A National Step Forward for Brain Health

Food for the Brain awarded an Innovate UK grant to advance early dementia detection and prevention

We are delighted to announce that Food for the Brain Foundation has been awarded a prestigious grant from Innovate UK, part of UK Research and Innovation (UKRI) – national recognition of our pioneering work in dementia prevention and early detection.

Importantly, this funding marks a milestone for us as a UK-based research charity. It also represents a significant step forward for our global community of citizen scientists, clinicians, and individuals dedicated to preventing Alzheimer’s, dementia, and cognitive decline.

For us, this is not just a charity and research achievement – it’s a sign that the world is waking up to prevention.

Why this matters?

Right now, someone in the UK develops dementia every three minutes. Across the globe, it’s every three seconds. And despite this, dementia cost the world over US$1.3 trillion in 2019, yet countless cases remain undiagnosed.

For nearly two decades, we have led the charge in prevention. So far, over 400,000 people worldwide have taken our Cognitive Function Test (CFT) – a free, validated online tool that helps you understand your brain health, assess your risks, and take action to improve.

This grant from Innovate UK, part of the UK’s national innovation agency, provides crucial funding to further validate and expand our tools for early dementia detection and – ultimately – prevention.

It forms part of the Blood Biomarker Challenge, a UK-wide research initiative led by Professor Vanessa Raymont at the University of Oxford, which aims to integrate blood-based biomarker testing into NHS diagnostic pathways.

Our Cognitive Function Test (CFT) has been selected to assess cognitive performance in the READ-OUT trial – part of this Innovate UK-funded programme, supported by the Department of Health and Social Care, the NIHR, and Alzheimer’s Research UK.

It will allow us to:

Integrate our Cognitive Function Test into NHS-linked research, workflows, and clinical studies, thereby bridging science and healthcare delivery.
Further expand access to our evidence-based prevention tools – making them mobile-friendly, multilingual, and culturally inclusive for global use.

About Innovate UK

Innovate UK is the UK government’s innovation agency, supporting organisations that deliver real-world impact across science, technology, and health. Each year, it invests over £1 billion in ideas that can transform industries, economies, and lives – from sustainable energy and biotech to healthcare innovation.

Receiving an Innovate UK grant means your project has been rigorously evaluated for its scientific quality, innovation, feasibility, and potential global impact.

What this means for global brain health and dementia detection?

Our Cognitive Function Test (CFT) is the only freely available online tool that measures cognitive performance. It also provides a personalised Dementia Risk Index, based on eight key lifestyle and biological factors.

With this grant, we can now take the next step – integrating this digital test with blood test data from our DRIfT (Dementia Risk Index Functional Test).

The DRIfT test measures five critical nutritional biomarkers proven to influence cognitive ageing:

Omega-3 Index – vital brain fats that support memory and neuronal health

Vitamin D – essential for mood, immunity, and brain protection

Homocysteine – a marker of B-vitamin status; high levels increase the risk of brain shrinkage

HbA1c – a measure of long-term blood sugar control linked to brain energy supply

Glutathione Index – the body’s master antioxidant defence

Combining these markers with our multilingual, free Cognitive Function Test means that more and more people can detect early warning signs of cognitive decline. This can happen decades before diagnosis. This empowers them to take action early – and prevent it. Together, these innovations represent the future of dementia detection and prevention.

Why prevention and early dementia detection must come first?

Despite billions spent on drug development, no Alzheimer’s medication to date has shown meaningful improvement in cognitive outcomes. In fact, many come with serious side effects, including brain swelling and bleeding. (Read more Alzheimer’s drugs here and here.)

That’s why our focus, and now Innovate UK’s, is on early dementia detection.

Identifying risk early, addressing nutritional and metabolic imbalances, and protecting the brain before damage occurs.

Take part – protect your brain, advance the science, stay sharp for life

Ultimately, this work only matters if people like you take part.

By joining our global citizen-science movement, you’ll help us refine and accelerate the world’s first large-scale dementia prevention database.

Step 1: Take the free Cognitive Function Test

A quick, 20-minute online test that shows you how well your brain is performing and what to do next.

Take the free CFT now

Step 2: Complete the DRIFT biomarker test

A simple at-home finger-prick blood test that measures your omega-3, vitamin D, B-vitamin, blood sugar, and antioxidant status.

Order your DRIFT test

Step 3: Become a FRIEND of Food for the Brain

For just £50 a year or £5 a month, you can support our research and charitable work. You’ll also gain access to – your personalised brain upgrade programme. Additionally, enjoy monthly group coaching sessions and live webinars.

Become a FRIEND here

Looking ahead: the future of dementia detection and prevention

With the support of Innovate UK, the NHS, and thousands of citizen scientists and Friends, we’re building a future where Alzheimer’s is preventable, not inevitable.

Ultimately, this grant strengthens our ability to deliver credible, evidence-based tools that empower everyone to take charge of their cognitive health – starting today.

Take the test. Join the study. Be part of prevention.
👉 foodforthebrain.org/tests | foodforthebrain.org/driftstudy

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

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

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

Reference:

1 https://www.alzint.org/about/dementia-facts-figures/

2 UK Research and Innovation 

3  UK Government Press Release)

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

by Greg Potter

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.

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

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

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

Reference:

1 https://pubmed.ncbi.nlm.nih.gov/30066063/

2 https://www.nature.com/articles/s41586-025-09335-x

3 https://pubmed.ncbi.nlm.nih.gov/38657568/

4 https://pubmed.ncbi.nlm.nih.gov/22746245/

5 https://pubmed.ncbi.nlm.nih.gov/36640269/

6 https://pubmed.ncbi.nlm.nih.gov/35252091/

7 https://pubmed.ncbi.nlm.nih.gov/25126078/

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

9 https://pubmed.ncbi.nlm.nih.gov/27068460/

10 https://pubmed.ncbi.nlm.nih.gov/34532960/

11 https://pubmed.ncbi.nlm.nih.gov/38697859/

12 https://pubmed.ncbi.nlm.nih.gov/33650218/

13 https://pubmed.ncbi.nlm.nih.gov/3313443/

14 https://pubmed.ncbi.nlm.nih.gov/38810780/

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

—

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

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

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

They wrote:

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

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

A Systematic Omission

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

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

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

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

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

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

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

Criticism 1: Misunderstanding Who Benefited in the VITACOG Trial

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

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

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

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

Criticism 2: No Benefit in the Hong Kong Trial?

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

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

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

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

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

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

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

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

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

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

What Does the Evidence Really Say?

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

Their conclusion is clear:

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

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

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

The perfect time to start? Today.

What Can You Do?

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

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

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

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

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

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

—

What can you do, practically and quickly, to reduce your risk of developing Alzheimer’s?

The International Alzheimer’s Prevention Expert Group, including our founder Patrick Holford, has identified four key areas that could cut your future risk by over 80% – down to less than a quarter – if addressed early.

The four “quick wins”? Increase your vitamin D, omega-3, and B vitamins, and reduce your intake of sugar and refined carbs.

1. Vitamin D: The Sunshine Factor

Vitamin D is primarily made in your skin through sun exposure, particularly at midday in the summer. However, in the winter – especially in the UK and other northern countries – you cannot make enough, so supplementation is essential. A Dutch study found that people with low levels of vitamin D, omega-3s, and B vitamins were over four times more likely to develop dementia¹. Those who supplement with vitamin D have around a third less risk².

Even levels below 62.5 nmol/L (25 ng/mL) increase risk. A French study found that low vitamin D levels tripled Alzheimer’s risk³. The darker your skin, the more sun exposure you need – which makes supplementation all the more vital for many.

2. Omega-3: Feed Your Brain with Fish

Fish is a true brain food – rich in omega-3s, vitamin D, and B12. Eating fish at least once a week reduces Alzheimer’s risk by a third⁴. A recent review confirmed that a daily serving cuts the risk of cognitive decline by 30%⁵.

Omega-3 fats (especially DHA) quite literally build brain cells. The UK Biobank study of over 250,000 people found that those with higher omega-3 levels had a 20% lower risk of dementia⁶. A US study also found that a higher omega-3 index correlated with more white matter in the brain and better cognitive function⁷.

Professor William Harris of the Fatty Acid Research Institute calls it “a safe, simple, cheap and effective tool to forestall Alzheimer’s.”

3. B Vitamins: The Brain Fixers

B6, B12, and folate don’t just support brain function – they’re essential for fixing omega-3s into your brain’s cell membranes. Without them, homocysteine – a toxic amino acid – builds up in your blood. High levels (above 11 μmol/L) are strongly linked to brain shrinkage and Alzheimer’s.

Half of people over 60 in the US have homocysteine levels above 11. The Dutch study found that risk rises even above 8 – a level many people exceed.

As Professor Joshua Miller from Rutgers University says, raised homocysteine is an early warning sign: “a canary in the coal mine.” The good news? It’s easily lowered with a B vitamin supplement – ideally one containing 500 mcg of B12, methylfolate, and B6.

More greens, beans, nuts, and lentils also help. A recent study showed that replacing just one serving of processed meat with nuts or beans (rich in folate) cut dementia risk by 19%⁸.

4. Sugar and Refined Carbs: Silent Brain Saboteurs

The more sugar a person eats – including refined white carbohydrate foods such as bread, pastries, pasta, and rice – the higher their risk of both diabetes and dementia. Fizzy drinks and ultra-processed foods, sweetened with high-fructose corn syrup, are particularly bad for the brain.
“The brain needs the most energy of any organ, so it has the most mitochondria to make it. Sugar damages mitochondria,” says Dr Robert Lustig from the University of California, San Francisco.

A study just published this month in Neurology involving 2 million people shows that those with sugar problems (metabolic syndrome) are 24% more likely to develop dementia early¹⁰.
Keeping blood glucose levels in the low–normal range is reflected by a low glycosylated haemoglobin (HbA1c), which is the blood test doctors use to diagnose diabetes. Having a lower HbA1c is associated with reduced risk for dementia in several studies⁹. A recent study of 374,021 older men with diabetes found that keeping HbA1c stable over three years cut the risk of dementia by a third¹¹.

Want to know what’s driving your brain risk?

Take our free 3-minute Alzheimer’s Prevention Check at alzheimersprevention.info – or, for the full picture, order the four-in-one home blood test to measure your omega-3 index, vitamin D, homocysteine and HbA1c: foodforthebrain.org/tests

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

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

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

References:

1  van Soest APM., et al Alzheimers Dement. 2024 Jul;20(7):4594-4601

2 Ghahremani M, et al. Vitamin D supplementation and incident dementia: Effects of sex, APOE, and baseline cognitive status. Alzheimers Dement (Amst). 2023 Mar;15(1):e12404. doi: https://doi.org/10.1002/dad2.12404

 3 Feart C, et al. 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: https://doi.org/10.1016/j.jalz.2017.03.003

4 Beydoun MA, et al. Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis. BMC Public Health. 2014;14:643. doi: https://doi.org/10.1186/1471-2458-14-643

5 Godos J, et al. Fish consumption, cognitive impairment and dementia: an updated dose-response meta-analysis of observational studies. Aging Clin Exp Res. 2024;61:3731–3739. doi: https://doi.org/10.1007/s40520-024-02823-6

6 Sala-Vila A, et al. Plasma Omega-3 Fatty Acids and Risk for Incident Dementia in the UK Biobank Study: A Closer Look. Nutrients. 2023 Nov;15(23):4896.

7 Loong S, et al. Omega-3 Fatty Acids, Cognition, and Brain Volume in Older Adults. Brain Sci. 2023;13:1278. doi: https://doi.org/10.3390/brainsci13091278

8 Li Y, et al. Long-term intake of red meat in relation to dementia risk and cognitive function in US adults. Neurology.2025;104(3):e210286. doi: https://doi.org/10.1212/WNL.0000000000210286

9 Luchsinger JA, et al. Hyperinsulinemia and risk of Alzheimer disease. Neurology. 2004;63(7):1187–92. doi:https://doi.org/10.1212/01.WNL.0000140292.04932.04932.87;  see also Abbatecola AM, et al. Insulin resistance and executive dysfunction in older persons. J Am Geriatr Soc.2004;52(10):1713–

8. https://doi.org/10.1111/j.1532-5415.2004.52466.x ;see also Xu WL, et al. Uncontrolled diabetes increases the risk of Alzheimer’s disease: a population-based cohort study. Diabetologia. 2009;52(6):1031–

9. doi: 10.1007/s00125-009-1323-x ;see also Hassing LB, et al. Type 2 diabetes mellitus contributes to cognitive decline in old age: a longitudinal population-based study. J Int Neuropsychol Soc. 2004;10(4):599–607. https://doi.org/10.1017/S1355617704104165
; see also Yaffe K, et al. Glycosylated hemoglobin level and development of mild cognitive impairment or dementia in older women. J Nutr Health Aging. 2006;10(4):293–5. https://pubmed.ncbi.nlm.nih.gov/16886099/ ; see also Roberts RO, et al. Diabetes and elevated hemoglobin A1c levels are associated with brain hypometabolism but not amyloid accumulation. J Nucl Med. 2014;55(5):759–64. https://jnm.snmjournals.org/content/55/5/759 

10  Lee JY, Han K, Kim J, Lim JS, Cheon DY, Lee M. Association Between Metabolic Syndrome and Young-Onset Dementia: A Nationwide Population-Based Study. Neurology. 2025 May 27;104(10):e213599. doi: 10.1212/WNL.0000000000213599. Epub 2025 Apr 23. PMID: 40267374.11 Underwood PC, et al. HbA1c time in range and dementia. JAMA Netw Open. 2024;7(8):e2425354. doi: https://doi.org/10.1001/jamanetworkopen.2024.25354

Patrick Holford’s new book claims that almost no one needs to develop Alzheimer’s.

Fewer than 1% of Alzheimer’s cases are genetic, and amyloid deposits – long targeted by new drugs – are neither the cause of the disease nor its cure.

Alzheimer’s is the consequence of a ‘perfect storm’ – a combination of poor diet, unhealthy lifestyle and harmful environmental factors that affect the structure, function or utilisation of the brain, says Patrick Holford,  our founder and author of Alzheimer’s: Prevention is the Cure. He says: “Every single known risk factor affects one of these, and it is combinations of these risk factors – which are under our control – that lead to cognitive decline, first experienced as brain fog and forgetfulness”.

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The book stems from a major global Alzheimer’s prevention project by the charity Food for the Brain, which has assessed the cognitive function of hundreds of thousands of people through a free test, followed by a comprehensive diet and lifestyle questionnaire that calculates their future risk – and shows how to lower it.

“We can detect declining cognitive function from as young as 18. The youngest non-genetic Alzheimer’s diagnosis is just 19,” says Holford, who founded the charity to help prevent Alzheimer’s. “We see a steady decline in cognitive function from the early twenties, with most people starting to show significant cognitive impairment in their seventies and eighties. But this decline cannot only be arrested – it can be reversed with the right diet, supplements and lifestyle choices.”

“Becoming an Alzheimer’s patient is almost always a choice,” says neurologist Dr David Perlmutter, a member of the charity’s Alzheimer’s Prevention Expert Group who also believes that diet and lifestyle, much more than genes, are driving the increase in Alzheimer’s.

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The book  (out today!) explains all the known risk factors we can change – and the extent to which doing so reduces future risk. Particularly important are what Holford calls ‘the four horsemen of the brain health apocalypse’: lack of brain fats, lack of B vitamins, lack of antioxidants, and too much sugar and refined foods. Increasing omega-3 intake from oily fish and supplements cuts risk by about 20%, as does optimising vitamin D levels. Vitamin D is produced in the skin when exposed to sunlight, with some also obtained from oily fish, but supplementation is needed during the winter months. Those who supplement with vitamin D have about one third less risk of developing dementia.

The single biggest–and most easily eliminated–risk factor, is lack of B vitamins, leading to high levels of the toxic amino acid homocysteine. “Homocysteine, if raised above 11 µmol/L, causes brain shrinkage and cognitive decline. If lowered with B vitamins, both shrinkage and decline are arrested. It is the only risk factor for which the evidence is strong enough to say it is causal.” says Holford. “Mine is 7 µmol/L but my wife’s, despite eating the same food, was 15µmol/L – right in the brain-shrinking zone. She now supplements high-dose B12, B6 and folate and her level has dropped to the same as mine. You would never know without testing. We are both in our sixties.” He estimates that half of those over-60 have a homocysteine level above 11, increasing their risk by about one-third.

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“This is why we are now testing people, with a home-test kit, for homocysteine, vitamin D and omega-3 index. If the omega-3 index is below 8% – as it is for many – that predicts cognitive decline and loss of brain density.”

The test kit also measures HbA1c, which GPs use to diagnose diabetes. However, the optimal level for Alzheimer’s prevention is lower than the threshold used to diagnose diabetes. Eating less sugar, fewer refined and ultra-processed foods, and reducing total carbohydrate intake also cuts dementia risk by about 20%.

Another big risk reducer is increasing intake of fruits and vegetables rich in antioxidants, and supplementing with vitamin C. Those in the top third of antioxidant intake have half the risk of cognitive decline, according to a study of 2,716 people over age 60 (1). The home-test kit also measures antioxidant status, specifically glutathione levels.  Greens and beans are rich sources of the B vitamin folate. A recent study found that swapping one serving of processed meat for a serving of nuts or beans – foods high in folate – was associated with a 19% lower risk of dementia (2).

Getting your diet right is only half the story, says Holford. “Minimising alcohol, not smoking, staying physically active, and having a socially and intellectually stimulating lifestyle are all vital parts of dementia-proofing. So too are getting enough sleep, managing stress, and ensuring good hearing and vision. Cataracts, for example, increase risk, but having cataract surgery significantly lowers it. Women also need to support hormonal health after menopause. Often using ‘natural’ HRT makes a big difference.”

The book is out in the UK, EU today and you can pre-order for USA & Australia too (they will be shipped ot you in 3-5 weeks) .

Also join us in May for the Alzheimer’s Prevention Day

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

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

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

By Patrick Holford

Recently, the Telegraph reported: “Statins can reduce the risk of dementia among those who already have low cholesterol.” The article claimed that those on statins were less likely to develop dementia – even Alzheimer’s – and that low LDL cholesterol was somehow protective.

Frankly, this is dangerous misinformation.

Why? Because it contradicts robust scientific evidence that low cholesterol – particularly below 4 mmol/l – increases the risk for dementia. That’s hardly surprising when you consider that 25% of the cholesterol in your body is in your brain. Cholesterol is a vital component of neuronal membranes – it’s not just blood fat, it’s brain fuel.

And as for statins? There’s no credible evidence that they prevent dementia. Quite the opposite: the evidence points to statins lowering brain-essential cholesterol and raising dementia risk. So I asked cholesterol expert Dr Malcolm Kendrick for his take on the study in question.

His response was blunt but justified: “This study is horseshit. Here’s why…”

Dr Kendrick Key Critiques:

LDL measurement was vague. It’s unclear if they even measured LDL directly- most studies use the Friedewald formula, known to be wildly inaccurate, especially with high triglycerides or low HDL.

Only one measurement. LDL was recorded once at the study’s start – never again. That’s like measuring someone’s blood pressure once and claiming to predict their lifetime stroke risk.

Bizarre cohort overlap. Somehow, 170,174 participants were in both high and low LDL groups? That’s statistically and biologically nonsensical.

Alzheimer’s exclusion unexplained. Those with pre-existing Alzheimer’s were removed, but with no breakdown of their LDL levels – crucial missing data.

Propensity score manipulation. This “retrospective matching” excluded over 350,000 people, distorting the natural associations. Diabetes and hyperlipidaemia were artificially balanced between groups, masking real-world relationships.

Key confounder: statin timing. Participants were only included after being prescribed statins, meaning LDL levels were already artificially lowered. So “low LDL” here is post-drug, not natural. The entire premise collapses.

This study, like too many others published today, exemplifies what Drummond Rennie famously criticised:

“There is no study too fragmented, no hypothesis too trivial, no design too warped, no analysis too self-serving for it to be published.”

So what do we actually know? Here is an extract from Patrick’s new book – Alzheimers: Prevention is the Cure.

Cholesterol and the Brain – The Real Story

Your brain needs cholesterol. Low cholesterol (<4 mmol/l) is a clear risk factor for dementia. One biomarker study found that high homocysteine and low cholesterol were the best predictors of dementia risk【1】.

And what’s a common cause of low cholesterol in the elderly? Statins. These drugs have consistently failed to show benefits in preventing cognitive decline【2】.

This fits what we know genetically. The ApoE gene governs how cholesterol gets into neurons. Those with ApoE4 are less efficient at this – that’s why they’re more prone to cognitive decline.

It’s not high cholesterol itself that’s dangerous – it’s cholesterol mismanagement in the brain.

Yes, very high cholesterol (above 6.5 mmol/l) is statistically linked to increased dementia risk – but modest elevations, particularly with a healthy lifestyle, are not a problem【3】. And even that data is shaky. One meta-analysis of over a million people showed only a 14% increased dementia risk with “high” cholesterol. But the thresholds varied – some studies defined “high” as anything over 6.2 mmol/l【3】.

More importantly, people with higher cholesterol often eat more sugar, processed foods, and trans fats – all factors known to fuel inflammation and oxidative stress in the brain.

The Lancet Commission, which makes the anti-cholesterol case, even acknowledged this diet–dementia link: in a cohort of 94,184 Danes, poor diet predicted both high LDL and dementia risk【4】.

So maybe it’s not the cholesterol – it’s what comes with it.

Statins and the Hope for Vascular Dementia 

Originally, statins were hyped for vascular dementia – about 20% of all dementia cases – because of their supposed blood vessel–protective effects. But that theory has fallen flat. A Cochrane review found no benefit from statins for dementia prevention【6】.

And the best independent trial – not funded by drug companies – also found no cardiovascular benefit for statins in older adults【5】.

There’s no data supporting the notion that statins protect the brain. Yet the Lancet Commission listed “high cholesterol” as contributing 7% to dementia risk, which will no doubt spur even more statin prescriptions【4】.

The Optimum Nutrition Perspective

From an optimum nutrition standpoint, we view cholesterol differently.

If your total cholesterol is up to 6.5 mmol/l – but you have high HDL, low triglycerides, low homocysteine, and a healthy diet low in sugar and refined carbs – you’re not at risk. In fact, you’re likely protected.

One recent study showed that higher HDL in midlife predicted significantly lower future dementia risk【7】. Low HDL, not high total cholesterol, is a hallmark of metabolic syndrome – the precursor to diabetes, heart disease, and yes, dementia.

The evidence is clear: cholesterol is essential for brain health. Statins do not prevent dementia – and may contribute to cognitive decline by pushing cholesterol levels too low.

Instead of dumbing down the brain with unnecessary statins, we need to smarten up with nutrients that build brain health: omega-3 fats, phospholipids, B vitamins, and a low-sugar diet.

Doctors prescribing statins as dementia prevention are not only missing the mark – they may be making things worse.

Let’s change the narrative. Let’s put nutrition – not cholesterol fear – at the top of the brain health agenda. Find out more in Patrick’s new book – Alzheimer’s: Prevention is the Cure.

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

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

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

References

1  Gong, Q., Xie, L., Bi, M., & Yu, L. (2021). A probability formula derived from serum indicators, age, and comorbidities as an early predictor of dementia in elderly Chinese people. Brain and Behavior 11, e2236. https://doi.org/10.1002/brb3.2236

2 Peters, R, Breitner, J, James, S, et al. Dementia risk reduction, why haven’t the pharmacological risk reduction trials worked? An in-depth exploration of seven established risk factors. Alzheimer’s Dement. 2021; 7:e12202. https://doi.org/10.1002/trc2.12202 

3 Wee J, Sukudom S, Bhat S, Marklund M, Peiris NJ, Hoyos CM, Patel S, Naismith SL, Dwivedi G, Misra A. The relationship between midlife dyslipidemia and lifetime incidence of dementia: A systematic review and meta-analysis of cohort studies. Alzheimers Dement (Amst). 2023 Mar 8;15(1):e12395. doi: 10.1002/dad2.12395. PMID: 36911359; PMCID: PMC9993469.

4  Kjeldsen EW, Thomassen JQ, Rasmussen KL, Nordestgaard BG, Tybjærg-Hansen A, Frikke-Schmidt R. Adherence to dietary guidelines and risk of dementia: a prospective cohort study of 94 184 individuals. Epidemiol Psychiatr Sci 2022; 31: e71. 

5  Han BH, Sutin D, Williamson JD, Davis BR, Piller LB, Pervin H, Pressel SL, Blaum CS; ALLHAT Collaborative Research Group. Effect of Statin Treatment vs Usual Care on Primary Cardiovascular Prevention Among Older Adults: The ALLHAT-LLT Randomized Clinical Trial. JAMA Intern Med. 2017 Jul 1;177(7):955-965. doi: 10.1001/jamainternmed.2017.1442. PMID: 28531241; PMCID: PMC5543335.

6  McGuinness B, Craig D, Bullock R, Passmore P. Statins for the prevention of dementia. Cochrane Database Syst Rev 2016;1: CD003160. 

7 Zhang X, Tong T, Chang A, Ang TFA, Tao Q, Auerbach S, Devine S, Qiu WQ, Mez J, Massaro J, Lunetta KL, Au R, Farrer LA. Midlife lipid and glucose levels are associated with Alzheimer’s disease. Alzheimers Dement. 2023 Jan;19(1):181-193. doi: 10.1002/alz.12641. Epub 2022 Mar 23. PMID: 35319157; PMCID: PMC10078665.

A recent study of 1,178 women found that those carrying the APOE4 gene taking Hormone Replacement Therapy (HRT) had a better delayed memory score compared to APOE4 carriers that were not taking HRT, and to non-APOE4 carriers.[1] They also had slightly larger brain volumes in certain areas. This study suggested that HRT may help to prevent Dementia. This study was an observational trial, not a clinical trial, meaning the statement remains a hypotheses and requires further randomised controlled trials to investigate further. We analysed the paper and provided our comments below.

Clinical Trials on HRT

Clinical trials to date have not shown benefit of HRT with improving cognitive function. A systematic review of the clinical trial evidence for the effect of HRT on cognitive outcomes did not find benefit.[2] The Women’s Health Initiative Memory Study (WHIMS) conducted a double-blind, placebo-controlled clinical trial examining 8300 women 65 years of age or older over a 2- year period to observe the effects of HRTs and dementia progression. The trial failed to find a beneficial effect for HRT in reducing dementia risk, instead finding an increase in all types of dementia.[3]

The ApoE4 Gene

Roughly 1 in 5 people carry the ApoE4 gene, which accounts for 4 to 6% of risk for dementia and can be modified, downregulating the gene, with positive diet, nutritional supplement and lifestyle changes.[1]

Find out your risk for Dementia

In our Dementia Risk Index, as part of the Cognitive Function test, and COGNITION programme to reduce dementia, we excluded HRT because the evidence was not conclusive or consistent.

Have you tried our free Cognitive Function Test yet? Find out your Alzheimer’s disease risk using our evidence backed Dementia Risk Index. If your risk is high, our clever new programme COGNITION can help you make the right nutrition and lifestyle changes to help improve your score.

References

[1] Saleh RNM, Hornberger M, Ritchie CW, Minihane AM. Hormone replacement therapy is associated with improved cognition and larger brain volumes in at-risk APOE4 women: results from the European Prevention of Alzheimer’s Disease (EPAD) cohort. Alzheimers Res Ther. 2023 Jan 9;15(1):10. doi: 10.1186/s13195-022-01121-5. PMID: 36624497; PMCID: PMC9830747.

[2] Marjoribanks J, Farquhar C, Roberts H, Lethaby A, Lee J. Long-term hormone therapy for perimenopausal and postmenopausal women. Cochrane Database Syst Rev. 2017;1(1):CD004143.

[3] Shumaker SA, Legault C, Rapp SR, et al. Estrogen plus progestin and the incidence of dementia and mild cognitive impairment in post- menopausal women: the Women’s Health Initiative Memory Study: a randomized controlled trial. JAMA. 2003;289(20):2651-2662.

Exercise plays an important role in cognition. In this TED talk listen to expert Dr Wendy Suzuki explaining in more detail.

Dr Wendy Suzuki – The Brain Changing Benefits of Exercise (TED).

This study investigate bilingualism & cognition. The study was a meta analysis of studies. Inclusion criteria was studies investigating bilingualism in the elderly with relation to Alzheimer’s disease risk. 6 prospective cohort studies were selected and 8 retrospective studies were selected. Of the 14 studies, only 2 had a monolingual control group. 14 studies selected for analysis. Study indicated that bilingualism may be protective against memory decline in older adults.

Results:

Meta analysis indicates that one exception, the studies support the idea that bilingualism reduces risk of memory decline. . However, only a small sample of studies included, although selected studies generally of a good sample size (>500). Only two of the studies included participants with Alzheimer’s disease diagnosis. Moreover, only two studies had a control group. Further, two of the studies included only Hispanic subjects, which may have impacted results.

A notable limitation of the meta analysis is that it did not include any statistical analysis methods (i.e p value) and this is a significant limitation. Further large scale research is required to explore effects of bilingualism on cognition, and whether bilingualism may be protective against cognitive decline.

Abstract available here

Klimova, B., Valis, M., and Kuca, K. (2017). Bilingualism as a strategy to delay the onset of Alzheimer’s disease. Clin. Interv. Aging 12, 1731–1737.

This study investigated bilingualism & cognition. Study included 28 older adult participants – 14 monolingual participants and 14 bilingual participants (who had been bilingual since before age 11). All participants were subjected to a fMRI and had no diagnosed mental health conditions.

Results indicated:

Bilingual participants performed better on tasks and had better working memory (p<0.01) and better connectivity (p=0.002), compared with the monolingual group (p=0.17)

Results observed for other types of memory were not significant

Study size was small. Further large scale warranted. Study did not specify regarding bilingualism, as to whether participants spoke more than 2 languages, or whether certain type and complexity of language afford greater protection (i.e romance languages, Germanic languages etc.). Further research merited to explore effects of bilingualism on other types of memory.

Abstract available here

Grady, C. L., Luk, G., Craik, F. I., and Bialystok, E. (2015). Brain network activity in monolingual and bilingual older adults. Neuropsychologia 66, 170–181. doi: 10.1016/j.neuropsychologia.2014.10.042