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Magnesium for Brain Function

Magnesium for brain function icon featuring an orange periodic table style element tile with the symbol

Magnesium for Brain Function

When people think about nutrients that support the brain, omega-3 fats, B vitamins, and vitamin D usually get most of the attention. However, magnesium for brain function, including focus and memory, is just as important and often overlooked.

Yet there is another nutrient that may deserve a place on that list.

Magnesium is involved in more than 300 biochemical reactions throughout the body. It helps regulate nerve signalling, supports energy production, influences sleep quality, helps control blood sugar, and plays a critical role in the brain’s ability to learn, adapt, and form memories.

Despite this, many people consume less magnesium than they need.

As rates of cognitive decline, anxiety, sleep problems, and metabolic disease continue to rise, researchers are increasingly investigating whether magnesium status could play a role in protecting brain health throughout life.

Why does magnesium matter for the brain?

Your brain is an energy-hungry organ.

Although it accounts for only around 2% of body weight, it uses approximately 20% of the body’s energy supply. To function well, brain cells require a constant supply of nutrients that support energy production, communication between neurons, and protection from oxidative stress.

Magnesium contributes to all three.

It helps regulate neurotransmitters, supports healthy nerve-cell communication, and is required for the production of ATP, the molecule that powers every cell in the body. Magnesium also influences NMDA receptors, which are involved in learning, memory formation, and neuroplasticity, the brain’s ability to adapt and create new connections.¹

Low magnesium levels have been linked to increased inflammation, greater oxidative stress, and impaired glucose regulation, all of which are recognised contributors to cognitive decline and dementia risk.²

Magnesium and cognitive decline

One of the most interesting areas of research concerns magnesium and long-term cognitive health.

Several large population studies have found that people with higher magnesium intake or higher blood magnesium levels tend to have a lower risk of cognitive impairment and dementia.³⁻⁵ In a study published in Neurology, individuals with optimal blood magnesium levels had a significantly lower risk of developing dementia compared with those with lower levels.⁴

A recent systematic review concluded that magnesium appears to play an important role in maintaining cognitive health throughout ageing, although researchers emphasise that more intervention studies are needed to establish cause and effect.²

This does not mean magnesium is a magic bullet for preventing dementia, but it does suggest that ensuring adequate magnesium intake may be one of several important factors that help support a healthy brain as we age.

Could magnesium help with brain fog?

Many people first become interested in magnesium because they feel mentally tired, forgetful, or unable to concentrate.

While brain fog is not a medical diagnosis, it is often associated with poor sleep, chronic stress, blood sugar instability, and low energy production, all areas in which magnesium plays an important role. It also helps regulate the body’s response to stress. Chronic stress can deplete magnesium stores, while low magnesium levels may make us more vulnerable to the effects of stress, creating a vicious cycle.⁶

For some people, improving magnesium status may help support mental clarity simply by improving sleep quality, reducing stress reactivity, and supporting stable energy production.

Magnesium, mood and sleep

The relationship between magnesium and mental wellbeing has been studied for decades.

Research suggests that magnesium may help support healthy mood regulation and stress resilience, particularly in individuals with inadequate magnesium intake.⁶

Magnesium is also commonly used to support sleep. It helps regulate the nervous system and appears to influence melatonin production and GABA activity, both of which are involved in sleep regulation.

While magnesium is not a sleeping tablet, some people report improvements in sleep quality, reduced nighttime waking, and a calmer mind when magnesium intake is optimised.

Since poor sleep is increasingly recognised as a risk factor for cognitive decline and Alzheimer’s disease, supporting healthy sleep may be one of the ways magnesium contributes to long-term brain health.

Before reaching for a supplement, it’s worth looking at your diet. The richest sources of magnesium include:

  • Pumpkin seeds

  • Chia seeds

  • Almonds and cashews

  • Beans and lentils

  • Spinach and leafy greens

  • Whole grains

  • Dark chocolate

Many people can substantially improve their magnesium intake simply by eating more magnesium-rich foods, including leafy greens, beans, nuts and seeds. Although modern farming and soil quality may have reduced the magnesium content of some foods compared with the past, food should still be your first source wherever possible. Supplements are best considered a complement to diet, not a replacement for it.

Which type of magnesium is best?

One of the most confusing aspects of supplementation is the number of different forms available.

The truth is that there is no single “best” magnesium. Different forms may be more suitable, depending on your goals.

Magnesium glycinate combines magnesium with the amino acid glycine. It is well absorbed and gentle on the stomach. Although it is widely recommended to support sleep and relaxation, there is currently little direct evidence that it is more effective than other well absorbed forms of magnesium. Its popularity is based largely on its favourable absorption, the calming properties of glycine, and positive clinical experience.

Magnesium L-threonate has attracted attention because it appears to increase magnesium levels within the brain more effectively than some other forms.

Animal studies have shown improvements in learning and memory, while early human studies suggest potential benefits for cognitive function.¹ ⁷

The evidence remains preliminary, but this is currently the form generating the most interest for memory and cognitive health.

Magnesium citrate is widely available and generally well absorbed. It is often used when constipation is also an issue because it can have a mild laxative effect.

Magnesium malate combines magnesium with malic acid, a compound involved in cellular energy production.

Some practitioners favour this form for people experiencing fatigue, although the evidence supporting its superiority for energy is limited.

Magnesium oxide contains a high amount of elemental magnesium but is relatively poorly absorbed.

For brain health purposes, there are usually better options available.

The bottom line: what this means for you

Magnesium is not a miracle nutrient, nor is there one form that’s right for everyone. The best choice depends on your individual needs, goals, and overall health. For some people, simply eating more magnesium-rich foods may be enough, while others may benefit from supplementation.

What the evidence does tell us is that magnesium is fundamental to healthy brain function. It supports energy production in every cell, helps nerve cells communicate, contributes to healthy sleep and stress regulation, and plays an important role in learning and memory. Maintaining healthy magnesium levels may therefore be one of the many ways we can support our brains as we age. (2-8)

Brain health is rarely transformed by a single nutrient, supplement, or food. It’s the result of consistently supporting the systems your brain depends on through good nutrition, regular movement, restorative sleep, stable blood sugar, social connection, and other healthy lifestyle habits.

Magnesium isn’t the whole picture, but it is an important piece of it. Making sure you’re getting enough, whether through your diet or, where appropriate, a well-chosen supplement, is one simple step towards supporting your brain for years to come.

References
  1. Ozawa M, Ohara T, Ninomiya T, et al. Dietary patterns and risk of dementia in an elderly Japanese population: the Hisayama Study. Am J Clin Nutr. 2013;97(5):1076-82.
  2. Kieboom BCT, Niemeijer MN, Leening MJG, et al. Serum magnesium and the risk of dementia. Neurology. 2017;89(16):1716-22.
  3. Slutsky I, Abumaria N, Wu LJ, et al. Enhancement of learning and memory by elevating brain magnesium. Neuron. 2010;65(2):165-77.
  4. Zhang C, Hu Q, Li S, Dai F, Qian W, Hewlings S, et al. A Magtein® magnesium L-threonate-based formula improves brain cognitive functions in healthy Chinese adults. Nutrients. 2022;14(24):5235. doi:10.3390/nu14245235.
  5. Vink R. Magnesium in the CNS: recent advances and developments. Magnes Res. 2016;29(3):95–101. doi:10.1684/mrh.2016.0408.
  6. Slutsky et al. (2010), Neuron — rat study, magnesium-L-threonate improved learning and memory. DOI: 10.1016/j.neuron.2009.12.026
  7. Liu et al. (2016), Journal of Alzheimer’s Disease — randomised, double-blind, placebo-controlled human trial in older adults with cognitive impairment, using MMFS-01 (a magnesium-L-threonate compound). DOI: 10.3233/JAD-15053

Further info

The Best Foods to Help Lower Homocysteine Naturally

The Best Foods to Help Lower Homocysteine Naturally

Foods that lower homocysteine including leafy greens, salmon, eggs, beans, whole grains, broccoli, asparagus, dairy, and nuts

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

NutrientRole in homocysteine metabolismFood sources
FolateSupports conversion of homocysteine back into methionineSpinach, kale, broccoli, asparagus, lentils and chickpeas
Vitamin B12Works with folate in homocysteine recyclingSalmon, sardines, shellfish, eggs, dairy products and liver
Vitamin B6Helps convert homocysteine into cysteinePoultry, salmon, chickpeas, potatoes and bananas
RiboflavinSupports folate metabolism and MTHFR activityEggs, milk, yoghurt, mushrooms and almonds
CholineSupports an alternative methylation pathwayEggs, liver, fish and soybeans
BetaineActs as a methyl donor in homocysteine recyclingBeetroot, spinach, quinoa and wholegrains

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

The richest dietary sources include:

  • Spinach
  • Kale
  • Broccoli
  • Brussels sprouts
  • Asparagus

These foods offer far more than folate alone. They also provide fibre, antioxidants and hundreds of naturally occurring plant compounds that support healthy blood vessels, reduce inflammation and contribute to overall brain health.

Folate-rich foods that lower homocysteine including spinach, kale, broccoli, Brussels sprouts, and asparagus

Beans and lentils

Legumes are another valuable source of folate. Good choices include:

  • Lentils
  • Chickpeas
  • Black beans
  • Kidney beans
  • Peas

Beans and lentils also provide fibre, plant protein and vitamin B6.

Rather than relying on one particular vegetable or legume, aim to include a wide variety throughout the week. Consistency is far more important than perfection.

Folate-rich legumes including lentils, chickpeas, black beans, kidney beans, and peas

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

Among the richest natural sources of vitamin B12 are fish and seafood, particularly:

  • Salmon
  • Sardines
  • Trout
  • Mussels
  • Oysters

Fish also provides omega-3 fatty acids, which may work alongside B vitamins in supporting brain health.

Homocysteine lowering foods including salmon, oysters, mussels, and sardines rich in vitamin B12

Eggs and dairy

Useful amounts of vitamin B12 are provided by eggs, milk, yoghurt, and cheese.

Eggs are particularly valuable because they also provide choline, another nutrient involved in homocysteine metabolism and healthy methylation.

Foods with vitamin B12 including eggs, milk, yogurt, butter, and cheese

Meat and liver

Beef, poultry and liver also provide vitamin B12.

For many people, improving dietary intake is an excellent place to start. For others, particularly if absorption has declined, supplementation may become necessary to restore adequate levels.

Foods that lower homocysteine with vitamin B12 including beef, chicken, and beef 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

A meal pattern that supports homocysteine metabolism might include:

  • Breakfast:Eggs with spinach and wholegrain toast.
  • Lunch:A lentil, beetroot and leafy green salad.
  • Dinner:Salmon with broccoli and quinoa.
  • Snack:Yoghurt with almonds or hummus with vegetables.

This is only an example. The goal is not to follow a rigid meal plan, but to combine foods that provide folate, vitamin B12, vitamin B6, riboflavin, choline and betaine throughout the day.

Sample homocysteine diet featuring eggs, salmon, leafy greens, whole grains, and fresh vegetables

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.

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

Frequently asked questions

What foods lower homocysteine fastest?

No individual food lowers homocysteine directly or works instantly.
Foods rich in folate, vitamin B12, vitamin B6, riboflavin, choline and betaine provide the nutrients your body uses to recycle homocysteine.
How quickly your level changes depends on your starting level, nutrient status, absorption, genetics, medications and any underlying medical conditions.

Which vitamin is most important for homocysteine?

Folate, vitamin B12 and vitamin B6 all play important but different roles in homocysteine metabolism.
Folate and vitamin B12 help recycle homocysteine back into methionine, while vitamin B6 helps convert it into cysteine.
Riboflavin, choline and betaine also support related pathways. For this reason, there is no single vitamin that is universally most important for everyone.

Are eggs good for homocysteine?

Eggs provide vitamin B12, vitamin B6, riboflavin and choline, all of which are involved in homocysteine metabolism.
They can form part of a balanced diet that supports healthy homocysteine levels, but eggs alone should not be expected to correct elevated homocysteine.

Is coffee bad for homocysteine?

The evidence is mixed.
Moderate coffee consumption has been associated with several health benefits, but some studies suggest that high consumption may increase homocysteine.
You may not need to stop drinking coffee, but maintaining a nutrient-rich diet is particularly important if you regularly consume several cups each day.

Can a vegetarian or vegan diet raise homocysteine?

A well-planned vegetarian or vegan diet can provide abundant folate and vitamin B6.
However, vitamin B12 is found mainly in animal-derived foods, so people following a vegan diet need a reliable source through fortified foods or supplements.
Low vitamin B12 status can contribute to raised homocysteine, even when folate intake is high.

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.

References
  1. Smith AD, Refsum H. Homocysteine: from disease biomarker to disease prevention. J Intern Med. 2021.
  2. 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: a randomized controlled trial. PLoS One. 2010;5(9):e12244.

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‘Our Children No Longer Need to Worry About Our Cognitive Decline’

Our Children No Longer Need to Worry About Our Cognitive Decline

man and woman walking on the beach image for Our Children No Longer Need to Worry About Our Cognitive Decline article

What one family learned from living through dementia and why they decided to take action.

When dementia affects a family, the impact often extends far beyond the person who receives the diagnosis. Many people begin to worry about cognitive decline, wondering whether it is an inevitable part of ageing or whether there is anything they can do to reduce their risk.In this story, Peter shares how watching his mother develop dementia changed the way he and his wife thought about ageing, why they decided to take a more proactive approach to their brain health, and how that decision ultimately gave their children something they hadn’t expected: peace of mind.

Most people do not start thinking seriously about dementia until it touches someone they love. Yet every day in the UK, around 790 people receive a dementia diagnosis, the equivalent of seven double-decker buses full of families beginning a journey they never expected to take.

Why One Family Decided Not to Worry About Cognitive Decline

For Peter and his family, dementia was not something they read about in the news or encountered through awareness campaigns. It arrived at their front door.

As his mother’s dementia progressed, the family witnessed first-hand how profoundly the condition could affect daily life. For a period, she lived with Peter and his wife, giving them a close-up view of the challenges, heartbreak, and uncertainty that often accompany cognitive decline.

Their children were young when their grandmother first became unwell and were old enough to witness much of what followed. They saw the gradual changes in her memory, independence, and ability to live the life she had once enjoyed. Like many families affected by dementia, they adapted as best they could, but experiences like these leave their mark.

Should You Worry About Cognitive Decline if Dementia Runs in Your Family?

At first, the family’s focus was entirely on supporting a much-loved mother and grandmother. Then, as they watched dementia unfold over many years, the children naturally started asking questions about the future. What would happen to their parents? Was this simply what ageing looked like? Could anything be done to reduce the risk of dementia?

For Peter, this became one of the most difficult parts of the journey.

“It wasn’t fair that they should have this burden so young.”

When his mother died in 2016, he and his wife found themselves reflecting on everything the family had been through. They knew there were no guarantees when it came to health and ageing, but they also felt increasingly uncomfortable with the idea of simply hoping for the best.

Instead, they made a decision. Rather than focusing on what they could not control, they would focus on what they could.

“We decided to do something about it. We wanted to keep our physical and cognitive health together for as long as possible.”

That decision marked the beginning of a journey that continues today.

What to Do Instead of Worrying About Cognitive Decline

Peter’s interest in health had not appeared overnight.

Years earlier, they had discovered Patrick Holford’s work and become increasingly interested in nutrition and healthy ageing. Like many people, they had spent years trying to understand how food, lifestyle, and everyday habits influence long-term wellbeing.

Dementia, however, gave that interest a new urgency, as brain health was no longer an abstract topic. It had become deeply personal.

Instead of feeling powerless, they wanted to understand more about the factors associated with cognitive decline and, more importantly, what practical steps they could take to support healthy brain ageing. This led them to Food for the Brain’s educational resources, the Cognitive Function Test, and DRIfT biomarker testing.

They were not looking for guarantees or predictions about the future. They wanted a clearer understanding of where they stood and, perhaps more importantly, what they could actually do about it.

Measuring What Matters

The first steps? Understanding where they actually stood.

After years of watching dementia affect someone they loved, they wanted more than good intentions. They wanted a clearer picture of their current health and a better understanding of where they should focus their efforts.

The Cognitive Function Test provided one piece of that picture. Having first completed the assessment many years ago, Peter returned to it years later with a renewed interest in dementia prevention and healthy ageing. His score improved from 51 to 73.

The score itself was only part of the story. What mattered more was having a way to check in on how things were going. After everything the family had been through, it felt reassuring to have something tangible to measure rather than simply wondering whether their efforts were making a difference.

Alongside cognitive testing, they also began monitoring several biomarkers associated with brain health through DRIfT testing and implementing the guidance they were given along the way. The results showed encouraging changes across a number of areas:

Key Changes Over Time

FromTo
Cognitive Function Test5173
Homocysteine11.9 µmol/L 7.16 µmol/L
HbA1c5.5% 5.1%
Omega-3 Index 7.69%10.3%

His homocysteine level proved particularly useful information. Although he had already made a number of dietary and lifestyle changes, his levels remained higher than he would have liked, hovering at around 12 µmol/L across several tests. Regular testing allowed him to identify the issue, make further adjustments, and see how his body responded over time. After introducing vitamin B12, his homocysteine eventually reduced from 11.9 µmol/L to 7.16 µmol/L.

Without testing, he would never have known that this important marker remained elevated, as it is not something you can feel. Equally, without repeating the test, he would never have known whether the changes he made were having the desired effect. never have known whether the changes he made were having the desired effect.

Lifestyle Changes That Reduced Their Worry About Cognitive Decline

There was no single intervention that transformed their health overnight. Instead, they gradually reshaped the way they lived. Ultra-processed foods disappeared from the shopping trolley, wheat was removed from the diet, fermented foods became a regular feature at mealtimes, and targeted supplements were added where testing suggested they might be beneficial. Alongside this, they stayed physically active, walked regularly, and continued to challenge themselves mentally through activities such as completing The Times crossword.

Like many people who successfully improve their health over the long term, they did not follow a perfect plan or look for a magic solution. They focused on making changes they could sustain and enjoy, building habits that fitted naturally into the life they wanted to lead in retirement.

In many ways, their experience reflects what the research increasingly tells us about brain health: it is rarely one single intervention that matters most, but the cumulative effect of multiple factors working together over time, from nutrition and exercise to sleep, metabolic health, social connection, and lifelong learning.

The Difference It Made

Over time, they began to notice subtle shifts. Their thinking felt clearer, they felt more optimistic about ageing, and they gained confidence from seeing improvements in some of the markers they were tracking. Yet perhaps the biggest change was not physical at all. For years, dementia had been something that happened to their family. Now, instead of feeling defined by that experience, they felt they were actively shaping what came next.

The conversations within the family began to change, too. Their children and their children’s partners became more interested in brain health, nutrition, and prevention, turning what began as one family’s experience of dementia into a wider conversation about healthy ageing. Rather than seeing cognitive decline as an inevitable part of getting older, the family started to see it through a different lens, one that recognised the role informed choices can play in supporting long-term brain health.

When asked what has mattered most, Peter does not talk about biomarkers, supplements, or cognitive test scores. He returns instead to the concern that first motivated him and his wife to take action. Watching their grandmother’s decline had left a deep impression on the children, who naturally worried about what the future might hold for their parents. Those concerns did not disappear overnight, but they gradually eased as they saw their parents taking positive action, learning more about brain health, and making it a priority.

Reflecting on everything that had changed, Peter felt one thing stood out above all the others. He said “our children no longer need to worry about our cognitive decline.”

For Peter, that is the result that matters most.

Want to understand your own brain health?

Peter’s experience is not really about a test score, a supplement, or a blood result. Those were simply tools that helped him and his wife better understand their health, make informed decisions, and feel more confident that they were moving in the right direction.

At its heart, this is a story about a family who experienced dementia first-hand and decided not to leave the future entirely to chance. It is about protecting independence, preserving memories, staying connected to the people we love, and approaching later life with greater confidence and optimism.

At Food for the Brain, we believe more people deserve the opportunity to do the same. As a research and education charity, our mission is to make dementia prevention and optimal brain health possible by translating the latest science into practical, accessible actions that people can take today. Through research, education, testing, and behaviour-change programmes, we help people understand their brain health and take positive action while there is still time.

Whether you are simply curious about your brain health or looking for ways to reduce your risk, you can get started by:

  1. Taking the free Cognitive Function Test and tracking your progress over time.

  2. Exploring DRIfT biomarker testing to gain deeper insight into key areas of brain health.

  3. Becoming a FRIEND of Food for the Brain and gaining access to the COGNITION programme, educational webinars, group coaching and ongoing support


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Algae Oil vs Fish Oil for Brain Health: What’s the Difference?

Algae Oil vs Fish Oil for Brain Health: What’s the Difference?

Algae Oil vs Fish Oil for Brain Health

If you’ve spent any time reading about brain health, you’ve probably come across omega-3s. When it comes to choosing a source of these essential nutrients, many people weigh up Algae Oil vs Fish Oil. They are one of the most researched nutrients in dementia prevention, cognitive function and healthy ageing, yet one surprisingly common question remains:

Does it matter where your omega-3s come from?

For years, fish oil was considered the gold standard. More recently, algae oil has emerged as an alternative that is popular with vegetarians, vegans and those who simply prefer a tasteless supplement. But does algae oil offer the same brain health benefits as fish oil, or is one genuinely better than the other?

The answer is more interesting than you might think.

Why Omega-3s Matter for Brain Function and Healthy Ageing

When we talk about omega-3s and brain health, we are mainly referring to two fatty acids: EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid).

DHA is particularly important because it forms part of the structure of brain cells themselves. In fact, DHA is one of the most abundant fats found within the brain, helping maintain healthy cell membranes and supporting communication between neurons.

EPA appears to play a slightly different role. It is involved in regulating inflammation, blood flow and a number of processes linked to mood and cognitive function.

Research has consistently linked higher omega-3 status with better cognitive performance, healthier brain ageing and a lower risk of cognitive decline. Some of the most fascinating findings come from the Oxford VITACOG studies, which examined the relationship between omega-3s, B vitamins and brain ageing.

Researchers found that participants with higher blood levels of omega-3s gained significantly greater benefits from homocysteine-lowering B vitamins than those with lower omega-3 levels. Those with both adequate omega-3 status and B vitamin support experienced slower rates of brain atrophy and reduced cognitive decline compared with those who had lower omega-3 levels [3,4].

Interestingly, emerging research suggests that maintaining adequate omega-3 levels may be particularly important for women. Hormonal changes associated with ageing can influence brain health, inflammation and cognitive resilience, making omega-3 status an important consideration throughout later life. You can learn more in our article on why women’s brains need omega-3 now.

The simple takeaway is that omega-3s appear to be an important part of protecting the brain as we age. They also do not work in isolation. Like most nutrients, they seem to be most effective when part of a wider network of nutrients and healthy lifestyle factors.

Want a quick overview before we compare algae oil and fish oil? This short video explains why omega-3s are so important for brain health and healthy ageing.

Algae Oil vs Fish Oil: What’s the Difference?

Fish oil is extracted from oily fish such as sardines, anchovies and mackerel and has been the most widely used source of EPA and DHA for decades.

Algae oil, on the other hand, is derived directly from marine microalgae.

This distinction is important because fish do not actually produce omega-3 fats themselves. Instead, they accumulate EPA and DHA by consuming algae and other organisms within the marine food chain [5].

In other words, algae are the original source of the omega-3 fats found in fish.

From a nutritional perspective, both fish oil and algae oil can provide the same biologically active forms of omega-3. The main differences relate to dietary preference, manufacturing methods and the specific balance of EPA and DHA provided by individual products.

If you’re considering an omega-3 supplement, it’s worth understanding the differences between EPA and DHA, how much you may need, and what to look for when choosing a quality product. Our comprehensive guide to omega-3 supplements covers the evidence, recommended intake levels and key considerations before you buy.

Algae Oil vs Fish Oil: Key Differences

Fish OilAlgae Oil
SourceFishMarine algae
Vegan-FriendlyNoYes
EPA & DHAHighDHA-focused (some EPA)
TasteMay cause fishy aftertasteNeutral
SustainabilityVariesMore sustainable
Best ForTraditional omega-3 supportPlant-based omega-3 support

Is Algae Oil as Effective as Fish Oil?

Fish oil still has one clear advantage: it has been studied for much longer.

As a result, there is currently a larger body of research investigating fish oil supplementation and health outcomes. That does not necessarily mean fish oil is superior, only that it has a longer research history.

More recently, scientists have started directly comparing fish oil and algae oil. A 2025 human trial found that algae-derived EPA and DHA were absorbed just as effectively as omega-3s from fish oil when equivalent doses were provided [6].

This is an important finding because it suggests the body is able to utilise EPA and DHA from algae in much the same way as EPA and DHA from fish oil. For people who do not eat fish, follow a plant-based diet or simply prefer a tasteless source of marine omega-3s, algae oil appears to be a credible alternative rather than a compromise.

Omega-3s, B Vitamins and Dementia Prevention

There are two topics we love talking about at Food for the Brain: omega-3s and homocysteine. While they might seem unrelated, some of the most exciting dementia prevention research suggests they may be more connected than we once thought.

One reason omega-3s have become such an important focus in dementia prevention research is their relationship with homocysteine. Homocysteine is a naturally occurring amino acid that, when elevated, is associated with a greater risk of cognitive decline and dementia. B vitamins, particularly folate, vitamin B12 and vitamin B6, help keep homocysteine levels under control.

In the landmark VITACOG trial, homocysteine-lowering B vitamins significantly slowed the rate of brain shrinkage in older adults with mild cognitive impairment [1]. Further analysis showed that these benefits were strongest among participants with higher omega-3 levels [3,4].

This helps explain why many practitioners now assess both homocysteine and omega-3 status when considering an individual’s long-term brain health. This highlights an important lesson in nutrition: it is rarely one nutrient acting alone. The greatest benefits usually come from the interaction between multiple nutrients and healthy lifestyle factors working together. (Which is why we have our 8 nutrition and lifestyle domains in the COGNITION online community and programme.)

Don’t Guess Your Omega-3 Status

One of the biggest misconceptions about omega-3 supplementation is that taking a supplement automatically means your levels are optimal.

In reality, omega-3 status varies considerably from person to person. Genetics, absorption, diet, dosage and supplement quality can all influence the amount that ultimately reaches your bloodstream. Two people taking the same supplement may achieve very different results.

That is why, at Food for the Brain, we believe testing is often more useful than guessing.

The DRIfT test measures several important biomarkers linked to brain health, including omega-3 status, homocysteine, vitamin D, HbA1c and glutathione. Rather than assuming your current diet or supplement routine is working, testing can help identify where support is needed and allow you to take a more personalised approach to protecting your brain health.

Algae Oil and Fish Oil: Key Takeaways for Cognitive Health

Both fish oil and algae oil provide the EPA and DHA associated with healthy brain ageing and cognitive function.

Fish oil remains the most extensively studied source and continues to have the largest body of evidence behind it. However, current research suggests that algae oil can raise blood levels of EPA and DHA just as effectively, making it a viable option for those who prefer not to use fish-derived products [6].

Perhaps the most important lesson from the research is that taking an omega-3 supplement is only part of the story. What ultimately matters is whether those omega-3s are reaching meaningful levels in your bloodstream and, ultimately, your brain.

The real question might not be whether your omega-3 comes from fish or algae.

The real question is whether your brain is getting enough.

Next Steps:

  1. Find out your omega-3 status with our DRIfT at-home blood test.

    It measures omega-3 levels alongside homocysteine, vitamin D, HbA1c and glutathione.

  2. Already focused on omega-3s?

    Order a standalone Omega-3 Test to see whether your current diet and supplements are achieving optimal levels.

References
  1. 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: a randomized controlled trial. PLoS One. 2010;5(9):e12244.
  2. de Jager CA, Oulhaj A, Jacoby R, Refsum H, Smith AD. Cognitive and clinical outcomes of homocysteine-lowering B-vitamin treatment in mild cognitive impairment: a randomized controlled trial. Int J Geriatr Psychiatry. 2012;27(6):592-600.
  3. Jernerén F, Cederholm T, Refsum H, Smith AD, Turner C, Palmblad J, et al. 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):215-221.
  4. Oulhaj A, Jernerén F, Refsum H, Smith AD, de Jager CA. Omega-3 fatty acid status enhances the prevention of cognitive decline by B vitamins in mild cognitive impairment. J Alzheimers Dis. 2016;50(2):547-557.
  5. Doughman SD, Krupanidhi S, Sanjeevi CB. Omega-3 fatty acids for nutrition and medicine: considering microalgae oil as a vegetarian source of EPA and DHA. Curr Diabetes Rev. 2008;4(3):198-203.

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Chromium, Blood Sugar and Brain Health: The Overlooked Connection

Chromium, Blood Sugar and Brain Health: The Overlooked Connection

Foods high in chromium, including whole grains, broccoli, grapes, eggs, nuts, legumes, and dairy, surrounding a chalkboard marked 'Cr' for sugar cravings and insulin resistance

How Blood Sugar Regulation Affects Brain Function?

When people think about protecting their brain, they often focus on keeping mentally active, reducing alcohol, or hoping they avoid dementia as they get older, somehow? But nutrients and minerals like chromium may also play a role in brain health.

Few think about blood sugar.

Yet every thought, memory, conversation, and decision relies on a constant supply of energy. Increasingly, researchers are discovering that how effectively we regulate blood sugar and respond to insulin may play an important role in how our brains function and age. (1)

This is where chromium enters the story.

Although only required in tiny amounts, chromium plays an important role in normal carbohydrate, fat, and protein metabolism. Its best understood role is helping insulin do its job more effectively. Insulin is the hormone that helps move glucose from the bloodstream into cells, where it can be used for energy, and chromium appears to support this process. (2)

The Brain’s Energy Demand and Glucose Supply

The brain represents only around 2% of body weight, yet uses roughly 20% of the body’s energy. (3) To function properly, brain cells require a continuous supply of fuel. Most of the time, that fuel comes from glucose, although the brain can also use ketones under certain circumstances.

When insulin is working well, glucose can be transported efficiently to the cells that need it. When cells become less responsive to insulin, a state known as insulin resistance develops. Blood sugar levels may rise, inflammation can increase, and energy production becomes less efficient.

Importantly, insulin resistance does not just affect muscles, fat tissue, and the liver. It also affects the brain.

Researchers have linked impaired insulin signalling with changes in brain structure and function, while people with type 2 diabetes consistently show a higher risk of cognitive decline and dementia than those with healthy glucose regulation. (4)

This growing body of evidence is changing how scientists think about brain health. Protecting the brain is not only about keeping it stimulated and active. It also depends on how effectively the body produces, regulates, and delivers energy to brain cells throughout life.

Chromium and Blood Sugar Regulation

Chromium is found naturally in foods including shellfish, meat, eggs, broccoli, and whole grains.

In terms of how it works, you can think of insulin as a key trying to unlock the door to a cell, and chromium appears to help that key work more efficiently, allowing glucose to move where it is needed and be used for energy. (2)

This has led researchers to investigate whether chromium supplementation might support healthy blood sugar regulation. Results have been mixed, but overall, the evidence suggests chromium may help improve fasting glucose in some individuals, particularly those with impaired glucose control or type 2 diabetes. (5)

That does not make chromium a miracle nutrient, nor does it mean everyone should supplement with it. What it does suggest is that even relatively small nutrient deficiencies may influence how effectively the body’s blood sugar regulation systems operate.

Insulin Resistance, Dementia and Brain Health

Unlike omega-3 DHA and B vitamins, which work together to support the formation, maintenance, and communication of brain cells, chromium’s role appears to be less about building brain tissue directly and more about helping to regulate the energy supply those cells depend upon.

Its potential relevance lies in the fact that the brain is one of the most energy-demanding organs in the body. If insulin resistance increases the risk of cognitive decline, it is reasonable to ask whether nutrients involved in healthy insulin function might also matter for long-term brain health.

We do not yet have evidence that chromium supplementation directly reduces dementia risk. However, the connection between insulin resistance and brain health is now difficult to ignore, making nutrients that support healthy glucose regulation increasingly worthy of attention.

In other words, chromium is interesting not because it is a brain nutrient, but because it sits within a system that appears to be highly relevant to how the brain functions and ages.

Chromium, Mood and Sugar Cravings

Interestingly, chromium’s effects may extend beyond glucose regulation.

Several small studies have explored chromium supplementation in people with atypical depression, particularly where symptoms include fatigue, increased appetite and carbohydrate cravings. Some reported improvements in mood and reductions in cravings, while researchers have also proposed possible effects on neurotransmitter systems involved in mood regulation. (6)

These studies are small and far from definitive, but they point towards something that is becoming increasingly clear: metabolism and mental health may be far more connected than we once believed. So much so that entire fields such as metabolic psychiatry and nutritional psychiatry have emerged in recent years. Researchers including Christopher Palmer and Georgia Ede are helping to challenge the idea that mental health exists solely in the brain, highlighting the important role that blood sugar regulation, nutrient status, inflammation and cellular energy production may play in our mental health and resliency.

Why Metabolic Health and Chromium Matters for the Brain

The story of chromium is not really about chromium.

It is about systems.

For decades we have tended to separate brain health from metabolic health. We talk about memory, dementia and cognition on one side, and blood sugar, insulin and diabetes on the other.

Increasingly, the science suggests these systems are deeply interconnected.

Reducing excess sugar intake remains one of the most important things we can do for long-term health. But this also raises an interesting question. What if someone is already eating relatively well, yet their blood sugar regulation remains less than optimal? Could nutrient status be part of the picture?

Chromium is unlikely to be the missing piece for everyone. In fact, many multivitamins already contain small amounts. But it serves as a useful reminder that healthy insulin regulation depends on more than simply avoiding sugar. It relies on a network of nutrients, hormones and metabolic processes working together.

This is one reason we include HbA1c in the DRIfT blood test. HbA1c provides insight into how effectively blood sugar has been regulated over the previous two to three months and can help identify an often-overlooked aspect of brain health long before symptoms appear.

Next Steps:

  1. Complete the Cogntive Function Test

    It is a free validated online assessment that gives you personalised results on your current brain health and the simple things you could do to improve it.

References
  1. de la Monte SM. Insulin resistance and Alzheimer’s disease. BMB Rep. 2009;42(8):475-481.
  2. Arnold SE, Arvanitakis Z, Macauley-Rambach SL, Koenig AM, Wang HY, Ahima RS, et al. Brain insulin resistance in type 2 diabetes and Alzheimer disease. Nat Rev Neurol. 2018;14(3):168-181.
  3. Vincent JB. Chromium: celebrating 50 years as an essential element? Dalton Trans. 2010;39(16):3787-3794.
  4. Harris JJ, Jolivet R, Attwell D. Synaptic energy use and supply. Neuron. 2012;75(5):762-777.
  5. Biessels GJ, Despa F. Cognitive decline and dementia in diabetes mellitus: mechanisms and clinical implications. Nat Rev Endocrinol. 2018;14(10):591-604.
  6. Davidson JR, Abraham K, Connor KM, McLeod MN. Effectiveness of chromium in atypical depression: a placebo-controlled trial. Biol Psychiatry. 2003;53(3):261-264.
  7. Docherty JP, Sack DA, Roffman M, Finch M, Komorowski JR. A double-blind, placebo-controlled, exploratory trial of chromium picolinate in atypical depression. Int Clin Psychopharmacol. 2005;20(5):245-249.
  8. Attenburrow MJ, Odontiadis J, Murray BJ, Cowen PJ, Franklin M. Chromium treatment decreases the sensitivity of 5-HT2A receptors. Psychopharmacology (Berl). 2002;163(2):216-221.

Further info

Is China’s Alzheimer’s Nightmare Becoming Our Reality?

Is China’s Alzheimer’s Nightmare Becoming Our Reality?

Patrick Holford examines how China is advancing Alzheimer’s prevention through nutrition, lifestyle and digital health initiatives, while questioning the pace of policy action in the UK.

The Race to Prevent Alzheimer’s in China

If there is one country that has to move fast to prevent Alzheimer’s, it is China. And it is.

With almost a quarter of its population over 60, some 320 million people, and an estimated 20 million expected to have Alzheimer’s by 2030, costing close to a trillion dollars a year, government health officials are taking prevention very seriously indeed.

Those over 60 are not called old, elderly, or senior, but “silver-haired“, a growing community that is at the heart of China’s health prevention strategies.

The doctor in charge of the Silver-Haired Healthy Lifestyle campaign is Dr Zhang Lei. He is a famous TV doctor and former surgeon.

I asked him if he believed there would ever be a cure for Alzheimer’s.

Prevention is the cure,” he said. “And I want to make a special announcement. Next year, when your excellent book Alzheimer’s: Prevention is the Cure is published in Chinese, we will use this book as the cornerstone of our national prevention campaign. We already have direct access to 20 million people through our networks, but our ambition is to reach as many as 100 million. We will encourage everyone to take the online Cognitive Function Test from Food for the Brain. This book and this tool together will be our roadmap for a prevention revolution in China.”

Prevention-First Approach

I attended and spoke at the 2nd Silver-Haired Healthy Lifestyle Conference, where I met hundreds of silver-haired people like myself. The event was attended by 2,500 people and broadcast to 10 million people across twenty TV channels.

Other speakers included leading professors of public health, nutrition, gerontology and geriatrics, all delivering positive and progressive messages about prevention, including eating more seafood and vegetables, stopping smoking, cutting right back on sugar, sleeping better and taking 10,000 steps a day.

I spoke about the essential need for, and codependence of, omega-3, phospholipids and B vitamins. If omega-3 were the man and phospholipids, rich in eggs and seafood, were the woman, then B vitamins are the priest, I said. When they are married in your brain, magic happens. Together, they are the three building blocks of every brain cell.

You could have heard a pin drop. Everyone was listening and, in China, action is taken quickly.

The former Health Minister said that “diet, supplements and lifestyle” are the cornerstones of prevention. “We need education, not medication.

No one was talking about anti-amyloid treatments.

Prevent Alzheimer’s at Scale

Next year, when the 3rd Healthy Lifestyle Conference coincides with the Chinese publication of my book Alzheimer’s: Prevention is the Cure, I have been invited to speak at universities and health departments across China.

Many silver-haired people in China do not have computers, but they all have smartphones. There are virtually no physical wallets. Communication and payment are conducted through the WeChat app.

The professors and public health officials were therefore very excited about our online digital test. They want to get everyone using Food for the Brain’s Cognitive Function Test. The COGNITION questionnaire then helps people understand which specific prevention steps are most relevant to them.

The experts, health authorities and policymakers understand that changing behaviour is the hardest part, and that this kind of personalised digital technology is key to motivating individuals and measuring change to find out what really works. It is big-data science helping to sharpen prevention strategies.

Why China Is Embracing Nutrition Over Medication for Brain Health

Traditionally, Chinese culture sees food as medicine, which may be one reason people are more open to optimum nutrition. There is also a long tradition of using natural compounds to support health, so supplements are a natural extension of this way of thinking.

Not one person repeated the old myth that “you can get all the nutrients you need from a well-balanced diet“.

The stark ignoring of established scientific facts about, for example, B vitamins and omega-3, which have outperformed anti-amyloid treatments, by our politicians and health ministers is verging on outrageous when the lives and brains of so many are at stake.

China’s High-Speed Lesson for Alzheimer’s Prevention

As I sat on a high-speed train travelling 1,200 kilometres from Shanghai to Beijing in just 3.5 hours, faster than taking a plane, and capable of speeds of 650 kilometres an hour, I found myself contemplating how the UK has yet to deliver the promised high-speed rail line from London to Birmingham, a little over 100 miles, despite more than a decade of work, a projected cost of over £100 billion, and a journey time saving of less than half an hour.

If this same failure to translate prevention science into policy continues, as it has over the past two decades, offering platitudes about the importance of prevention but little action, while continuing to avoid the scientific evidence of what actually works, then China’s nightmare of a large proportion of its silver-haired population slipping into dementia will become our reality.

Alzheimer’s is preventable. That is a fact, not a belief.

Those who say it cannot be done should not stand in the way of those who are doing it.

Patrick Holford.

Founder of the Food for the Brain Foundation and the Institute for Optimum Nutrition,  Chair of the Scientific Advisory Board

Further info

Amyloid isn’t Alzheimer’s – How NOT to Study a Disease

Amyloid isn’t Alzheimer’s – How NOT to Study a Disease

by Patrick Holford

alzheimers drugs

Alzheimer’s disease has, for decades, been framed primarily as a problem of amyloid plaques building up in the brain.

It is a compelling idea. It is measurable, visible on brain scans, and has shaped billions in research funding and drug development. There’s just one problem.

It doesn’t adequately explain what we see in people.

Many individuals with significant amyloid in their brains remain cognitively normal. Others develop clear dementia with little or no amyloid present (1). Treatments that successfully reduce amyloid have, at best, produced only modest effects on slowing decline, with no meaningful reversal of symptoms (2).

Amyloid is associated with Alzheimer’s disease, but association is not the same as causation.

And that distinction changes everything.

This growing tension between theory and evidence is explored in depth by neurobiologist Karl Herrup in How Not to Study a Disease, where he challenges how the field has come to define and pursue Alzheimer’s.

Some people develop increasingly severe cognitive decline as they age. This affects roughly one in ten older adults. We call this dementia. In some cases, brain scans show clear shrinkage in key regions, particularly the medial temporal lobe, which is then used to diagnose Alzheimer’s disease. So we have two observable features: a decline in cognitive function and measurable loss of brain tissue.

The question that follows is simple, but critical.

What is actually causing this process?

What causes Alzheimer’s?

Amyloid has long been positioned as the answer. Yet the evidence tells a more complicated story.

A significant proportion of older adults have amyloid plaques in their brains and remain cognitively normal. At the same time, some individuals with clear dementia show little or no amyloid pathology. Amyloid is associated with Alzheimer’s, but that is not the same as being the cause.

If amyloid were the primary driver, then reducing it should meaningfully change the course of the disease. However, interventions designed to reduce amyloid have consistently lowered amyloid burden in the brain, yet produced, at best, modest effects on slowing decline, often measured as very small changes on cognitive scales. There has been no meaningful reversal of symptoms. In some cases, safety concerns have emerged, including brain bleeding and swelling.

Recent large-scale evidence (6) now reinforces this point. A 2026 Cochrane review concluded that although anti-amyloid monoclonal antibodies can remove amyloid from the brain, this does not appear to translate into clinically meaningful effects for people with mild cognitive impairment or mild dementia due to Alzheimer’s disease, while increasing the risk of amyloid-related imaging abnormalities.

From a scientific perspective, this adds to an already substantial body of evidence suggesting that amyloid accumulation, on its own, does not explain the disease process. It may be part of the picture, but it is not the engine driving it.

And yet, the field has remained heavily focused on this single pathway.

When a hypothesis becomes a lens

Research tends to follow what is measurable, fundable, and already established. Over time, this can narrow the lens rather than expand it.

Amyloid has become that lens. As Karl Herrup argues in his book, once a hypothesis becomes dominant, it can begin to shape not just what is studied, but how results are interpreted and what gets funded next.

The result is that vast resources have been invested in understanding and modifying amyloid biology, while other avenues have received comparatively less attention. We have learned a great deal about amyloid itself, but we are not significantly closer to preventing or reversing the condition that matters most to patients, which is cognitive decline.

This is not unusual in science. Once a model becomes dominant, it shapes the direction of funding, research questions, and even how people interpret results.

Fig. 1. How lowering homocysteine stops p-tau formation.

A similar pattern is now emerging with another biomarker, p-tau.

Tau is a normal protein that, under certain conditions, becomes altered and associated with the tangles seen in Alzheimer’s pathology. Higher levels of p-tau are linked with increased risk, but again, association does not establish causation. Many individuals have elevated levels without clinical symptoms.

As with amyloid, the risk is that a marker becomes mistaken for the mechanism.

What does influence the disease process?

This is where the picture becomes more interesting.

There are factors that sit upstream of both amyloid and tau, influencing the environment in which brain cells function or fail. One of the most studied is homocysteine, a marker of methylation and B vitamin status.

Unlike amyloid, intervention trials have shown that homocysteine influences outcomes. In the VITACOG study, lowering elevated homocysteine with targeted B vitamins significantly slowed the rate of brain atrophy in individuals with mild cognitive impairment, with corresponding effects on cognitive decline. This is much closer to what we would describe as a disease-modifying effect (3,4). It also raises questions explored in Apparently healthy but diagnosed with Alzheimer’s about whether current diagnostic models are identifying true disease drivers or simply biomarkers.

That does not mean homocysteine is the only cause. It is one piece of a larger system. But it illustrates an important point. When you influence the underlying biology of the brain, rather than a downstream marker, you begin to see meaningful change.

A systems problem, not a single cause

Alzheimer’s does not behave like a single-cause disease.

It is better understood as the result of multiple interacting processes. These include inflammation, oxidative stress, insulin resistance, mitochondrial dysfunction, and impaired methylation, among many others (5). Each of these affects how brain cells are built, maintained, and powered.

Individually, they may not be sufficient to cause disease. Together, they can create the conditions in which the brain becomes vulnerable.

This is closer to how we understand most chronic conditions. Not as a single fault, but as a convergence of pressures that eventually exceed the system’s ability to compensate. A more useful way to think about it is not as one switch flipping, but as several dials turning in the wrong direction at the same time.

Why this matters

If we continue to focus primarily on downstream markers such as amyloid or p-tau, we risk missing the broader picture.

If instead we look at the upstream drivers, the factors that influence brain structure, function, and energy supply, we open up a different set of possibilities. Not just for treatment, but for prevention.

These are not fringe ideas. They are part of a growing shift in how Alzheimer’s is being understood, questioned, and re-examined. Researchers like Karl Herrup are helping to bring that conversation into the open, challenging long-held assumptions and asking more useful questions about what truly drives the disease.

It’s a conversation that is only just beginning to reach wider audiences.

This is exactly what we’ll be exploring at Alzheimer’s Prevention: New Frontiers conference, where leading researchers and clinicians will come together to look beyond single-cause models and towards a more complete understanding of brain health and cognitive decline.

Is prevention the real solution?

The prevailing model in medicine has been to identify a single cause and target it with a treatment. That works well for some conditions. It is less suited to complex, multifactorial diseases like Alzheimer’s.

A systems-based approach asks a different question.
What combination of factors leads to decline, and how do we shift that combination in the opposite direction?

This is the approach we take at Food for the Brain. By combining cognitive testing with blood testing and lifestyle information, it becomes possible to see patterns, not just isolated variables. Over time, this allows us to understand what drives resilience as well as risk.

It is likely that we will not find a single primary cause of Alzheimer’s. What we may find is something more useful: a set of modifiable factors that, together, determine whether the brain maintains function or begins to decline.

In that sense, prevention may not just be part of the solution.

It’s the solution.

Find out more with Alzheimer’s: Prevention is the Cure book here

Learn more about our Alzheimer’s Prevention: New Frontiers Conference here.

References
  1. Jack CR Jr, Bennett DA, Blennow K, et al. NIA-AA Research Framework: Toward a biological definition of Alzheimer’s disease. Alzheimers Dement. 2018;14(4):535–562.
  2. van Dyck CH, Swanson CJ, Aisen P, et al. Lecanemab in early Alzheimer’s disease. N Engl J Med. 2023;388:9–21.
  3. de Jager CA, Oulhaj A, Jacoby R, et al. Cognitive and clinical outcomes of homocysteine-lowering B-vitamin treatment in mild cognitive impairment. Int J Geriatr Psychiatry. 2012;27(6):592–600.
  4. Livingston G, Huntley J, Sommerlad A, et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. Lancet. 2020;396(10248):413–446.
Further info

How to Keep your Brain Young with Antioxidants

How To Keep Your Brain Young with Antioxidants?

How To Keep Your Brain Young with Antioxidants?

Being alive is a balancing act between making energy by combusting glucose with oxygen and generating ‘oxidant’ exhaust fumes that must then be neutralised. This process, known as oxidative stress, is a key contributor to ageing. Over time, if oxidants outpace your body’s ability to disarm them, damage accumulates in cells and tissues, including the brain.[8]

The brain is particularly vulnerable. It consumes a high proportion of the body’s oxygen, is rich in fats that are susceptible to oxidation, and has relatively limited antioxidant defences compared with other tissues. This makes maintaining an effective antioxidant defence system essential for long-term cognitive health.

However, this process is not fixed. You can influence it. Improving your intake of antioxidants and polyphenols, and supporting your body’s internal defence systems, can help shift the balance and support brain resilience over time.

To explore this idea further, watch the film Keeping Your Brain Young with Antioxidants’ below.

The Science Behind Eating the Rainbow

You’ve heard it before, but the science behind it matters.

Different colours in plant foods reflect different polyphenols and antioxidant compounds, each with distinct biological effects. These compounds do more than just neutralise oxidants. Many also act as signalling molecules, influencing inflammation, blood flow, and cellular pathways linked to brain function and ageing.[9]

Mustard and turmeric, for example, are strong yellows. Dijon mustard is great, with no added sugar, and traditional English mustard is also beneficial. Turmeric, rich in curcumin, can be added to steam-fries, curries, or soups, grated into a tea, and even used in a turmeric latté.

Bright oranges such as butternut squash, sweet potato, and carrots provide carotenoids that support cellular protection. Tomatoes are particularly rich in lycopene, associated with reduced oxidative damage. Strawberries are a lower glycaemic fruit option, and peppers of all colours are rich in vitamin C, which plays a central role in antioxidant recycling.

Anything purple, magenta, or blue is especially valuable. From beetroot to blueberries, blackberries, and raspberries, these foods are rich in anthocyanidins, a class of polyphenols associated with improved vascular and cognitive function.

Strong greens remain foundational. Spinach, kale, Brussels sprouts, broccoli, watercress, rocket, asparagus, and green beans all contribute a wide spectrum of antioxidants, minerals, and phytonutrients that support detoxification and cellular defence.

Eating the rainbow is not a nice idea. It’s an essential part of upgrading and protecting your brain at any age.

The Best Fruits and Vegetables for Brain Health

But are there any particular vegetables or fruits that pack the biggest punch as far as polyphenols and antioxidants are concerned? Or, if you know you can’t or don’t like to eat a huge variety of fruit and veg, are there particular ones to focus on eating to get the most benefit?

Foods that are high in ‘polyphenols’, which refers to the structure of plant-based compounds, seem especially beneficial for protecting your brain. You might have heard of flavonoids in berries, quercetin in red onions, anthocyanidins in blue and red foods, and isoflavones in beans. These are all examples of polyphenols. Herbs and spices such as peppermint, basil, oregano, cumin, and curcumin in turmeric contain high levels of polyphenols and potent antioxidants.

But there are other criteria by which to judge a plant, including its ability to influence pathways linked to cellular ageing. Certain polyphenols, such as resveratrol, interact with sirtuin pathways involved in cellular repair and longevity.[10] For example, olives, blueberries, and kale support these processes.

Then there’s a group of compounds called ‘salvestrols’, generally only found in organic fruit, vegetables, herbs, and spices, which turn out to be anti-cancer.[1] They’re produced in plants as part of their self-defence system against invaders such as fungi. If the plant is sprayed with fungicides, it won’t produce them.

Taking all these factors into account, including the GL, antioxidants, polyphenols, salvestrols, and sirtuin-related activity, these are the dozen best-rated fruits and vegetables. (This list is not definitive. More and more research continues to reveal the healing power of nature’s fruits and vegetables.)

So, if eating the ‘rainbow’ feels like too much pressure or is difficult to achieve, think about incorporating some of the above into your meals each day.

Our Top 13 to Help Keep Your Brain Young

 Lowest GLAntioxidantPolyphenolSalvestrolSirtuin Act.
Olives***************
Blueberries**************
Kale**************
Blackcurrants*************
Broccoli*********** 
Artichokes*********** 
Cabbage (red)*********** 
Asparagus********** 
Onions (red)****** ***
Avocado********** 
Apples**********
Beetroot*****  
Cherries******  

Top Up Brain-Friendly Antioxidant Nutrients: Consider Supplementation

Antioxidants Work as a Network

Much like dementia prevention is a combination of the 8 domains, which all influence each other, antioxidants are part of a network keeping you healthy.

A number of key vitamins, as measured in food and in the blood, do correlate with decreased dementia risk. This is hardly surprising, since the brain is made of complex fats that can easily be damaged by oxidants. It makes sense that having a high intake of antioxidants would protect the brain from damage. Antioxidants disarm oxidants by teamwork. You need a combination of nutrients, not just vitamin C or vitamin E.

Evidence for Antioxidant Protection

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.[2]

A study of 4,740 Cache County, Utah, older residents found that those supplementing both vitamin E and C cut their risk of developing Alzheimer’s by two thirds. A trend toward lower Alzheimer’s risk was also evident in those who took vitamin E supplements together with multivitamins containing vitamin C, but there was no evidence of a protective effect in those taking only vitamin E or vitamin C supplements alone, with multivitamins alone, or with vitamin B-complex supplements. Lowest risk was reported in those supplementing at least 1000 mg a day of vitamin C together with at least 1000 IU a day of vitamin E.[3]

However, vitamin E on its own doesn’t seem to work. In a double-blind study, people with mild cognitive impairment were randomly assigned to receive 2000 IU a day of vitamin E or placebo for three years. There were no significant differences in the rate of progression to AD between the vitamin E and placebo groups at any point.[4]

Building Your Antioxidant Defences

Your best bet is probably to both eat 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 – protects the memory-friendly neurotransmitter acetylcholine and dampens brain oxidation and inflammation.[5]

Glutathione[6] or N-acetyl cysteine[7] (NAC) – protects the brain and improves methylation, thus having potential in dementia prevention.

It doesn’t really make a lot of sense to give one without the others. All those listed above, vitamin C, E, glutathione, N-acetyl cysteine, Coenzyme Q10 and resveratrol, work together. There are many other team player ‘cousins’, from B vitamins to minerals such as magnesium, zinc and selenium.

The first step is to eat ‘whole’ foods, especially fresh plant foods that are more likely to contain these kinds of nutrients. However, there are some nutrients, such as vitamin C, for which just eating whole foods doesn’t guarantee you are achieving optimum nutrition.

Most nutritional therapists supplement extra vitamin C, and some supplement an all-round antioxidant supplement providing the nutrients listed above. There is very good logic, and supporting evidence, to do this, especially if you’re over 50 years old, even if there isn’t yet that definitive ‘randomised placebo controlled trial’.

Other key antioxidant nutrients include:

Vitamin A, C and E – associated with reduced Alzheimer’s risk

Lipoic acid – supports mitochondrial function and reduces oxidative stress and inflammation.[5]

Glutathione or N-acetyl cysteine (NAC) – supports detoxification, antioxidant recycling and methylation, with potential relevance for cognitive ageing.[6][7]

Coenzyme Q10 and resveratrol – support cellular energy and protection

There are also important supporting nutrients, including B vitamins, which contribute to methylation and help regulate homocysteine, a compound associated with oxidative stress and cognitive decline when elevated.[12]

Why Food Comes First but Supplements May Still Be Needed

We are Food for the Brain, so the first step is always to eat whole foods, focusing especially on fresh plant foods that are naturally rich in antioxidants and polyphenols.

However, achieving optimal levels of certain nutrients through diet alone is not always guaranteed. Factors such as soil depletion, food storage, genetics, individual absorption, age, and increased physiological demand all play a role.

For this reason, targeted supplementation, particularly for nutrients such as vitamin C and those involved in the antioxidant network, may be beneficial. There is strong rationale, and supporting evidence, for this approach, especially in individuals over 50 or those with increased oxidative load. Read more about supplementation here.

From General Brain Health Advice to Personalised Insight

Why Antioxidant Needs Differ and Why Testing Matters

Eating a diet rich in colourful plant foods is a powerful place to start. But the real question is whether your unique body has the antioxidant capacity to meet your current level of demand.

Or, said another way, how do you know if you are eating enough to protect your brain and your future?

Oxidative stress is influenced by far more than diet alone. Age, stress, environmental toxins, blood sugar balance, genetic variations, nutrient status, and individual biochemistry all play a role. Two people can eat similarly and have very different levels of oxidative damage and antioxidant protection.

This is where testing becomes valuable.

One of the most informative markers is glutathione, often referred to as the body’s master antioxidant. It sits at the centre of your antioxidant defence system, helping to neutralise oxidative damage and recycle other antioxidants. If levels are low, it can indicate that your overall antioxidant capacity is under strain.

Rather than guessing whether you are getting enough antioxidant support, testing allows you to see what is actually happening inside your body. (Historically, glutathione has been hard to test, but we developed new technology with our lab partners to now be able to do this accurately with an at home finger prick blood test.)

Understanding Your Brain Health More Clearly

The DRIfT 5-in-1 test shows you what is actually happening inside your body, across the key drivers of cognitive decline, including oxidative stress, inflammation, blood sugar balance, nutrient status, and essential fats. It moves you beyond general advice and highlights exactly where your biggest risks and opportunities lie.

If your focus is antioxidant capacity, testing glutathione offers direct insight into whether your body is under oxidative strain and how well your defence system is functioning. Find out more here.

Alongside this, our free Cognitive Function Test provides a practical way to track how your brain is performing today, while contributing to ongoing research into what truly works in preventing cognitive decline.

Understanding your results allows you to move from general advice to a more targeted, personalised approach, so you can support your brain with greater precision and confidence.

When you join COGNITION and become a FRIEND, you get access to our new Digital education platform and our new COGNITION programme. You can also register FREE for both our monthly guest speaker webinars and our monthly live COGNITION Coaching – this is an hour live with our Food for the Brain health coaches and there is a Q&A at the end (you also get access to the past coaching workshop recordings).

On April 22nd April, our COGNITION Coaching Workshop is all about antioxidants and attendees will get a mini-ebook on antioxidants and 2 delicious, anti-oxidant rich recipes. You can become a FRIEND by clicking the link below:

References:

[1] Potter, G.A. & Burke, M.D. (2006) Salvestrols – Natural Products with Tumour Selective Activity. Journal of Orthomolecular Medicine. 21(1): 34-36.

[2] Yu JT, Xu W, Tan CC, et al. Evidence-based prevention of Alzheimer’s disease: systematic review and meta-analysis. J Neurol Neurosurg Psychiatry. 2020;91(11):1201–1209.

[3] Zandi PP, et al. Reduced risk of Alzheimer disease in users of antioxidant vitamin supplements. Arch Neurol. 2004;61:82–98.

[4] Petersen RC, et al. Vitamin E and donepezil for the treatment of mild cognitive impairment. N Engl J Med. 2005;352:2379–2388.

[5] Maczurek A, et al. Lipoic acid as an anti-inflammatory and neuroprotective treatment. Adv Drug Deliv Rev. 2008;60(13-14):1463–1470.

[6] Pocernich CB, Butterfield DA. Elevation of glutathione as a therapeutic strategy. Biochim Biophys Acta. 2012;1822(5):625–630.

[7] Hara Y, et al. Evaluation of N-acetylcysteine for cognitive ageing. J Prev Alzheimers Dis. 2017;4(3):201–206.

[8] Halliwell B. Oxidative stress and neurodegeneration. J Neurochem. 2006;97(6):1634–1658.

[9] Spencer JPE. The impact of flavonoids on memory. Chem Soc Rev. 2009;38(4):1152–1161.

[10] Baur JA, Sinclair DA. Therapeutic potential of resveratrol. Nat Rev Drug Discov. 2006;5(6):493–506.

[11] Sekhar RV, et al. Glutathione synthesis is diminished in older adults. Am J Clin Nutr. 2011;94(3):847–853.

[12] Smith AD, Refsum H. Homocysteine, B vitamins, and cognitive impairment. Annu Rev Nutr. 2016;36:211–239.

Further info

Dr Tommy Wood: Why Brain Health Needs a Systems-Based Approach

Dr Tommy Wood: Why Brain Health Needs a Systems-Based Approach

Dr Tommy Wood: Why Brain Health Needs a Systems-Based Approach blog post image

Dr Tommy Wood brain health research shows that we now know more than ever about protecting the brain, yet many people still feel overwhelmed by disconnected advice.

A headline about blood sugar here. A podcast on omega-3 there. A post about sleep, a study on exercise, a warning about stress.

Useful, yes. But also fragmented.

What Dr Tommy Wood brain health research offers is something more valuable than another isolated tip. He brings a framework.

As Head of Research at Food for the Brain, Associate Professor of Pediatrics and Neuroscience at the University of Washington, and author of the forthcoming book The Stimulated Mind, Tommy brings something rare to this field. He helps connect the dots. His work focuses on how brain health is shaped across the lifespan and why protecting cognitive function means thinking in systems, not silos.

Dr Tommy Wood Brain Health Framework

One of the reasons brain health can feel confusing is that it is often presented as a list:
A long list of risk factors. Nutrients to take, habits to adopt, or a long list of things to avoid.

But the brain does not work like a checklist: it works as a living, dynamic system. It responds to what it is supplied with, how it is used, and whether it has the conditions it needs to recover and adapt.

That is the core idea behind a systems-based approach to brain health.

Instead of asking “What is the one thing that protects the brain?”, it asks three bigger questions:

  • Does the brain receive enough oxygen, nutrients and stable energy to function well?
  • How well is it being stimulated to stay active, adaptable and resilient?
  • Are the foundations for repair and recovery in place, such as good sleep, stress regulation and metabolic health?

When you look at brain health this way, something important changes.

Many people understandably hope for a “magic bullet”. One supplement. One diet. One breakthrough drug that protects the brain.

But science tells a different (more hopeful) story. Cognitive resilience is shaped by the interaction between many systems in the body. Blood flow, nutrient status, sleep, movement, learning, stress and social connection all influence how the brain functions and adapts.

The encouraging part is that this gives us many entry points for change. You do not have to get everything perfect, and small improvements across several areas can work together to create meaningful protection for the brain over time.

That is why a systems-based approach is not more complicated. In practice, it is far more empowering.

Why this matters for prevention?

One of the most important insights in Tommy’s work is that cognitive decline does not happen in isolation.

The brain changes in response to how we live. Blood flow, nutrient status, movement, learning, sleep, stress and social connection all shape how the brain ages and how resilient it remains.

This is also why Tommy’s forthcoming book, The Stimulated Mind, focuses on the interaction between stimulation, sleep and nutrient supply as key drivers of lifelong brain health.

This perspective is closely aligned with the mission of Food for the Brain. For years we have been communicating that dementia risk is not fixed. By understanding and addressing modifiable factors across the lifespan, it is possible to protect your mind and keep the brain healthier for longer.

Tommy’s leadership as Head of Research helps bring greater scientific clarity to this systems-based approach to prevention.

Watch: A systems-based approach to cognitive function

If you want to hear Tommy explain this approach in more depth, his lecture from the Upgrade Your Brain Conference is one of the clearest introductions we have shared.

Watch the lecture below.

What Tommy offers is not another list of things to do. It is a framework. A way to understand why so many different factors matter and how they fit together.

Learn More About Dr Tommy Wood Brain Health Research

If this approach resonates with you, Tommy will be going deeper in our upcoming webinar, How to Keep Your Brain Young.

In this session he will explore the science of cognitive resilience and share practical ways to stimulate the brain, support long-term brain health and reduce lifetime dementia risk.

Food for the Brain will host the webinar on 19th March 2026 at 6 pm GMT.

Tommy’s new book is available to pre-order

The Stimulated Mind: Future-Proof Your Brain from Dementia and Stay Sharp at Any Age

Tommy’s new book, The Stimulated Mind, is also available to pre-order now.
In it, he explores how the brain develops, adapts, and stays resilient across the lifespan, and why everyday factors such as movement, learning, sleep, nutrition, and social connection play such an important role in shaping long-term brain health.

Pre-order your copy today before the book releases on 26th March 2026.

Final thought

For many people, the challenge with brain health is not a lack of information. It is knowing where to start.

When advice comes as scattered tips, nutrients, tests, and lifestyle changes, it can feel difficult to turn good science into clear action.

What Tommy’s work offers is a framework: a way of understanding how the different pieces of brain health fit together and why small changes across several areas can have a powerful cumulative effect.

At Food for the Brain, this systems-based approach sits at the heart of COGNITION, our brain upgrade programme.

COGNITION helps you understand your personal risk factors, learn the most important steps to protect your brain, and put them into practice with guidance and support.

The programme has recently been upgraded and is now available globally for just £5 per month or £50 a year, making it accessible to anyone who wants to take their brain health seriously.

If Tommy’s lecture resonates with you, COGNITION is the natural next step.

Because protecting your brain is not about doing everything perfectly.

It is about understanding the system and taking the next right step.

Further info

The Biggest Myths About Alzheimer’s – And What the Science Actually Shows

The Biggest Myths About Alzheimer’s – And What the Science Actually Shows

The Biggest Myths About Alzheimer’s blog post image

Alzheimer’s disease is one of the most feared diagnosis of modern life. And where there is fear, myths flourish. Many of the biggest myths about Alzheimer’s have become widely accepted beliefs. We are told it is purely genetic, that it is an inevitable part of ageing, and that the main hope lies in new drugs targeting amyloid in the brain.

The science tells a far more complex and, importantly, far more hopeful story.

Myth #1 in the biggest myths about Alzheimer’s: ‘It’s all in your genes’

When Alzheimer’s runs in families, it is natural to assume destiny is fixed. Both your grandmothers had it, so you assume you will too.

Yet fewer than 1% of cases are caused by rare deterministic mutations in APP, PSEN1 or PSEN2 genes that lead to early-onset familial Alzheimer’s disease [1].

The vast majority of Alzheimer’s cases are late-onset and multifactorial. That means risk is shaped by multiple influences across a lifetime.

What about APOE4?

Celebrities like Chris Hemsworth have put the APOE4 gene on the map and into the public sphere and it is the strongest common genetic risk factor for late-onset Alzheimer’s. Having one copy increases risk; two copies increase it further [2]. But it does not determine outcome, as many APOE4 carriers never develop dementia. Many people with Alzheimer’s do not carry APOE4.

Genes influence vulnerability but they do not dictate your future.

APOE4 affects lipid transport, inflammatory signalling and neuronal repair. These processes are influenced by metabolic health, vascular function, nutrient status, sleep, stress physiology and lifestyle.

One of the most important things to remember is that gene expression is not static, as genes respond to the environment they are in.

The most important question is not necessarily ‘How do I check my genes?’ The question is ‘What environment are your genes operating in?’ Because you cannot change your genes but you can influence how they function and are expressed.

Myth #2 in the biggest myths about Alzheimer’s: ‘Nothing can be done’

This is the most damaging myth of all.

The 2020 Lancet Commission concluded that around 40% of dementia cases worldwide are attributable to modifiable risk factors [3]. The 2024 update increased that estimate to approximately 45% [4].

Nearly half of all cases.

And this is mainstream consensus. (Read more about the Alzheimer’s Prevention Expert Group’s APEG response to this recent Lancet report here).

The identified risk factors include hypertension, diabetes, obesity, physical inactivity, smoking, depression, hearing loss and social isolation. Importantly, Alzheimer’s risk is not fixed, it develops gradually over decades.

However, many researchers (ourselves included) believe even 45% may underestimate the true preventable proportion.

A large UK Biobank analysis published in the journal Nature Human Behaviour modelled a broader range of modifiable factors and estimated that up to around 73% of dementia cases could be attributable to modifiable influences [8]. Professor David Smith of Oxford University, co-author of that study, member of our Scientific Advisory Board, and lead investigator of the VITACOG trial, has suggested this may still be conservative, as certain blood biomarkers were not included in the modelling.

Whether the true figure is closer to 45% or 73%, the direction of evidence is consistent.

A large proportion of dementia and Alzheimer’s is preventable and you can modify your risk with simple changes.

Why biology supports prevention

Alzheimer’s develops through interacting processes such as impaired glucose metabolism, vascular dysfunction, inflammation and elevated homocysteine.

Raised homocysteine, reflecting impaired methylation and B vitamin status, is associated with increased dementia risk and accelerated brain atrophy [5].

In the VITACOG trial, homocysteine-lowering B vitamins significantly slowed whole-brain atrophy in people with mild cognitive impairment [6]. The benefit was strongest in those with adequate omega-3 status [7].

That is structural brain change.

(When compared to anti-amyloid drug trials, which show modest slowing of decline in already symptomatic patients, VITACOG demonstrated slowing of brain shrinkage itself in an at-risk group.)

Once significant neuronal loss has occurred, reversal is unlikely, but years before diagnosis, measurable risk is accumulating and that is where prevention has its power.

alzheimer's modifiable risks

Myth #3 in the biggest myths about Alzheimer’s: ‘It has a single cause

The reductionist model searches for one target and one solution.

Alzheimer’s reflects the interaction of multiple biological systems:

  • Glucose regulation
  • Vascular health
  • Lipid transport
  • Inflammation
  • Oxidative stress
  • Methylation
  • Sleep and stress regulation
  • Hormonal balance

People arrive at cognitive decline through different combinations of biological drivers. For some, insulin resistance may be central. For others, vascular stiffness and hypertension. In others, chronic inflammation and elevated homocysteine may play a key role. The destination may look similar, but the route is not.

This systems view explains why targeting one downstream marker, such as amyloid, yields modest slowing. Correcting multiple upstream drivers is biologically more plausible for meaningful long-term risk reduction.

Watch the video below to learn how Food for the Brain uses a systems-based approach.

Myth #4 in the biggest myths about Alzheimer’s: ‘It’s inevitable with ageing’

Age increases risk. However, that is only part of the story.

There are many individuals in their 80s and 90s with preserved cognition. The difference often lies in lifelong vascular, metabolic and lifestyle patterns, also known as patterns for prevention.

It is clear from what you have read so far that this is not an inevitable part of getting older. With the right knowledge and habits, it is something most people can avoid.

And that is why Food for the Brain exists, because not enough people know this and not enough people know what action they need to take to protect their brain.

A More Accurate Framework

Ageing is not the enemy. It is a privilege denied to many.

The goal is not to avoid growing older. It is to protect the brain as we do.

Alzheimer’s is not a single event. It reflects decades of interacting biological stress: metabolic strain, vascular change, inflammation and nutrient imbalance. These processes build slowly and often silently.

By the time symptoms appear, significant damage has already occurred.

The science is clear that a substantial proportion of dementia risk is modifiable [6,10]. That does not mean guarantees. It means opportunity.

You cannot change your genes and you cannot stop the passage of time.

Yet, you can influence how your brain responds to both.

And you can start today!

Gain personalised insight into your current cognitive performance and identify potential areas of vulnerability early.

Order our at-home blood test to assess homocysteine, omega-3 status, and other key markers linked to long-term brain resilience.

Our six-month brain upgrade programme provides structured guidance, accountability and expert support to help you translate knowledge into meaningful and lasting change.

Prevention is possible. It begins with measurement, and it progresses with action.

.

References
  1. Bekris LM, Yu CE, Bird TD, Tsuang DW. Genetics of Alzheimer disease. J Geriatr Psychiatry Neurol. 2010;23(4):213–27.
  2. Corder EH, Saunders AM, Strittmatter WJ, et al. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late onset families. Science. 1993;261(5123):921–3.
  3. Livingston G, Huntley J, Sommerlad A, et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. Lancet. 2020;396(10248):413–46.
  4. Hooshmand B, Polvikoski T, Kivipelto M, et al. Plasma homocysteine, Alzheimer and cerebrovascular pathology: a population-based autopsy study. Brain. 2013;136(9):2707–16.
  5. Jernerén F, Elshorbagy AK, Oulhaj A, et al. Brain atrophy in cognitively impaired elderly: the importance of long-chain omega-3 fatty acids and B vitamin status. Am J Clin Nutr. 2015;102(1):215–21.

Further info