do just that. It measures the percentage of your red blood cells that are sugar-damaged or ‘glycosylated’. It’s called glycosylated haemoglobin, or HbA1c. This simple pinprick blood test is, in effect, measuring the total blood sugar spikes you experienced over the past three months (red blood cells, called haemoglobin, live for three months).

—

What should you be aiming for?

Ideally, it should be 5% (31mmol/mol) or less. That’s healthy.

Above 5.4% (36) and in studies you can already pick up brain shrinkage and cognitive decline.

Above 6% (42) is considered pre-diabetic.

6.5% (48) or higher is considered diabetic.

For both brain and body health you certainly want it to be below 5.4%

(It’s measured slightly differently in the UK, in mmol/mol, which is the number shown in brackets.)

A recent study in Denmark of 20,000 people in their 60’s, published in the British Medical Journal [1], found that one in nine with an HbA1c of 6-6.1% developed diabetes in the next three years and one in five in the next five years. One in ten died. 

—

How to lower your score?

It is easy to lower, if you need to. But first, you need to know where you are starting from. Then you can retest three months later and find out if what you’ve done has worked.

There are several approaches. 

A low GL diet (read Patrick Holford’s Low GL Diet Cookbook). 
An intermittent fasting approach, doing all your eating in a six hour window with dinner at eg 7pm then lunch at 1pm. 
Going ‘keto’, which Dr Georgia Ede explained in our recent webinar which you can watch here.
There are even supplements that can help – chromium, HCA (Hydroxycitric acid) found in a type of tamarind and glucomannan fibre. 

You will learn about all these and more if you’ve signed up for the COGNITION programme by becoming a FRIEND and select the ‘Low carbs and GL’ section. Jill, a retired teacher, lost almost a stone following this advice. 

—

But first, we suggest you measure your baseline HbA1c.

It’s more predictive of your blood sugar control than just your weight or waist circumference. In fact, it is the single most important measure of your glucose balance ‘resilience’ which is why it’s one of the four ‘essentials’ in our DRIfT test – the others being vitamin D, omega-3 and homocysteine (B vitamins).

We want to wish you a Healthy Easter by giving you £10 off your HBA1c test when you buy before Easter. 

So that’s £39.95, not £49.95. 

Also, if you book a repeat test in 3 months, which is how long it takes to ‘renew’ all your red blood cells, hopefully no longer sugar-coated, you’ll save a further 6%, bringing the cost down to £37.55, saving you £12.40 now and in 3 months time. That’s £24.80 in total. This offer ends on April 10th 2024.

Use the coupon code: easter at check out to save

(Discount applies to the HBa1c test only.)

Remember every test kit you order will not only help you upgrade your brain it will also help us in our vital research – you will become a part of our ‘Citizen Science’ team and be donating to our wider charitable work and research.

Thank you!

Thank you for reading!

Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References:

1 http://dx.doi. org/10.1136/bmjdrc-2022- 002946

By Patrick Holford

Read part one here to learn about the first two ‘horsemen’ – Brain Fats & Methylation.

—

Few people realise the catastrophic decline in mental health that has occurred over the past 50 years.

‘Brain health conditions have become a global health emergency,’ according to the Federation of European Neuroscience Societies last year (1).

The big question is: why?

—

Introducing the four horsemen (recap)

I’m proposing that there are four main biological drivers of our demise which I’m calling the four horsemen of the mental health apocalypse: a lack of brain fats, messed up methylation, loss of glucose control and excessive oxidation.

The first two – brain fats and methylation – are vital for the integral structure of neuronal membranes.

The second two are vital for the function of brain cells, supplying fuel and coping with the oxidant ‘exhaust fumes’ of energy metabolism.

—

—

Brain fuel

While omega-3 and B vitamins literally build a healthy brain, it is glucose and ketones that fuel it.

As a result of this process, oxidants are created which age the brain through the process of oxidation. Of course, oxidation can also occur through external causes, which is why smoking and air pollution are also established risk factors for Alzheimer’s.

Which leads us to the next two ‘horses of the mental health apocalypse’: the brain’s fuel supply and antioxidant protection. The brain consumes more energy than any other organ of the body. Neurons can only run on glucose or ketones. The irony is that the consequence of eating too many carbs and sugar is that the brain develops insulin resistance – effectively blocking the glucose from entering the mitochondria within the neurons. Starved of their energy source, we experience the consequences as mental fatigue and forgetfulness. According to Dr Robert Lustig,  Emeritus Professor of Pediatrics at the University of California, San Francisco and a member of our Scientific Advisory Board, “This cognitive decline starts young. Cognitive decline in overweight children is associated with a high GL diet (1), and adolescents with metabolic dysfunction, driven by a high GL diet, have been shown to have shrinkage of the hippocampal area of the brain, as well as other structural changes and cognitive deficits (2).” This particular study showed actual shrinkage of the Alzheimer’s associated area of the brain in teenagers with metabolic syndrome as a consequence of too much sugar and ‘white’ carbs. The youngest age of an Alzheimer’s diagnosis, which requires proof of shrinkage of the hippocampal area of the brain, is age 19, in a young man in China who had no genetic risk factors (2).

It’s a biochemical storm.

As well as the fuel starvation that insulin resistance generates, the converse of blood sugar spikes, create Advanced Glycation End-products, or AGEs, that literally damage neurons. This ‘glycosylation’ is also seen in red blood cells, and why the HbA1c test which measures glycosylated haemoglobin is so good at predicting our health. If over 6.5% (or 48 mmol/mol) of these erythrocytes are sugar damaged, it’s a clear basis for a diabetes diagnosis. Just as for the omega-3 index, HbA1c is a reliable long-term measure showing the average sugar spikes over the past three months. You can assume what’s happening in the membranes of red blood cells is also happening to the neuronal membranes in the brain. 

This is why the next brain essential is to measure HbA1c.

If 6.5% is the cut-off for a diabetes diagnosis, the ideal level is actually considerably lower. In what is usually considered to be the ‘normal range’, teenagers with HbA1c above 5.4% show cognitive decline and shrinkage of the hippocampus in the central area of the brain compared to those with lower HbA1c levels (3). “In teenagers with raised, but normal levels of HbA1c, there is clear evidence of the same kind of memory problems, and the same areas of brain shrinkage seen in patients with Alzheimer’s Disease” says Dr Robert Lustig.

Shrinkage of the hippocampus is the hallmark of Alzheimer’s and is used to diagnose the disease. A new study shows that 40-year-old adults with so-called normal glucose levels, but at the higher end of the normal range, have increased their risk of Alzheimer’s by 15%. (4) 

A primary function of sleep is to repair all the neuronal membrane damage that occurs during the day. No sleep, no repair and the brain ages fast. This is mainly why lack of sleep is also a strong risk factor for Alzheimer’s.

(Click here to test your HbA1c and be a part of our Citizen Science Research)

—

Do ketones fill the energy gap?

There’s a growing interest in the role of ketogenic diets and ketone promoting supplements for brain health. Professor Stephen Cunnane, our expert in the new science of ‘keto therapeutics’ has shown that giving C8 oil or supplementing ketones can help to prevent Alzheimer’s, slow down cognitive decline, improve mood and lessen anxiety. His studies showed, in those with mild cognitive impairment, that taking 30g (two tablespoons) of mainly C8 oil, resulted in a 230% increased brain energy production from ketones with no change in energy derived from glucose (5), thus filling the ‘energy gap’ so often experienced by older people or those drifting towards insulin resistance. “Our research shows that the areas of the brain that have trouble using glucose for energy are able to use ketones perfectly well, even in moderately advanced dementia. This may explain why many people later in life who are given a supplement of C8 oil or MCT oil have improvements on a battery of cognitive tests. They often feel it brings their brain power back to life” says Cunnane. 

Many people also report feeling calmer, less anxious and less depressed on ketogenic diets. A new book, Change Your Diet, Change Your Mind, out next month by psychiatrist Dr Georgia Ede digs deep into the growing evidence that a ketogenic diet, or at least one low in carbohydrates, is brain-friendly and helps people out of various mental health disorders. Or you can watch the recent webinar she did with us here.

—

Antioxidant and polyphenol power

The more biologically active an essential fat is (with DHA at the top), the more prone it is to oxidation.

It is literally this ability of DHA to absorb energy (photons from light) that creates the impulse that passes information from the eye to the brain. It explains the origin of the brain and nervous system, going back a billion years to a rudimentary single cell called dynoflagellate. This little organism basically used the electric shock from photons to create the first ‘twitch’ towards light. Where there was light, there was food, and ultimately the evolution of the nervous system and brain. In simple terms, we can see that the brain is really an extension of the eye. How do we see with such precision and speed? Until now, no-one has been able to explain this satisfactorily. At the age of 93, Professor Michael Crawford, who helped our charity get started, has worked out how this occurs and how we see in colour. It requires knowledge of quantum physics, explained in a recent paper entitled ‘Docosahexaenoic Acid Explains the Unexplained in Visual Transduction’.(6)

With all this volatile fatty acid and mitochondrial energy production, cleaning up the oxidant exhaust fumes is a vital function for a healthy brain. So how do we achieve protection and how do we measure it?

There are hundreds, if not thousands of antioxidants and polyphenols in our food. Foods can be measured for their ‘Total Antioxidant Capacity’ or TAC for short. It’s worked out from an equation involving eight key antioxidants from vitamin A, carotenes (think carrots), lycopenes (rich in tomatoes), lutein and zeaxanthine (rich in green vegetables), vitamin E (in nuts and seeds), but most of all vitamin C (rich in berries, broccoli, peppers and other vegetables).

Vitamin C is a keystone nutrient as far as swinging the antioxidant equation in our favour. Individually, the impact of these nutrients on our health may be less than when combined. For example, a study of 4,740 Cache County Utah elderly residents found that those supplementing both vitamin E and C cut their risk of developing Alzheimer’s by two thirds (66%). Taking just one cut the risk by a mere quarter (25%).  (7)

The higher the TAC score of our diet, the lower our risk of memory decline becomes. This was the finding of a recent study of 2,716 people over age 60. Higher TAC scores correlated with better memory function (8). Those in the highest quarter of TAC scores had half the risk of decreasing memory. Powerful stuff!

Tea, cacao, red wine, red onions, olives and berries are rich sources of polyphenols. Many of these polyphenol-rich foods improve circulation, lower blood pressure and dampen down inflammation which lies behind many brain and heart health problems. 

More than a decade ago research in Norway (9) found that the more tea you drink the better; a small glass of wine (125ml) a day (preferably red, as it is rich in resveratrol) reduces the risk of cognitive decline. Cacao is also beneficial, ideally no more than 10g, (about 3 pieces) of dark, 70 percent or more. Other studies based on adding cacao to the diet have shown improved cognition, possibly by improving circulation. This was recently confirmed in a big ‘COSMOS’ trial involving over 20,000 people given a cacao extract supplement versus a placebo for five years (10). The reduction in cardiovascular risk was even greater than that of a Mediterranean diet.

The take-away message? Polyphenols are a vital part of a healthy diet for both our heart and our brain.

So, what do we need to eat and drink to protect our brain and body? Basically, eat a Mediterranean-style ‘rainbow coloured’ diet. A Mediterranean diet has more fish, less meat and dairy, more olive oil, fruit and vegetables including tomatoes, legumes (beans and lentils), and whole grain cereals than a standard Western diet. It also includes small quantities of red wine. There are variations of this kind of diet, called the MIND diet and the DASH diet, but the core components are the same. As researchers drill down, we are learning what to eat and drink and how much, to keep our minds sharp and brain young.

The trick is to really start thinking of the colours we are eating and gravitate to the strong colours, choosing organic where possible. Mustard and turmeric, for example, are strong yellows. Bright oranges include butternut squash, sweet potato, carrots. For red, think tomatoes and watermelons. Anything purple, magenta or blue is brilliant for us too. From beetroots (eat them raw, grated into salads) to blueberries, blackberries to raspberries, all these foods are fantastically good for us, so tuck in!

In addition to food, as a health aspiring 65-year-old, I both supplement 1 gram of vitamin C twice a day and take an AGE Antioxidant containing Co-Q10, alpha lipoic acid, n-acetyl cysteine (NAC – as a precursor to glutathione which is the master antioxidant) and resveratrol as well as vitamin E and A – both beta-carotene and retinol. Many people think that there is no point supplementing glutathione because it is so rapidly oxidised, or sacrificed, to disarm oxidants, but it is also rapidly recycled by anthocyanidins in blue/red berries. So, combining the two reloads glutathione. This film shows how.

But how do we measure our antioxidant status?

My research team is working on exactly this challenge and we are finding that the ratio between reduced glutathione (GSH) and oxidised glutathione (GSSG) in red blood cells is probably the best biological determinant. We hope to introduce that into our panel of functional indicators, and research how it correlates with dietary intake and lifestyle habits as well as cognitive function.

We are due to launch a DRIfT Test as part of a global prevention initiative, which will be a 4 in 1 test

The UK Biobank has collected data on 500,000 people since 2006, inviting people to fill in questionnaires, give blood and carry out certain tests. We are funded by ‘Friends’ who pay £50/$60/€60 a year.  So far we have collected data on 410,000 people and this number is growing by about a hundred a day. 

In addition to taking the blood test, participants are invited to complete a validated online Cognitive Function Test (not a questionnaire), followed by a comprehensive 144 question Dementia Risk Index diet and lifestyle questionnaire which takes 20-25 minutes. This works out a person’s future risk and shows what’s driving the risk. This is a free service.

We run the UK’s leading dementia prevention charity which is running the prevention project together with Dr Tommy Wood, Assistant Professor at the University of Washington. “By tracking a person’s blood sugar, vitamin B, D and omega-3 status against changes in cognitive function over time, in addition to lifestyle factors such as sleep and physical activity, we can learn what really helps prevent cognitive decline.” says Dr Wood, the principal investigator for the study. 

Citizen Science

All donations are put back into research, and the results of the research are shared back to the people. 

This is science for the people, funded by the people, shared back with the people. We call them Citizen Scientists and we hope to reach a million people around the world within a year or so making this the biggest prevention-focussed study of its kind. The purpose of research is to help people. Too often great scientists do great studies, which get published and ignored. We have to face the fact that, in the UK as an example, the Government has commissioned four reports on mental health and Wellcome did a further independent report, all showing we have a cerebral tsunami with brain and mental health disorders ahead of every other disease.

They have ignored every single one.

Change is not going to come from the Government or the NHS. It is going to have to come from us, the people. I urge everyone in natural medicine to take the test themselves, share it with others and support us by becoming Friends and donating £50 a year, getting so much in return.

This is how we are funding our amazing research team. We are a lean, keen, small but mighty team. 

Every donation, big or small, goes right back into helping people prevent these preventable and terrible diseases such as dementia. 

Together, we can change the world. 

We need to because time is running out. 

We will lose our humanity if we don’t stop this brain drain.

—

Want to learn more about homocysteine and how to reclaim your brain? Join us for the Homocysteine Unplugged webinar.

Thank you for reading!

Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References

1 Lakhan, S.E., Kirchgessner, A. The emerging role of dietary fructose in obesity and cognitive decline. Nutr J 12, 114 (2013). 

2 https://www.psychiatrist.com/news/a-19-year-old-is-youngest-ever-to-be-diagnosed-with-alzheimers/

3 Yau PL, Castro MG, Tagani A, Tsui WH, Convit A. Obesity and metabolic syndrome and functional and structural brain impairments in adolescence. 

Pediatrics. 2012 Oct;130(4):e856-64. doi: 10.1542/peds.2012-0324. Epub 2012 Sep 

4  Zhang X, et al Midlife lipid and glucose levels are associated with Alzheimer’s disease. Alzheimers Dement. 2023

5  Fortier M, Castellano CA, St-Pierre V, Myette-Côté É, Langlois F, Roy M, Morin MC, Bocti C, Fulop T, Godin JP, Delannoy C, Cuenoud B, Cunnane SC. A ketogenic drink improves cognition in mild cognitive impairment: Results of a 6-month RCT. Alzheimers Dement. 2021 Mar;17(3):543-552. doi: 10.1002/alz.12206. Epub 2020 Oct 26. PMID: 33103819; PMCID: PMC8048678.

6 Crawford, M.A..; Sinclair, A.J.; Wang, Y.;
Schmidt, W.F.; Broadhurst, C.L.; Dyall, S.C.; Horn, L.; Brenna, J.T.; Johnson, M.R.; Docosahexaenoic Acid Explains the Unexplained in Visual Transduction. Entropy 2023, 25, x. https://doi.org/10.3390/xxxxx 

7  Basambombo LL, Carmichael PH, Côté S, Laurin D. Use of Vitamin E and C Supplements for the Prevention of Cognitive Decline. Ann Pharmacother. 2017 Feb;51(2):118-124. doi: 10.1177/1060028016673072. Epub 2016 Oct 5. PMID: 27708183.

8 Peng, M., Liu, Y., Jia, X. et al. Dietary Total Antioxidant Capacity and Cognitive Function in Older Adults in the United States: The NHANES 2011–2014. J Nutr Health Aging 27, 479–486 (2023). https://doi.org/10.1007/s12603-023-1934-9

9 Nurk E, Refsum H, Drevon CA, Tell GS, Nygaard HA, Engedal K, Smith AD. Intake of flavonoid-rich wine, tea, and chocolate by elderly men and women is associated with better cognitive test performance. J Nutr. 2009 Jan;139(1):120-7. doi: 10.3945/jn.108.095182. Epub 2008 Dec 3. PMID: 19056649.

10 Sesso HD, Manson JE, Aragaki AK, Rist PM, Johnson LG, Friedenberg G, Copeland T, Clar A, Mora S, Moorthy MV, Sarkissian A, Carrick WR, Anderson GL; COSMOS Research Group. Effect of cocoa flavanol supplementation for the prevention of cardiovascular disease events: the COcoa Supplement and Multivitamin Outcomes Study (COSMOS) randomized clinical trial. Am J Clin Nutr. 2022 Jun 7;115(6):1490-1500. doi: 10.1093/ajcn/nqac055. PMID: 35294962; PMCID: PMC9170467.

By Patrick Holford. This is part one, read part two here.

Few people realise the catastrophic decline in mental health that has occurred over the past 50 years.

—

‘Brain health conditions have become a global health emergency,’ according to the Federation of European Neuroscience Societies last year (1).

Globally, 15 per cent of all disability is due to brain and mental health disorders. The lifetime cost of Alzheimer’s in 2022 was estimated to be €1.2 trillion across the EU which is half the UK’s total GDP! This burden and costs exceeds that of all diseases, including cancer and heart disease. But most worrying are the trends of falling IQ at a rate of about 7 per cent a generation and the steady increase in young people with four in ten now reporting persistent feelings of sadness or hopelessness and almost a quarter (22 per cent) contemplating suicide (2).

On this flight path, by 2080, suicide may well become the leading cause of death in those under 24. Also, more than a third of children will have severe neurodevelopmental impairment, defined as significantly below the norm for IQ. That’s the conclusion of Professor Michael Crawford who discovered the essentiality of omega-3 DHA for the brain. Alarmingly, brain size, deduced from cranial capacity of skulls, has shrunk by a staggering 20 per cent over a mere 30,000 years. It took over six million years for brain size to increase from that of a chimpanzee (350cc) to a peak of 1,600 to 1,700 cc with Cro Magnon man thirty thousand years ago. Today, brain size averages 1,350cc (3). There is no question that we are devolving mentally with an endless escalation of rates of ADHD, autism, depression, anxiety, insomnia, schizophrenia, dementia and Alzheimer’s, as well as strokes, Parkinson’s and multiple sclerosis.

The big question is: why?

—

Introducing the four horsemen…

I’m proposing that there are four main biological drivers of our demise which I’m calling the four horsemen of the mental health apocalypse: a lack of brain fats, messed up methylation, loss of glucose control and excessive oxidation.

The first two – brain fats and methylation – are vital for the integral structure of neuronal membranes. The second two are vital for the function of brain cells, supplying fuel and coping with the oxidant ‘exhaust fumes’ of energy metabolism.

—

Brain fats in short supply

The dry weight of the brain is 60 per cent fat, and omega-3 DHA makes up the majority of the structural fat of neurons, followed closely by Arachidonic Acid (AA), an omega-6 fat. ALL BRAINS OF ALL ANIMALS contain predominantly these two essential brain fats. It is the available supply of these that determine whether an animal ends up with a big or small brain. The link between omega-3 DHA and brain function is beyond doubt, with study after study confirming the scientific evidence. Only last month, a study from the UK BioBank reported a 30 per cent lower risk of dementia in those with a higher omega-3 status in their blood (4). This confirmed the results of a US study (5) that found a 49 per cent reduced risk for dementia in those with the highest DHA level (top fifth) in their red blood cells versus the lowest (bottom fifth). A meta-analysis of 48 studies in the American Journal of Clinical Nutrition in 2023 (6) concludes that ‘a moderate-to-high level of evidence suggested that dietary intake of omega-3 fatty acids could lower risk of all-cause dementia or cognitive decline by about 20 per cent, especially for docosahexaenoic acid (DHA) intake’. Each 100mg increment of DHA was associated with an 8–10 per cent lower risk of dementia. And a 2023 study, by psychologists at the Linda Loma University in California and published in the journal Brain Sciences (7), reported that the higher a person’s omega-3 blood index was, the more white matter there was in their brain, and the better they performed on cognitive tests that predict less risk for dementia.

It’s compelling science. That is why my first recommendation is to always test your omega-3 index.

This is the percentage of omega-3 DHA and EPA in the membrane of red blood cells, and it is a direct reflector of the membrane levels in your brain. Red cells last for three months so this is a long-term measure of your omega-3 status. In countries such as Japan, known for a high fish diet, the omega-3 index is around 10 per cent on average. Ideally, a level of above 8 per cent is optimal. I thought I was doing well, supplementing daily 575mg of EPA and DHA combined, plus eating oily fish three times a week but I scored just under – 7.7 per cent. I’ve since upped my intake of DHA by 500 mg, to 750 mg total daily intake.

In its pure form, DHA isn’t enough, it has to become ‘phosphorylated’ to work. It’s a bit like using those glues where you have two tubes and have to mix a squeeze of one with the other for the glue to work. The ‘mixer’ in this case is the B vitamins in your body attaching the DHA to the phospholipids such as phosphatidylcholine (PC). If you have no phospholipids, or no DHA or B vitamins, the mix is not going to work. While the body can synthesise DHA, to reach the levels we need requires good quality food sources such as seafood, by far the richest source of (already) phosphorylated DHA. If fish isn’t your thing, supplementing with lecithin (granules or capsules) is a must – aim for two 1200mg capsules or 250mg of PC per day.

—

Vitamin D is a mental health essential

The other essential brain fat, which is actually a hormone, is vitamin D.

A large-scale study earlier this year, involving over twelve thousand dementia-free 70+ year olds (8), found that more than a third (37 per cent) took supplements of vitamin D and those that did had a 40 per cent lower incidence of dementia. Many nutrition professionals recommend supplementing around 3,000 iu in the winter to achieve an adequate blood level of 75 nmol/L or more, advice that is backed up by a consortium of some 35 vitamin D researchers.(9)  The UK Government also recommends supplementing vitamin D, although the recommended 400iu falls far short of the amount needed for brain health. In a study in France, those with low vitamin D levels, below 50 nmol/L, had a nearly three-fold increased risk of Alzheimer’s (10) and worryingly, over sixty per cent of people in the UK have lower levels than this (11), while half are unaware of the need to supplement in the winter and only one in ten actually do (12). (Back in 2010, I was reported to the Advertising Standards Agency for suggesting that people had to supplement vitamin D in the winter because diet alone was not sufficient – how times change!)

Research continues to investigate whether having a higher blood level of vitamin D, perhaps 100 nmol/L, is even better for brain health. If you know your vitamin D level, you can help with this research by completing the Cognitive Function Test, and providing your vitamin D level. Or you can join our MIND project which includes a home test kit to measure your vitamin D level. We’ve tested 410,000 people’s cognitive function so far but need more people who know, or are willing to test their vitamin D.

Methylation and homocysteine-lowering B vitamins

Omega-3 DHA can only become active by the process of methylation, which attaches the DHA to a phospholipid and thereby enables it to be incorporated into the neuronal membrane. The process of methylation is totally dependent on vitamins B6, B12 and folate. Our methylation-ability is beautifully defined by our homocysteine level. Homocysteine rises if the biochemical pathway between the amino acid methionine converting to the methyl-donor SAMe is blocked. Without adequate vitamin B6, B12, folate or, in the liver, zinc and tri-methyl glycine (TMG), homocysteine will rise.

Lowering homocysteine with B vitamins is the greatest evidenced disease-modifying treatment, as shown in the best meta-analysis of 396 trials (13) by China’s leading Alzheimer’s prevention expert, Professor Jin-Tai Yu, whom we are honoured to have in our Scientific Advisory Board. It was also rated so by the US National Institutes of Health researchers (14). 

Homocysteine is also a biomarker for over 100 diseases including almost all mental and neurological diseases. The seminal paper by Professors David Smith and Helga Refsum on the subject is vital for all to read. For example, just one recent meta-analysis showed that both homocysteine, vitamin B12, and folic acid predict the onset and development of Parkinson’s. Homocysteine levels above 11µmol/L are a clear indicator that the brain is shrinking. Professor David Smith, another member of our Scientific Advisory Board, recommends treatment with B vitamins for anyone with a homocysteine above 10µmol/L , giving 20 mg of B6, 400 mcg of methylfolate and 500µg of B12.

Increasingly, raised homocysteine is extremely common. In America, 40 per cent of those over 60 have a homocysteine of over 11 (15). In China ‘the mean (average) homocysteine levels in adult males less than 30 years of age and greater than 60 years were higher than the upper limit of normal (15 µmol/L).’ And in the UK, two in five adults over 61 have insufficient B12 to prevent accelerated brain shrinkage (16).

Homocysteine not only predicts Alzheimer’s dementias but also vascular dementia which, combined, make up almost 90 per cent of all dementias. Raised homocysteine is a major driver of cardiovascular and cerebrovascular disease. Raised homocysteine increases the risk of cerebrovascular disease by seventeen times (17)! Joe Rogan dedicated his recent show to exactly this (18) and stressed why testing homocysteine is vital for anyone with any form of cardiovascular, neurological or mental health disease.

The trouble with homocysteine is you just don’t know if your level is raised without testing it, which is why we have create our own at-home, highly accurate test kit. While up to 20 per cent of people have a methylation gene mutation (MTHFR677TT) making them more likely to have a raised level, it’s likely that most people with raised homocysteine are just not good at absorbing vitamin B12, a condition that becomes more common with age. This is why antacid proton pump inhibitor (PPI) drugs are such bad news. They drive down B12 and four years use cranks up Alzheimer’s risk by over 33 per cent (19). 

Breakthrough in homocysteine testing

It is essential to test homocysteine level for anyone over 50 and anyone with any brain or mental health or cardiovascular disorder including hypertension. Treatment with B vitamins is also essential if the level is above 10µmol/L. While a homocysteine level above 11 means increased brain shrinkage, research shows that even a homocysteine level of above 9 during pregnancy predicts more problems, specifically withdrawn behaviour, anxiety/depression, social problems and aggressive behaviour in the child by the age of six (20). Raised homocysteine is a well known predictor of miscarriage and pregnancy problems, which is why I recommend that women can best prepare for a healthy pregnancy by ensuring their homocysteine level is below 7.5 mcmol/l. Above this, the evidence points to chromosomal damage (21).

All these studies refer to plasma homocysteine, that is the level found in the clear serum part of blood (rather than the red blood cells). The difficulty with many test kits is the need to separate or spin the blood shortly after taking the sample or pass the blood through a plasma separator. Many fall short of the correlation with serum/plasma homocysteine, the gold standard of testing. Excitingly, a breakthrough with both the fixing of blood (taken using a dry blood spot) and the testing process now means that we now have an accurate and inexpensive way to test homocysteine with our home test kit. This is going to be made available all over the world, starting with the UK and EU in January 2024. The validation of this test is extremely good, with no false positives or negatives. Accuracy can be further improved if the test is taken after fasting for 12 hours with water only. Both coffee and alcohol affect homocysteine levels, as does eating a protein-rich meal.

Please, join our Citizen Science research by both testing homocysteine and completing the Cognitive Function Test here

A consensus of world experts (22) has concluded that lowering homocysteine with B vitamins is the easiest and most cost-effective prevention action, which Oxford University’s health economists estimate would save the UK £66 million per year (23).

However, it’s vital to test both homocysteine and Omega-3 levels, as they are co-dependent. Homocysteine-lowering B vitamins only work in those with sufficient omega-3, and omega-3 only works if homocysteine is low. This short film shows how this works here.

It explains why studies giving omega-3 or giving B vitamins have not consistently been effective. However, in re-analyses of three studies, B vitamins are highly effective, both in reducing the rate of brain shrinkage and improving cognition, in those with sufficient omega-3, and conversely, omega-3 is highly effective, but only in those with homocysteine below 11 mcmol/L (24). 

…Read part two here!

Want to learn more about homocysteine and how to reclaim your brain? Join us for the Homocysteine Unplugged webinar.

Thank you for reading!

Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References

1 https://www.politico.eu/sponsored-content/global-data-is-key-to-tackling-the-rise-in-brain-health-conditions/

2  van Os J, Guloksuz S. Population Salutogenesis—The Future of Psychiatry? JAMA Psychiatry. Published online December 20, 2023. doi:10.1001/jamapsychiatry.2023.4582

3 Crawford M, Marsh, D ‘The Shrinking Brain’ 2023

4 Sala-Vila, A.; Tintle, N.; Westra, J.; Harris, W.S. Plasma Omega-3 Fatty Acids and Risk for Incident Dementia in the UK Biobank Study: A Closer Look. Nutrients 2023, 15,4896. https://doi.org/10.3390/ nu15234896

5 Sala-Vila, A.; Satizabal, C.L.; Tintle, N.; Melo van Lent, D.; Vasan, R.S.; Beiser, A.S.; Seshadri, S.; Harris, W.S. Red Blood Cell DHA Is Inversely Associated with Risk of Incident Alzheimer’s Disease and All-Cause Dementia: Framingham Offspring Study. Nutrients 2022, 14, 2408. https://doi.org/10.3390/ nu14122408

6 Wei BZ, Li L, Dong CW, Tan CC; Alzheimer’s Disease Neuroimaging Initiative; Xu W. The Relationship of Omega-3 Fatty Acids with Dementia and Cognitive Decline: Evidence from Prospective Cohort Studies of Supplementation, Dietary Intake, and Blood Markers. Am J Clin Nutr. 2023

7 Loong, S.; Barnes, S.; Gatto, N.M.; Chowdhury, S.; Lee, G.J. Omega-3 Fatty Acids, Cognition, and Brain Volume in Older Adults. Brain Sci.2023,13,1278. https://doi.org/ 10.3390/brainsci13091278 

8 Ghahremani M et al. Vitamin D supplementation and incident dementia: Effects of sex, APOE, and baseline cognitive status. Alzheimers Dement (Amst). 2023 Mar 1;15(1):e12404. doi: 10.1002/dad2.12404. PMID: 36874594; PMCID: PMC9976297.

9 Płudowski P et al Guidelines for Preventing and Treating Vitamin D Deficiency: A 2023 Update in Poland. Nutrients. 2023 Jan 30;15(3):695. doi: 10.3390/nu15030695. PMID: 36771403; PMCID: PMC9920487.

10 Jia J et al. Effects of vitamin D supplementation on cognitive function and blood Aβ-related biomarkers in older adults with Alzheimer’s disease: a randomised, double-blind, placebo-controlled trial. J Neurol Neurosurg Psychiatry. 2019 Dec;90(12):1347-1352. doi: 10.1136/jnnp-2018-320199. Epub 2019 Jul 11. PMID: 31296588.

11 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7353432/pdf/nutrients-12-01868.pdf

12 https://www.nutrition.org.uk/news/2021/british-nutrition-foundation-survey-reveals-49-adults-unaware-of-uk-government-guidelines-for-vitamin-d/

13 Yu JT, Xu W, Tan CC, Andrieu S, Suckling J, Evangelou E, Pan A, Zhang C, Jia J, Feng L, Kua EH, Wang YJ, Wang HF, Tan MS, Li JQ, Hou XH, Wan Y, Tan L, Mok V, Tan L, Dong Q, Touchon J, Gauthier S, Aisen PS, Vellas B. Evidence-based prevention of Alzheimer’s disease: systematic review and meta-analysis of 243 observational prospective studies and 153 randomised controlled trials. J Neurol Neurosurg Psychiatry. 2020 Nov;91(11):1201-1209. doi: 10.1136/jnnp-2019-321913. Epub 2020 Jul 20. PMID: 32690803; PMCID: PMC7569385.

14 Beydoun MA, Beydoun HA, Gamaldo AA, Teel A, Zonderman AB, Wang Y. Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis. BMC Public Health. 2014 Jun 24;14:643. doi: 10.1186/1471-2458-14-643. PMID: 24962204; PMCID: PMC4099157.

15 Pfeiffer C, Clin Chem. 2008; R. Xu, Nature Scientific Reports 2022; Vogiatzlou A, Neurology, 2008

16 Vogiatzoglou A, Refsum H, Johnston C, Smith SM, Bradley KM, de Jager C, Budge MM, Smith AD. Vitamin B12 status and rate of brain volume loss in community-dwelling elderly. Neurology. 2008 Sep 9;71(11):826-32. doi: 10.1212/01.wnl.0000325581.26991.f2. PMID: 18779510.

17 Teng Z, Feng J, Liu R, Ji Y, Xu J, Jiang X, Chen H, Dong Y, Meng N, Xiao Y, Xie X, Lv P. Cerebral small vessel disease mediates the association between homocysteine and cognitive function. Front Aging Neurosci. 2022 Jul 15;14:868777. doi: 10.3389/fnagi.2022.868777. PMID: 35912072; PMCID: PMC9335204.

18  See the Joe Rogan show https://www.youtube.com/watch?v=-oqYoNwnOs0.

19 Northuis CA, Bell EJ, Lutsey PL, George KM, Gottesman RF, Mosley TH, Whitsel EA, Lakshminarayan K. Cumulative Use of Proton Pump Inhibitors and Risk of Dementia: The Atherosclerosis Risk in Communities Study. Neurology. 2023 Oct 31;101(18):e1771-e1778. doi: 10.1212/WNL.0000000000207747. Epub 2023 Aug 9. PMID: 37558503; PMCID: PMC10634644.

20 Roigé-Castellví J, Murphy M, Fernández-Ballart J, Canals J. Moderately elevated preconception fasting plasma total homocysteine is a risk factor for psychological problems in childhood. Public Health Nutr. 2019 Jun;22(9):1615-1623. doi: 10.1017/S1368980018003610. Epub 2019 Jan 14. PMID: 30636652; PMCID: PMC10261079.

21 Fenech M, Aitken C, Rinaldi J. Folate, vitamin B12, homocysteine status and DNA damage in young Australian adults. Carcinogenesis. 1998 Jul;19(7):1163-71. doi: 10.1093/carcin/19.7.1163. PMID: 9683174.

22 Smith AD, Refsum H, Bottiglieri T, Fenech M, Hooshmand B, McCaddon A, Miller JW, Rosenberg IH, Obeid R. Homocysteine and Dementia: An International Consensus Statement. J Alzheimers Dis. 2018;62(2):561-570. doi: 10.3233/JAD-171042. PMID: 29480200; PMCID: PMC5836397.

23 Tsiachristas A, Smith AD. B-vitamins are potentially a cost-effective population health strategy to tackle dementia: Too good to be true? Alzheimers Dement (N Y). 2016 Aug 11;2(3):156-161. doi: 10.1016/j.trci.2016.07.002. PMID: 29067302; PMCID: PMC5651357.

24 Jernerén F, Elshorbagy AK, Oulhaj A, Smith SM, Refsum H, Smith AD (2015). Brain atrophy in cognitively impaired elderly: the importance of long-chain ω-3 fatty acids and B vitamin status in a randomized controlled trial. Am J Clin Nutr. 2015 Jul;102(1):215-21; see also van Soest, A.P.M., van de Rest, O., Witkamp, R.F. et al. DHA status influences effects of B-vitamin supplementation on cognitive ageing: a post-hoc analysis of the B-proof trial. Eur J Nutr 61, 3731–3739 (2022). https://doi.org/10.1007/s00394-022-02924-w; see also Jernerén F, Cederholm T, Refsum H, Smith AD, Turner C, Palmblad J, Eriksdotter M, Hjorth E, Faxen-Irving G, Wahlund LO, Schultzberg M, Basun H, Freund-Levi Y. Homocysteine Status Modifies the Treatment Effect of Omega-3 Fatty Acids on Cognition in a Randomized Clinical Trial in Mild to Moderate Alzheimer’s Disease: The OmegAD Study. J Alzheimers Dis. 2019;69(1):189-197. doi: 10.3233/JAD-181148. PMID: 30958356.

25 Lakhan, S.E., Kirchgessner, A. The emerging role of dietary fructose in obesity and cognitive decline. Nutr J 12, 114 (2013). 

—

Back in the decade that gave us neon shell suits, the first space shuttle, and the birth of the pop video (the unforgettable 1980s) we also believed that glucose (the sugar used by our bodies) gave us extra energy. Lucozade, a liquid form of glucose with a good dose of preservatives, artificial sweeteners and artificial colourants, was advertised as ‘energy for the human race.’ 

—

Yet, new studies are showing that too much glucose, and especially fructose, over time starves the brain of energy, leading to both memory loss and brain shrinkage.

These two sugars interfere with the energy factories within cells, called mitochondria, and deprive the brain of the energy it needs to function properly.

The link between diabetes and dementia is well known – those with diabetes have four times the risk of dementia. 

Haemoglobin A1c (HbA1c) is a long-term measure of glucose bound to red blood cells (haemoglobin) and is used by doctors to diagnose diabetes and monitor its therapy. HbA1c is a measure of damage produced by sugar spikes on red blood cells; a HbA1c of 6.5% or greater is diagnostic of diabetes. But long before this, in what is usually considered to be the ‘normal range’ teenagers with HbA1c above 5.4% show cognitive decline and shrinkage of the hippocampus in the central area of the brain compared to those with lower HbA1c levels (1). 

Shrinkage of the hippocampus is the hallmark of Alzheimer’s and is used to diagnose the disease. A new study shows that 40-year-old adults with so-called normal glucose levels, but at the higher end of the normal range, have increased their risk of Alzheimer’s by 15% (2). 

Furthermore, “In teenagers with raised, but normal levels of HbA1c, there is clear evidence of the same kind of memory problems and the same areas of brain shrinkage seen in patients with Alzheimer’s Disease” says Robert Lustig, Emeritus Professor of Pediatrics at University of California, San Francisco.

—

“Keeping your HbA1c below 5.4% with a no-added-sugar diet, and for some a low-carbohydrate diet, is one of the most direct ways you can protect your brain at any age.” says Lustig. 

“The irony is that having too much sugar over a number of years makes a person resistant to insulin. We need insulin in order to deliver glucose into our brain cells, so insulin resistance, the direct consequence of too much glucose, ends up starving the brain of energy with the consequent loss of concentration and memory.” says nutritionist and psychologist Patrick Holford, our CEO and founder.

“We are calling for people to test both their cognitive function with our free online test and measure their HbA1c with our new home pin prick blood test kit, so we can really find out when problems occur and how to prevent cognitive decline.” So far, over 400,000 people have done our Cognitive Function Test – our FREE, validated, online cognitive function test which tells you your future dementia risk and what to do to lower it.

Professor Robert Lustig thinks the problem got even worse when the food industry switched from sucrose, derived from cane, to high-fructose corn syrup, derived from corn; “High-fructose corn syrup is not more biologically evil; it’s economically evil, because it’s half the price of sucrose, so it found its way into all sorts of foods…

“The key message is to test HbA1c early if it is over 5.4% and act to bring it down by cutting right back on foods and drinks with added sugar including carbohydrate-rich foods such as bread, rice, pasta, potatoes, and especially fruit juice. Nature never provides fructose without the requisite fibre. When God made the poison, he packaged it with the antidote. Eat your fruit, don’t drink it.” says Lustig.

Thank you for reading!
Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

REFERENCES

BRAIN SHRINKAGE IN ADOLESCENTS

Yau PL, et al Obesity and metabolic syndrome and functional and structural brain impairments in adolescence. Pediatrics. 2012 

MIDLIFE GLUCOSE INCREASING ALZHEIMER’S DISEASE RISK

 Zhang X, et al Midlife lipid and glucose levels are associated with Alzheimer’s disease. Alzheimers Dement. 2023

BACKGROUND ON SUGAR AND DEMENTIA

foodforthebrain.org/eat-a-low-glycaemic-load-gl-diet/

and 

foodforthebrain.org/is-sugar-killing-your-brain/

¹ Yau PL, et al Obesity and metabolic syndrome and functional and structural brain impairments in adolescence. Pediatrics. 2012 

² Zhang X, et al Midlife lipid and glucose levels are associated with Alzheimer’s disease. Alzheimers Dement. 2023

By Patrick Holford

Did you know the length of your shadow can tell you if you’re able to generate vitamin D from sunlight?

If your shadow is longer than your body – you can’t produce vitamin D from sunlight. If you are in winter and live in a country of higher latitude (like the UK), this is happening now!

Vitamin D is an all-rounder as far as your brain and mental health is concerned.

It helps neurotransmission and exerts anti-inflammatory and neuroprotective activities within the brain by reducing both inflammation and oxidative stress (1).  

—

We are all deficient in winter

Generally speaking, the lower your vitamin D, the worse your mood which makes vitamin D especially important to supplement from October to March if you live in the UK or a similar latitude, when the angle of the sun is too low and you’re also less likely to get outdoors exposing your skin to sunlight. It’s best to assume that we are all deficient in winter, unless you travel to the sun, and therefore need to supplement at least 25mcg (1000iu) although two or three times may be optimal and necessary to correct deficiency.

—

Vitamin D and depression

The lower your vitamin D level, the more depressed you are likely to feel. If your mood takes a dip in winter months this is a key sign that you might need more. That’s what researchers at the University of Tromso in Norway found on testing 441 volunteers who were given a test for depression and also a test for blood levels of vitamin D. The volunteers were then given Vitamin D supplements or placebo. Tested one year on, those given vitamin D, but not those given the placebos, had substantially lower depression ratings (2).

However, you don’t have to wait for a year to get a lift in your mood. An eight-week study in Australia found that some of those given vitamin D supplements had an improvement in mood in only five days (3). Another study, in Iran, gave a single vitamin D injection and reported improvement in depression when measured 3 months on (4).

Since vitamin D stores, there is no need to supplement daily. You can take a weekly dose. In the Norwegian study above they gave 20,000iu or 40,000iu weekly. Both worked and there wasn’t a big difference in the effects on mood. So, you can assume that 20,000iu weekly, or 3,000iu daily would likely be sufficient.

It’s what is in your blood that matters

However, the yardstick for what you need is really whatever gets your blood level into the optimal range.

In the study above, those given 20,000iu a week averaged a blood level of 88 nmol/l, while those given 40,000iu averaged 111nmol/l. It is now well recognised that levels above 75nmol/l (30 ng/ml) correlate with good health for many health measures, while levels above 100nmol/l (40ng/ml) might be even better in some respects. My recommendation is to test yourself and consider anything below 50 to be deficient, and above 75 to be sufficient with an optimal level being closer to 100nmol/l (40ng/ml). If you then supplement 3,000iu daily, or seven times this weekly, especially from October to March, retest yourself against these yardsticks.

It’s not JUST about vitamin D

But it isn’t just vitamin D we need – it’s sunlight.

During the summer months, if you are spending half an hour outdoors, with short sleeves, shorts or even more skin exposure, in the sunlight, even a multivitamin that provides you 800iu (a quarter of what you need in the darker months) might be sufficient.

Sunlight promotes serotonin, the happy neurotransmitter.

Having good vitamin D levels is a vital part of your brain upgrade since it helps optimise your brain’s serotonin levels. That’s because a vital enzyme called TPH, which converts the amino acid tryptophan into serotonin, is enhanced in the brain by vitamin D, and selectively shut down in the gut. So, with sufficient vitamin D you get higher brain levels of serotonin, promoting good mood, and lower serotonin levels in the gut (5), protecting against gut inflammation. 

The other way to boost your light exposure is with light therapy. Canadian researchers compared the effects of an anti-depressant (fluoxetine), placebo or 30 minutes daily of light therapy as soon as possible on waking for people with major depression. Light therapy was both superior to placebo and anti-depressants, which were also no better than placebo. I have a full spectrum light in my study, which I put on in the winter, when I’m writing in the early morning, before the sun comes up.

—

Vitamin D and addiction

Interestingly, vitamin D deficiency is also associated with greater opioid addiction (7), suggesting the need to up vitamin D intake to reduce cravings. There’s also something else interesting about vitamin D, sun exposure and addiction. People can become addicted to sunbeds. In relation to opioids, the lower one’s vitamin D levels, the more addictive they become. Sun exposure, which promotes higher vitamin D levels, reduces opioid addiction.

—

What to eat?

The best food sources of vitamin D are oily fish and eggs. A serving of salmon or mackerel is likely to give you 400iu of vitamin D. Two eggs will provide about 130iu. In some countries, not the UK, milk is fortified with vitamin D but otherwise, it is not a great source. Some mushrooms are purposely fortified with vitamin D by exposing them to UV light.

In summary, the way up from down is to eat a low GL diet, with plenty of oily fish and eggs, avoid sugar, cut back on stimulants and alcohol, and make sure your daily supplements include omega-3, B vitamins, with extra B12 if your homocysteine level is high, vitamin D, zinc, magnesium, chromium, plus the amino acids 5-HTP with is the precursor of serotonin.

—

Vitamin D protects your brain and memory.

Vitamin D deficiency increases the risk of Alzheimer’s (9). In a study in France involving 912 elderly patients followed for 12 years, a total of 177 dementia cases occurred. Those with low vitamin D levels had a nearly three-fold increased risk of Alzheimer’s (10). Supplementing 800iu (20mcg) a day for 12 months has also been shown to improve cognitive function (11). 

Supplements may also help ward off dementia, according to a recent, large-scale study involving over twelve thousand dementia-free 70+ year-olds in the US (12). More than a third (37%) took supplements of vitamin D. Those who did had a 40% lower incidence of dementia. Professor Zahinoor Ismail, of the University of Calgary and University of Exeter, who led the research, said: “We know that vitamin D has some effects in the brain that could have implications for reducing dementia, however so far, research has yielded conflicting results. Overall, we found evidence to suggest that earlier supplementation might be particularly beneficial, before the onset of cognitive decline.”

—

Vitamin D helps recovery from strokes and brain injury

Having a higher vitamin D level or supplementing vitamin D at levels above 2,000iu a day also helps people recover from strokes (13) and other forms of brain injury.

I recommend 3,000iu a day or 21,000iu a week in winter but most importantly, monitoring your vitamin D level to keep it above 75nmol/l (30 ng/ml). A level of 100nmol/l may be optimal. That is why testing is so vital as winter approaches. Test again 3 months later so you know if you’re taking enough or too much and that will give you a good gauge as spring approaches when you can probably lower your intake to 600 to 1,000iu depending on sun exposure and diet to top up to over 1,000iu.

Vitamin D is vital in pregnancy and for children

A breastfeeding mother must, at least, supplement omega-3 fish oils and ensure enough B vitamins for homocysteine to be below 7 mcmol/L, but many other nutrients are also necessary. Low vitamin D status in both the mother and newborn baby increases the likelihood of developing autistic spectrum disorder by 54% (14).

Without sufficient nutrients not only do brain cells not make the connections but the production and flow of neurotransmitters doesn’t happen optimally. Bruce Ames, Emeritus professor of Biochemistry and Molecular Biology at the University of California, thinks that “serotonin synthesis, release, and function in the brain are modulated by vitamin D and the 2 marine omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).” He says that ”insufficient levels of vitamin D, EPA, or DHA, in combination with genetic factors and at key periods during development, would lead to dysfunctional serotonin activation and function and may be one underlying mechanism that contributes to neuropsychiatric disorders and depression in children”. (15) 

A study in Northern Ireland found that half of schoolchildren were deficient in vitamin D, with a level below 50nmol/l (I recommend above 75 nmol/l). Another finds that low vitamin D levels in childhood are related to behaviour problems in adolescence (16). Is it any wonder so many children are neurodivergent?

A placebo-controlled trial giving ADHD children magnesium together with vitamin D for eight weeks showed a major reduction in emotional, conduct and peer problems and improved socialisation compared with children treated with the placebo (17).

—

The bottom line – we all need to supplement vitamin D

The bottom line is everyone, from children to older people, and especially anyone considering pregnancy, suffering with low mood or memory problems, must test their vitamin D, ideally, at the start of winter to guide them as to what to supplement, during winter perhaps at 3 months, and 6 months later, to learn what amount of vitamin D supplementation they need in summer and winter.

In summary, you want to get your blood level above 75nmol/l (30 ng/ml) which usually means supplementing 3,000iu from October to March for those in the Northern Hemisphere. The optimal level is, however,  likely to be above 100nmol/l (40mg/ml).  Your need for vitamin D is likely to be greater if you are overweight and have darker skin and live further North.

When spring returns, and throughout summer, 1,000iu a day may be enough depending on your sun exposure.

Thank you for reading!
Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References

¹ Jayedi A, Rashidy-Pour A, Shab-Bidar S. Vitamin D status and risk of dementia and Alzheimer’s disease: A meta-analysis of dose-response †. Nutr Neurosci. 2019 Nov;22(11):750-759. doi: 10.1080/1028415X.2018.1436639. Epub 2018 Feb 15. PMID: 29447107

² Jorde R, Sneve M, Figenschau Y, Svartberg J, Waterloo K. Effects of vitamin D supplementation on symptoms of depression in overweight and obese subjects: randomized double blind trial. J Intern Med. 2008 Dec;264(6):599-609. doi: 10.1111/j.1365-2796.2008.02008.x. Epub 2008 Sep 10. PMID: 18793245.

³ Khoraminya N, Tehrani-Doost M, Jazayeri S, Hosseini A, Djazayery A. Therapeutic effects of vitamin D as adjunctive therapy to fluoxetine in patients with major depressive disorder. Aust N Z J Psychiatry. 2013 Mar;47(3):271-5. doi: 10.1177/0004867412465022. Epub 2012 Oct 23. PMID: 23093054. Xxxx check the some in 5 days

⁴ Mozaffari-Khosravi H, Nabizade L, Yassini-Ardakani SM, Hadinedoushan H, Barzegar K. The effect of 2 different single injections of high dose of vitamin D on improving the depression in depressed patients with vitamin D deficiency: a randomized clinical trial. J Clin Psychopharmacol. 2013 Jun;33(3):378-85. doi: 10.1097/JCP.0b013e31828f619a. PMID: 23609390.

⁵ Patrick RP, Ames BN. Vitamin D hormone regulates serotonin synthesis. Part 1: relevance for autism. FASEB J. 2014 Jun;28(6):2398-413. doi: 10.1096/fj.13-246546. Epub 2014 Feb 20. PMID: 24558199.

⁶ Lam RW, Levitt AJ, Levitan RD, Enns MW, Morehouse R, Michalak EE, Tam EM. The Can-SAD study: a randomized controlled trial of the effectiveness of light therapy and fluoxetine in patients with winter seasonal affective disorder. Am J Psychiatry. 2006 May;163(5):805-12. doi: 10.1176/ajp.2006.163.5.805. PMID: 16648320.Psychiary, No015

⁷ Kemény LV, Robinson KC, Hermann AL, Walker DM, Regan S, Yew YW, Lai YC, Theodosakis N, Rivera PD, Ding W, Yang L, Beyer T, Loh YE, Lo JA, van der Sande AAJ, Sarnie W, Kotler D, Hsiao JJ, Su MY, Kato S, Kotler J, Bilbo SD, Chopra V, Salomon MP, Shen S, Hoon DSB, Asgari MM, Wakeman SE, Nestler EJ, Fisher DE. Vitamin D deficiency exacerbates UV/endorphin and opioid addiction. Sci Adv. 2021 Jun 11;7(24):eabe4577. doi: 10.1126/sciadv.abe4577. PMID: 34117054; PMCID: PMC8195487.

⁸ Jayedi A, Rashidy-Pour A, Shab-Bidar S. Vitamin D status and risk of dementia and Alzheimer’s disease: A meta-analysis of dose-response †. Nutr Neurosci. 2019 Nov;22(11):750-759. doi: 10.1080/1028415X.2018.1436639. Epub 2018 Feb 15. PMID: 29447107

⁹ Chai B, Gao F, Wu R, Dong T, Gu C, Lin Q, Zhang Y. Vitamin D deficiency as a risk factor for dementia and Alzheimer’s disease: an updated meta-analysis. BMC Neurol. 2019 Nov 13;19(1):284. doi: 10.1186/s12883-019-1500-6. PMID: 31722673; PMCID: PMC6854782.

10 Jia J, Hu J, Huo X, Miao R, Zhang Y, Ma F. Effects of vitamin D supplementation on cognitive function and blood Aβ-related biomarkers in older adults with Alzheimer’s disease: a randomised, double-blind, placebo-controlled trial. J Neurol Neurosurg Psychiatry. 2019 Dec;90(12):1347-1352. doi: 10.1136/jnnp-2018-320199. Epub 2019 Jul 11. PMID: 31296588.

11 Feart C, Helmer C, Merle B, Herrmann FR, Annweiler C, Dartigues JF, Delcourt C, Samieri C. Associations of lower vitamin D concentrations with cognitive decline and long-term risk of dementia and Alzheimer’s disease in older adults. Alzheimers Dement. 2017 Nov;13(11):1207-1216. doi: 10.1016/j.jalz.2017.03.003. Epub 2017 May 16. PMID: 28522216.

12 Ghahremani M, Smith EE, Chen HY, Creese B, Goodarzi Z, Ismail Z. Vitamin D supplementation and incident dementia: Effects of sex, APOE, and baseline cognitive status. Alzheimers Dement (Amst). 2023 Mar 1;15(1):e12404. doi: 10.1002/dad2.12404. PMID: 36874594; PMCID: PMC9976297.

13 Marek K, Cichoń N, Saluk-Bijak J, Bijak M, Miller E. The Role of Vitamin D in Stroke Prevention and the Effects of Its Supplementation for Post-Stroke Rehabilitation: A Narrative Review. Nutrients. 2022 Jul 4;14(13):2761. doi: 10.3390/nu14132761. PMID: 35807941; PMCID: PMC9268813.

14 Wang Z, Ding R, Wang J. The Association between Vitamin D Status and Autism Spectrum Disorder (ASD): A Systematic Review and Meta-Analysis. Nutrients. 2020 Dec 29;13(1):86. doi: 10.3390/nu13010086. PMID: 33383952; PMCID: PMC7824115.

15 Patrick RP, Ames BN. Vitamin D and the omega-3 fatty acids control serotonin synthesis and action, part 2: relevance for ADHD, bipolar disorder, schizophrenia, and impulsive behavior. FASEB J. 2015 Jun;29(6):2207-22. doi: 10.1096/fj.14-268342. Epub 2015 Feb 24. PMID: 25713056.

16 Sonia L Robinson, Constanza Marín, Henry Oliveros, Mercedes Mora-Plazas, Betsy Lozoff, Eduardo Villamor, Vitamin D Deficiency in Middle Childhood Is Related to Behavior Problems in Adolescence, The Journal of Nutrition, Volume 150, Issue 1,

2020, Pages 140-148, ISSN 0022-3166, https://doi.org/10.1093/jn/nxz185.

17 Hemamy M, Pahlavani N, Amanollahi A, Islam SMS, McVicar J, Askari G, Malekahmadi M. The effect of vitamin D and magnesium supplementation on the mental health status of attention-deficit hyperactive children: a randomized controlled trial. BMC Pediatr. 2021 Apr 17;21(1):178. doi: 10.1186/s12887-021-02631-1. Erratum in: BMC Pediatr. 2021 May 12;21(1):230. PMID: 33865361; PMCID: PMC8052751.

By Patrick Holford

What does any animal, perhaps your dog, do after exercising or going for a walk?

Sleep.

Sleep is how the brain recovers. There is now overwhelming evidence that sleep is a ‘brain essential’ and just like Goldilocks, it seems we need just the right amount. Getting too much, or too little, increases our risk for cognitive decline.

The optimal amount of sleep for brain health appears to be a total of seven hours. This does not necessarily need to be in one uninterrupted stretch – a study found that napping after physical activity can reduce the risk of cognitive impairment (1).

However, those consistently getting less than seven hours of sleep may be doubling their risk of age-related cognitive decline (2). A UK study of Whitehall civil servants, which began in the 1980s, found that persistent short sleep at ages 50, 60, and 70 was associated with a 30% increased risk of dementia (3). Sleep loss does not just increase long-term dementia risk – it also reduces empathy, increases negative emotions, and impairs next-day functioning (4).

Why Sleep Is Essential to Brain Health?

Think of sleep as the brain’s housekeeper. During sleep, circulation of blood and cerebrospinal fluid improves, helping to clear out waste products from brain metabolism (5). These include harmful oxidants and amyloid protein, the latter linked to Alzheimer’s and brain inflammation – which can begin accumulating after just one night of poor sleep (6).

One key agent in this nightly brain cleanse is melatonin. As night falls, our brains convert serotonin into melatonin, primarily in the pineal gland – referred to by Descartes as the seat of the soul, and known in yoga as the ‘third eye’ chakra.

Sensitive to light via receptors behind the eyes, the pineal gland is the only endocrine organ in direct contact with the external world. Darkness triggers melatonin production, while exposure to light – including screen use before bed – suppresses it.

Melatonin helps keep us in sync with the circadian cycle. Some frequent flyers even use melatonin supplements to overcome jet lag and adjust their sleep rhythms more easily (7).

More than just a sleep aid, melatonin acts as a powerful antioxidant – disarming damaging oxidants, restoring mitochondrial energy production, and acting as an anti-inflammatory. It has been used to support recovery in cancer, COVID-19, and cardiovascular conditions (8,9). Reduced brain melatonin levels and circadian disruption are also observed in individuals with cognitive decline.

Why Dreaming Matters?

Sleep isn’t just for rest – it’s a deeply active process. About 30 minutes after falling asleep, we enter deep sleep, marked by slower breathing, a reduced heart rate, and lower blood pressure. This phase restores and repairs bodily tissues. About 90 minutes in, we shift into REM (rapid eye movement) sleep – where most dreaming occurs.

REM sleep is critical for brain health. Each night, we cycle between deep, light, and REM sleep three to five times, with REM ideally making up about 25% of total sleep.

REM and deep sleep phases also see increased production of growth hormone, which supports tissue repair. Meanwhile, melatonin helps clear metabolic waste. However, under stress, cortisol levels rise and suppress REM sleep and growth hormone production, reducing the brain’s ability to recover. Sleep-deprived individuals tend to experience more REM when they finally do sleep, suggesting REM plays a key role in emotional processing.

One theory suggests that dreams help us metabolise suppressed emotions – fear, anger, sadness – stored during our busy days. If you have a vivid, emotional dream, it may be worth tracing it back to unresolved feelings from the previous day.

How Chronic Stress Disrupts Sleep and Brain Function?

Chronic or intense stress – such as bereavement, illness, or financial strain – has been shown to increase the risk of cognitive decline and dementia (10). However, good sleep can help process a stressful day.

The perception of control matters, too. Studies show that high job demands combined with low control are strongly linked to an increased risk of depression and cognitive impairment (11). Examples might include caregiving for a loved one with dementia while navigating health services, or working in a high-stress job without the resources to make meaningful changes.

Your Brain on Cortisol: The Hippocampus Feedback Loop

Two hormones mediate stress: adrenaline (short-acting) and cortisol (longer-acting). Adrenaline prepares you to act quickly – it’s the fight-or-flight hormone. Cortisol helps regulate energy and alertness throughout the day.

In the morning, cortisol naturally rises to get us going. It should fall in the evening to support sleep. But chronic stress disrupts this rhythm. If cortisol stays high at night, sleep is disturbed. If it’s too low in the morning, you may feel foggy and reach for caffeine.

Excess cortisol impairs memory, slows thinking, lowers social functioning, and raises the risk of dementia (12). What’s happening in the brain is that cortisol overstimulates the hippocampus, which is responsible for memory and emotional regulation. With prolonged stress, this feedback loop fails – the hippocampus shrinks, and cortisol levels remain elevated, accelerating brain ageing.

Short-Term Relief, Long-Term Harm: Sugar and Alcohol as Stress Crutches

Oscar Ichazo described how we reach for compensations under stress. Unfortunately, many – like alcohol and sugar – backfire.

Alcohol temporarily boosts GABA, calming the nervous system and reducing adrenaline. But the effect is short-lived. Drinking too much reduces GABA receptor sensitivity the next day, leaving us more anxious. In the long term, alcohol is neurotoxic and increases dementia risk (12). It also disrupts sleep architecture, impairing the brain’s ability to repair itself.

Sugar triggers dopamine and activates the brain’s reward circuits, making us crave more. It also spikes the adrenal system, amplifying stress and cortisol levels (13). Fats and proteins do not have this effect – this is unique to sugar.

So, when we use sugar or alcohol to manage stress, we often wake up feeling more anxious and foggy. This leads us to reach for caffeine and more sugar, which spikes cortisol again, leaving us even more depleted by evening – creating a cycle of stress, poor sleep, and accelerated brain ageing.

Simple Ways to Break the Cycle

The good news? You can reverse this pattern. Start here:

Become a FRIEND and get access to your personalised COGNITION® programme which which includes:
– A whole module dedicated to sleep and calm
– Another focused on helping you reduce sugar
– Plus monthly live group coaching to help you stay focused and on track
Prioritise seven hours of quality sleep each night.
Identify and reduce common stress triggers.
Be mindful of alcohol and sugar intake.
Find positive outlets: yoga, walking, journaling, a good book – like Upgrade Your Brain.

–

Thank you for reading!
Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

———

References:

¹ Qian YX, Ma QH, Sun HP, Xu Y, Pan CW. Combined effect of three common lifestyle factors on cognitive impairment among older Chinese adults: a community-based, cross-sectional survey. Psychogeriatrics. 2020 Nov;20(6):844-849. doi: 10.1111/psyg.12604. Epub 2020 Aug 31. PMID: 32869429.

² Bubu OM, Brannick M, Mortimer J, Umasabor-Bubu O, Sebastião YV, Wen Y, Schwartz S, Borenstein AR, Wu Y, Morgan D, Anderson WM. Sleep, Cognitive impairment, and Alzheimer’s disease: A Systematic Review and Meta-Analysis. Sleep. 2017 Jan 1;40(1). doi: 10.1093/sleep/zsw032. PMID: 28364458.

³ Sabia S, Fayosse A, Dumurgier J, van Hees VT, Paquet C, Sommerlad A, Kivimäki M, Dugravot A, Singh-Manoux A. Association of sleep duration in middle and old age with incidence of dementia. Nat Commun. 2021 Apr 20;12(1):2289. doi: 10.1038/s41467-021-22354-2. PMID: 33879784; PMCID: PMC8058039.

⁴ Krause AJ, Simon EB, Mander BA, Greer SM, Saletin JM, Goldstein-Piekarski AN, Walker MP. The sleep-deprived human brain. Nat Rev Neurosci. 2017 Jul;18(7):404-418. doi: 10.1038/nrn.2017.55. Epub 2017 May 18. PMID: 28515433; PMCID: PMC6143346.

5⁶ Xie L, Kang H, Xu Q, Chen MJ, Liao Y, Thiyagarajan M, O’Donnell J, Christensen DJ, Nicholson C, Iliff JJ, Takano T, Deane R, Nedergaard M. Sleep drives metabolite clearance from the adult brain. Science. 2013 Oct 18;342(6156):373-7. doi: 10.1126/science.1241224. PMID: 24136970; PMCID: PMC3880190.

⁶ Shokri-Kojori E, Wang GJ, Wiers CE, Demiral SB, Guo M, Kim SW, Lindgren E, Ramirez V, Zehra A, Freeman C, Miller G, Manza P, Srivastava T, De Santi S, Tomasi D, Benveniste H, Volkow ND. β-Amyloid accumulation in the human brain after one night of sleep deprivation. Proc Natl Acad Sci U S A. 2018 Apr 24;115(17):4483-4488. doi: 10.1073/pnas.1721694115. Epub 2018 Apr 9. PMID: 29632177; PMCID: PMC5924922.

⁷ Herxheimer A, Petrie KJ. Melatonin for the prevention and treatment of jet lag. Cochrane Database Syst Rev. 2002;(2):CD001520. doi: 10.1002/14651858.CD001520. PMID: 12076414.

⁸ Keithahn C, Lerchl A. 5-hydroxytryptophan is a more potent in vitro hydroxyl radical scavenger than melatonin or vitamin C. J Pineal Res. 2005 Jan;38(1):62-6. doi: 10.1111/j.1600-079X.2004.00177.x. PMID: 15617538.

⁹ Chitimus DM, Popescu MR, Voiculescu SE, Panaitescu AM, Pavel B, Zagrean L, Zagrean AM. Melatonin’s Impact on Antioxidative and Anti-Inflammatory Reprogramming in Homeostasis and Disease. Biomolecules. 2020 Aug 20;10(9):1211. doi: 10.3390/biom10091211. PMID: 32825327; PMCID: PMC7563541; regarding covid see also Tan DX, Reiter RJ. Mechanisms and clinical evidence to support melatonin’s use in severe COVID-19 patients to lower mortality. Life Sci. 2022 Apr 1;294:120368. doi: 10.1016/j.lfs.2022.120368. Epub 2022 Jan 30. PMID: 35108568; PMCID: PMC8800937.; see also Begum R, Mamun-Or-Rashid ANM, Lucy TT, Pramanik MK, Sil BK, Mukerjee N, Tagde P, Yagi M, Yonei Y. Potential Therapeutic Approach of Melatonin against Omicron and Some Other Variants of SARS-CoV-2. Molecules. 2022 Oct 16;27(20):6934. doi: 10.3390/molecules27206934. PMID: 36296527; PMCID: PMC9609612.; regarding cancer see Reiter RJ, Rosales-Corral SA, Tan DX, Acuna-Castroviejo D, Qin L, Yang SF, Xu K. Melatonin, a Full Service Anti-Cancer Agent: Inhibition of Initiation, Progression and Metastasis. Int J Mol Sci. 2017 Apr 17;18(4):843. doi: 10.3390/ijms18040843. PMID: 28420185; PMCID: PMC5412427.

¹0 Franks KH, Bransby L, Saling MM, Pase MP. Association of Stress with Risk of Dementia and Mild Cognitive Impairment: A Systematic Review and Meta-Analysis. J Alzheimers Dis. 2021;82(4):1573-1590. doi: 10.3233/JAD-210094. PMID: 34366334.

¹1 Wang HX, Wahlberg M, Karp A, Winblad B, Fratiglioni L. Psychosocial stress at work is associated with increased dementia risk in late life. Alzheimers Dement. 2012;8(2):114-20. doi: 10.1016/j.jalz.2011.03.001. PMID: 22404853; see also Gonzalez-Mulé, E., & Cockburn, B. S. (2021). This job is (literally) killing me: A moderated-mediated model linking work characteristics to mortality. Journal of Applied Psychology, 106(1), 140–151. https://doi.org/10.1037/apl0000501; see also Gonzalez-Mulé E, Kim MM, Ryu JW. A meta-analytic test of multiplicative and additive models of job demands, resources, and stress. J Appl Psychol. 2021 Sep;106(9):1391-1411. doi: 10.1037/apl0000840. Epub 2020 Sep 21. PMID: 32955269.

¹2 Ouanes S, Popp J. High Cortisol and the Risk of Dementia and Alzheimer’s Disease: A Review of the Literature. Front Aging Neurosci. 2019 Mar 1;11:43. doi: 10.3389/fnagi.2019.00043. PMID: 30881301; PMCID: PMC6405479.¹3 Gonzalez-Bono E, Rohleder N, Hellhammer DH, Salvador A, Kirschbaum C. Glucose but not protein or fat load amplifies the cortisol response to psychosocial stress. Horm Behav. 2002 May;41(3):328-33. doi: 10.1006/hbeh.2002.1766. PMID: 11971667.

Keeping our brain’s structure and neural network healthy may seem like a mystery at times, but often the best advice is simple: ‘use it or lose it!’

The exercise and stimulation your brain gets from an active physical, social and intellectual lifestyle is vital to keeping it healthy. Just like our bodies need movement and exercise to function well, our brains need their own workout to thrive, too.

Lifestyle expert at Food for the Brain, Assistant Professor Tommy Wood, from the University of Washington has advised people at the top of their game, from Formula 1 drivers and Olympians to world champions, on how to maximise their performance, both mentally and physically.  His top tip for keeping our brains sharp?  

“In short, use it or lose it. The brain is an amazing organ, and it’s more resilient and adaptable than we’ve been led to believe. I’m sure you’ve heard that adults have a fixed amount of brain cells. Then, as we get older (or every time we take a sip of wine) we “lose” some of those brain cells as part of an unstoppable decline towards dementia or Alzheimer’s disease.”

“That’s not necessarily true” says Professor Wood. “I like to think about the brain like I think about muscles. In order to grow our muscles, we need to provide a stimulus – like lifting weights in the gym – followed by a period of rest. The opposite also happens – if we stop going to the gym or if we stop using a limb after breaking a bone – our muscles get smaller. Most have experienced this personally, and there’s every indication that your cognitive “muscle” behaves in the same way.”

A classic example of this is a study of London taxi drivers in training who have to learn ‘The Knowledge’. Many spend three years driving the 25,000 streets of London, logging up tens of thousands of miles, on foot or on a scooter. Not all pass the first time. Katherine Woollett at University College London decided to find out if acquiring the knowledge actually changed a person’s brain by measuring the density of grey matter as an indicator of brain volume. About half of her group of training taxi drivers passed first time and the other half failed. She also had a control group of people of the same age, most in their late 30’s with similar other demographics such as IQ. Sure enough, those who passed had increased their brain density of grey matter, and specifically in the central hippocampus area most associated with cognitive resilience. (1)

Keep Cognitively Active

There’s a pattern in our society – we are meant to learn every day as we go through school in childhood and teenage years, then we get a job, which, past a training phase, may not require much more learning, then around 65 we are meant to retire, with no more ‘need’ to work or learn.

Every indicator that you can think of – leaving school early, having a lower educational standard (2), or retiring early (3), has been associated with an increasing risk of cognitive decline.

When Professor May Beydoun, at the US National Institutes of Health (NIH) did a comprehensive study of the biggest risk factors for developing Alzheimer’s, she attributed 24% of risk to educational status and 32% of risk to physical activity(4). So, using our brains, reflected in educational and physical activity, is a huge part of keeping your brain healthy. (It’s worth remembering that  omega-3/seafood and homocysteine-lowering B vitamins account for 22% each while smoking racks up 31% in the risk stakes).

Think about how you use your mind. How much time do you spend stimulated, learning something? How much time do you spend engaged in relatively mindless mental activities? 

Television can be stimulating, or mind-numbing – engaging your attention but not really making you think. Social media activity, like scrolling through TikTok or Instagram, could be mind-numbing, while digital engagement with others could be stimulating. A simple yardstick is to ask ‘am I learning anything? Am I using my mind?’ 

While these activities are keeping your brain busy, what our brains really needs is to be engaged in learning or working something out, ideally without too much stress. Many films are designed to engage you by stimulating a stress response, keeping you on the edge of our seat. On the other hand, doing Wordle or a crossword, or playing a game of backgammon or chess involves concentration and thinking without cranking up your stress response. 

Two high-rating apps designed to engage our minds Brain HQ and Lumosity. Brain HQ (www.brainhq.com) adapts according to your needs – do you want better memory, better attention or faster processing? Three 20-minute sessions weekly are recommended. Lumosity (www.lumosity.com) is also adaptive and achieves much the same improvement in cognition. In just the same way you become physically fitter by increasing the duration or intensity of an exercise, it seems the same is true with your mind.

Reading books, or listening to podcasts can also be a great way to stimulate the old grey matter, mind but it does depend on what you are reading or listening to. The golden question is  ‘am I learning anything from this?’. Even better – join a bookclub for the social stimulation, sharing views, hearing others, and working out where you stand. 

Learn by failing

Land on any social media platform and we are bombarded with stories of people succeeding, urging us to try the latest self-help, diet or exercise programme, meditation or music app (who didn’t try and learn the guitar in lockdown!) but failure, according to Professor Tommy Wood, is when the magic really happens for our brains:

“Failure constitutes protective cognitive demand. The cocktail of hormones released as we try, fail, repeat, and learn, provides the ideal environment for the brain to grow and adapt. This is a real sticking point for improving brain health – as adults we hate the feeling of being bad at something.”

Professor Wood recommends picking an activity that’s truly challenging. “Cognitive demand requires failure, so pick something you’ll be bad at initially. What’s cognitively challenging is personal, but learning a new language is better than sudoku, picking up a guitar is better than listening to music, building model airplanes is probably better than reading the news, and playing chess is definitely better than scrolling through Instagram. As you get better, add challenges to keep stimulating your brain.”

“A fascinating study looked at the brains of musicians.  While both professional and amateur musicians’ brains looked younger compared to non-musicians of the same age, the benefit was greatest in amateur musicians (5) – it’s harder, so they got more benefit. The cocktail of hormones released as we try, fail, repeat, and learn, provides the ideal environment for the brain to grow and adapt.”

In fact, learning an instrument, or a language, are considered heavy lifters when it comes to brain stimulation – it’s challenging and can take a long time to become completely proficient. But every step along the way, even just a few minutes a day, learning new words, processing the grammar, learning chords and finger positions, is a significant mental challenge.  And there are so many language learning apps, like DuoLingo now, playing on the ‘reward’ and game theory to keep us cognitively engaged and coming back for more. 

Speaking two languages is not only associated with less risk of cognitive decline but, according to one study, ‘the neuroprotective effects of lifelong bilingualism act both against neurodegenerative processes and through the modulation of brain networks connectivity.’ (6) Your brain ends up more connected – literally hardwired for brain health.

Keep physically active

The brain also benefits from physical exercise, especially if it involves complex movements and learning – think dance, yoga or t’ai chi or trail running or walking on uneven surfaces. The brain is processing a lot of information, triggering patterns of muscle movement, keeping you in balance. You want a bit of both – movement and balance. Just working out on a fixed machine or walking on a flat, straight, tarmacked path, is not nearly as challenging as hill walking up an uneven path, cycling, surfing, skateboarding or anything where your body is micro-adjusting to keep you in balance.

One study of retired people assigned to walk briskly for 40 minutes three times a week showed increased hippocampal brain volume (7).  Another study showed benefits from doing one or two sessions of resistance or strength training twice a week (8).

Of all the measures relating to how fit or fat we are, muscle mass best predicts brain volume and risk of cognitive decline in later years. 

One big study from the UK Biobank data found that those with a lower fat-to-muscle ratio) in their legs had around 40% less risk for dementia later in life (9). Muscle uses energy and ‘soaks up’ glucose. This helps keep your blood sugar stable and prevent insulin resistance. Often, as we age, it can seem like an uphill battle to keep our weight down, even if we are not eating any more than we used to. This is often simply because we’ve lost muscle mass with age. So hitting those weights can be extra beneficial in later years and many gyms offer classes especially for older clients. Even body weight exercise can build resistance, though, and there are plenty of free videos on the internet – just check with your GP first.

Step it up

A good general guideline is to aim for 30 minutes of brisk walking every day. Some days you may do none and others twice this, so this is a good weekly average to shoot for. Over time you can step it up by walking faster, jogging or including some hills in your circuit. 

A good way to monitor and up our exercise level is to count steps. Smart phones and watches have apps that do this for you. Shoot for increasing daily steps between 10% and 20% a week. If you start at 2,000 and add 200 steps per day each week, that’s a great start. If you’re at 4,000 steps already then getting up to 4,400 daily in this week is also going to stimulate our muscles and brains. While 8,000 steps a day is considered optimal, what’s much more important is to make sustainable improvements as you ‘activate’ your lifestyle.

But, we don’t need to limit ourselves to ‘exercise’. Gardening, mowing the lawn, playing a sport, vigorous cleaning, or clearing out a yard – anything that gives us a faster heart rate, a bit of sweat and engages different sets of muscles, thus including ‘resistance’(10), counts as well, especially if we can do them faster or more energetically.

Aerobic plus resistance exercise anti-ages your brain

As previously mentioned, of all the measures relating to how fit or fat we are, muscle mass best predicts brain volume and risk of cognitive decline in later years. 

Including exercise that helps build and maintain muscle tone correlates most strongly with brain health. A good weekly guideline is to include two resistance training sessions a week. Perhaps you are a member of a gym, go to a pilates or yoga class or have some equipment at home for your own workout.

If you’re not sure where to start, “Burn Fat Fast” (Piatkus, 2013), written by Patrick Holford and exercise guru and former Gladiator (Zodiac) Kate Staples, is a great resource.  Staples devised a series of strength building exercises that anyone can do at home in eight minutes, three times a week, including  beginner version, and intermediate and advanced versions (light to medium weight dumbbells (2kg – 6kg) are needed for these).

The exercises are all explained in the book and  Kate Staples demonstrates each one HERE so you can follow along until you feel comfortable. A five minute warm-up (marching on the spot is great, or stepping side to side) will get your heart rate up and help avoid injury. 

The beginner sequence includes wall sits and reverse lunges, while the advance sequence progresses to jumping squats and mountain climbers. It’s important to build up gradually, keep hydrated, and learn to do the moves safely, so watching the videos is a great way to get started. 

The secret is to find an activity that engages both mind and body, builds muscle, and is not too repetitive. As an example, our very own Patrick Holford says “I’ve taken up paragliding, and qualified at the age of 65. I had to pass an exam on meteorology, aerodynamics and air law, and failed the first time, but now I have to think about these things before and during flight. Then there’s the exercise of carrying an 11 kg pack up a mountain, and the balance and strength and adjustments my brain is having to make to keep the canopy stable even before take off.” This may not be your thing but it shows how one activity can tick so many brain boxes. It is good to learn new sports for this very reason.

Be Social

A lack of meaningful social interaction, and loneliness, is also a major driver of both low mood and cognitive decline later in life (11). 

How often do you go to social gatherings, meet new people and have engaging conversations? This could be meeting friends, going to the movies, a museum, a gallery, a show, church or temple, or a restaurant?

There are times in your lives where you might find yourself more isolated. For example, when relationships break up and you lose connection with ‘their’ friends, or if a partner dies and most of your social interaction was with them. These are extremely challenging times, but facing our fears and getting out there to meet friends can help us on the road to recovery. 

Unset your mind

It’s all too easy to get locked into routines that remove any form of challenging social interaction yet this is not only how we learn, it also nourishes the social aspect of who we are. A good strategy is to make sure you have a significant social event or interaction every week, starting with this week.

As we age, and friends move away, or pass on, it’s important to find ways to expose ourselves to new ideas and new ways of thinking and feeling differently and swapping ideas. Travelling and exploring other cultures can be an incredibly enriching way to broaden our mindset and there are lots of companies that cater for the solo traveller these days.

But there’s no need to go far from home to get the benefits of brain gain. There are many opportunities to ‘use it or lose it’, for example, volunteering at a local garden or school or supporting the local arts club. The brain boost from being out of your comfort zone will reap dividends, whether it’s joining a group of new people, engaging in a new activity you’ve never tried, like drawing, writing or yoga – or even just catching up with old friends you haven’t seen for ages, or striking up a conversation with someone you meet on the daily dog walk.

Local bookshops, art centres, churches or schools can be great sources of information, so check them out. 

Be inquisitive

As Tommy Wood says “The key is to push right at the boundaries of what you’re capable of – with occasional failure showing that you’re at the right level of difficulty. Keep at it, and you’ll be more likely to be healthy and sharp for decades to come.”

And if you want more personalised information on how you can improve and support your brain through nutrition and lifestyle changes then make sure you complete our Cognitive Function Test. A FREE, online and validated test to assess your current cognitive function and dementia risk and then get a clear plan of action on how you can improve your brain health and score over the next 6 months.

—-

Thank you for reading!
Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References:

¹ Woollett K, Maguire EA. Acquiring “the Knowledge” of London’s layout drives structural brain changes. Current biology: CB. 2011;21(24):2109-14. Epub 2011/12/08. doi: 0.1016/j.cub.2011.11.018. PubMed PMID: 22169537.

² Yu JT, Xu W, Tan CC, Andrieu S, Suckling J, Evangelou E, Pan A, Zhang C, Jia J, Feng L, Kua EH, Wang YJ, Wang HF, Tan MS, Li JQ, Hou XH, Wan Y, Tan L, Mok V, Tan L, Dong Q, Touchon J, Gauthier S, Aisen PS, Vellas B. Evidence-based prevention of Alzheimer’s disease: systematic review and meta-analysis of 243 observational prospective studies and 153 randomised controlled trials. J Neurol Neurosurg Psychiatry. 2020;91(11):1201-9. Epub 2020/07/22. doi: 10.1136/jnnp-2019-321913. PubMed PMID: 32690803; PMCID: PMC7569385.

³ Hale JM, Bijlsma MJ, Lorenti A. Does postponing retirement affect cognitive function? A counterfactual experiment to disentangle life course risk factors. SSM – Population Health. 2021;15:100855. doi: https://doi.org/10.1016/j.ssmph.2021.100855; see also Dufouil C, Pereira E, Chêne G, Glymour MM, Alpérovitch A, Saubusse E, Risse- Fleury M, Heuls B, Salord JC, Brieu MA, Forette F. Older age at retirement is associated with decreased risk of dementia. Eur J Epidemiol. 2014;29(5):353-61. Epub 2014/05/06. doi: 10.1007/s10654-014-9906-3. PubMed PMID: 24791704.

⁴ Beydoun MA, Beydoun HA, Gamaldo AA, Teel A, Zonderman AB, Wang Y. Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis. BMC Public Health. 2014 Jun 24;14:643. doi: 10.1186/1471-2458-14-643. PMID: 24962204; PMCID: PMC4099157.

⁵ Erickson KI, Voss MW, Prakash RS, Basak C, Szabo A, Chaddock L, Kim JS, Heo S, Alves H, White SM, Wojcicki TR, Mailey E, Vieira VJ, Martin SA, Pence BD, Woods JA, McAuley E, Kramer AF. Exercise training increases size of hippocampus and improves memory. Proceedings of the National Academy of Sciences. 2011;108(7):3017. doi: 10.1073/pnas.1015950108.

⁶ Sala A, Malpetti M, Farsad M, Lubian F, Magnani G, Frasca Polara G, Epiney JB, Abutalebi J, Assal F, Garibotto V, Perani D. Lifelong bilingualism and mechanisms of neuroprotection in Alzheimer dementia. Hum Brain Mapp. 2022;43(2):581-92. Epub 2021/11/04. doi: 10.1002/hbm.25605. PubMed PMID: 34729858; PMCID: PMC8720191.

⁷ Ludyga S, Gerber M, Pühse U, Looser VN, Kamijo K. Systematic review and meta- analysis investigating moderators of long-term effects of exercise on cognition in healthy individuals. Nature Human Behaviour. 2020;4(6):603-12. doi: 10.1038/s41562-020-0851-8.

⁸ Herold F, Törpel A, Schega L, Müller NG. Functional and/or structural brain changes in response to resistance exercises and resistance training lead to cognitive improvements – a systematic review. Eur Rev Aging Phys Act. 2019;16:10. Epub 2019/07/25. doi: 10.1186/s11556-019-0217-2. PubMed PMID: 31333805; PMCID: PMC6617693.

⁹ Wang W, Luo Y, Zhuang Z, Song Z, Huang N, Li Y, Dong X, Xiao W, Zhao Y, Huang T. Total and regional fat-to-muscle mass ratio and risks of incident all-cause dementia, Alzheimer’s disease, and vascular dementia. J Cachexia Sarcopenia Muscle. 2022 Oct;13(5):2447-2455. doi: 10.1002/jcsm.13054. Epub 2022 Jul 20. PMID: 35856185; PMCID: PMC9530585.

¹⁰0 Gallardo-Gómez D, Del Pozo-Cruz J, Noetel M, Álvarez-Barbosa F, Alfonso-Rosa RM, Del Pozo Cruz B. Optimal dose and type of exercise to improve cognitive function in older adults: A systematic review and bayesian model-based network meta-analysis of RCTs. Ageing Res Rev. 2022 Apr;76:101591. doi: 10.1016/j.arr.2022.101591. Epub 2022 Feb 17. PMID: 35182742.

¹¹1 Penninkilampi R, Casey AN, Singh MF, Brodaty H. The Association between Social Engagement, Loneliness, and Risk of Dementia: A Systematic Review and Meta-Analysis. J Alzheimers Dis. 2018;66(4):1619-33. Epub 2018/11/20. doi: 10.3233/jad- PubMed PMID: 30452410.

Dopamine and the Brain: Is Modern Life Hijacking Your Reward System?

By Patrick Holford. In this article, we explore the important relationship between dopamine and the brain.

We already know that today’s diet is low in brain-friendly fats and nutrients and high in sugar and ultra-processed food. It’s likely shrinking our brains, dumbing us down, and driving the rise in mental health problems. But diet isn’t the only thing engineering our mental decline. Tech, sugar, caffeine and alcohol are all pulling the same lever in your brain: dopamine.

Dopamine makes us want the reward. It isn’t what makes us enjoy it. It drives the urge to check, eat, drink or scroll again. That distinction matters, because marketers behind our food, phones and drinks have got very good at triggering the itch without ever satisfying it. That’s why you can eat a whole packet of biscuits, or scroll for an hour, and still feel restless afterwards.

The mechanism: variable reward

This was first identified in the 1930s by psychologist B.F. Skinner. He found that mice responded most frequently to a reward-associated lever when rewards arrived unpredictably. The mouse never knew which press would pay off. We’re wired the same way: if a reward feels random, and checking for it costs us nothing, we end up checking compulsively. It’s the exact mechanism behind a fruit machine, and it’s the exact mechanism behind your phone’s notification badge.

This manipulation of the brain’s stress-and-reward response is one of its oldest systems: essential for survival, but also what makes us impulsive, manipulable, and, frankly, easier to sell to. Multinational companies have learned to get us neurochemically hooked on their products. They use the language of happiness to sell us pleasure: the happy hour, the happy meal, happiness in a can. But joy and contentment are governed by serotonin, not sugar or a special offer, and chasing dopamine too hard actively undermines it. This relationship between dopamine and the brain helps explain why repeated rewards can become so difficult to resist.

Dopamine, pleasure and the brain hijack

“The more pleasure you seek, the more unhappy you get,” says Professor Robert Lustig, author of The Hacking of the American Mind. Too much dopamine suppresses serotonin, leaving you feeling flat, restless or low once the initial hit fades. He describes this constant cycle of stimulation and reward-seeking as a kind of “brain hijack”, and one possible piece of a much bigger mental health picture. And that picture is concerning: in England, 92.6 million antidepressant items were dispensed in 2024/25 alone, up almost 4% on the year before,[1] while in the US, 19.3% of adults reported taking prescription medication for their mental health in 2024.[2]

“We are the most in debt, the most obese, the most medicated and the most drugged-up adult population in human history,” Lustig argues. We’ve learned to fool our own brains. In doing so, we’ve fooled ourselves by engineering addictive foods and behaviours around us.

Sugar, dopamine and the brain: not so different from cocaine

Sugar stimulates dopamine and endorphins in much the same way as cocaine and heroin. It triggers the reward system and, with overuse, can lead to reward deficiency, where you need more to feel the same lift.[3] Dr Candace Pert, the neuroscientist who discovered the opiate receptor, was among the first to say this outright: “I consider sugar to be a drug, a highly purified plant product that can become addictive. Relying on an artificial form of glucose, sugar, to give us a quick pick-me-up is analogous to, if not as dangerous as, shooting heroin.”[4] That was heresy when she said it. It’s now closer to conventional wisdom, but it’s still not sugar acting alone.

Why sugar and fat are a powerful combination

Neuropharmacologist Professor Paul Kenny discovered the real driver almost by accident, feeding rats different diets in his Mount Sinai lab. Rats fed only sugary food, or only fatty food, barely gained weight: they self-regulated. But rats fed a 50/50 combination of sugar and fat, the cheesecake diet, “dive head first into a slice and gorge so vigorously that it covered its fur in blobs.” They kept eating as if the “I’m full” switch had stopped working, stopped exercising, and gained significant weight within a week.[5] When Kenny then offered them an electric shock as a warning before the food arrived, rats on a normal diet fled. The cheesecake rats ignored the shock and kept eating anyway; their reward-seeking had overridden their own self-preservation.

Dopamine resistance and food addiction

This is the pattern behind food addiction more broadly. In some people, the reward system becomes so overstimulated that it overpowers the normal “stop eating” signal. As with alcohol and drugs, the more you have, the more you need, and dopamine receptors gradually shut down in response, a cycle researchers call dopamine resistance. People with fewer dopamine D2 receptors are, in fact, at greater genetic risk of both obesity and addiction. So if this feels like an uphill battle for you specifically, that’s not just willpower.[6,7] Counter-intuitively, some studies suggest people people with a higher weight respond less strongly to food reward, not more. This means they may need to eat more just to feel the same lift a leaner person gets from less.

No single ingredient drives this as reliably as the fat-and-sugar combination together, at high calorie density.[8,9] Think biscuits, doughnuts, chocolate, ice cream, cakes and many fast ultra processed foods. Nature simply doesn’t produce foods like this; only manufacturing does.

Sugary drinks exploit the reward system in a slightly different way. The same logic explains a can of cola. Caffeine, sugar and salt combined to make you drink more, with fructose (rather than glucose) doing extra work, because your body is slower to register “enough” from fructose, so you keep consuming past the point you’d normally stop. That’s also why fructose, often as high-fructose corn syrup, has quietly become the default sweetener in ultra-processed food.

Are you addicted to your smartphone? Dopamine and the brain in the digital age

Of everything that’s changed this century, the digital revolution has reshaped daily life most completely. It has changed not just what we do, but the sheer pace we live at. People everywhere are sleeping less, resting less, and burning out faster, and it shows up in rising work absence, anxiety and depression, especially in cities.

Phone-checking estimates vary enormously depending on who’s asking and how. A 2026 US survey put the average at 186 checks a day, down from 205 the year before, roughly once every five minutes of waking time.[10] A separate, larger commercial survey in 2022 put the figure far higher, at 352 checks a day, up from just 96 in the same survey’s 2019 run.[11] The truth is that “checks per day” is measured differently by almost everyone who studies it, so treat any single number as an illustration of scale rather than a precise fact; the honest takeaway is that the frequency has clearly risen, by a lot, in a few years.

How smartphones keep us checking

Whatever the exact count, the direction is the same. Our phones have become almost constant companions, including at moments we’d probably rather they weren’t. A 2026 study published in JAMA Pediatrics found that over 70% of parents and nearly 70% of children used a phone or other digital device during their family’s most recent meal together.[12] What’s better established: separate UK research from January 2025 found 81% of Britons reach for their phone as one of the first things they do after waking,[13] and a May 2025 US survey found 43% of adults use their phone within ten minutes of trying to fall asleep, and 44% within ten minutes of waking, rising to around 60% among under-30s.[14]

Social media, dopamine and the brain reward loop

Why does it work so well? To sell things. “I feel tremendous guilt,” Chamath Palihapitiya, Facebook’s former Vice President of User Growth, told an audience of Stanford students. “The short-term, dopamine-driven feedback loops that we have created are destroying how society works.” Every major platform is built the same way. It captures your attention, then serves ads tailored to what it has learned about you. A red notification badge, a “like” or an unexplained ping can provide a small hit of validation. Facebook has even been documented timing notifications for when a user is likely to be feeling insecure or bored, when that validation may land hardest.

There’s a genuinely useful finding buried in the research here. A study of 143 University of Pennsylvania undergraduates found that limiting social media use to 30 minutes a day significantly reduced loneliness and depression.[15] The researchers’ own conclusion was blunt: “limiting social media use to approximately 30 minutes per day may lead to significant improvement in well-being.” That’s not a difficult habit to test on yourself for two weeks.

Whether it’s a text, a “like” or a notification, the mechanism is identical to sugar: a dopamine hit, scheduled by an algorithm built to know exactly when a variable reward will keep you coming back. This constant cycle of dopamine and reward can train the brain to seek stimulation more frequently, making it harder to switch off.

Your brain’s reward system, in one paragraph : dopamine and the brain

All of this (sugar, phones, gambling, gaming, alcohol) routes through the same small structure: the nucleus accumbens, the brain’s dopamine-based reward hub. The more dopamine you release chasing something, the more your receptors down-regulate in response, so you need progressively more stimulation to feel the same lift. That’s the hijack. It’s not a character flaw; it’s the same ancient survival circuit being pulled by people who’ve studied exactly how to pull it. Understanding dopamine and the brain helps explain why these everyday rewards can become so compelling.

Alcohol, dopamine and the brain: reward disguised as relaxation

Alcohol might seem different from sugar, ultra-processed food or social media, but it taps into the same reward circuitry. The difference is that while we often reach for sugar, caffeine or our phones for stimulation, alcohol is frequently used for the opposite reason: to switch off, unwind or take the edge off stress. Yet it still acts on the brain’s reward system, which is part of what can make that evening drink so easy to repeat. Over time, tolerance can creep up: a glass a night becomes two, then half a bottle, then more.

Alcohol is a well-established neurotoxin,[16] and perhaps the most normalised drug of the lot. Smoking has become socially unacceptable in a single generation; drinking, outside of visibly heavy use, largely hasn’t. Yet alcohol remains a major cause of premature death and disability. The World Health Organization estimates that it was responsible for 2.6 million deaths worldwide in 2019, with 13% of deaths among 20 to 39-year-olds attributable to alcohol.[17] In the UK, 9,809 alcohol-specific deaths were registered in 2024, still substantially above pre-pandemic levels.[18] Despite this scale of harm, alcohol remains deeply embedded in how we socialise, celebrate and switch off. It is another example of how dopamine and the brain can shape repeated reward-seeking behaviour.

How much alcohol is too much?

What’s less well known is that the health risk from alcohol isn’t confined to heavy drinkers. It rises with the amount consumed, even at moderate levels. The encouraging flip side is that reducing consumption reduces risk. To make that concrete, a 12.5%-ABV bottle of wine contains about 75g of alcohol. Two large glasses, roughly two-thirds of a bottle, contain about 50g, while one medium 175ml glass contains about 17.5g.

More recent research adds to the case for keeping alcohol intake low. A 2022 study of 36,678 UK Biobank participants found that consuming more than one unit of alcohol per day was associated with progressively lower grey and white matter volume in the brain.[25] Neuropsychopharmacologist Professor David Nutt has advocated lower-risk daily alcohol limits. He recommends around 15g for women and 20g for men, with alcohol-free days each week. The current UK Chief Medical Officers’ guideline remains no more than 14 units a week for both men and women. That’s about 112g of pure alcohol, spread over three or more days rather than concentrated into one or two sessions.[19] Nutt was dismissed as chair of the government’s Advisory Council on the Misuse of Drugs in 2009. He had repeatedly challenged drug harm classifications, arguing that alcohol and tobacco were more harmful than several illegal drugs, including ecstasy.[20]

Are you addicted to stimulants?

The other major, socially glorified drug is caffeine, mostly as coffee, though strong tea carries a similar caffeine load to a regular cup of coffee. Like sugar, alcohol and your phone, it stimulates dopamine release and a genuine hit of reward. This connection between dopamine and the brain is part of what makes caffeine so effective at reinforcing the habit of reaching for another cup. Picture a day with no coffee, tea, chocolate or that end-of-day drink. If your instinctive reaction is “absolutely not,” there’s a real chance you have some level of dependence, anywhere from mild and manageable to something quietly running your day.

Whatever the level, the net effect of stimulant dependence is always less energy, not more. One of my clients, Bobbie, is a good example. She already ate well and took a sensible, targeted supplement programme. Her only real complaints were low morning energy and occasional headaches, and her only vice was three cups of coffee a day. She agreed, reluctantly, to drop the coffee for a month. Her energy came back, and the headaches stopped.

Like Bobbie, it’s worth auditing your own stimulant intake occasionally, honestly, not the version you’d tell your doctor. Try asking yourself:

Do you ever buy sweets and hide the wrappers so no one else knows you’ve eaten them?
Do you swoon at the dessert menu before you’ve even ordered a main course?
How much do you think about, or look forward to, your morning coffee, or the second cup?
How important is the after-work drink, really?
Does everyone around you actually know how much you smoke?
Has your “normal” coffee crept up to a double-espresso equivalent, more coffee at home than you used to make?
Do you still get a noticeable “kick” from caffeine, or does it now just relieve the fuzzy tiredness of not having had it yet?

None of these are shameful on their own; they’re just useful, honest data. What they point to, taken together, is a chemical dependency that quietly drains your energy and mood, and at its more extreme end, feeds into genuine mental health problems.

Caffeine, withdrawal and sleep

If you wake up feeling fine and function well without coffee, that’s a good sign. If you also sleep normally, one daily coffee isn’t necessarily a problem worth solving. The real test of your relationship with caffeine is what happens when you stop. No effect suggests little or no physical dependence, while headaches, fatigue and irritability are well-established signs of caffeine withdrawal.[21] Withdrawal can begin within 12 to 24 hours and typically peaks within one to two days. It usually resolves within several days. For some people, just 100mg of caffeine a day, roughly one cup of coffee, can cause withdrawal symptoms when stopped abruptly.[22]

It’s also worth knowing that caffeine can interfere with sleep even when consumed several hours before bed. One controlled study found that a 400mg dose taken six hours before bedtime significantly reduced sleep. The effect of a normal-strength cup of coffee is likely to be smaller.[23] If sleep is already a struggle, a simple experiment is to set a caffeine cut-off around noon and see whether sleep improves.

Tea or coffee?

Both raise adrenaline, cortisol and dopamine while blocking adenosine, the brain’s natural calming chemical. That adrenaline spike gives you a lift now, but often leaves you flatter and more fatigued later, and if you respond by having more caffeine, you end up agitated by day and wired-but-tired by night. It’s another important connection between dopamine and the brain when looking at everyday stimulant use.

Tea contains caffeine, but also theanine, a calming amino acid. Theanine has been shown to support cognitive performance [24] and protect GABA receptors, effectively the brain’s adrenaline off-switch. On balance, tea comes out ahead of coffee. Green tea edges out black tea because it retains more antioxidants and polyphenols.

Benefits, or just good excuses?

There’s no shortage of research on the upsides of tea, coffee and even moderate alcohol, from resveratrol in red wine to polyphenols in coffee and cacao and antioxidants in tea.

But almost any dependency generates its own psychological alibi: “it’s just a nice sauce” (sugar), “a little of what you fancy never hurt anyone,” “I’m too stressed not to have a drink,” “I need a coffee to focus.” These substances work. That’s precisely why we reach for them. Used with real intention, in the right moment, that’s not automatically a problem. A sugary drink after a genuine shock, or caffeine to get through a late deadline, are reasonable uses of a tool.

The problem comes when these habits start to stack up. Sugar, caffeine, alcohol, tech and social media can combine into a system that leaves you more tired, anxious and low than if you’d never reached for any of them.

The good news is that this is genuinely reversible. It doesn’t require an overhaul, just a few deliberate changes to how you use each of these levers.

Simple ways to win back your brain

Want to understand whether food or drink has hijacked your own reward system, and what you can do about it? Watch our webinar with psychologist Dr Jen Unwin to discover how to recognise and break the cycle of food and drink addiction. You can also become a FRIEND and get support to build healthier habits that help protect your brain for the long term.

None of this replaces individual medical advice. If drinking, medication, sleep or your mood feel genuinely out of your control, talk to your GP or a qualified practitioner alongside making these changes.

——–

Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a FRIEND of Food for the Brain.

Related reading:

Coffee and Brain Health? We Investigate…
Alcohol, caffeine and cognitive deficits (2021)
Coffee – Good or Bad for your Brain?

—–

By Patrick Holford

Life is a balancing act between making energy by combusting glucose or ketones with oxygen, which generates ‘oxidant’ exhaust fumes and dealing with these ‘oxidant fumes’ which harm the body.

Skin goes crinkly, age spots develop all due to oxidation. That’s what makes apples go brown, leaves change colour and iron rust. In the end, we lose, which is why all oxygen-based life forms have a finite life – and why your brain and body do inevitably age.

However, you can not only add years to your life, but also life to your years by improving your intake of antioxidants and polyphenols found in whole foods, fruits, vegetables and herbs and spices. A study in Finland and Sweden compared those with a ‘healthy’ versus ‘unhealthy’ diet in mid-life for future risk of developing Alzheimer’s disease and dementia 14 years later (1). Those who ate the healthiest diet had an 86-90% decreased risk of developing dementia and a 90-92% decreased risk of developing Alzheimer’s disease. Some of the benefit comes from low sugar diets, high in omega-3 and B vitamins and some from foods high in antioxidants and polyphenols which we will focus on here.

Your intake of these versus your intake and generation of oxidants, for example from smoking and pollution, is a major determinant of brain health. An illustration of this is the fact that both smoking and pollution exposure increase risk of cognitive decline and dementia, while vitamin C, which is the antioxidant par excellence, reduces risk.

(This is why we have developed our brand new Glutathione at home blood test – the first of its kind where you can accurately test your antioxidant status from home and support our further research into this important area. You can find out more and pre order the test here )

—

Oxidants vs antioxidants – moving the balance in your favour

Smoking increases risk of Alzheimer’s just as much as having low B vitamin or omega-3 status, according to the US National Institute of health’s analysis (2). Smoking is something a person can easily change. Air pollution, for many, is not. It is measured in the amount of particulate matter (PMs) and people living in polluted cities are exposed to more. A study of women living in cities in the US found that those exceeding the ‘safe’ levels (greater than 12 μg/m3) had ‘increased the risks for global cognitive decline and all-cause dementia respectively by 81% and 92%’. (3)

While you may not be able to change where you live, can you mitigate the effects of pollution? The answer is yes – in two ways. Firstly, by increasing your intake of antioxidants and also by improving your B vitamin status since the body detoxifies many toxins, including toxic metals from lead to mercury, by methylation. A similar study to the one above found that residing in locations with PM exposure above the safe level was associated with a higher risk of dementia but only among people with lower intakes of the homocysteine lowering B vitamins (B6, folate, b12) (4). ‘Vitamin C in the diet or taken as supplements might help’ concludes another.(5)

Smokers need at least twice as much vitamin C as non-smokers just to have basic vitamin C levels in their blood (serum). Men do worse than women. Even with an intake of 200mg a day they do not achieve this basic blood level, which is already two to three times the recommended dietary intake and what you’d get in four oranges (6). It is certainly wise for any smoker to supplement vitamin C, perhaps adding 50mg per cigarette – 500mg if you smoke 10 a day, although there is a good case for everyone to supplement 1,000mg a day, or 2,000mg a day if over 50.

Nature always provides a solution to help us with our evolution. It seems obvious to me we need vitamin C to combat excessive pollution.

Vitamin C is a keystone nutrient as far as swinging the antioxidant equation in your favour. It’s made in all living things, from animals to plants, including yeasts and funghi. It’s probably been the essential ‘exhaust recycler’ of all oxygen-based lifeforms. Production is even activated when oxidants are sensed. Animals also make more when stressed or exposed to viruses. Us humans, and all other primates, are one of very few species who can’t make it. The first non-vitamin C making animal to be discovered was the guinea pig. That’s how it became the ‘guinea pig’ for research since, like us, it’s dependent every second of every day on vitamin C from diet. Bats, a few birds and the teleost family of fish have also lost the ability to make vitamin C. 

You’ll see in this figure below and from watching the film above, that vitamin C disarms water-based oxidants, such as smoke, and vitamin E disarms fat-based oxidants such as burnt fat. Then, there are other key antioxidant team players that help to neutralise the reactive oxidants that damage our brain and body.

—

—

Your best bet is probably to both eat a diet with a broad spectrum of antioxidants and also supplement them. The older you are the more you are likely to need. Key antioxidants are:

Vitamin A, C and E – associated with reducing Alzheimer’s risk
Lipoic acid (7) – protects the memory-friendly neurotransmitter acetylcholine and dampens down brain oxidation and inflammation)
Glutathione (8) or N-acetyl Cysteine (NAC)(9) – protects the brain and improves methylation thus having potential in dementia prevention.
Co-enzyme Q10 – protects the mitochondria in the brain from oxidative stress (10)
Resveratrol – resveratrol has antioxidant, anti-inflammatory and neuroprotective properties and prevents hippocampal brain damage. (11)

It doesn’t really make a lot of sense to supplement one without the others.

Individually, their impact on your brain health may be less than when combined. A study of 4,740 Cache County Utah elderly residents found that those supplementing both vitamin E and C cut their risk of developing Alzheimer’s by two thirds. Taking either cut risk by a quarter (12). A recent meta-analysis of all studies on factors that could prevent Alzheimer’s by one of our Scientific Advisory Board members – Professor Jin Tai Yu of Fudan University in Shanghai, China – shows that ‘either a high vitamin E or C intake showed a trend of attenuating risk by about 26%’ making these nutrients ‘grade 1’ top level prevention risk factors (13).

All those listed above – vitamin C, E, glutathione and N-acetyl cysteine, Coenzyme Q10 and resveratrol – work together and are often found in combined antioxidant supplement formulas. There are many other team player ‘cousins’ from B vitamins to minerals such as magnesium, selenium and zinc found respectively in greens, seafood, nuts and seeds.

There are two ways to increase your intake – through food and from supplements. Foods can be measured for their ‘Total Antioxidant Capacity’ or TAC for short. It’s worked out from an equation involving eight key antioxidants from vitamin A, carotenes (think carrots), lycopenes (rich in tomatoes), lutein and zeaxanthine (rich in green vegetables), vitamin E (is nuts and seeds), but most of all vitamin C (rich in berries, broccoli, peppers and other vegetables).

(Click here to read our guidance on supplements)

The higher the TAC score of your diet the lower is your risk of cognitive and memory decline. This was the finding of a recent study of 2,716 people over age 60. The researchers measured the TAC score from their diet, splitting them into the highest to lowest quarter of TAC score, and compared this to a number of memory tests. Those in the highest quarter, eating the most antioxidant-rich foods had half the risk of decreasing memory. The higher the TAC score the better their memory function was. (14)

—

Go Rainbow, ‘Mediterranean’ and eat five or more servings of fruit and vegetables a day

So, what do you need to eat and drink to preserve your memory and protect your brain?

Basically, eat a Mediterranean style ‘rainbow coloured’ diet. A Mediterranean diet has more fish, less meat and dairy, more olive oil, fruit and vegetables including tomatoes, legumes (beans and lentils) and whole grain cereals than a standard Western diet. It also includes small quantities of red wine. There are variations of this kind of diet, called the MIND diet and the DASH diet, but the core components are the same and as researchers drill down, we are learning what to eat and drink to keep your mind sharp and brain young, and how much.

The trick is to really start thinking of the colours you’re eating and gravitate for the strong colours.

Mustard and turmeric, for example, are strong yellows. Dijon mustard is great – no sugar. But if you like good old-fashioned English mustard go for it. Have a teaspoon every other day.

Add turmeric to almost any steam-fry, curry or soup. 

Bright oranges include butternut squash, sweet potato, carrots – but do buy organic. Translucent mass produced carrots are tasteless and have a higher water content, ie less actual carrot. 

Tomatoes are particularly good for you. Buy seeded, not seedless watermelons. Blend the flesh in a blender, perhaps with some ice. The black husk of the seeds drops to the bottom. The flesh of the seeds, full of essential nutrients, becomes part of this mouth-wateringly refreshing drink. Great for detox. Strawberries are a low GL fruit. Red, yellow, green and orange peppers are all rich in vitamin C.

Anything purple, magenta or blue is brilliant for you. From beetroots (eat them raw, grated into salads) to blueberries, blackberries and raspberries. Strawberries are particularly good. According to a study, part of the Rush Memory and Aging Project at Rush University, Chicago, having a higher intake cut Alzheimer’s risk by a quarter. They are high in both vitamin C and flavanoids, a high level of which were also confirmed to cut risk by a third. (15)

Strong greens are always beneficial – from spinach, kale, Brussels sprouts, broccoli, tender stem, watercress, rocket, asparagus, artichoke, green beans, peas, kohlrabi, and cauliflower (although not green).

Polyphenol power

Some of these foods are particularly rich in ‘polyphenols’ a group of health promoting molecules which also includes flavonoids, sometimes called flavanols.  Blue foods such as blueberries contain another polyphenol called anthocyanins. Tea, the cacao in chocolate, red wine, red onions, olives and all the blueish berries are rich sources of polyphenols. Many of these polyphenol rich foods act as antioxidants but they do much more than this. They improve circulation in the brain, lower blood pressure and dampen down inflammation which lies behind many conditions from depression to dementia. Once again, the principle of what’s good for the heart is good for the brain.

One of the first important studies was carried out in Norway more than a decade ago by Eha Nurk and Helga Refsum and colleagues in Norway. (16)(17) They found that:

Tea – the more you drink the better. The tea benefit has been confirmed more recently in a study in Singapore, with green tea being marginally better than black tea.(18) However, this benefit was not found in a UK Biobank study, which reported tea and coffee drinking to be associated with worsening cognition compared to abstainers. (19)

Chocolate – peaks at 10g, or about 3 pieces – and let’s say dark, 70 or more percent, thus with less sugar, is likely to be better, as sugar is a strong indicator of cognitive decline. If a chocolate is 80% cacao that means almost 20% will be sugar. More recent studies giving cocoa, a rich source of flavanols, have shown improved cognition, possibly by improving circulation.(20) This has been confirmed in a big COSMOS trial involving over 20,000 people given a cacao extract supplement rich in flavanols versus a placebo for five years. (21) The reduction in cardiovascular risk was even greater than that of a Mediterranean diet.

Wine – consumption reduces risk of cognitive decline up to an intake of 125ml a day, which is a small glass. A thorough study in the British Medical Journal in 2018, which had followed over 9,000 people over 23 years, showed that both abstinence and drinking more than 14 units of alcohol a week, which is equivalent to a medium glass of wine (2.3 units) every day, also increases risk (22). This is consistent with studies showing that a small glass of wine a day decreases risk of cardiovascular disease. Red wine, high in resveratrol is likely to be most beneficial.

All the above are rich in a polyphenol called epicatechin. Jeremy Spencer, an advisor to Food for the Brain, who is Professor of Nutritional Biochemistry and Medicine at the University of Reading, where he specialises in studying the health benefits of polyphenols and other compounds in plants, has shown that these polyphenol rich plants improve blood brain flow in specific regions of the brain that improve attention, decision-making, impulse control and emotion, thus improving overall ‘executive’ function (23). What’s more, the level of flavanols you have in your bloodstream predicts your memory. The biggest impact of increasing flavanols, was seen in the COSMOS study, in those in the lowest third for dietary intake specifically seeing improvement in aspects of memory that link to the hippocampus, that central area of the brain that degenerates in Alzheimer’s (24).

—

The Best Fruit and Veg to Eat for Your Brain

Which vegetables pack the biggest punch as far as polyphenols and antioxidants are concerned and are also lower in sugar or low GL?

Taking all these factors into account – the GL, antioxidants and polyphenols these are the dozen best rated fruit and veg. But do not think of this list as finite as more and more research reveals the amazing healing power of nature’s fruits and vegetables.

—

—

The optimal intake for brain protection is 5 to 6 servings of fruit and veg a day. 

Half a plate of a main meal counts as two. A handful of berries would count as one. So, if half your plate for two main meals is vegetables, and you had some berries with your breakfast and another piece of fresh fruit or perhaps some broccoli heads or tenderstem or carrots dipped in hummus as a snack, or half an avocado with some high polyphenol olive oil, you’ve achieved six servings.

The first step is to eat ‘whole’ foods, and especially fresh plant foods with an emphasis on those listed above that are more likely to be high in antioxidants and polyphenols. (Also see the Alzheimers Prevention Diet.) There are some nutrients such as vitamin C for which just eating whole foods doesn’t guarantee you are achieving an optimal intake and are well worth supplementing.

My advice is to supplement 500mg to 1,000mg of vitamin C twice a day and also take an antioxidant formula or antioxidant rich multivitamin containing vitamins A, C, E, lipoic acid, glutathione or NAC, resveratrol and CoQ10.

Summary

Support our research and be one of the first to test your antioxidant status with the Glutathione Index test. Pre order here
Take the FREE Cognitive Function Test here.
Want to get recipes to help you increase your antioxidant intake? Pre order the Upgrade Your Brain Cook App here

—

Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References

Eskelinen MH, Ngandu T, Tuomilehto J, Soininen H, Kivipelto M. Midlife healthy-diet index and late-life dementia and Alzheimer’s disease. Dement Geriatr Cogn Dis Extra. 2011 Jan;1(1):103-12. doi: 10.1159/000327518. Epub 2011 Apr 27. PMID: 22163237; PMCID: PMC3199886.
Beydoun MA, Beydoun HA, Gamaldo AA, Teel A, Zonderman AB, Wang Y. Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis. BMC Public Health. 2014 Jun 24;14:643. doi: 10.1186/1471-2458-14-643. PMID: 24962204; PMCID: PMC4099157.
Cacciottolo M, Wang X, Driscoll I, Woodward N, Saffari A, Reyes J, Serre ML, Vizuete W, Sioutas C, Morgan TE, Gatz M, Chui HC, Shumaker SA, Resnick SM, Espeland MA, Finch CE, Chen JC. Particulate air pollutants, APOE alleles and their contributions to cognitive impairment in older women and to amyloidogenesis in experimental models. Transl Psychiatry. 2017 Jan 31;7(1):e1022. doi: 10.1038/tp.2016.280. PMID: 28140404; PMCID: PMC5299391.
 Chen C, Whitsel EA, Espeland MA, Snetselaar L, Hayden KM, Lamichhane AP, Serre ML, Vizuete W, Kaufman JD, Wang X, Chui HC, D’Alton ME, Chen JC, Kahe K. B vitamin intakes modify the association between particulate air pollutants and incidence of all-cause dementia: Findings from the Women’s Health Initiative Memory Study. Alzheimers Dement. 2022 Nov;18(11):2188-2198. doi: 10.1002/alz.12515. Epub 2022 Feb 1. PMID: 35103387; PMCID: PMC9339592.
 Yu JT, Xu W, Tan CC, Andrieu S, Suckling J, Evangelou E, Pan A, Zhang C, Jia J, Feng L, Kua EH, Wang YJ, Wang HF, Tan MS, Li JQ, Hou XH, Wan Y, Tan L, Mok V, Tan L, Dong Q, Touchon J, Gauthier S, Aisen PS, Vellas B. Evidence-based prevention of Alzheimer’s disease: systematic review and meta-analysis of 243 observational prospective studies and 153 randomised controlled trials. J Neurol Neurosurg Psychiatry. 2020 Nov;91(11):1201-1209. doi: 10.1136/jnnp-2019-321913. Epub 2020 Jul 20. PMID: 32690803; PMCID: PMC7569385.
 Carr AC, Lykkesfeldt J. Factors Affecting the Vitamin C Dose-Concentration Relationship: Implications for Global Vitamin C Dietary Recommendations. Nutrients. 2023 Mar 29;15(7):1657. doi: 10.3390/nu15071657. PMID: 37049497; PMCID: PMC10096887.
 A. Maczurek, et al., ‘Lipoic acid as an anti-inflammatory and neuroprotective treatment for Alzheimer’s disease’, Advance Drug Delivery Review, 2008;60(13-14):1463-70 
 Pocernich CB, Butterfield DA. Elevation of glutathione as a therapeutic strategy in Alzheimer disease. Biochim Biophys Acta. 2012 May;1822(5):625-30. doi: 10.1016/j.bbadis.2011.10.003. Epub 2011 Oct 12. PMID: 22015471; PMCID: PMC3277671.
 Hara Y, McKeehan N, Dacks PA, Fillit HM. Evaluation of the Neuroprotective Potential of N-Acetylcysteine for Prevention and Treatment of Cognitive Aging and Dementia. J Prev Alzheimers Dis. 2017;4(3):201-206. doi: 10.14283/jpad.2017.22. PMID: 29182711.
 Yang X, Zhang Y, Xu H, Luo X, Yu J, Liu J, Chang RC. Neuroprotection of Coenzyme Q10 in Neurodegenerative Diseases. Curr Top Med Chem. 2016;16(8):858-66. doi: 10.2174/1568026615666150827095252. PMID: 26311425.
 Gomes BAQ, Silva JPB, Romeiro CFR, Dos Santos SM, Rodrigues CA, Gonçalves PR, Sakai JT, Mendes PFS, Varela ELP, Monteiro MC. Neuroprotective Mechanisms of Resveratrol in Alzheimer’s Disease: Role of SIRT1. Oxid Med Cell Longev. 2018 Oct 30;2018:8152373. doi: 10.1155/2018/8152373. PMID: 30510627; PMCID: PMC6232815.
 Basambombo LL, Carmichael PH, Côté S, Laurin D. Use of Vitamin E and C Supplements for the Prevention of Cognitive Decline. Ann Pharmacother. 2017 Feb;51(2):118-124. doi: 10.1177/1060028016673072. Epub 2016 Oct 5. PMID: 27708183.
 See reference 5.
 Peng, M., Liu, Y., Jia, X. et al. Dietary Total Antioxidant Capacity and Cognitive Function in Older Adults in the United States: The NHANES 2011–2014. J Nutr Health Aging 27, 479–486 (2023). https://doi.org/10.1007/s12603-023-1934-9
 Agarwal P, Holland TM, Wang Y, Bennett DA, Morris MC. Association of Strawberries and Anthocyanidin Intake with Alzheimer’s Dementia Risk. Nutrients. 2019 Dec 14;11(12):3060. doi: 10.3390/nu11123060. PMID: 31847371; PMCID: PMC6950087.
 Nurk E, Refsum H, Drevon CA, Tell GS, Nygaard HA, Engedal K, Smith AD. Intake of flavonoid-rich wine, tea, and chocolate by elderly men and women is associated with better cognitive test performance. J Nutr. 2009 Jan;139(1):120-7. doi: 10.3945/jn.108.095182. Epub 2008 Dec 3. PMID: 19056649.
 Nurk E, Refsum H, Drevon CA, Tell GS, Nygaard HA, Engedal K, Smith AD. Cognitive performance among the elderly in relation to the intake of plant foods. The Hordaland Health Study. Br J Nutr. 2010 Oct;104(8):1190-201. doi: 10.1017/S0007114510001807. Epub 2010 Jun 16. PMID: 20550741.
 Feng L, Chong MS, Lim WS, Lee TS, Kua EH, Ng TP. Tea for Alzheimer Prevention. J Prev Alzheimers Dis. 2015;2(2):136-141. doi: 10.14283/jpad.2015.57. PMID: 29231231.
 Cornelis MC, Weintraub S, Morris MC. Caffeinated Coffee and Tea Consumption, Genetic Variation and Cognitive Function in the UK Biobank. J Nutr. 2020 Aug 1;150(8):2164-2174. doi: 10.1093/jn/nxaa147. PMID: 32495843; PMCID: PMC7398783.
 Lamport DJ, Pal D, Moutsiana C, Field DT, Williams CM, Spencer JP, Butler LT. The effect of flavanol-rich cocoa on cerebral perfusion in healthy older adults during conscious resting state: a placebo controlled, crossover, acute trial. Psychopharmacology (Berl). 2015 Sep;232(17):3227-34. doi: 10.1007/s00213-015-3972-4. Epub 2015 Jun 7. PMID: 26047963; PMCID: PMC4534492.
 Sesso HD, Manson JE, Aragaki AK, Rist PM, Johnson LG, Friedenberg G, Copeland T, Clar A, Mora S, Moorthy MV, Sarkissian A, Carrick WR, Anderson GL; COSMOS Research Group. Effect of cocoa flavanol supplementation for the prevention of cardiovascular disease events: the COcoa Supplement and Multivitamin Outcomes Study (COSMOS) randomized clinical trial. Am J Clin Nutr. 2022 Jun 7;115(6):1490-1500. doi: 10.1093/ajcn/nqac055. PMID: 35294962; PMCID: PMC9170467.
 Sabia S, Fayosse A, Dumurgier J, Dugravot A, Akbaraly T, Britton A, Kivimäki M, Singh-Manoux A. Alcohol consumption and risk of dementia: 23 year follow-up of Whitehall II cohort study. BMJ. 2018 Aug 1;362:k2927. doi: 10.1136/bmj.k2927. PMID: 30068508; PMCID: PMC6066998.
 See Professor Peremy Spencer’s presentation at the Alzheimer’s is preventable masterclass (2022); also see Spencer JP. The impact of fruit flavonoids on memory and cognition. Br J Nutr. 2010 Oct;104 Suppl 3:S40-7. doi: 10.1017/S0007114510003934. PMID: 20955649.
 Brickman AM, Yeung LK, Alschuler DM, Ottaviani JI, Kuhnle GGC, Sloan RP, Luttmann-Gibson H, Copeland T, Schroeter H, Sesso HD, Manson JE, Wall M, Small SA. Dietary flavanols restore hippocampal-dependent memory in older adults with lower diet quality and lower habitual flavanol consumption. Proc Natl Acad Sci U S A. 2023 Jun 6;120(23):e2216932120. doi: 10.1073/pnas.2216932120. Epub 2023 May 30. PMID: 37252983; PMCID: PMC10265949.

This was the title of a report in the British Medical Journal (1), pointing out that choline is an essential nutrient, much like omega-3 fats, that is vital for health and especially the brain, but not sufficiently supplied in many people’s diets, and especially those who are largely vegan.

While the body can make a little, it does not make enough and thus choline is being reclassified as an essential nutrient with an adequate intake defined as between 400mg and 520mg a day, the latter for pregnant and breast-feeding women. But these levels don’t relate to brain function. They relate to the EFSA allowed claims of “choline is needed for lipids metabolism”, “maintaining healthy liver functioning” and “reduction in homocysteine levels”. You need choline to do the right thing with cholesterol in the liver. 

But even more important is choline’s role in building and maintaining a healthy brain. A pregnant woman’s intake defines the cognitive abilities of their child. Twenty years ago we knew that pregnant rats fed choline half way through their pregnancy have more connections between brain cells, plus improved learning ability and better memory recall. Now we know it’s true for babies. In fact, a lack of choline can lead to a shrinking of a woman’s brain as the foetus robs their brain to build its own – a case of ‘Mummy I shrank your brain’. Babies are born with blood choline levels three times higher than their mother, illustrating how vital this nutrient is for building neuronal connections, which newborn babies do at a rate of up to a million new connections a second! An optimal intake for brain function is likely to be a lot higher than the 400mg recommended for adults.

Brain cells are made of a membrane containing choline (and other phospholipids) attached to the omega-3 fat DHA. Without choline the omega-3 doesn’t work. The attaching of the two depends on methylation, a process that is dependent on B vitamins, especially B12, folate and B6. Choline helps methylation and healthy methylation, indicated by low homocysteine, helps synthesize choline.

The reason the BMJ says ‘crisis’ is that more people are eating a plant-based diet and shunning eggs, fish and meat, which are the best sources of, not only choline, but also B12. There’s a tiny bit of choline in broccoli and in nuts, but not enough. An egg provides around 120mg, a 50g beef or salmon steak around 50mg. The same amount of almonds or broccoli is about 25mg. Cow’s milk has a little, but a fraction of that found in human milk. Beef liver is the richest source.

Twenty years ago I found the evidence sufficiently compelling to recommend eating an egg a day, three servings of fish and one of meat (or another portion of fish) a week, a handful of nuts, plus daily supplementation of circa 100mg, which is what I do in my ‘brain food’ formula. If you also ate a serving of broccoli a day, you’d be achieving something like 2,100mg a week, or 300mg a day – still short of daily requirements.

If you don’t eat eggs, fish or meat and don’t supplement there’s no way of getting even close. That’s why it’s time to add choline, along with omega-3 DHA and B12, to the list of nutrients that must be supplemented by those eating a vegan diet. Lecithin granules and capsules are the richest vegan source of choline, derived from soya. It will not work in building the brain, without a source of DHA which can be derived, in supplements, from algae or seaweed. 

If you want more strategies on what to eat and do to support ad upgrade your brain make sure you complete the Cognitive Function Test below to get your plan of action for improving your brain over the next 6 months.

Reference:

Derbyshire E. ‘Could we be overlooking a potential choline crisis in the United Kingdom?’ BMJ Nutrition, Prevention and Health, 2019; 0:1–4

Our brains have a dual fuel mechanism. The brains of large-brained animals like us can run on either glucose or ketones, derived from fat. If given the choice they prefer ketones. The rise in popularity in high fat ketogenic diets is partly to do with the ability of ketones to nourish and improve brain function when things go wrong, as well as weight loss benefits and the potential to reverse diabetes.

Epilepsy, for example, has been successfully treated in both children and adults with a high-fat ketogenic diet since the 1920’s often halving the frequency of fits. A recent study on people with Parkinson’s found that those placed on a high-fat diet had 41 per cent reduction in shaking, compared to 11 percent on a low-fat diet. There’s also a potential benefit in chronic fatigue syndrome.

The reason these high-fat keto diets work is that if a cell’s sugar metabolism is all messed up, a consequence of insulin resistance promoted by a high-sugar diet, then the cell struggles to get enough energy and you feel mentally and physically tired. But if, like a hybrid car, you can switch to a different fuel, ketones, then the cell comes back to life. This is especially true in struggling brain cells. When you fast, and switch to burning your body fat, the brain derives two-thirds of its energy from ketones.

Ketones are made from medium-chain triglycerides, known as MCTs. The rise in sales of MCT oil, which can be derived from palm or coconut oil. Also gaining in popularity are ketone salts and pure synthetic ketones, although these are yet to clear EU Novel Foods so are not yet available in Europe.

Fats are chains of carbon molecules and MCTs contain C6, C8, C10 and C12 oil. Of these C8 oil (called tricaprylin or caprylic acid triglyceride) makes ketones fastest. While coconut oil is 60 percent MCTs only 12 percent of MCTs is C8. That means that only 7 percent of coconut oil is C8.

The growth in bullet-proof coffee, adding a blob of coconut oil to your morning brew, is one way to up ketone levels but it’s much less effective than adding pure C8 oil. Patrick Holford’s Hybrid Latté – a coffee with carb-free almond milk, almond butter, C8 oil, cacao and cinnamon, is a step up. While coffee gives you energy like a bank loan gives you wealth it does speed up conversion to running on ketones.

Case studies with coconut oil have shown short-term beneficial effects in people with Alzheimer’s, with improved mental clarity. Two breakthrough studies in Canada, by Dr Melanie Fortier and Professor Stephen Cunnane from Sherbrooke University in Canada have established that C8 oil can be extremely helpful as an energy source for those with cognitive decline. Cunnane is an expert on fatty acid metabolism in the brain who has held the ‘Canada Research Chair on Dietary Fatty Acids and Cognitive Function during Ageing’.

Are there any downsides? A few people report abdominal or stomach discomfort. This can be minimized by building up slowly – starting with a teaspoon, then a dessert spoon, then a tablespoon, then two, then three tablespoons taken at different times of day, with food or in drinks or neat.

If glucose is petrol ketones are electricity. If your brain needs a service, switching from running on carbs to running on ketones by eating a low-carb, high-fat diet for a week, may be a good idea. It takes only 12 hours to start to run out of glucose fuel and start switching to ketones. Also good is an 18-hour carb fast – eg dinner at 6pm, lunch at 1pm. My brain stays sharp and I don’t feel hungry.

Want to know more about ketones and your brain? Then make sure you join us for our webinar: KETONES – A Key Brain Fuel During Ageing’ With Professor Stephen Cunnane

Find out more about the Ketones Webinar HERE >>>

References

 M. Nei et al., Seizure. 2014;23(6):439-42.
 M. Phillips et al., Movement Disorders 2018; 33(8):1306-1314 
 Craig C. Med Hypotheses. 2015;85(5):690-3
 C. Vandenberghe et al., Current Developments in Nutrition 2017; 1(4):e000257
 Vanderberghe et al., Can J Physiol Pharmacol. 2017 Apr;95(4):455-458.

By Research Professor Tommy Wood from the University of Washington

Most of us have two types of elderly relatives.

One of them is old – they have trouble walking, they’re in and out of the doctor’s office, and they always seem to repeat the same stories. The other type seems younger than their years they play tennis twice a week, they’re social, and they’re sharp as a tack. How can we become part of the latter group?

When it comes to aging in general and cognitive function in particular, genes obviously play a role, but did you know that lifestyle choices matter even more?[1] So, what are the top lifestyle choices to keep our brains sharp into old age?

As a neuroscientist, this is a question I often get.

Besides the obvious ones – physical activity, strength, sleep, a healthy diet, not smoking – my top tip is this: If you want to stay mentally sharp into old age, keep your brain active. In short, “use it or lose it”.

But what does “using it” look like? In this post I’ll cover some of the evidence around cognitive decline, as well as some practical take-aways for anybody wanting to improve their brain health as they get older.

—

Use it or lose it

The brain is an amazing organ, and it’s more resilient and adaptable than we’ve been led to believe. I’m sure you’ve heard that adults have a fixed amount of brain cells. Then, as we get older (or every time we take a sip of wine) we “lose” some of those brain cells as part of an unstoppable decline towards dementia or Alzheimer’s disease.

But that’s not necessarily true. I like to think about the brain like I think about muscles. In order to grow our muscles, we need to provide a stimulus – like lifting weights in the gym – followed by a period of rest. The opposite also happens – if we stop going to the gym or if we stop using a limb after breaking a bone – our muscles get smaller. Most have experienced this personally, and there’s every indication that your cognitive “muscle” behaves in the same way.

How do we know this? One type of evidence is that longer education seems to reduce dementia in later life. [2]* You might think of education as early cognitive muscle building that you then benefit from throughout life. We see similar effects from other forms of early cognitive stimulus – like protection from neurodegenerative disease in people who grew up bilingual.[3]

But we’re not cognitively doomed after adolescence. One of my favourite studies looked at adults studying “The Knowledge” – memorising ~25,000 streets in central London to become a taxi driver. These participants were in their 30s or 40s, yet they saw a significant increase in the size of the hippocampus, the brain region associated with memory.[4]

We also see the opposite effect – less cognitive stimulus increases the risk of cognitive decline and dementia. This is most easily studied by looking at retirement. Multiple studies in populations across the US, China, and Europe, show that the risk of cognitive decline accelerates after retirement.[5-8] Those that retire later are protected against cognitive decline, even after considering factors that might force early retirement such as poor health. Overall, a recent meta-analysis looking at health and lifestyle factors associated with cognitive decline found that cognitive activity was the single most protective factor – halving the risk of Alzheimer’s disease.[2] This really emphasises the lesson: use it or lose it. What counts as ‘protective cognitive demand’? Doing something badly.

The evidence around retirement and cognitive decline suggests that work is where adults tend to get most of their cognitive activity. However, it’s important to unpick what constitutes cognitive activity that is protective. We may feel that our work demands a lot from our brain, but being “busy” does not necessarily benefit the brain. In fact, it’s often the opposite. Being “busy” tends to come with stress, and though stress is very personal, chronic stress is associated with an increased risk of Alzheimer’s disease.[9] What keeps us busy and stressed – sitting in meetings, reading emails, inputting data – may be time consuming, but rarely requires much brain power.

So, what constitutes protective cognitive demand? Failure.

Activities that provide the greatest cognitive stimulus involve learning and skill development. That means we’re initially bad at them and occasionally fail before we get better. This is the real sticking point for improving brain health – as adults we hate the feeling of being bad at something. Failing is, however, when the magic happens. A fascinating study looked at the brains of musicians.[10] While both professional and amateur musicians’ brains looked younger compared to non-musicians of the same age, the benefit was greatest in amateur musicians. The researchers suggested that playing music is more of a cognitive stimulus for amateurs – it’s harder, so they get more benefit. The cocktail of hormones released as we try, fail, repeat, and learn, provides the ideal environment for the brain to grow and adapt.

How to “use it”

So, how should we apply this knowledge? Below are some of the best and easiest ways to build in cognitive stimuli you can benefit from for years to come.

1 | Pick an activity that’s truly challenging
Cognitive demand requires failure, so pick something you’ll be bad at initially. What’s cognitively challenging is personal, but learning a new language is better than sudoku, building model airplanes is probably better than reading the news, and playing chess is definitely better than scrolling through Instagram. As you get better, add challenge to keep stimulating your brain.

2 | Start small and do something you enjoy
Skill development should be a lifelong process, which means it should be a routine. Start small – for instance 2 minutes a day of playing an instrument or learning a new language. Make sure your new skill is something you enjoy – that makes it easier to stick to and keep as a part of your life.

3 | Move – with a skill component
Movement has some of the best evidence on improving brain health. One of the first studies to show that the hippocampus can grow in adults of retirement age (or older) used a walking intervention – just 40 minutes of brisk walking 3x per week.[11] Other studies have showed increased brain connectivity and function in adults doing resistance training 1-2 times per week.[12] Best is movement that includes balance or motor skills: the added challenge of coordination seems to be particularly protective against cognitive decline.[13] Think yoga, dance, or even skateboarding

4 | Try a new skill that’s social
Social interaction is its own form of cognitive stimulus: social connection is protective of cognitive function, while social isolation has the opposite effect.[14] So what’s better than simply learning a new skill? Doing so with friends. Start a book club to discuss the books you read. Join a knitting circle, language group, or dance class. Volunteer for a local charity. All of these help you learn new skills, with the added benefit of social interaction.

5 | Repeat, repeat, repeat
There are no hard and fast rules about how much or how often to work on a new skill, but once a week is a good start. If it’s a class or a movement practice, maybe 1-3 times per week. If it’s something you can do on your own, you may prefer more frequent, smaller bouts of focused practice. Try using a Pomodoro timer to dig in for 20-30 minutes – a suitable time for most people to keep their undivided attention.
The key is to push right at the boundaries of what you’re capable of – with occasional failure showing that you’re at the right level of difficulty. Keep at it, and you’ll be more likely to be healthy and sharp for decades to come.

Footnote
*It’s worth noting that those who stay in education for longer also tend to be socioeconomically advantaged, but the benefit of longer education seems to hold even accounting for that.

Thank you for reading!

Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References

Lourida I, Hannon E, Littlejohns TJ, Langa KM, Hyppönen E, Kuźma E, Llewellyn DJ. Association of Lifestyle and Genetic Risk With Incidence of Dementia. Jama. 2019;322(5):430-7. doi: 10.1001/jama.2019.9879.
Yu JT, Xu W, Tan CC, Andrieu S, Suckling J, Evangelou E, Pan A, Zhang C, Jia J, Feng L, Kua EH, Wang YJ, Wang HF, Tan MS, Li JQ, Hou XH, Wan Y, Tan L, Mok V, Tan L, Dong Q, Touchon J, Gauthier S, Aisen PS, Vellas B. Evidence-based prevention of Alzheimer’s disease: systematic review and meta-analysis of 243 observational prospective studies and 153 randomised controlled trials. J Neurol
Neurosurg Psychiatry. 2020;91(11):1201-9. Epub 2020/07/22. doi: 10.1136/jnnp-2019-321913. PubMed PMID: 32690803; PMCID: PMC7569385.
Sala A, Malpetti M, Farsad M, Lubian F, Magnani G, Frasca Polara G, Epiney JB, Abutalebi J, Assal F, Garibotto V, Perani D. Lifelong bilingualism and mechanisms of neuroprotection in Alzheimer dementia. Hum Brain Mapp. 2022;43(2):581-92. Epub 2021/11/04. doi: 10.1002/hbm.25605. PubMed PMID: 34729858; PMCID: PMC8720191.
Woollett K, Maguire EA. Acquiring “the Knowledge” of London’s layout drives structural brain changes. Current biology : CB. 2011;21(24):2109-14. Epub 2011/12/08. doi: 0.1016/j.cub.2011.11.018. PubMed PMID: 22169537.
Hale JM, Bijlsma MJ, Lorenti A. Does postponing retirement affect cognitive function? A counterfactual experiment to disentangle life course risk factors. SSM – Population Health. 2021;15:100855. doi: https://doi.org/10.1016/j.ssmph.2021.100855.
Dufouil C, Pereira E, Chêne G, Glymour MM, Alpérovitch A, Saubusse E, Risse- Fleury M, Heuls B, Salord JC, Brieu MA, Forette F. Older age at retirement is associated with decreased risk of dementia. Eur J Epidemiol. 2014;29(5):353-61. Epub 2014/05/06. doi: 10.1007/s10654-014-9906-3. PubMed PMID: 24791704.
Nikolov P, Adelman AM. Do Pension Benefits Accelerate Cognitive Decline? Evidence from Rural China. Labor: Public Policy & Regulation eJournal. 2019. Sundström A, Rönnlund M, Josefsson M. A nationwide Swedish study of age at retirement and dementia risk. Int J Geriatr Psychiatry. 2020;35(10):1243-9. Epub 2020/06/20. doi: 10.1002/gps.5363. PubMed PMID: 32557831.
Ye Y, Li J, Yuan Z. Effect of antioxidant vitamin supplementation on cardiovascular outcomes: A meta-analysis of randomized controlled trials. PloS One. 2013;8:e56803. doi:10.1371/journal.pone.0056803.
Rogenmoser L, Kernbach J, Schlaug G, Gaser C. Keeping brains young with making music. Brain Struct Funct. 2018;223(1):297-305. Epub 2017/08/18. doi: 10.1007/s00429-017-1491-2. PubMed PMID: 28815301.
Erickson KI, Voss MW, Prakash RS, Basak C, Szabo A, Chaddock L, Kim JS, Heo S, Alves H, White SM, Wojcicki TR, Mailey E, Vieira VJ, Martin SA, Pence BD, Woods JA, McAuley E, Kramer AF. Exercise training increases size of hippocampus and improves memory. Proceedings of the National Academy of Sciences. 2011;108(7):3017. doi: 10.1073/pnas.1015950108.
Herold F, Törpel A, Schega L, Müller NG. Functional and/or structural brain changes in response to resistance exercises and resistance training lead to cognitive improvements – a systematic review. Eur Rev Aging Phys Act. 2019;16:10. Epub 2019/07/25. doi: 10.1186/s11556-019-0217-2. PubMed PMID: 31333805; PMCID: PMC6617693.
Ludyga S, Gerber M, Pühse U, Looser VN, Kamijo K. Systematic review and meta- analysis investigating moderators of long-term effects of exercise on cognition in healthy individuals. Nature Human Behaviour. 2020;4(6):603-12. doi: 10.1038/s41562-020-0851-8.
Penninkilampi R, Casey AN, Singh MF, Brodaty H. The Association between Social Engagement, Loneliness, and Risk of Dementia: A Systematic Review and Meta-Analysis. J Alzheimers Dis. 2018;66(4):1619-33. Epub 2018/11/20. doi: 10.3233/jad- PubMed PMID: 30452410.

Neurons, that is brain and nerve cells, are primarily made out of what’s called ‘phosphorylated DHA’. That means the omega-3 fat DHA that is bound to a kind of fat called a phospholipid, as shown in the figure below. 

Seafood contains phosphorylated DHA but DHA supplements, whether derived from fish oil or algae, is not phosphorylated. Hence, it needs to be attached to phospholipids to work. This attachment is done by a B vitamin dependent process called methylation. 

There are several different kinds of phospholipids with strange names all starting with ‘phosphatidyl’ such as phosphatidyl choline, phosphatidyl serine, phosphatidyl inositol and phosphatidyl ethanolamine.  To a large extent these can be made from phosphatidyl choline. As a group of nutrients they are classified as ‘semi-essential’ because we can make some, but not enough for optimal health and especially optimal brain health. 

As a consequence there are moves afoot to classify choline (which can be easily attached to the ‘phosphatidyl’ part) as an essential nutrient with a recommended intake. This has come about due to the growing evidence that insufficient choline in pregnancy leads to cognitive impairment and developmental delay. This is particularly important for vegans because, like the omega-3 fatty acid DHA, there’s not much choline in plant-based foods, but there is some in foods such as quinoa, soya, beans, nuts and broccoli.

Currently an adequate intake of choline is defined as between 400mg and 520mg a day, the latter for pregnant and breast-feeding women. This is based on how much choline you need for healthy fat metabolism, liver function and reducing homocysteine levels. You also need choline to process cholesterol in the liver and brain. As you’ll see in the figure above, cholesterol is a vital brain component. But these levels don’t take into account what’s being learnt about choline’s role in brain development.. A good estimate of optimum daily choline intake would be at least 500mg and maybe double this in pregnancy. 

Most important is choline’s role in building, and maintaining, a healthy brain. A pregnant woman’s intake defines the cognitive abilities of their child. Twenty years ago we knew that pregnant rats fed choline half way through their pregnancy have more connections between brain cells, plus improved learning ability and better memory recall. Now we know it’s true for babies with several recent trials showing similar results indicating that more choline in pregnancy enhances cognitive development.

An example of this is a study which gave women in their third trimester of pregnancy either 480mg of choline or almost double this – 930mg. They then tested the babies’ information processing speed at 4,7,10 and 13 months. Not only were the babies of the mothers given the higher dose faster but also the longer the mother had been given even the lower dose the faster were the child’s reactions. The authors concluded that “even modest increases in maternal choline intake during pregnancy may produce cognitive benefits for offspring ”. Seven years later, there will still memory advantages in the children whose mother had extra choline during pregnancy.

Babies are born with blood choline levels three times higher than their mother, illustrating how vital this nutrient is for building neuronal connections, which newborn babies do at a rate of up to a million new connections a second! An optimal intake for brain function is likely to be a lot higher than the 400 to 500mg recommended for adults, and higher still in pregnancy.

Since brain cells are made of a membrane containing choline (and other phospholipids) attached to the omega-3 fat DHA, without choline the omega-3 doesn’t work. The attaching of the two depends on methylation, a process that is dependent on B vitamins, especially B12, folate and B6. Choline helps methylation and healthy methylation, indicated by a low blood level of homocysteine, helps synthesize choline. You need all three – DHA, choline and B vitamins especially B12. So, if you are lacking in DHA, or in vitamin B12, then you’ll be doubly dependent on getting enough choline.

Choline rich foods – are vegans at risk of deficiency? 

While the richest dietary sources are fish, eggs and organ meats there is significant amounts of choline in plant-based foods, notably soya as in tofu and soya milk, quinoa, nuts and seeds including flax seeds, almonds and peanuts, and cruciferous vegetables including broccoli, cauliflower and Brussels sprouts.

While, on the face of it, it does appear than vegans, especially those planning pregnancy, need to become choline focused in relation to choosing the right daily foods, and possibly supplementing, there is not yet conclusive evidence showing that vegan mothers are at risk, although it is likely that they are. One of the learnings that has come out of studies on omega-3 DHA is than vegan mothers may convert more vegan omega-3 ALA into DHA as an evolutionary imperative – not that a top up with supplementation isn’t still the recommendation. Could it be that vegan mothers make more choline if needed since it is so important for brain development? There are very few studies of vegans to know the answer to this question.

One recent study looked at choline levels in breast-milk of vegans, versus vegetarians and non-vegetarians. There was no significant difference with the author of the study concluding “This suggests that maternal plant-based diet by itself is not a risk factor for low breast-milk choline.” 

The vegan community is certainly divided on this issue. Of course, the safe or cautious position, while the science unravels, is to supplement choline during pregnancy.

What intake of choline can you achieve from a vegan diet alone? Here’s a list of the best plant-based food for choline, compared to egg and fish as a yardstick, listed in order of how much you could get in a reasonable serving*:

FOOD CHOLINE PER SERVING PER 100g

An egg (all in the yolk) 50g 113mg  226mg

Fish eg salmon (100g/3oz) 90mg 90mg

Soya milk (cup – 250g) 57mg 23mg

Shiitake mushrooms (1 cup/145g) 54mg 37mg

Soya flour 12.5g (a cake slice) 24mg 192mg

Peas (1 cup -160g) 47mg 30mg

Quinoa, raw (1/3 cup 60g) 42mg 70mg 

Beans, raw (1/3 cup – 60g) 40mg 67mg

black, white, pinto, kidney

Broccoli, cauliflower 

or sprouts (1 cup/91g) 36mg 40mg  

Tofu (half a cup-125g) 35mg  28mg

Hummus (1/2 cup) 34mg 28mg

Chickpeas (1/4 can) 33mg 33mg

Baked beans (1/4 can) 31mg 31mg

Flaxseeds (small handful) 22mg 78mg

Pistachio (small handful) 20mg 71mg

Pine nuts (small handful) 18mg 65mg

Cashews (small handful) 17mg 61mg

Wholegrain bread (2 slices – 50g) 17mg 34mg

Avocado (1/2) 14mg 28mg

Almonds 50g (small handful) 12mg 42mg

Peanuts (small handful) 12mg 42mg

Wheatgerm (tablespoon 7g) 12mg 178mg

Almonds or peanut butter (tbsp) 10mg 61mg

Source: USDA choline content database and https://nutritiondata.self.com

*Many foods have not been analysed for choline, and measurements do vary, so this is a guide rather than a definitive list.

What does this mean for your daily diet? Here’s a typical vegan daily menu aimed to maximise choline intake and how much it would give you (I’m not including all foods and recipes, just those ingredient that deliver significant amount of choline):

BREAKFAST

A cup of soya milk 57mg

Small handful of nuts or seeds 20mg

(Flax, chia, almonds etc)

LUNCH

A cup of cooked quinoa (1/3 cup raw) 43mg

A serving (100g) of either broccoli, 36mg

cauliflower or Brussels sprouts

Avocado (1/2) 14mg

SNACKS

A tablespoon of almond or peanut butter 10mg

Hummus (1/2 cup) 34mg

Two slices of wholegrain bread 17mg

DINNER

A serving of tofu (125g) or beans 35-40mg

Half a cup of shiitake mushrooms 27mg

A serving (100g) of either broccoli, 36mg

cauliflower or Brussels sprouts

TOTAL 332mg

In reality you are unlikely to achieve this every day, and it would be quite limiting on your food choices, so a realistic target would be to achieve 300mg of choline from food. If you are aiming to achieve 500mg, which is the low end of optimal – more than this may be optimal in pregnancy – that leaves a shortfall of around 200mg of choline, suggesting the need for supplementation.

The most direct source of choline is from soya-derived lecithin granules and capsules. A flat tablespoon of lecithin granules (7.5g), which has a neutral and pleasant taste and can be sprinkled on cereals, in shakes and soups or eaten as is, provides 1,500 mg of phosphatidylcholine and around 200mg (13 per cent) of choline. Some ‘high phosphatidyl choline’ lecithin, sometimes called ‘high PC lecithin’ is 18 per cent choline, thus you need less – approximately a flat dessertspoon.

One tablespoon of lecithin granules equals three 1,200mg lecithin capsules (if ‘high PC’ two capsules would suffice). We suggest that this is a sensible addition to a completely vegan diet. (If you aspire to be plant-based most, but not all of the time the addition of two eggs, or an egg and a fish serving, would achieve 500mg a day of choline.)

You can also find ‘brain food’ supplements providing a combination of different kinds of phospholipids, not just choline, but its hard to get enough choline from these if your only other food sources are plant-based foods. 

In summary, we need both omega-6 and omega-3 fats, as well as phospholipids.

Have one or two servings a day of dark green, leafy veg – especially those that grow in colder climates such a kale, broccoli, brussels sprouts, or a serving of seaweed as sources of both choline and omega-3.
Have a serving of quinoa, beans or tofu every day, if not two, for choline.
Have a dessertspoon of high PC lecithin, or two capsules of high PC lecithin granules every day. These guidelines are especially important if you are planning a pregnancy, pregnant or breast-feeding.

If you are not completely vegan the best food source for phospholipids and choline are eggs. Eat six eggs a week. The choline is in the yolk. The advice regarding omega-3 – eat three servings of fish a week, is good for choline too but it is present in all fish, not just oily fish high in omega-3 fats.

Have you taken the Cognitive Function Test to find out your Dementia Risk Index score? It’s completely FREE and you can choose to pay for the COGNITION programme afterwards if you need personalised recommendations to help you put diet and lifestyle tips into action.

Brain Fats – Seafood, Omega-3 PUFAs, Phospholipids and Vitamin D

The omega-3 fat, docosahexaenoic acid (DHA) is the most abundant PUFA in the brain, concentrated in the grey matter and, particularly at the synapses.¹ DHA is incorporated into membrane phospholipids, where it affects the properties of the membrane, for example, maintaining membrane fluidity. DHA, along with other omega-3 fats EPA, DPAn-3 and their mediators are involved in a wide variety of processes in the brain, such as making new neurons, synaptic connections and the regulation of inflammation.²

Fish, especially cold-water oily fish, contain high levels of DHA and EPA,  and epidemiological studies consistently suggest that an elevated fish intake is associated with decreased risk of neurodegenerative diseases, such as Alzheimer’s disease.³ Recent estimates suggest that worldwide many populations are currently consuming DHA and EPA at levels well below the recommendations issued by many international authorities (GOED), with and blood levels of EPA and DHA have been estimated to be low to very low for most of the world, which may increase global risk for chronic disease.⁴

Interestingly, positive associations have also been found between walnut consumption and cognitive performance.⁵ Walnuts are a source of omega-3 fat, alpha-linolenic acid (ALA) and also a range of antioxidants.

Omega-3 Supplementation and cognitive decline

DHA supplementation appears to show the greatest promise in the early stage before the onset of memory loss symptoms,¹ and at levels at or above 1000 mg per day (Ismail 2015).⁶

A study of healthy 50-75 year olds were given 2,200 mg a day of omega 3 fish oils for six months not only reported significant increase in executive function, one aspect of cognition that is a hallmark of Alzheimer’s, but also beneficial structural changes in white matter integrity and grey matter volume in the brain. The cognitive improvement correlated with blood levels of omega-3 PUFAs.⁷

A randomized, double-blind, placebo-controlled, clinical study, gave 900 mg of DHA a day for 24 weeks and reported an improvement in learning and memory function in those with age-related cognitive decline.⁸ In a further trial by the same research group, giving 2,000 mg a day of DHA or placebo to 402 people with mild to moderate Alzheimer’s disease, therefore further along the disease process, for a period of 18 months found no cognitive improvement.⁹

Phospholipids

Phospholipids, rich in eggs and seafood, are abundant in the brain. They make up the membranes of the different types of cells in the brain. These include Phosphatidylethanolamine (PE) and phosphatidylserine (PS) phosphatidylcholine (PC) and phosphatidylinositol (PI). They become attached to omega-3 DHA. (see film ‘Build Your Brain‘) Phosphatidylethanolamine (PE) and phosphatidylserine (PS) are enriched in DHA, whereas much lower levels are found in phosphatidylcholine (PC) and phosphatidylinositol (PI).³ Attaching DHA to phospholipids is a process that requires methylation, which is dependent on B vitamins.⁹ Interestingly, although DHA is typically found high in PS, levels have been found to be low in PS in post-mortem samples from Alzheimer’s disease patients.¹⁰ PS supplementation may benefit cognition in the elderly,¹¹ but as PS is highly enriched with DHA, it is currently unclear whether the potential beneficial effects of PS on cognition are due to the intact PS or DHA.  Although PC is not highly enriched in DHA, higher plasma concentrations of PC-DHA are associated with reduced risk of dementia and AD,¹² and post mortem samples from AD shows depletion of PC-DHA in grey matter.¹³

Supplementation

A number of trials have investigated the effects of providing multinutrient supplements containing a range of nutritional factors with the aim of supporting phospholipid biosynthesis. Our recent systematic review identified that omega-3 PUFAs and B vitamins as part of these multinutrient formulas confers benefits on cognition in older adults across a range of different types of measures of cognition in older adults.¹⁴ Furthermore, 12-week trial of citicoline has shown cognitive benefits in healthy older adults.¹⁵

Vitamin D

The primary source of vitamin D is exposure to sunlight. Seafood provides the most dietary vitamin D. Vitamin D deficiency increases risk of AD.^161,17,18  Supplements of vitamin D can be derived from animal or fungal sources (mushrooms and yeast). Supplementing 800iu (20mg) a day for 12 months has been shown to improve cognitive function and lessen amyloid protein markers.¹⁹

In a study in France involving 912 elderly patients followed for twelve years, a total of 177 dementia cases (124 AD) occurred: 25(OH)D deficiency was associated with a nearly three-fold increased risk of AD.²⁰

References

1.Dyall, S. C. (2015, 2015-April-21). Long-chain omega-3 fatty acids and the brain: A review of the independent and shared effects of EPA, DPA and DHA [Review]. Frontiers in Aging Neuroscience, 7(52). https://doi.org/10.3389/fnagi.2015.00052

2. Dyall, S. C., Balas, L., Bazan, N. G., Brenna, J. T., Chiang, N., da Costa Souza, F., Dalli, J., Durand, T., Galano, J. M., Lein, P. J., Serhan, C. N., & Taha, A. Y. (2022, Apr). Polyunsaturated fatty acids and fatty acid-derived lipid mediators: Recent advances in the understanding of their biosynthesis, structures, and functions. Prog Lipid Res, 86, 101165. https://doi.org/10.1016/j.plipres.2022.101165

3. Dyall SC, Michael-Titus AT. Neurological benefits of omega-3 fatty acids. Neuromolecular Med. 2008;10(4):219-35. doi: 10.1007/s12017-008-8036-z. Epub 2008 Jun 10. PMID: 18543124.

4. Stark, K. D., Van Elswyk, M. E., Higgins, M. R., Weatherford, C. A., & Salem, N., Jr. (2016, Jul). Global survey of the omega-3 fatty acids, docosahexaenoic acid and eicosapentaenoic acid in the blood stream of healthy adults. Prog Lipid Res, 63, 132-152. https://doi.org/S0163-7827(15)30033-3 [pii]10.1016/j.plipres.2016.05.001 Alzheimers Dement. 2017 Nov;13(11):1207-1216. doi: 10.1016/j.jalz.2017.03.003. Epub 2017 May 16

5. Theodore LE, Kellow NJ, McNeil EA, Close EO, Coad EG, Cardoso BR. Nut Consumption for Cognitive Performance: A Systematic Review. Adv Nutr. 2021 Jun 1;12(3):777-792. doi: 10.1093/advances/nmaa153. PMID: 33330927; PMCID: PMC8166568.

6. Ismail

7. A. Veronica Witte, Lucia Kerti, Henrike M. Hermannstädter, Jochen B. Fiebach, Stephan J. Schreiber, Jan Philipp Schuchardt, Andreas Hahn, Agnes Flöel, Long-Chain Omega-3 Fatty Acids Improve Brain Function and Structure in Older Adults, Cerebral Cortex, Volume 24, Issue 11, November 2014, Pages 3059–3068, https://doi.org/10.1093/cercor/bht163

8. Yurko-Mauro K, McCarthy D, Rom D, et al; Beneficial effects of docosahexaenoic acid on cognition in age-related cognitive decline. Alzheimers Dement. 2010; 6, 456-64

9. Quinn JF, Raman R, Thomas RG, et al; Docosahexaenoic acid supplementation and cognitive decline in Alzheimer disease: a randomized trial. JAMA, 2010; Nov 3;304(17):1903-11.

10. A David Smith, Fredrik Jernerén, Helga Refsum, ω-3 fatty acids and their interactions, The American Journal of Clinical Nutrition, Volume 113, Issue 4, April 2021, Pages 775–778, https://doi.org/10.1093/ajcn/nqab013

11. Cunnane, Stephen & Schneider, Julie & Tangney, Christine & Tremblay-Mercier, Jennifer & Fortier, Mélanie & Bennett, David & Morris, Martha. (2012). Plasma and Brain Fatty Acid Profiles in Mild Cognitive Impairment and Alzheimer’s Disease. Journal of Alzheimer’s disease : JAD. 29. 691-7. 10.3233/JAD-2012-110629.

12. Richter Y, Herzog Y, Lifshitz Y, Hayun R, Zchut S. The effect of soybean-derived phosphatidylserine on cognitive performance in elderly with subjective memory complaints: a pilot study. Clin Interv Aging. 2013;8:557-63. doi: 10.2147/CIA.S40348. Epub 2013 May 21. PMID: 23723695; PMCID: PMC3665496.

13. Schaefer EJ, Bongard V, Beiser AS, Lamon-Fava S, Robins SJ, Au R, Tucker KL, Kyle DJ, Wilson PW, Wolf PA. Plasma phosphatidylcholine docosahexaenoic acid content and risk of dementia and Alzheimer disease: the Framingham Heart Study. Arch Neurol. 2006 Nov;63(11):1545-50. doi: 10.1001/archneur.63.11.1545. PMID: 17101822.

14. Yuki D, Sugiura Y, Zaima N, Akatsu H, Takei S, Yao I, Maesako M, Kinoshita A, Yamamoto T, Kon R, Sugiyama K, Setou M. DHA-PC and PSD-95 decrease after loss of synaptophysin and before neuronal loss in patients with Alzheimer’s disease. Sci Rep. 2014 Nov 20;4:7130. doi: 10.1038/srep07130. PMID: 25410733; PMCID: PMC5382699.

15. Fairbairn, P., Dyall, S. C., & Tsofliou, F. (2022, Apr 27). The Effects of Multi-Nutrient Formulas containing a Combination of Omega-3 Polyunsaturated Fatty Acids and B vitamins on Cognition in the older adult: A Systematic Review and Meta-analysis. Br J Nutr, 1-42. https://doi.org/10.1017/S0007114522001283

16. Nakazaki E, Mah E, Sanoshy K, Citrolo D, Watanabe F. Citicoline and Memory Function in Healthy Older Adults: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial. J Nutr. 2021 Aug 7;151(8):2153-2160. doi: 10.1093/jn/nxab119. PMID: 33978188; PMCID: PMC8349115.

17. Sommer I, Griebler U, Kien C, Auer S, Klerings I, Hammer R, Holzer P, Gartlehner G. Vitamin D deficiency as a risk factor for dementia: a systematic review and meta-analysis. BMC Geriatr. 2017 Jan 13;17(1):16. doi: 10.1186/s12877-016-0405-0. PMID: 28086755; PMCID: PMC5237198;

18. Jayedi A, Rashidy-Pour A, Shab-Bidar S. Vitamin D status and risk of dementia and Alzheimer’s disease: A meta-analysis of dose-response †. Nutr Neurosci. 2019 Nov;22(11):750-759. doi: 10.1080/1028415X.2018.1436639. Epub 2018 Feb 15. PMID: 29447107;

19. Chai B, Gao F, Wu R, Dong T, Gu C, Lin Q, Zhang Y. Vitamin D deficiency as a risk factor for dementia and Alzheimer’s disease: an updated meta-analysis. BMC Neurol. 2019 Nov 13;19(1):284. doi: 10.1186/s12883-019-1500-6. PMID: 31722673; PMCID: PMC6854782.

20. Jia J, Hu J, Huo X, Miao R, Zhang Y, Ma F. Effects of vitamin D supplementation on cognitive function and blood Aβ-related biomarkers in older adults with Alzheimer’s disease: a randomised, double-blind, placebo-controlled trial. J Neurol Neurosurg Psychiatry. 2019 Dec;90(12):1347-1352. doi: 10.1136/jnnp-2018-320199. Epub 2019 Jul 11. PMID: 31296588.

21. Feart C, Helmer C, Merle B, Herrmann FR, Annweiler C, Dartigues JF, Delcourt C, Samieri C. Associations of lower vitamin D concentrations with cognitive decline and long-term risk of dementia and Alzheimer’s disease in older adults. Alzheimers Dement. 2017 Nov;13(11):1207-1216. doi: 10.1016/j.jalz.2017.03.003. Epub 2017 May 16. PMID: 28522216.

By Robert H. Lustig, MD, MSL

Most people know that refined sugar is not good for you, but what is it about sugar that’s particularly bad for your brain? Why is it essential, not only for brain health and dementia prevention, to reduce your intake of not only sugar but refined carbohydrates in general? (By refined, I mean those whose fiber has been processed away – not ‘whole’ as in vegetables, whole fruit (not juice), beans, and whole grains.

Let’s start at the extreme. What happens if you lived at the North Pole, and ate virtually no carbohydrates, or at least so little as to force your body and brain to switch to a kind of fuel, ketones, produced from fat? This is often called a “very low carb high fat” (LCHF) or “ketogenic” diet. Would you get sick? This is what Vilhjamur Steffanson did, when his Arctic exploration shipwrecked in 1913, and he was forced to live amongst the Inuit for two years. He noted that there was no diabetes, no cancer — and no Alzheimer’s. In 1928, he and his colleague checked themselves into Bellvue hospital, and ate only meat for one year.[1]They were healthier than the researchers who studied them! 

Your brain likes ketones

Ketones are made in the liver from fat – either breaking down your own fat (for example, if you were fasting, eating very little or exercising a lot), or from ingestion of a type of fat containing ‘medium chain triglycerides’ (MCTs). Coconut oil is approximately 54% MCTs and contains all 4 MCTs (C6, C8, C10, C12), but it turns out that one particular kind of MCT, called C8 because it is 8 carbons long, is the best fat for the liver to convert into ketones.

You may be surprised to know that your brain can run well on glucose (the kind of sugar that is fuel for our cells), but even better on ketones. The reason is that ketones cross into the brain easily, rapidly, and without a biochemical transporter. This is why children with severe epilepsy improve on a ketogenic diet. Watch this short film ‘Fuel your Brain’.

Brain benefits of a low-carb ketogenic diet

In fact, brain cells prefer ketones. In two studies, one on people with Alzheimer’s and the other on those with pre-dementia or mild cognitive impairment, giving 2 tablespoons of C8 oil (called capricin or caprylic acid triglyceride), brain energy derived from ketones went up by 230% and memory and mental acuity improved in those with Minimal Cognitive Impairment (MCI).[2,3]

A ketogenic diet has been shown to reduce schizophrenia symptoms, help reduce shaking in Parkinson’s, and slow down cognitive decline in those with dementia or pre-dementia. In fact, the ketogenic diet has been used to effectively treat childhood epilepsy for over 100 years! There’s a good review on the current status of the ketogenic diet in psychiatry here^.[4]

Ketogenic diets may help in many ways. Firstly, when a person eats too much carbohydrate, sugar, but especially fructose, damages the energy burning factories in cells, called mitochondria, so their ability to produce chemical energy for the neuron is greatly reduced. Switching to burning ketones instead can increase mitochondria number and function. A recent study also shows that a ketogenic diet has a positive effect on the gut microbiome,[5] and this might be one way the diet helps reduce fits in people with epilepsy.[6] Fructose, on the other hand, disrupts the gut microbiome in a negative way.

How sugar damages your brain

But what is it about a ketogenic diet that is good for your brain? Is it the ketones, the lowering of insulin, the type of fat, the elimination of carbohydrate, or specifically the elimination of sugar? We don’t yet know – I ask this question of every Alzheimer’s and metabolic researcher I know, and no one can tell me – just that it works.

There are a few possible mechanisms. First, the more carbs and sugar you eat, the more resistant you become to the hormone insulin. Insulin not only drives glucose into cells (including brain cells), but also sends excess sugar to the liver to turn into fat. When a person becomes insulin resistant, ironically, glucose transport is negatively impacted, reducing brain energy availability. Insulin resistance is a major driver of depression.[7] A ketogenic diet can reverse that. 

Fructose, which comprises half of sucrose (‘white’ or ‘table’ sugar), and half of ‘high-fructose corn syrup’ (added to numerous processed foods), damages our mitochondria, which leads to less brain energy availability. One study showed that fructose reduces liver mitochondrial function, while glucose stimulates it^.[8]  “The most important takeaway of this study is that high fructose in the diet is bad,” said Dr. C. Ronald Kahn from the Joslin Diabetes Center.  “It’s not bad because it’s more calories, but because it has effects on liver metabolism to make it worse at burning fat. As a result, adding fructose to the diet makes the liver store more fat, and this is bad for the liver and bad for whole body metabolism.”

Fructose is the main sugar in most fruits. People then extrapolate, “oh fruit must be bad for you.” Not true. Whole fruit has fibre (both soluble and insoluble); together they slow down glucose and fructose absorption in the GI tract limiting both liver and brain exposure, and they also help feed the gut bacteria (microbiome), so actually you get less fructose entering the bloodstream. Juicing the fruit removes the protective fiber, and juice has been shown to be just as dangerous to metabolism as is soda. So, eat your fruit — don’t drink it!

Carbohydrates and fructose age your brain

There’s another reason why sugar, and especially fructose, is bad for your brain and body. They produce Advanced Glycation Endpoints or AGEs, which damage the brain. These ‘oxidise’ proteins (so does cigarette smoke), rendering them useless , allowing them to aggregate into clumps, and use up valuable antioxidants in your diet such as vitamin C and E.

Fructose acts on your liver to switch your metabolism away from fat burning to fat making and storing, and inhibits an anti-ageing process called ‘autophagy’ which helps clean up and remove damaged mitochondria in order to regenerate new, healthier cells.

Why sweet foods are so addictive

So far we’ve only explored why sugar is bad for your “physical” brain. Knowing this is a good start. But why does your “emotional” brain keep telling you that you want it? Why do people find it so hard to resist, and so many become sugar addicts? The answer is that fructose activates the “reward system” in the brain. It causes dopamine release, the motivational neurotransmitter associated with ‘reward’. Any chemical that does so can be addictive – cocaine, heroin, alcohol, nicotine, or example. The trouble is the more you have, the more your brain ‘down-regulates’, i.e. becomes less responsive to your own natural feel-good dopamine, so you end up needing more sugar to get the hit and, in the end, you get no hit at all but feel thoroughly awful without it. That’s the Law of Diminishing Returns. That’s addiction.

Blood sugar control reduces dementia risk

Keeping blood glucose levels in the low-normal range is reflected by a low blood glycosylated haemoglobin (HbA1C) level, which means ‘sugar-coated red blood cells’. A low HbA1c is good and is a proxy for improved insulin sensitivity, associated with reduced risk for dementia in several studies.[9,10,11,12,13,14] 

A new study also shows that, in 40 year old adults with so-called normal glucose levels but at the higher end of the normal range, have increased their risk of Alzheimer’s by 15% [37]

Type 2 diabetes, the net result of losing blood sugar control, almost doubles the risk for dementia.[15,16] Diabetes is also associated with more rapid brain shrinkage.[17,18] Even people in the upper normal range of blood glucose have increased brain atrophy, impaired cognition, and increased risk of dementia.[19,20]

For instance, one trial measured HbA1c and glucose levels in several thousand elderly people over the course of almost seven years. In that time, slightly more than a quarter of the participants developed dementia, and the bottom line was that rising glucose levels were associated with increased risk of developing the condition, irrespective of whether the participants also had diabetes. Non-diabetics who experienced a modest increase in blood sugar levels had an 18% increased risk of dementia, as compared to those who already had diabetes at the start of the study or developed it within the trial period, who had a 40% increased risk.[21]

Prevention action – how to cut down your sugar load

In practical terms, preventing dementia today means avoiding sugar as much as possible.  If you’re going to eat carbohydrate, eat ‘whole’ carbohydrate foods such as whole vegetables, fruits (not juice), beans, only wholegrain bread (labelled as ‘100% wholegrain’, or pasta in small quantities. 

Starchy carbohydrates such as pasta, rice and potatoes benefit from being cooked and cooled, then eaten cold or re-heated, as some of the carbohydrate is converted into resistant starch – a type of fibre we can’t digest but which has the added benefit of fermenting and feeding our gut bacteria.

Make sure the carbohydrate comes with its inherent fibre. Oat cakes would be better than bread since the fibre in these foods helps ‘slow release’ the sugars. Eating white bread is associated with a poorer cognitive test performance, whereas high fibre bread is associated with better performance.[34] Eating carbohydrate foods with protein, for example brown rice with fish, or porridge oats with seeds, or fruit with nuts, further reduces the glycemic load (GL) of a meal. The best fruits in this respect are low-sugar high-fiber fruits like berries, cherries, and plums.

These kinds of foods are consistent with a Mediterranean diet which has also been shown to reduce risk.[35] Conversely, grapes, raisins, and bananas are high GL. A study in Finland and Sweden compared those with a healthy versus unhealthy diet, including the above criteria, in mid-life for future risk of developing Alzheimer’s disease and dementia 14 years later. Those who ate the healthiest diet had an 88% decreased risk of developing dementia and a 92% decreased risk of developing Alzheimer’s disease.[36] 

The take-home message is, if you are going to eat complex carbohydrates, eat them with fibre, fat and protein.

However, if you want to go one step further, you can switch to eating a ketogenic low-carb, high fat diet. The problem with the ketogenic diet is staying on it – there’s so much carbohydrate out there it’s hard to avoid it. But there are now breath monitors (e.g. Ketoscan, BioSense from ReadOut Health) that can help you stay in ketosis. A good book to help you explore and put into practice either a low carb ketogenic diet or a low GL diet is ‘The Hybrid Diet’ by Patrick Holford & Jerome Burne. And to understand how processed food is your enemy, take a look at my book ‘Metabolical’.

And if you want to know how sugar is impacting your body and brain then you can take one of our at-home, pin-prick, DRIfT blood test so you can know exactly how sugar is impacting your body and also become a part of our vital research into this area.

Become a Citizen Scientist & Join our Research today!

Food for the Brain is a non-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices

Please support our research by becoming a Friend of Food for the Brain.

References:

1. Heinbecker P. STUDIES ON THE METABOLISM OF ESKIMOS. Journal of Biological Chemistry. 1928 Dec;80(2):461–75.

2. Fortier M, Castellano C-A, St-Pierre V, Myette-Côté É, Langlois F, Roy M, et al. A ketogenic drink improves cognition in mild cognitive impairment: Results of a 6-month RCT. Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association [Internet]. 2020 Oct 26; Available from: https://pubmed.ncbi.nlm.nih.gov/33103819/

3. Croteau E, Castellano C-A, Richard MA, Fortier M, Nugent S, Lepage M, et al. Ketogenic Medium Chain Triglycerides Increase Brain Energy Metabolism in Alzheimer’s Disease. Journal of Alzheimer’s disease: JAD [Internet]. 2018;64(2):551–61. Available from: https://pubmed.ncbi.nlm.nih.gov/29914035/

4. Bostock ECS, Kirkby KC, Taylor BVM. The Current Status of the Ketogenic Diet in Psychiatry. Frontiers in psychiatry [Internet]. 2017;8:43. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28373848

5. Paoli A, Mancin L, Bianco A, Thomas E, Mota JF, Piccini F. Ketogenic Diet and Microbiota: Friends or Enemies? Genes. 2019 Jul 15;10(7):534

6. Olson CA, Vuong HE, Yano JM, Liang QY, Nusbaum DJ, Hsiao EY. The Gut Microbiota Mediates the Anti-Seizure Effects of the Ketogenic Diet. Cell [Internet]. 2018 Jun [cited 2019 Apr 17];173(7):1728-1741.e13. Available from: https://www.cell.com/cell/pdf/S0092-8674(18)30520-8.pdf

7. Watson K, Nasca C, Aasly L, McEwen B, Rasgon N. Insulin resistance, an unmasked culprit in depressive disorders: Promises for interventions. Neuropharmacology [Internet]. 2018 Jul 1 [cited 2022 Aug 5];136(Pt B):327–34. Available from: https://pubmed.ncbi.nlm.nih.gov/29180223/

8. Softic S, Meyer JG, Wang G-X, Gupta MK, Batista TM, Lauritzen HPMM, et al. Dietary Sugars Alter Hepatic Fatty Acid Oxidation via Transcriptional and Post-translational Modifications of Mitochondrial Proteins. Cell Metabolism [Internet]. 2019 Oct;30(4):735-753.e4. Available from: https://www.cell.com/cell-metabolism/pdfExtended/S1550-4131(19)30504-2

9. Luchsinger JA, Tang M-X ., Shea S, Mayeux R. Hyperinsulinemia and risk of Alzheimer disease. Neurology. 2004 Oct 11;63(7):1187–92.

10. Abbatecola AM, Paolisso G, Lamponi M, Bandinelli S, Lauretani F, Launer L, et al. Insulin Resistance and Executive Dysfunction in Older Persons. Journal of the American Geriatrics Society. 2004 Oct;52(10):1713–8.

11. Xu WL, von Strauss E, Qiu CX, Winblad B, Fratiglioni L. Uncontrolled diabetes increases the risk of Alzheimer’s disease: a population-based cohort study. Diabetologia. 2009 Mar 12;52(6):1031–9.

12. Hassing Lb, Grant Md, Hofer Sm, Pedersen Nl, Nilsson Se, Berg S, et al. Type 2 diabetes mellitus contributes to cognitive decline in old age: A longitudinal population-based study. Journal of the International Neuropsychological Society. 2004 Jul;10(4):599–607.

13. Yaffe K, Blackwell T, Whitmer RA, Krueger K, Barrett Connor E. Glycosylated hemoglobin level and development of mild cognitive impairment or dementia in older women. The Journal of Nutrition, Health & Aging [Internet]. 2006 Jul 1 [cited 2022 Aug 5];10(4):293–5. Available from: https://pubmed.ncbi.nlm.nih.gov/16886099/

14. Roberts RO, Knopman DS, Cha RH, Mielke MM, Pankratz VS, Boeve BF, et al. Diabetes and Elevated Hemoglobin A1c Levels Are Associated with Brain Hypometabolism but Not Amyloid Accumulation. Journal of Nuclear Medicine. 2014 Mar 20;55(5):759–64.

15. Arvanitakis Z, Wilson RS, Bienias JL, Evans DA, Bennett DA. Diabetes mellitus and risk of Alzheimer disease and decline in cognitive function. Arch Neurol. 2004 May;61(5):661-6. doi: 10.1001/archneur.61.5.661. PMID: 15148141.

16. Yaffe K, Blackwell T, Kanaya AM, Davidowitz N, Barrett-Connor E, Krueger K. Diabetes, impaired fasting glucose, and development of cognitive impairment in older women. Neurology [Internet]. 2004 Aug 24 [cited 2022 Mar 16];63(4):658–63. Available from: https://n.neurology.org/content/63/4/658

17. Tiehuis AM, van der Graaf Y, Visseren FL, Vincken KL, Biessels GJ, Appelman APA, et al. Diabetes Increases Atrophy and Vascular Lesions on Brain MRI in Patients With Symptomatic Arterial Disease. Stroke. 2008 May;39(5):1600–3.

18. Samaras K, Lutgers HL, Kochan NA, Crawford JD, Campbell LV, Wen W, et al. The impact of glucose disorders on cognition and brain volumes in the elderly: the Sydney Memory and Ageing Study. AGE [Internet]. 2014 Jan 9 [cited 2022 Aug 5];36(2):977–93. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4039246/

19. Mortby ME, Janke AL, Anstey KJ, Sachdev PS, Cherbuin N. High “normal” blood glucose is associated with decreased brain volume and cognitive performance in the 60s: the PATH through life study. PLoS One. 2013 Sep 4;8(9):e73697. doi: 10.1371/journal.pone.0073697. PMID: 24023897; PMCID: PMC3762736.

20. Crane PK, Walker R, Hubbard RA, Li G, Nathan DM, Zheng H, Haneuse S, Craft S, Montine TJ, Kahn SE, McCormick W, McCurry SM, Bowen JD, Larson EB. Glucose levels and risk of dementia. N Engl J Med. 2013 Aug 8;369(6):540-8. doi: 10.1056/NEJMoa1215740. Erratum in: N Engl J Med. 2013 Oct 10;369(15):1476. PMID: 23924004; PMCID: PMC3955123.

21. Crane PK, Walker R, Hubbard RA, Li G, Nathan DM, Zheng H, Haneuse S, Craft S, Montine TJ, Kahn SE, McCormick W, McCurry SM, Bowen JD, Larson EB. Glucose levels and risk of dementia. N Engl J Med. 2013 Aug 8;369(6):540-8. doi: 10.1056/NEJMoa1215740. Erratum in: N Engl J Med. 2013 Oct 10;369(15):1476. PMID: 23924004; PMCID: PMC3955123.

22. Luchsinger JA, Tang MX, Shea S, Mayeux R. Hyperinsulinemia and risk of Alzheimer disease. Neurology. 2004 Oct 12;63(7):1187-92. doi: 10.1212/01.wnl.0000140292.04932.87. PMID: 15477536.

23. Abbatecola AM, Paolisso G, Lamponi M, Bandinelli S, Lauretani F, Launer L, Ferrucci L. Insulin resistance and executive dysfunction in older persons. J Am Geriatr Soc. 2004 Oct;52(10):1713-8. doi: 10.1111/j.1532-5415.2004.52466.x. PMID: 15450050.

24. Ye X, Gao X, Scott T, Tucker KL. Habitual sugar intake and cognitive function among middle-aged and older Puerto Ricans without diabetes. Br J Nutr. 2011 Nov;106(9):1423-32. doi: 10.1017/S0007114511001760. Epub 2011 Jun 1. PMID: 21736803; PMCID: PMC4876724.

25. Seetharaman S, Andel R, McEvoy C, Dahl Aslan AK, Finkel D, Pedersen NL. Blood glucose, diet-based glycemic load and cognitive aging among dementia-free older adults. J Gerontol A Biol Sci Med Sci. 2015 Apr;70(4):471-9. doi: 10.1093/gerona/glu135. Epub 2014 Aug 22. PMID: 25149688; PMCID: PMC4447796.

26. Power SE, O’Connor EM, Ross RP, Stanton C, O’Toole PW, Fitzgerald GF, Jeffery IB. Dietary glycaemic load associated with cognitive performance in elderly subjects. Eur J Nutr. 2015 Jun;54(4):557-68. doi: 10.1007/s00394-014-0737-5. Epub 2014 Jul 18. PMID: 25034880.

27. Taylor MK, Sullivan DK, Swerdlow RH, Vidoni ED, Morris JK, Mahnken JD, Burns JM. A high-glycemic diet is associated with cerebral amyloid burden in cognitively normal older adults. Am J Clin Nutr. 2017 Dec;106(6):1463-1470. doi: 10.3945/ajcn.117.162263. Epub 2017 Oct 25. PMID: 29070566; PMCID: PMC5698843.

28. Taylor MK, Sullivan DK, Swerdlow RH, Vidoni ED, Morris JK, Mahnken JD, Burns JM. A high-glycemic diet is associated with cerebral amyloid burden in cognitively normal older adults. Am J Clin Nutr. 2017 Dec;106(6):1463-1470. doi: 10.3945/ajcn.117.162263. Epub 2017 Oct 25. PMID: 29070566; PMCID: PMC5698843.

29. Gentreau M, Raymond M, Chuy V, Samieri C, Féart C, Berticat C, Artero S. High Glycemic Load Is Associated with Cognitive Decline in Apolipoprotein E ε4 Allele Carriers. Nutrients. 2020 Nov 25;12(12):3619. doi: 10.3390/nu12123619. PMID: 33255701; PMCID: PMC7761247.

30. M.E. Mortby et al., ‘High “normal” blood glucose is associated with decreased brain volume and cognitive performance in the 60s: the PATH through Life Study’, PLoS One (2013), vol 8:e73697.

31. Lakhan, S.E., Kirchgessner, A. The emerging role of dietary fructose in obesity and cognitive decline. Nutr J 12, 114 (2013). https://doi.org/10.1186/1475-2891-12-114

32. Yau PL, Castro MG, Tagani A, Tsui WH, Convit A. Obesity and metabolic syndrome and functional and structural brain impairments in adolescence. Pediatrics. 2012 Oct;130(4):e856-64. doi: 10.1542/peds.2012-0324. Epub 2012 Sep 3. PMID: 22945407; PMCID: PMC3457620.

33. Mangone A, Yates KF, Sweat V, Joseph A, Convit A. Cognitive functions among predominantly minority urban adolescents with metabolic syndrome. Appl Neuropsychol Child. 2018 Apr-Jun;7(2):157-163. doi: 10.1080/21622965.2017.1284662. Epub 2017 Feb 22. PMID: 28631969.

34. Loef M, Walach H. Fruit, vegetables and prevention of cognitive decline or dementia: a systematic review of cohort studies. J Nutr Health Aging. 2012 Jul;16(7):626-30. doi: 10.1007/s12603-012-0097-x. PMID: 22836704.

35. Martínez-Lapiscina EH, Clavero P, Toledo E, Estruch R, Salas-Salvadó J, San Julián B, Sanchez-Tainta A, Ros E, Valls-Pedret C, Martinez-Gonzalez MÁ. Mediterranean diet improves cognition: the PREDIMED-NAVARRA randomised trial. J Neurol Neurosurg Psychiatry. 2013 Dec;84(12):1318-25. doi: 10.1136/jnnp-2012-304792. Epub 2013 May 13. PMID: 23670794.

36. Eskelinen MH, Ngandu T, Tuomilehto J, Soininen H, Kivipelto M. Midlife healthy-diet index and late-life dementia and Alzheimer’s disease. Dement Geriatr Cogn Dis Extra. 2011 Jan;1(1):103-12. doi: 10.1159/000327518. Epub 2011 Apr 27. PMID: 22163237; PMCID: PMC3199886.

37. Zhang X, Tong T, Chang A, Ang TFA, Tao Q, Auerbach S, Devine S, Qiu WQ, Mez J, Massaro J, Lunetta KL, Au R, Farrer LA. Midlife lipid and glucose levels are associated with Alzheimer’s disease. Alzheimers Dement. 2023 Jan;19(1):181-193. doi: 10.1002/alz.12641. Epub 2022 Mar 23. PMID: 35319157; PMCID: PMC10078665.

The mouth is a hub of activity, housing around 50–100 billion bacteria from 200 different bacterial species. The role of these resident bacteria in the mouth, also known as the oral microbiome, is an emerging area of research. Alterations in the oral microbiome may occur as a result of factors including consuming high amounts of sugar, smoking tobacco and experiencing chronic stress. Drinking large amounts of alcohol can also negatively impact the oral microbiome. Disruptions to the oral microbiome can lead to gut dysbiosis, which has been associated with increased permeability of the Blood Brain Barrier (BBB). 

Findings to date suggest that the oral microbiome, via interactions with the gut and brain (a network called the oral-gut-brain axis), may be a key consideration for brain health, and multiple associated conditions. This post will focus on three key areas where there is present research: autism, Down’s syndrome, and Alzheimer’s disease. 

Autism

Individuals with autism have been indicated to have alterations in their oral microbiome, as well as gut dysbiosis and related disruptions to the gut-brain axis. A study investigating the oral microbiome indicated that children with autism have a higher incidence of gastrointestinal disturbance and food allergies. Moreover, children with autism were observed to have a disruption to the ratio of Firmicutes: Bacteroidetes bacteria, in favour of Firmicutes. Balance of the Firmicutes: Bacteroidetes ratio is key for integrity of the gut, and disruptions to this ratio are indicative of gut dysbiosis.  

Moreover, two specific groups of bacteria, Brucella and Enterococcus faecalis were observed to be elevated in autistic children, whilst Flavobacterium sp. levels were demonstrated to be decreased. Research has suggested that individuals with autism have a higher risk of developing Alzheimer’s disease earlier in life. One potential mechanism for this could be due to alterations to the Firmicutes: Bacterodetes ratio.

Firmicutes and Bacteroidetes both utilise amyloids in the gut as structural material. Recognition of amyloids may become impaired by increased synthesis of inflammatory T cells by the innate immune system, as the result of intestinal permeability. Translocation of amyloids across the BBB has been hypothesised to be associated with enhanced Aβ deposit in the brain, although this requires further research.

Down’s Syndrome

Individuals with Down’s syndrome have been demonstrated to be more susceptible to periodontitis, or gum disease. One potential explanation for these findings could be due to alterations in oral microbiome composition. One study observed that individuals with Down’s syndrome have higher levels of Streptococcus mutans in their saliva. A further study observed increased levels of the pathogenic bacterial strains Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis.  Individuals with Down’s syndrome have an increased risk of developing Alzheimer’s disease later in life, with 50% of individuals >60 years of age meeting diagnostic criteria for dementia. One hypothesised mechanism for this is because of altered expression of inflammation and immune system modulating genes in periodontitis.

Alzheimer’s Disease

Individuals with Alzheimer’s disease have been observed to have higher levels of the oral bacteria, Treponema, in the brain. Moreover, disruptions to the oral-gut-brain axis has been associated with increased accumulation of beta amyloid and Tau, two key markers of Alzheimer’s disease.

Supporting the Oral-Gut-Brain Axis 

Supporting the oral-gut-brain axis is an area of research that is undeveloped, however, it seems logical that many of the measures employed for supporting gut and brain health would also be salient. 

Increase Fibre & Polyphenols

Consuming a wide array of colourful vegetables, fruits, herbs and spices is a great way of increasing prebiotic fibres, which help to support gut health via increasing production of SCFAs (short chain fatty acids), and polyphenols, plant compounds that have antioxidant properties and have been demonstrated to support the oral-gut-brain axis. 

Increase Omega-3 Fats

Omega-3 fats exert anti-inflammatory effects in the body, whilst increasing microbiome diversity via balancing the Firmicutes: Bacteroidetes ratio, which is essential for gut health and gut barrier integrity. Additionally, increased levels of omega-3 have been associated with reduced incidence of periodontitis. Ways to increase omega-3 include increasing consumption of oily fish such as salmon, mackerel and sardines, and also flaxseeds, walnuts and algae. 

Increase Fermented, Probiotic Foods

Probiotics have been associated with improved oral health due to decreased presence of pathogenic bacteria in the mouth. Examples of probiotic foods include fermented foods such as kimchi, kombucha, kefir, sauerkraut and sourdough bread.

Exercise plays an important role in cognition. In this TED talk listen to expert Dr Wendy Suzuki explaining in more detail.

Dr Wendy Suzuki – The Brain Changing Benefits of Exercise (TED).

Mental health conditions are on the rise and the statistics speak for themselves: a record 70 million antidepressant prescriptions were handed out in 2018, and an estimated 10 million people will be in need of mental health support in the next five years. Mood can of course be dependent on external factors, but internal factors such as fluctuations in hormones, neurotransmitters and nutrient availability can also exert considerable influence. In light of this, treating the mind and body separately does not make sense. 

Our Second Brain

Far from being distant organs, the gut and brain communicate through a complex network of neural, hormonal and immune pathways and messengers, called the “gut-brain axis”. The integrity of our digestive system directly impacts the information our brain receives, and the quality of the building blocks of the brain tissue itself.  

Poor mental health may be a symptom of imbalances in the gut-brain axis. More  than 100 million nerve cells line our gastrointestinal tract, working independently of our brains. We know that the gut-brain axis is a strong communication mechanism because anxiety and mood changes are correlated with irritable bowel syndrome and functional bowel problems such as constipation, diarrhea, bloating, pain and stomach upset.

Our mood can also be impacted by poor vagal tone. The vagus nerve connects our digestive system to our brain and is the major nerve in our ‘rest and digest’ nervous system. With busy and stressful lifestyles regularly triggering our ‘fight or flight’ response, this vagus nerve may not be functioning well, which can contribute to depression and indigestion. 

Mood and Immunity

The nervous and immune systems work together, with the brain housing specialised immune cells called microglia to help fight infections and clear away damaged cells. When stress is excessive, or when the immune system sends persistent distress signals, the inflammatory response triggered by the immune system has been linked with depression.  

Much of the immune system is housed in our gut, making sense when much of our environmental risk exposure enters the body through our food. Our gut, therefore, needs to be in good shape for our immune system to be working well.  

Maintaining Balance

Our blood sugar levels also impact our mood. Our brain is an energy hungry organ, using 25% of our total energy stores and preferring glucose to carbohydrates to keep it going. If our blood glucose levels are unstable, say from a high carbohydrate diet, this can be stressful for the brain to cope with and can cause mood swings or feeling ‘hangry’.   

Blood sugar swings can also make us feel fatigued and have a detrimental impact on an important protein, BDNF (brain-derived neurotrophic factor) essential for the survival and growth of brain cells. BDNF helps our brain cells communicate and promotes the calming neurotransmitter GABA, levels of which may be low in anxiety sufferers. It also supports how our body makes energy,  and therefore if levels of BDNF are low, we are more likely to feel fatigued, listless and at risk of experiencing mental ill health. 

Top Tip

Keeping our gut healthy with a Mediterranean style diet, abundant in fibre-rich fruit and vegetables, oily Omega-3 rich fish, and wholegrains enriched with B-vitamins, translates into increased brain health, in turn improving our mood and mental health. 

With thanks to Julie Pichler at Vagus Wellbeing for this article. Julie is a registered Nutritional Therapist and delivers our Workplace Wellbeing programme, offering educational and empowering webinars. Julie’s specialism is the gut-brain connection and how food impacts our mood and brain health.

Find out more about our webinars here and how they can support your employees’ mental wellbeing.

Methylation and mental health are intricately related. We take a deeper look into the association and why it is important.

What is methylation? 

Methylation has been a buzzword in the integrative health sphere for some time now. This is unsurprising considering its importance to our overall health and wellbeing. You may have heard of it before – or even googled it… Were you then promptly turned off by it after just one glance at its complexity?

We don’t blame you; understanding methylation is not for the faint-hearted. 

However, let us break it down for you into bite sized chunks. Hopefully you can finally make sense of it and apply this knowledge to your everyday life.

Think of it as a biological switch

Methylation is a critical biochemical process that happens billions of times in every single cell of the human body. It’s responsible for a vast range of biological functions such as: 

Detoxification
DNA expression
Neurotransmitter production
Hormone regulation

Whilst it can be complex in nature, the process of methylation simply entails the transfer of four atoms: one carbon atom and three hydrogen atoms. These are transferred from one substance to another.  

Let’s say that methylation is a type of biological switch that turns on and off to help keep our health in check. 

How does methylation impact mental health?

While we know that methylation plays an intrinsic role in many important body functions, for the purpose of this article, we will focus on its role in mental well-being and brain health. 

Put simply, methylation helps us make neurotransmitters, such as serotonin, dopamine, adrenaline, norepinephrine and melatonin. 

(For more in-depth information and references, please read the Upgrade Your Brain Book)

Methylation does this in a number of ways. It helps:

Convert tryptophan (building block for serotonin) to 5-HTP (precursor to serotonin) 
Transport dopamine, norepinephrine and adrenaline
Convert norepinephrine to adrenaline (important for focus and attention)
Lastly, convert serotonin to melatonin (sleep neurohormone) 

So as you can see, it’s pretty vital to a balanced mood and overall brain health. 

What impacts methylation? 

Unfortunately there are many things that can negatively impact methylation, such as our diet, exposure to environmental toxins, genetic factors and lifestyle habits. 

Let’s look at this in a little more detail. 

—

Anything that triggers oxidative stress can have a negative effect on methylation. Oxidative stress is a natural biological process that’s usually offset by our body’s own endogenous antioxidant production. But when there’s an imbalance between the two, and factors in our environment generating oxidative stress are tipping the scale in their favour, that’s when we can see prolonged inflammation and problems with methylation. 

What specific environmental factors can impact methylation?

Our modern environment is plagued with reactive oxygen species ROS that generate oxidative stress in the body. Key examples are environmental endocrine disruptors, like PCBs, herbicides, pesticides and plasticisers, as well as air pollution. 

Whilst we can’t necessarily fully control these aspects in our environment, we can control our defence against them, as well as making wise dietary choices that will have less of these substances in them. 

But first, let’s talk about what else can impact methylation.

Dietary factors and methylation

What you eat can impact how well you methylate, especially the intake of processed foods and sugars, which has been shown to play a negative role in methylation.

Perhaps unsurprisingly, research shows that eating a wholefood diet that includes wholemeal cereals, fish, legumes, fruits and vegetables can have a positive effect on methylation. 

Aside from dietary factors, there are a few nutrients that play a critical role in methylation.

Folate

Perhaps the most important nutrient is folate or B9. Methylation is almost entirely dependent on the availability of folate in the diet. It uses this nutrient to create the methyl donors – SAMe and methionine – to spark enzymatic reactions that are required for neurotransmitter production and transport. 

A large body of research (1) confirms that folate deficiency – something that is incredibly common – is frequently seen in those with depression, and is remediated with the supplementation of this nutrient.

When we consider the role that optimal methylation plays in producing serotonin and other neurotransmitters, it’s easy to see why folate is so important.

What about folic acid?

Many are drawn to supplementing folate in the form of folic acid, the synthetic version of this nutrient. You can often find folic acid in fortified foods such as breakfast cereals and breads. 

However, what people don’t realise is that this version of folate needs to be converted in the body to l-methylfolate and many people lack the ability to do this efficiently due to gene variations. 

This means the body is unable to utilise the folic acid properly.  We go into gene variants in a little more depth further down, so hold on for more information.

Where can we get folate in our diet? 

The best food sources of folate are dark leafy greens (like spinach and kale), legumes (such as lentils and chickpeas), liver, asparagus, Brussels sprouts, and fortified grains, so be sure to be getting these in your diet frequently. 

B12

Whereas folate is important to initiate the methylation cycle, B12 is required for the activation of folate from dietary folate to  5-methyltetrahydrofolate, so that it can go on to create the methyl groups – SAMe and methionine.  

If there isn’t enough B12 in the diet, folate can get stuck in the cycle, which halts methylation.

B12 is a nutrient that’s found in animal foods, such as meats, fish, eggs, poultry and dairy products. This means that if you’re vegan or vegetarian, you will likely need to supplement your B12 and consider eating fortified foods, such as plant milks.

Choline

Choline – plays an important role in various junctions in the methylation cycle. It is widely known that when folate is low, the body uses choline as its back up methyl donor to help keep methylation ticking along. 

It helps with activation of folate, as well as the recycling of homocysteine to methionine – a critical step in methylation.

The test that shows how well you are methylating…

Having high homocysteine is a key way of indicating whether your methylation is struggling and whether this recycling process isn’t functioning properly. 

We don’t want accumulating levels of homocysteine as it is a neurotoxin that has been linked to psychiatric disorders such as depression, schizophrenia, bipolar and Alzheimer’s disease (2). 

This is why if mental health is a concern, testing for homocysteine is a great way to find out whether you may have issues methylating. 
You can order and test your homocysteine level accurately from the comfort of your own home. Join our research and order your homocysteine test.

(Bear in mind that levels are not static and can change based on how well you’re methylating, as well as certain dietary factors, such as caffeine and alcohol consumption, which have been shown in some cases to tax methylation.)

Testing methylation

In addition to homocysteine, which is explained in further detail below, you can also take a DNA test to see whether you have any mutations on the MTHFR gene – the primary gene that is responsible for folate activation and homocysteine recycling – both of which are necessary for optimal methylation and therefore neurotransmitter production.

Testing for MTHFR

Variants or mutations on the MTHFR gene are inherited from your parents and can either be heterozygous (meaning you have one mutation) or homozygous (two mutations). 

It’s well known that having a homozygous mutation is more likely to cause health problems and having a heterozygous mutation is unlikely to cause issues. 

Common variants are:

C677T 
A1298C

Testing for these variants is done by a simple saliva test and is usually done privately. Here in the UK, there are various providers such as Lifecode GX, however, if you’re not based in the UK there are likely many more providers globally.

How do we optimise methylation?

As well as eating a wholefood diet that is devoid of sugar and processed foods, if you suspect methylation may be an issue for you, it’s important to take the environmental factors listed above into consideration. 

In order to avoid toxins and pollutants you can:

Eat organic produce as much as possible and wash any inorganic vegetables properly before consumption.
Drink filtered water
Buy toxin free cosmetics that don’t include typical endocrine disruptors such as parabens, benzophenones, bisphenols, and phthalates
Avoid plastics (bottled water, cling film, plastic tupperware etc)
If you smoke or vape – stop. 
Supplementation might also be considered, you can find out more about supplementation and brain health here.

Work with a nutritionist – find out more at our Brain Bio Centre Practitioners here.

Key takeaway: there is so much you can do to support your methylation pathways and support your mental health!

Eating a healthy, balanced diet, as well as engaging in healthy lifestyle practices as we outline in our COGNITION Programme, is key. We cannot change our genes but we can create the right environment for them.

When you become a FRIEND and gain access to your personalised 6-month COGNITION programme you will learn how to create the right environment to ‘upgrade your brain’.

—

Actions:

Order your homocysteine test here.
Dive deeper into the topic with our expert-led Methylation Webinar – you can get instant access here.
Complete the Cognitive Function Test here to get a personalised plan of action for upgrading your brain and to contribute to our research.
Become a FRIEND here

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References:
1 https://doi.org/10.1016/j.jpsychires.2017.07.019

2 Silva, V. C. da S., et al. (2015). “Homocysteine and Psychiatric Disorders.” Journal of Integrative and Environmental Sciences

Estimated reading time: 4mins

Despite the festivities and joy that Christmas celebrations can bring for some, for many, it can be a particularly painful time with heightened feelings of loneliness and despair. This may be especially true for those who are isolated or disconnected from their loved ones. With the extra pressures that this year brings, it’s important to have some strategies in place to help us find a sense of connection. 

An interesting recent study, offers some key information on how the brain is wired to seek social connection as if our survival depended on it, which helps us to understand why many of us feel such despair when we’re lonely. Neuroscientists at the University of Cambridge observed 40 participants in complete isolation for 10 hours, after which they were shown images of people socialising or playing sport. In response to these images, neurons in the midbrain – which is the part of the brain that is responsible for producing dopamine, our reward neurotransmitter – were stimulated. Interestingly, the same thing happened when these same participants – on a different day – were made to fast for 10 hours and then shown images of appetising food, like pizza and cake. This demonstrates how when we are lonely, we crave social connection in the same way that we crave food when we’re hungry. 

Connection to others is just as much of a necessity to survive as it is to eat, and it’s not the first time that science is showing this. For example, we know that loneliness is a significant risk factor for poorer cognitive health, as well as depression and mortality. So, in light of this, and with the added pressures of the pandemic, how can we nurture our connection with

others to help us thrive throughout the festive season? Here are a few tips that can help to boost our sense of connectedness:

1. Review which kinds of social interactions energise you the most 

This may be a time to reflect on which relationships/social circles you value the most and which ones may be leaving you a little drained. It is possible to feel lonely or disconnected, even when you’re with friends or family. Once you’ve determined those that you value the most, find time to nurture those connections away from distractions, such as phones or TV. Getting out in nature by finding a new park or green space you’ve never been to before and arranging a walk with a friend, or cooking a new recipe with your loved one and having a romantic dinner. The list is endless, but the most important thing is that it works for you. 

2. Find a volunteering opportunity

Science shows that altruistic behaviour, kindness and compassion, increase levels of endorphins and oxytocin, as well as creating new neural connections. Find a local food bank distribution venue or another cause that you resonate with where you can meet new people and help support others. 

3. Get creative

Getting involved in creative expression of any kind, from drawing and cooking, to gardening or dancing, can help to increase a sense of connection to ourselves and others. For example, making something creative with a friend or giving something creative as a gift, can be very therapeutic and rewarding, and has the added bonus of not requiring technology.

Final words…

It’s worth reiterating that loneliness can be a subjective experience, meaning that we can still be lonely despite having many loved ones around us. This highlights the need to take time to reflect and identify what makes each of us as individuals feel connected. 

Estimated reading time: 5 mins

The Gut Brain Axis

The gut microbiome, defined as the bacteria that colonises our digestive tract, seems to be a buzz word at the moment within the health industry, as a growing body of research is showing just how important quantity and quality of protective gut bacteria are for our health. But the most interesting recent discoveries concerning gut bacteria are how they interact with our brain, in a system that has been labelled the gut-brain axis. This axis represents a two-way relationship between the gut and the brain, whereby our bacteria help communicate messages to our brain and neurochemicals communicate from our brain to our gut. Not only have researchers found that gut bacteria are important for gut motility and nutrient absorption, but they are also finding that these 100 trillion microorganisms, that represent around 1000 different species, can actually modulate brain development and activity, as well as playing a role in conditions such as autism.

Autism and IBS

In the UK, there are over 700,000 people who are on the autism spectrum, which is a lifelong condition that can greatly impact the lives of those living with autism and their relatives. Research has continuously shown that those on the spectrum commonly have comorbidities related to digestive function, such as IBS. In a study of 255 (184 males/71 females) children with autism between two and 3.5 years of age and 129 (75 males/54 females) typically developing children in the same age group, it was found that preschool-aged children with autism were 2.7 times more likely to experience GI symptoms than their typically developing peers. Almost 50% of children with autism reported frequent GI symptoms — compared to 18% of children with typical development. It is not yet understood why this is the case, however the research on how our gut microbiome can influence brain activity is providing the grounds for new therapeutic measures for conditions like autism. 

The role of short chain fatty acids

The composition of our gut bacteria and its diversity is often dependent on the food that we eat. Insoluble fibre such as cellulose, xylans and inulin found in foods such as vegetables and whole grains, provide fuel for our gut bacteria to flourish and ferment to create short-chain fatty acids (SCFAs). These fatty acids, produced by protective bacteria, can reduce the production of proinflammatory molecules called cytokines and can enhance anti-inflammatory processes. SCFAs produced by certain strains of bacteria have also been found to be capable of producing neurotransmitters such as GABA, which is an inhibitory neurotransmitter that helps to regulate anxiety. Bacteria can also produce a set of neurotransmitters called monoamines such as dopamine, which helps control the brain’s reward and pleasure centres, serotonin, our mood stabilizer, and noradrenaline, a neurotransmitter that’s involved in our fight or flight stress response. The vagus nerve, which travels from the intestine to the brain, enables neurochemicals produced by the gut bacteria to be signalled to the brain.

SCFAs produced by pathogenic bacteria, such as the Clostridial species, have on the other hand, been shown to be elevated in those with autism. Disrupted gut bacteria has been frequently associated to autism in studies showing unfavourable amounts of pathogenic bacteria in stool samples and in biopsies of children on the autism spectrum. A variety of drivers such as early weaning from breast milk to infant formula, which was related to increased fecal concentrations of SCFAs produced by pathogenic bacteria, and genetic alterations that can negatively impact how food is digested, have been shown to play a role in symptoms associated to autism. 

Stress and the gut

Research has also shown how psychosocial stress can negatively impact our gut, by altering the composition of gut bacteria and thereby increasing inflammation. This is further evidence for the two-way relationship that exists between the brain and the gut, whereby externally-perceived stress can have a direct influence on the health of our digestive tract. A study measuring lactic acid bacteria (protective bacteria) in college students undergoing the stress of final examinations, found a significant decrease in this type of bacteria after the examination. In addition, studies observing the behaviour of bacteria-free mice, showed a wide range of deficits in brain and gut biochemistry, social behaviour and stress responses compared to mice inoculated with gut bacteria, again giving strong evidence for the role of gut bacteria in modulating brain activity.