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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.

Further info

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

Why “Normal” Vitamin D Levels May Not Be Protective for Women’s Brains

Why “Normal” Vitamin D Levels May Not Be Protective for Women’s Brains

Why “Normal” Vitamin D Levels May Not Be Protective for Women’s Brains

Science now recognises Vitamin D as far more than a bone-health nutrient. Over the past decade, it has become increasingly clear that vitamin D acts as a hormone regulator, playing an important role in brain health, immune regulation and inflammation, especially when considering optimal vitamin D levels for women’s brains.

What is discussed far less, is a more nuanced question…

If vitamin D matters for the brain, how much is actually enough and do vitamin D levels differ for women?

A growing body of research links lower vitamin D status with a higher risk of cognitive decline and Alzheimer’s disease. Yet most guidance still relies on population-based “normal” ranges that were never designed to protect the brain. This raises an important prevention question for women, who already carry a higher lifetime risk of Alzheimer’s disease.

What the research shows

A systematic review and meta-analysis in 2025 by Li et al. examined the relationship between circulating vitamin D levels and Alzheimer’s disease risk across multiple observational studies (1).

The findings were consistent:

• Lower vitamin D levels link to a higher risk of Alzheimer’s disease.
• Risk increased progressively as vitamin D levels declined
• Researchers observed this association across different populations and study designs.

Crucially, the authors did not claim that vitamin D deficiency causes Alzheimer’s disease. Instead, vitamin D status appears to track biological vulnerability in the brain and reflects processes such as neuroinflammation, immune dysregulation and vascular dysfunction, all recognised contributors to cognitive decline.

This distinction matters for prevention.

Why these findings matter particularly for women

Women account for around two thirds of Alzheimer’s diagnoses worldwide. Longevity alone cannot explain this difference.

Across midlife and later life, women experience biological changes that alter how the brain responds to metabolic, inflammatory and hormonal stress. The menopausal transition is a key inflection point. Declining oestrogen and progesterone influence immune signalling, cerebral blood flow and brain energy metabolism, all of which intersect with established dementia risk pathways (3). This helps explain why midlife can be a turning point for brain health in women, even when blood test results appear “normal”.

Vitamin D functions as a hormone-like regulator, with receptors widely distributed throughout the brain and immune system. Its actions include modulation of inflammatory responses, immune balance and neuronal protection. Hormonal changes appear to influence how effectively vitamin D signalling is utilised at a tissue level. This is supported by experimental and clinical research showing interactions between oestrogen, vitamin D receptors and immune signalling, although this is not always directly measured in large population studies. In practical terms, this means that a vitamin D level considered “normal” for the general population may not confer the same degree of neuroprotection in the ageing female brain.

This does not mean vitamin D requirements are definitively higher for every single woman, or that everyone should take high-dose supplementation. Excessive intakes via supplementation over time can be harmful, which is why context, testing and appropriate dosing matter. 

Prevention works best when it’s personal, based on what’s happening in your own brain and body, not just what’s considered “normal.”

The problem with “normal” ranges for vitamin D for women’s brains

Researchers established vitamin D reference ranges primarily to prevent overt deficiency-related disease, particularly rickets and osteomalacia. They did not design these ranges to define optimal levels for long-term brain resilience.

Population reference ranges do not account for factors that strongly influence dementia risk, including:

  • Chronic low-grade inflammation
  • Insulin resistance and blood sugar dysregulation
  • Oxidative stress (see our explainer video here)
  • Hormonal transitions across midlife
  • Genetic variation in vitamin D metabolism and receptor activity

As a result, vitamin D levels that fall within the laboratory “normal” range may still exist within a biological environment that favours cumulative brain damage over time. This limitation is not unique to vitamin D. It reflects a broader problem with single-nutrient or single-cause thinking in Alzheimer’s prevention.

Vitamin D does not act alone in protecting women’s brains

Vitamin D is not an isolated lever in brain health. Low vitamin D status frequently clusters with other modifiable biological risk factors, including:

• Low omega-3 fatty acid status
• Raised homocysteine, reflecting impaired B vitamin-dependent methylation, a process essential for maintaining brain cells
• Poor blood sugar control
• Reduced antioxidant capacity, including glutathione availability

Each of these factors independently links to cognitive decline. More importantly, they interact within the brain.

Alzheimer’s disease does not arise from a single deficiency, a single gene or one pathological protein.
It reflects the cumulative impact of multiple biological systems drifting out of balance over years or decades. This is why interventions that target a single marker so often produce disappointing results.

Prevention requires a broader, systems-based view.

Once you see vitamin D in this broader context, it becomes clear why testing a single marker in isolation can only ever give partial answers.

From nutrients to prevention systems

Testing vitamin D alone can identify a deficiency, but it cannot tell you whether the brain’s key protective systems are functioning together.

A prevention-led approach asks different questions:

  • How well is inflammation being regulated?
  • Are brain cell membranes supported by sufficient essential fats?
  • Is methylation, the nutrient-dependent process that supports DNA repair, neurotransmitter balance and brain structure, functioning effectively?
  • To what extent is blood sugar quietly damaging brain neurons over time?

These are not abstract concepts.

They are measurable, modifiable drivers of dementia risk that we assess through our at-home DRIfT blood test.

A smarter way to assess brain health

Many people reading this will have been told their vitamin D is “fine”. They may spend time outdoors, eat well, and still feel tired, foggy or not quite themselves. The problem is not that vitamin D doesn’t matter. It’s that a single number rarely tells the full story.

This systems-based understanding underpins our work at Food for the Brain. It is the heart of prevention.

Prevention is not about chasing one “perfect” nutrient level or one lifestyle change. 

It is about understanding how your body works as one connected system and acting early enough to change the trajectory.

If you want to begin supporting and upgrading your brain today:

Complete the Cognitive Function Test today if you haven’t done so yet.
It is free to everyone, validated and provides personalised insights into your current brain health.

Order your at-home DRIfT blood test to assess the key biological drivers of cognitive decline, including vitamin D, omega-3, homocysteine, blood sugar control and antioxidant status. Together, these results give you the information you need to move from awareness to meaningful prevention.

References:

Further info

Lithium and Brain Health: The Overlooked Mineral That Could Protect Your Mind

Lithium and Brain Health: The Overlooked Mineral That Could Protect Your Mind

by Greg Potter

Lithium and Brain Health: The Overlooked Mineral That Could Protect Your Mind

Lithium and brain health are more connected than many realise. One of the universe’s oldest elements could also be one of the brain’s most powerful protectors.

Long associated with bipolar treatment, lithium is often dismissed as a heavy-duty psychiatric drug – yet new research tells a different story. Trace amounts of lithium appear to influence mood, longevity and even cognitive decline. With dementia rates rising fast, scientists are revisiting this humble mineral to understand whether it could slow or prevent neurodegeneration altogether.

In this article, Dr Greg Potter, member of our Scientific Advisory Board and Sleep Scientist, explores the remarkable – and misunderstood – role of lithium in supporting brain health, from dementia protection to lifespan extension and neural resilience.


Lithium is one of three elements created during the Big Bang event that gave rise to the universe 13.8 billion years ago, and nowadays it’s mostly found in igneous rocks. 

Because lithium predates all life on Earth, it’s perhaps no surprise it plays a role in human biology. While lithium doesn’t seem to be a truly “essential” nutrient  (1) as it isn’t indispensable for any one biological process, lithium’s mood-stabilising actions have long been recognised. Specifically, lithium has primarily been used to help patients with bipolar disorder avert swings into sleepless mania. Despite its clinical utility, lithium has arguably been stigmatised due to its association with mental illness, its side effects at high doses, and perceptions that it’s an outdated drug with superior, more modern alternatives – a perspective that frankly defies reality. Some astute individuals have understood lithium’s greater promise for years; however, lithium was recently thrust back into the spotlight. 

A recent high-profile publication showing promise of lithium in mitigating Alzheimer’s in the prestigious journal Nature (2) means we are finally waking up to just how interesting and helpful lithium can be.

Could lithium help prevent or treat dementia?

Research into lithium effect on brain health goes back longer than many realise. Several studies have associated lithium use with reduced risk of dementia (3), and scientists have also considered lithium as an adjunct treatment for patients who already have dementia. An experiment (4) on Alzheimer’s disease patients found that supplementing just 300 mcg lithium (as carbonate) per day for 15 months prevented deterioration in cognitive function, which continued to decline in people taking a placebo. While not all research has reported such positive effects, the early evidence is encouraging, and discrepancies between studies might be explained by variables such as discrepant lithium forms and doses.

Returning to the 2025 publication that caused such a stir, the researchers undertook a range of experiments to try to decipher lithium’s effects. First, when they looked at levels of metals in the brains of cognitively healthy adults, people with mild cognitive impairment, or individuals with Alzheimer’s, they found higher levels of lithium in a part of the brain key to processes such as planning and decision making in the cognitively healthy. They also explored the effects of adding lithium orotate, a salt of lithium, to the drinking water of mice genetically engineered to develop a condition similar to familial Alzheimer’s, the aggressive, early-onset form of the disease that runs in families. Compared with the lithium-free condition, even very low doses of lithium orotate dramatically reduced the characteristic misfolded brain proteins that occur in Alzheimer’s, also potentially allaying cognitive decline. Promisingly, lithium also exerted similar protective effects in “wild type” mice. These mice lack the genetic changes that cause early-onset Alzheimer’s, making them a better model for most people.

Does Lithium Extend Lifespan? What the Evidence Suggests

My interest in lithium is tentative evidence from the last couple of decades positively associating intakes with lifespan. This link has been shown in the general population, but there’s also the intriguing finding that people medicated with lithium for psychiatric conditions live longer than their peers taking alternative medications (5). Some of lithium’s effects on mood might mediate the relationship between higher lithium intake and longer life. Tragically, suicide is a common driver of deaths in young adults, and studies of large groups of people have linked higher lithium intakes with lower suicidality (6), which by itself would extend lifespan a little. However, the effects of lithium on mood might not be the whole story, and scientists who study the biology of ageing (geroscientists) have started to test whether lithium extends lifespan in non-human animals. 

So far, the jury is out, for while lithium has been found to extend life in yeast, roundworms, and flies (7, 8 ,9), it didn’t do so in mice, although male mice consuming lithium did seem to have better body composition and blood sugar control (10). Again, perhaps lithium form, dose, and age of use matter though. Overall, lithium certainly doesn’t seem to hurt lifespan, and it might prove modestly beneficial for healthspan (let’s define this as days of life free from disease or disability) and lifespan in a subset of people – but more research needs to be done.

How Lithium Supports Brain Cells and Mood Stability

Regarding how lithium supports mood stability and protects the brain against degeneration (11), as usual, we’re not sure. Most of the relevant research has used the equivalent of very high lithium doses, but I’ll mention a few mechanisms that have substantial empirical support.

Lithium can enter cells through sodium channels, and by competing with sodium and magnesium it can reduce activity of enzymes activated by these other minerals. Perhaps the best-accepted instance of this is lithium’s inhibition of glycogen synthase kinase-3β, an enzyme so named because, among other actions, it reduces activity of an enzyme that synthesises the storage form of carbohydrate, glycogen. This, plus inhibition of other key enzymes, such as inositol monophosphate, set in motion changes in the expression of myriad gene networks involved in brain health, including enhancing clearance of dysfunctional cells and hence improving regulation of proteins in the brain, reducing brain inflammatory responses and hence collateral damage, and promoting the neuroplastic processes needed to remodel the brain to thrive in the dynamic environments in which we live. 

Interestingly, the kinds of high lithium doses used to treat bipolar also support body clock function and sleep, which often go awry before mental illness sets in. Lithium has been shown to influence the body clock at several levels of organisation, from individual cells to people’s rest-activity timing (12), shifting the sleep-wake cycle earlier, making the cycle more regular, and increasing its amplitude. High doses also tend to deepen sleep (13), and deep sleep is a key player in mood regulation and brain maintenance processes, such as waste clearance. (Incidentally, a big part of why appropriate exercise is so good for the brain is that it tends to deepen sleep.) Again, we’re talking about large doses here though.

How Much Lithium Do You Need – and Is Supplementation Safe?

Several factors make it difficult to give clear recommendations regarding lithium intakes.

Firstly, none of us really have any idea how much lithium we regularly consume. Lithium intakes vary enormously between populations, based partly on the physical geography of where people live (over half the world’s lithium is concentrated in Argentina and Chile). This affects how much lithium gets into local drinking water and food. Even then, in much of the world people drink water and eat food that doesn’t come from nearby. Next, your lithium intake would ideally map to your bodily lithium status and needs, and we don’t have good proxies for these at present. There’s also the fact that lithium comes in different salts. Lithium carbonate is most widely used in psychiatry, followed by lithium citrate. However, there’s experimental evidence that lithium orotate is more bioavailable than both, and this superiority of orotate was born out by the recent Nature publication, albeit for different reasons (related to reduced lithium uptake by amyloid). Finally, lithium is used as a medication and is quite tightly regulated in some parts of the world. The salt we know most about (carbonate) is therefore off limits for most of us, although given the early promise of lithium orotate, that might be no issue. 

I’m not a medical doctor and recommend running the supplements you take by a qualified medical professional – just bear in mind that most medical doctors know very little about nutrition and supplementation. I would consider a dose of up to 1 mg elemental lithium per day to be reasonable, provided it’s from a reputable manufacturer. People not very familiar with lithium doses might think of some of the adverse effects of high dose lithium intakes, which can include kidney toxicity. To be clear, my suggestion is well below the amount of lithium consumed from diet alone in much of the world, which most people have never thought twice about. 

I have no affiliation with either, but both Swanson and Life Extension sell low- or trace-dose lithium orotate, and the data I’ve seen suggest their products are high quality and contain what they claim they do. (In fact, there’s been research (14) showing the Swanson low-dose lithium orotate product raises brain lithium in adults.) Part of the difficulty here is that, in my opinion, the lithium doses in many supplements might be higher than is ideal. Based on the work on trace dose lithium use in dementia, plus the apparent higher bioavailability of lithium orotate (15), I think 300 to 400 mcg lithium orotate is an excellent starting point. That dose is more than conservative yet should be sufficient to be beneficial, and my approach to supplementation is generally to choose the lowest dose shown to have the effects you’re after. 

Parting words

In summary, while lithium is not an essential micronutrient, the human brain seems to thrive when it has enough lithium. To ensure you’re providing your brain with what it needs, a lithium supplement providing a trace dose (less than 5 mg elemental lithium) each day seems to be a reasonable, safe way to ensure this. If you’re interested in learning more about lithium, in 2024 I interviewed Dr Becci Strawbridge, an expert in low-dose lithium. The conversation is available on all major podcasting platforms. It’s also on YouTube here.

Note: These words are solely the opinions of the author. (He used no large language models to help write this article.)


About Greg Potter

Greg helps individuals and organisations sustainably improve their health and performance. He does this through developing and popularising innovative businesses and products, coaching, public speaking, consulting, and empowering people through educational resources such as e-books, articles, and courses. Among other roles, Greg is a Sleep Coach at the London Psychiatry Clinic and is Chief Science Officer at Coastline Longevity, where he leads the formulation of supplements to extend healthspan. He also hosts the Reason & Wellbeing podcast and YouTube channel.

Greg’s PhD research spanned sleep, circadian rhythms, nutrition, and metabolism. Highlights of Greg’s career include having this research featured in dozens of international news outlets, including the BBC, Reuters, and The Washington Post; having his writing featured in many newspapers and magazines, including The Metro, Stylist, and Newsweek; coaching a sprinter to four gold medals at the European Championships; and helping athletes break multiple World Records in ocean rowing.

Reference:

8 https://pubmed.ncbi.nlm.nih.gov/17959600/

15 https://pubmed.ncbi.nlm.nih.gov/37356352/

Further info

Why Women’s Brains Need Omega-3 Now

Why Women’s Brains Need Omega-3 Now

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

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

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

What The New Study Shows?

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

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

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

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

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

Why Omega-3 Is So Vital For The Brain?

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

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

Why Women’s Brains Need Special Attention After Menopause?

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

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

How Do You Know If You’re Protected?

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

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

The Bigger Picture Of Brain Health

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

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

Learn more

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

References

  1. Wretland A, et al. Lipid profiling shows reduced long-chain omega-3 lipids in individuals at risk for Alzheimer’s, especially women. Alzheimer’s Dement. 2024. PMID: 40832908.
  2. Crawford MA, et al. The role of essential fatty acids and phospholipids in brain development and health. Prostaglandins Leukot Essent Fatty Acids. 2001;64(2):95-111.
  3. Tan ZS, et al. Red blood cell omega-3 fatty acid levels and markers of accelerated brain aging. Neurology. 2012;78(9):658-664.
  4. Yassine HN, et al. Long-chain omega-3 fatty acids and brain health. Alzheimers Dement. 2016;12(7):759-768.
  5. Morris MC, et al. Fish consumption and the risk of Alzheimer disease. Arch Neurol. 2003;60(7):940-946.
  6. Smith AD, et al. Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment. Proc Natl Acad Sci U S A.
  7. Jernerén F, et al. Homocysteine-lowering B-vitamin treatment modifies the effect of omega-3 fatty acids on brain atrophy in mild cognitive impairment. Am J Clin Nutr. 2015;102(1):215-221.

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New Study: higher choline intake lowers the risk of dementia, Alzheimer’s, & cognitive decline

by Patrick Holford

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

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

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

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

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

Why does it matter?

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

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

What should you do or eat?

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

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

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

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

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

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Reference

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

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Your Brain Needs Supplements Beyond a ‘Well-Balanced Diet’…

By Patrick Holford

If you are eating a healthy whole food diet, do you need supplements? Surely the food you eat should be enough?

When it comes to supplements, the conventional view is based on government supported recommended intakes (RDAs, RNIs, NRVs or DRVs) designed to prevent classical symptoms of deficiency, such as scurvy in the case of vitamin C. The implication here is that if blood levels of nutrients are enough to prevent classical deficiencies then nutrient status is considered to be sufficient.  However, there is abundant evidence that even levels above those used to define ‘deficiency’, may still often be associated with adverse signs or symptoms or increased risk of diseases such as dementia. These levels therefore define a zone of ‘nutritional insufficiency’.

There is furthermore, a growing body of evidence from well-designed studies on specific mental health diseases, showing that supplements giving nutrients at levels beyond the basic ‘RDAs’, delay or reverse the disease or eliminate or ameliorate symptoms of disease, including cognitive decline. 

There are also many studies showing a steady reduction in symptoms or diseases, when blood levels of nutrients increase beyond the arbitrary cut-off levels, set to prevent classical deficiencies. Thus, neither RDAs nor normal reference ranges given for blood levels of nutrients, are ‘optimal’.

Outdated definitions

This illustrates that the definition of ‘deficiency’ is outdated. Deficiency means a lack of efficiency. If the definition of nutrient deficiency, and its counterpart, sufficiency, were to be defined as the level of a nutrient that relieves symptoms of disease or promotes its prevention, that definition is scientifically supportable. It also takes into account the unique biochemical individuality that occurs as a function of both genetics, environmental exposure, microbiomics and an individual’s ability to absorb nutrients.

While medical and advertising law prohibits the description of a nutritional supplement or food as ‘preventing, reversing or treating a disease’ this is scientifically not correct. Nutrients do prevent, reverse and treat disease.

The overarching principle of the Food for the Brain Foundation is that of scientific integrity – that is to be consistent with the prevailing science and share that growing body of knowledge in a way that enables people like you to restore, maintain and improve mental health.

What nutrients should we pay special attention to?

Four nutrients are especially significant in this regard.

Vitamin D – it is now well established that anyone living far from the Equator has to supplement vitamin D for several months (October to March in the UK and for cooler months in most of Europe, Australia, New Zealand and the US). The UK Government, in 2016, recommended that everyone should supplement during the Autumn and Winter. Almost a decade earlier, in 2007, I made the same point but was reported to the Advertising Standards Agency whose rule says “A well-balanced diet should provide the vitamins and minerals needed each day by a normal, healthy individual …”. I felt like reporting the government to the ASA!

Vitamin B12 – many people, especially people over age 50, simply do not absorb vitamin B12 well enough for food alone to be a sufficient supply. The ignorance regarding vitamin B12 is compounded by the inaccurate lower reference range for serum B12 in the UK of anything above 180pg/ml being sufficient (and the US level of 200pg/ml) being out of date and urgently in need of revision. In Europe and Japan anything below 500pg/ml is considered deficient. Against this yardstick, two in five over 60 have levels of B12 which are too low to stop accelerated brain shrinkage. 

Ignorance regarding B12, and the inability of doctors to prescribe it to those with cognitive concerns, is feeding the epidemic of dementia.

Omega-3 DHA – In the UK doctors are not allowed to prescribe omega-3 supplements for any condition, be it depression or dementia, despite all the evidence. I first wrote about omega-3 in 1981, and recommendations have gradually increased with each decade. However, there is still no official Nutrient Reference Value. The current guideline is to have 250mg of combined EPA and DHA a day but this is well below the level of DHA that confers the greatest protection from cognitive decline.

Choline – despite clear evidence of the need for choline, which makes the phospholipid phosphatidylcholine, in pregnancy for normal infant brain development, there is no recommended intake. Vegans can be assumed to be deficient unless supplementing.

I prefer to err on the side of caution, that is to provide the highest optimal level that research suggests would improve mood, memory, mental alertness and is consistent with minimising the risk of cognitive decline.

How many have developed dementia waiting for health officials to catch up?

Don’t be one of them and if you want to know more about what you can do to support your brain then make sure you:

1. Complete your DRIfT test to check your Omega-3 and Vitamin D status, alongside your HbA1c and Homocysteine markers. These are at home, pin-prick, accurate test kits available from UK, EU USA and soon Australia too!
(There is also the option of the DRIfT 5 in 1 test where you also test all of the above PLUS your antioxidant status via our unique Glutathione Index marker – find out more here.)
>> Learn about all our tests here.

2. Complete the FREE Cognitive Function Test. This validated online assessment will create a personalised set of results so you know exactly what you need to work on.
>> Do the online test here

3. Become a FRIEND. Join our mission and become one of our Citizen Scientists, you will get access to a community of like minded people in additionl to COGNITION, your 6-month interactive personalised programme to ensure you upgrade your brain.
>> Find out more here.

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Vitamin D – the Mind, Memory & Mood Essential

By Patrick Holford

Did you know the length of your shadow can tell you if you’re able to generate vitamin D from sunlight?

If your shadow is longer than your body – you can’t produce vitamin D from sunlight. If you are in winter and live in a country of higher latitude (like the UK), this is happening now!

Vitamin D is an all-rounder as far as your brain and mental health is concerned.

It helps neurotransmission and exerts anti-inflammatory and neuroprotective activities within the brain by reducing both inflammation and oxidative stress (1).  

We are all deficient in winter

Generally speaking, the lower your vitamin D, the worse your mood which makes vitamin D especially important to supplement from October to March if you live in the UK or a similar latitude, when the angle of the sun is too low and you’re also less likely to get outdoors exposing your skin to sunlight. It’s best to assume that we are all deficient in winter, unless you travel to the sun, and therefore need to supplement at least 25mcg (1000iu) although two or three times may be optimal and necessary to correct deficiency.

Vitamin D and depression

The lower your vitamin D level, the more depressed you are likely to feel. If your mood takes a dip in winter months this is a key sign that you might need more. That’s what researchers at the University of Tromso in Norway found on testing 441 volunteers who were given a test for depression and also a test for blood levels of vitamin D. The volunteers were then given Vitamin D supplements or placebo. Tested one year on, those given vitamin D, but not those given the placebos, had substantially lower depression ratings (2).

However, you don’t have to wait for a year to get a lift in your mood. An eight-week study in Australia found that some of those given vitamin D supplements had an improvement in mood in only five days (3). Another study, in Iran, gave a single vitamin D injection and reported improvement in depression when measured 3 months on (4).

Since vitamin D stores, there is no need to supplement daily. You can take a weekly dose. In the Norwegian study above they gave 20,000iu or 40,000iu weekly. Both worked and there wasn’t a big difference in the effects on mood. So, you can assume that 20,000iu weekly, or 3,000iu daily would likely be sufficient.

It’s what is in your blood that matters

However, the yardstick for what you need is really whatever gets your blood level into the optimal range.

In the study above, those given 20,000iu a week averaged a blood level of 88 nmol/l, while those given 40,000iu averaged 111nmol/l. It is now well recognised that levels above 75nmol/l (30 ng/ml) correlate with good health for many health measures, while levels above 100nmol/l (40ng/ml) might be even better in some respects. My recommendation is to test yourself and consider anything below 50 to be deficient, and above 75 to be sufficient with an optimal level being closer to 100nmol/l (40ng/ml). If you then supplement 3,000iu daily, or seven times this weekly, especially from October to March, retest yourself against these yardsticks.

It’s not JUST about vitamin D

But it isn’t just vitamin D we need – it’s sunlight.

During the summer months, if you are spending half an hour outdoors, with short sleeves, shorts or even more skin exposure, in the sunlight, even a multivitamin that provides you 800iu (a quarter of what you need in the darker months) might be sufficient.

Sunlight promotes serotonin, the happy neurotransmitter.

Having good vitamin D levels is a vital part of your brain upgrade since it helps optimise your brain’s serotonin levels. That’s because a vital enzyme called TPH, which converts the amino acid tryptophan into serotonin, is enhanced in the brain by vitamin D, and selectively shut down in the gut. So, with sufficient vitamin D you get higher brain levels of serotonin, promoting good mood, and lower serotonin levels in the gut (5), protecting against gut inflammation. 

The other way to boost your light exposure is with light therapy. Canadian researchers compared the effects of an anti-depressant (fluoxetine), placebo or 30 minutes daily of light therapy as soon as possible on waking for people with major depression. Light therapy was both superior to placebo and anti-depressants, which were also no better than placebo. I have a full spectrum light in my study, which I put on in the winter, when I’m writing in the early morning, before the sun comes up.

Vitamin D and addiction

Interestingly, vitamin D deficiency is also associated with greater opioid addiction (7), suggesting the need to up vitamin D intake to reduce cravings. There’s also something else interesting about vitamin D, sun exposure and addiction. People can become addicted to sunbeds. In relation to opioids, the lower one’s vitamin D levels, the more addictive they become. Sun exposure, which promotes higher vitamin D levels, reduces opioid addiction.

What to eat?

The best food sources of vitamin D are oily fish and eggs. A serving of salmon or mackerel is likely to give you 400iu of vitamin D. Two eggs will provide about 130iu. In some countries, not the UK, milk is fortified with vitamin D but otherwise, it is not a great source. Some mushrooms are purposely fortified with vitamin D by exposing them to UV light.

In summary, the way up from down is to eat a low GL diet, with plenty of oily fish and eggs, avoid sugar, cut back on stimulants and alcohol, and make sure your daily supplements include omega-3, B vitamins, with extra B12 if your homocysteine level is high, vitamin D, zinc, magnesium, chromium, plus the amino acids 5-HTP with is the precursor of serotonin.

Vitamin D protects your brain and memory.

Vitamin D deficiency increases the risk of Alzheimer’s (9). In a study in France involving 912 elderly patients followed for 12 years, a total of 177 dementia cases occurred. Those with low vitamin D levels had a nearly three-fold increased risk of Alzheimer’s (10). Supplementing 800iu (20mcg) a day for 12 months has also been shown to improve cognitive function (11). 

Supplements may also help ward off dementia, according to a recent, large-scale study involving over twelve thousand dementia-free 70+ year-olds in the US (12). More than a third (37%) took supplements of vitamin D. Those who did had a 40% lower incidence of dementia. Professor Zahinoor Ismail, of the University of Calgary and University of Exeter, who led the research, said: “We know that vitamin D has some effects in the brain that could have implications for reducing dementia, however so far, research has yielded conflicting results. Overall, we found evidence to suggest that earlier supplementation might be particularly beneficial, before the onset of cognitive decline.”

Vitamin D helps recovery from strokes and brain injury

Having a higher vitamin D level or supplementing vitamin D at levels above 2,000iu a day also helps people recover from strokes (13) and other forms of brain injury.

I recommend 3,000iu a day or 21,000iu a week in winter but most importantly, monitoring your vitamin D level to keep it above 75nmol/l (30 ng/ml). A level of 100nmol/l may be optimal. That is why testing is so vital as winter approaches. Test again 3 months later so you know if you’re taking enough or too much and that will give you a good gauge as spring approaches when you can probably lower your intake to 600 to 1,000iu depending on sun exposure and diet to top up to over 1,000iu.

Vitamin D is vital in pregnancy and for children

A breastfeeding mother must, at least, supplement omega-3 fish oils and ensure enough B vitamins for homocysteine to be below 7 mcmol/L, but many other nutrients are also necessary. Low vitamin D status in both the mother and newborn baby increases the likelihood of developing autistic spectrum disorder by 54% (14).

Without sufficient nutrients not only do brain cells not make the connections but the production and flow of neurotransmitters doesn’t happen optimally. Bruce Ames, Emeritus professor of Biochemistry and Molecular Biology at the University of California, thinks that “serotonin synthesis, release, and function in the brain are modulated by vitamin D and the 2 marine omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).” He says that ”insufficient levels of vitamin D, EPA, or DHA, in combination with genetic factors and at key periods during development, would lead to dysfunctional serotonin activation and function and may be one underlying mechanism that contributes to neuropsychiatric disorders and depression in children”. (15) 

A study in Northern Ireland found that half of schoolchildren were deficient in vitamin D, with a level below 50nmol/l (I recommend above 75 nmol/l). Another finds that low vitamin D levels in childhood are related to behaviour problems in adolescence (16). Is it any wonder so many children are neurodivergent?

A placebo-controlled trial giving ADHD children magnesium together with vitamin D for eight weeks showed a major reduction in emotional, conduct and peer problems and improved socialisation compared with children treated with the placebo (17).

The bottom line – we all need to supplement vitamin D

The bottom line is everyone, from children to older people, and especially anyone considering pregnancy, suffering with low mood or memory problems, must test their vitamin D, ideally, at the start of winter to guide them as to what to supplement, during winter perhaps at 3 months, and 6 months later, to learn what amount of vitamin D supplementation they need in summer and winter.

In summary, you want to get your blood level above 75nmol/l (30 ng/ml) which usually means supplementing 3,000iu from October to March for those in the Northern Hemisphere. The optimal level is, however,  likely to be above 100nmol/l (40mg/ml).  Your need for vitamin D is likely to be greater if you are overweight and have darker skin and live further North.

When spring returns, and throughout summer, 1,000iu a day may be enough depending on your sun exposure.



Thank you for reading!
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References

1 Jayedi A, Rashidy-Pour A, Shab-Bidar S. Vitamin D status and risk of dementia and Alzheimer’s disease: A meta-analysis of dose-response †. Nutr Neurosci. 2019 Nov;22(11):750-759. doi: 10.1080/1028415X.2018.1436639. Epub 2018 Feb 15. PMID: 29447107

2 Jorde R, Sneve M, Figenschau Y, Svartberg J, Waterloo K. Effects of vitamin D supplementation on symptoms of depression in overweight and obese subjects: randomized double blind trial. J Intern Med. 2008 Dec;264(6):599-609. doi: 10.1111/j.1365-2796.2008.02008.x. Epub 2008 Sep 10. PMID: 18793245.

3 Khoraminya N, Tehrani-Doost M, Jazayeri S, Hosseini A, Djazayery A. Therapeutic effects of vitamin D as adjunctive therapy to fluoxetine in patients with major depressive disorder. Aust N Z J Psychiatry. 2013 Mar;47(3):271-5. doi: 10.1177/0004867412465022. Epub 2012 Oct 23. PMID: 23093054. Xxxx check the some in 5 days

4 Mozaffari-Khosravi H, Nabizade L, Yassini-Ardakani SM, Hadinedoushan H, Barzegar K. The effect of 2 different single injections of high dose of vitamin D on improving the depression in depressed patients with vitamin D deficiency: a randomized clinical trial. J Clin Psychopharmacol. 2013 Jun;33(3):378-85. doi: 10.1097/JCP.0b013e31828f619a. PMID: 23609390.

5 Patrick RP, Ames BN. Vitamin D hormone regulates serotonin synthesis. Part 1: relevance for autism. FASEB J. 2014 Jun;28(6):2398-413. doi: 10.1096/fj.13-246546. Epub 2014 Feb 20. PMID: 24558199.

6 Lam RW, Levitt AJ, Levitan RD, Enns MW, Morehouse R, Michalak EE, Tam EM. The Can-SAD study: a randomized controlled trial of the effectiveness of light therapy and fluoxetine in patients with winter seasonal affective disorder. Am J Psychiatry. 2006 May;163(5):805-12. doi: 10.1176/ajp.2006.163.5.805. PMID: 16648320.Psychiary, No015

7 Kemény LV, Robinson KC, Hermann AL, Walker DM, Regan S, Yew YW, Lai YC, Theodosakis N, Rivera PD, Ding W, Yang L, Beyer T, Loh YE, Lo JA, van der Sande AAJ, Sarnie W, Kotler D, Hsiao JJ, Su MY, Kato S, Kotler J, Bilbo SD, Chopra V, Salomon MP, Shen S, Hoon DSB, Asgari MM, Wakeman SE, Nestler EJ, Fisher DE. Vitamin D deficiency exacerbates UV/endorphin and opioid addiction. Sci Adv. 2021 Jun 11;7(24):eabe4577. doi: 10.1126/sciadv.abe4577. PMID: 34117054; PMCID: PMC8195487.

8 Jayedi A, Rashidy-Pour A, Shab-Bidar S. Vitamin D status and risk of dementia and Alzheimer’s disease: A meta-analysis of dose-response †. Nutr Neurosci. 2019 Nov;22(11):750-759. doi: 10.1080/1028415X.2018.1436639. Epub 2018 Feb 15. PMID: 29447107

9 Chai B, Gao F, Wu R, Dong T, Gu C, Lin Q, Zhang Y. Vitamin D deficiency as a risk factor for dementia and Alzheimer’s disease: an updated meta-analysis. BMC Neurol. 2019 Nov 13;19(1):284. doi: 10.1186/s12883-019-1500-6. PMID: 31722673; PMCID: PMC6854782.

10 Jia J, Hu J, Huo X, Miao R, Zhang Y, Ma F. Effects of vitamin D supplementation on cognitive function and blood Aβ-related biomarkers in older adults with Alzheimer’s disease: a randomised, double-blind, placebo-controlled trial. J Neurol Neurosurg Psychiatry. 2019 Dec;90(12):1347-1352. doi: 10.1136/jnnp-2018-320199. Epub 2019 Jul 11. PMID: 31296588.

11 Feart C, Helmer C, Merle B, Herrmann FR, Annweiler C, Dartigues JF, Delcourt C, Samieri C. Associations of lower vitamin D concentrations with cognitive decline and long-term risk of dementia and Alzheimer’s disease in older adults. Alzheimers Dement. 2017 Nov;13(11):1207-1216. doi: 10.1016/j.jalz.2017.03.003. Epub 2017 May 16. PMID: 28522216.

12 Ghahremani M, Smith EE, Chen HY, Creese B, Goodarzi Z, Ismail Z. Vitamin D supplementation and incident dementia: Effects of sex, APOE, and baseline cognitive status. Alzheimers Dement (Amst). 2023 Mar 1;15(1):e12404. doi: 10.1002/dad2.12404. PMID: 36874594; PMCID: PMC9976297.

13 Marek K, Cichoń N, Saluk-Bijak J, Bijak M, Miller E. The Role of Vitamin D in Stroke Prevention and the Effects of Its Supplementation for Post-Stroke Rehabilitation: A Narrative Review. Nutrients. 2022 Jul 4;14(13):2761. doi: 10.3390/nu14132761. PMID: 35807941; PMCID: PMC9268813.

14 Wang Z, Ding R, Wang J. The Association between Vitamin D Status and Autism Spectrum Disorder (ASD): A Systematic Review and Meta-Analysis. Nutrients. 2020 Dec 29;13(1):86. doi: 10.3390/nu13010086. PMID: 33383952; PMCID: PMC7824115.

15 Patrick RP, Ames BN. Vitamin D and the omega-3 fatty acids control serotonin synthesis and action, part 2: relevance for ADHD, bipolar disorder, schizophrenia, and impulsive behavior. FASEB J. 2015 Jun;29(6):2207-22. doi: 10.1096/fj.14-268342. Epub 2015 Feb 24. PMID: 25713056.

16 Sonia L Robinson, Constanza Marín, Henry Oliveros, Mercedes Mora-Plazas, Betsy Lozoff, Eduardo Villamor, Vitamin D Deficiency in Middle Childhood Is Related to Behavior Problems in Adolescence, The Journal of Nutrition, Volume 150, Issue 1,

2020, Pages 140-148, ISSN 0022-3166, https://doi.org/10.1093/jn/nxz185.

17 Hemamy M, Pahlavani N, Amanollahi A, Islam SMS, McVicar J, Askari G, Malekahmadi M. The effect of vitamin D and magnesium supplementation on the mental health status of attention-deficit hyperactive children: a randomized controlled trial. BMC Pediatr. 2021 Apr 17;21(1):178. doi: 10.1186/s12887-021-02631-1. Erratum in: BMC Pediatr. 2021 May 12;21(1):230. PMID: 33865361; PMCID: PMC8052751.

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