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stigmatised due to its association with mental illness, its side effects at high doses, and perceptions that it’s an outdated drug with superior, more modern alternatives – a perspective that frankly defies reality.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/

Coffee – Good or Bad for your Brain?

by Patrick Holford

Coffee: Friend or Foe for Your Brain?

For many, the day doesn’t truly begin until that first cup of coffee hits the system. It sharpens the mind, lifts the fog, and gives an instant boost of focus – which explains why, in the UK alone, we drink an astonishing 100 million cups every single day, about two per person. But is this daily ritual really fuelling your brain, or quietly robbing it of long-term vitality?

Coffee is more than just a stimulant. Yes, it contains polyphenols – those antioxidant compounds that can protect the brain. But it also delivers caffeine, which fires up your adrenal hormones to give that short-term buzz. The problem is that this instant lift comes with a hidden cost: over time, it can deplete energy reserves and, more worryingly, raise homocysteine – one of the strongest predictors of dementia and Alzheimer’s.

The Hidden Brain Risk – Homocysteine

The homocysteine-raising effect is quite considerable. A group of doctors from University Hospital Nijmegen tested the effects of coffee by assigning volunteers to drink a litre of unfiltered coffee a day – that’s about four cups – for two weeks. At the start of the two weeks, their average homocysteine score was 12.8 µM, slightly above the national average of 10 to 11. At the end of the two weeks, their homocysteine score was 14. (1)

This homocysteine-raising effect was confirmed in another study by Dr Verhoef and colleagues at the Wageningen Centre for Food Sciences in the Netherlands, which showed that two cups of coffee increased homocysteine by 11% after four hours. Interestingly, caffeine tablets without coffee increased it by only 5%, suggesting that other compounds in coffee, such as theophylline and theobromine (also found in chocolate), may play a role. (2)

This means that if your homocysteine is already slightly raised, perhaps above 9 or 10, drinking coffee may be doing more harm than good, since the brain starts shrinking with homocysteine levels above 11. Also, if you do drink a lot of coffee, it’s a good reason to check your homocysteine level. 
(Order your homocysteine test here. An accurate and simple way to check your level via a quick pinprick test.)

How Much Coffee is Too Much?

So, does coffee protect against dementia – or put you at greater risk? The answer depends on quantity.  A UK Biobank study involving 400,000 participants compared those drinking 1-2 cups a day with those drinking six or more cups a day and found both a 53% increased risk of dementia and smaller brain volumes in those drinking 6 or more cups.(3)  The UK Biobank didn’t measure the homocysteine of the participants, but this is the most plausible mechanism.

A new 2025 analysis from the US NHANES database reached a similar conclusion: higher coffee consumption was associated with a greater risk of dementia (4).

Yet the story isn’t entirely one-sided. A review of all studies up to 2020 concluded: “Caffeine effects were more often positive when consumed in moderate quantities (100–400 mg/day), consumed in the form of coffee or green tea, and in women.” (5)  The most recent UK Biobank findings confirmed that moderate coffee or tea drinkers had a lower risk of cognitive decline than abstainers. (6)

A double espresso delivers 200–300 mg of caffeine, so moderation seems to mean no more than two to two and a half cups a day — and only if unsweetened.

Sweetened or Unsweetened – Does it Matter?

It matters a lot. The UK Biobank found a modest reduction in risk in those drinking up to 2.5 cups a day, compared with non-coffee consumers, but only in those drinking unsweetened coffee. Those drinking sweetened coffee had a higher risk. (7)

This is consistent with research at Canada’s University of Guelph. Participants were given a carbohydrate snack – such as a croissant, muffin, or toast – together with either a decaf or regular coffee. Those having the coffee-carb combo had triple the increase in blood sugar levels. In addition, insulin sensitivity, the hormone that controls blood sugar levels, was almost halved. (8)  The lesson? Enjoy your coffee on its own, without sugar or a carb-laden pastry.

Don’t Drink Coffee on Waking

Timing also matters. In the first hour after waking, your body naturally peaks in cortisol, the long-acting adrenal hormone that gets you going. (9)  That is why it is probably better not to have coffee, which further promotes adrenal hormones, for at least an hour after waking. Otherwise, you may stop producing enough of your own cortisol and become dependent on the caffeine hit.

In the evening, it’s the opposite story. Cortisol should be reducing and melatonin rising, but caffeine can affect this for up to 10 hours. The results? Over time, poorer sleep, which can contribute to a whole host of health problems, and greater difficulty waking in the morning, leading to a cycle of dependency on coffee.

One cup of coffee a day, in the morning, ideally not on waking but at least 30 to 60 minutes later, seems optimal. (10) However, the more tea you drink, the better, according to two studies, with green tea being the most beneficial.(11, 12)  This benefit, however, was not found in a UK Biobank study, which reported tea and coffee drinking to be associated with worsening cognition compared with abstainers.(13) 

The Japanese have a tradition of making a pot of green tea and, if they want a second, simply add hot water to the teapot. I do the same with coffee – if I have a second cup I run the coffee through the filter paper again. In this way it is progressively weaker.

But let’s be honest: coffee is an addictive stimulant and, while it may not be as harmful as alcohol, it is ultimately an energy robber. Having used coffee to help me through an intense month of early mornings and book writing, I quit and experienced a severe withdrawal headache that lasted 36 hours!

My Advice for the ‘Wired and Tired”

or those stuck in the vicious cycle – wired by coffee to stay awake, then relying on alcohol to switch off at night – my advice is simple: reset. Quit both for a time. Focus on consuming a low-sugar, low GL diet, along with supplements including B vitamins, plus extra vitamin C and omega-3 fish oil. All this advice and more is provided when you become a FRIEND of Food for the Brain and gain access to your six-month COGNITION™ brain upgrade programme. Click here to find out more.

Andrew was a case in point. Managing a chain of supermarkets had left him very stressed.

During the day, he drank coffee and in the evening, he relaxed with a beer or some wine as otherwise he would struggle to sleep. He was also gaining weight.

Andrew went on a low-GL diet, quit drinking coffee and alcohol, and took the recommended supplements. Three weeks later, he said: “My energy is through the roof, I don’t feel stressed, have no problem sleeping and I’m waking refreshed.” 

In Short …

One to two cups of unsweetened coffee a day, taken 30–60 minutes after waking, is probably optimal.
Avoid combining coffee with sugar or high-carbohydrate foods.  
Test your homocysteine levels, especially if you drink more than two cups a day.
Buy a single homocysteine test here or get it along with other important brain biomarkers in the DRIfT 5-in-1 test kit here (for best value).
Consider switching to green tea or more weakly brewed coffee where possible for a gentler stimulant effect.
Avoid caffeinated drinks after noon, especially if you have difficulty getting to sleep or staying asleep.
If you rely on caffeine to function or alcohol to unwind, it may be time for a reset.

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) Grubben MJ, Boers GH, Blom HJ, Broekhuizen R, de Jong R, van Rijt L, de Ruijter E, Swinkels DW, Nagengast FM, Katan MB. Unfiltered coffee increases plasma homocysteine concentrations in healthy volunteers: a randomized trial. Am J Clin Nutr. 2000 Feb;71(2):480-4. doi: 10.1093/ajcn/71.2.480. PMID: 10648261. https://pubmed.ncbi.nlm.nih.gov/10648261/

(2) Verhoef P, Pasman WJ, Van Vliet T, Urgert R, Katan MB. Contribution of caffeine to the homocysteine-raising effect of coffee: a randomized controlled trial in humans. Am J Clin Nutr. 2002 Dec;76(6):1244-8. doi: 10.1093/ajcn/76.6.1244. PMID: 12450889. https://pubmed.ncbi.nlm.nih.gov/12450889/

(3) Pham K, Mulugeta A, Zhou A, O’Brien JT, Llewellyn DJ, Hyppönen E. High coffee consumption, brain volume and risk of dementia and stroke. Nutr Neurosci. 2022 Oct;25(10):2111-2122. doi: 10.1080/1028415X.2021.1945858. Epub 2021 Jun 24. PMID: 34165394. https://pubmed.ncbi.nlm.nih.gov/34165394/

(4) Li, J., Yu, K., Bu, F. et al. Exploring the impact of coffee consumption and caffeine intake on cognitive performance in older adults: a comprehensive analysis using NHANES data and gene correlation analysis. Nutr J 24, 102 (2025). https://doi.org/10.1186/s12937-025-01173-x

(5) Alida Chen J et al, Associations Between Caffeine Consumption, Cognitive Decline, and Dementia: A Systematic Review Journal of Alzheimer’s Disease 78 (2020) 1519–1546 DOI 10.3233/JAD-201069 https://pubmed.ncbi.nlm.nih.gov/33185612/

(6)Rainey-Smith SR, Sewell KR, Brown BM, Sohrabi HR, Martins RN, Gardener SL. Moderate coffee and tea consumption is associated with slower cognitive decline. J Alzheimers Dis. 2025 Jul 21:13872877251361058. doi: 10.1177/13872877251361058. Epub ahead of print. PMID: 40686251.

(7) Tingjing Zhang, Jiangen Song, Zhenfei Shen, Kewan Yin, Feifei Yang, Honghao Yang, Zheng Ma, Liangkai Chen, Yanhui Lu, Yang Xia,

Associations between different coffee types, neurodegenerative diseases, and related mortality: findings from a large prospective cohort study, The American Journal of Clinical Nutrition, Volume 120, Issue 4, 2024, Pages 918-926, ISSN 0002-9165, https://doi.org/10.1016/j.ajcnut.2024.08.012. https://ajcn.nutrition.org/article/S0002-9165(24)00671-3/abstract

(8) Moisey LL, Kacker S, Bickerton AC, Robinson LE, Graham TE. Caffeinated coffee consumption impairs blood glucose homeostasis in response to high and low glycemic index meals in healthy men. Am J Clin Nutr. 2008 May;87(5):1254-61. doi: 10.1093/ajcn/87.5.1254. PMID: 18469247. https://pubmed.ncbi.nlm.nih.gov/18469247/

  (9) Debono M, Ghobadi C, Rostami-Hodjegan A, Huatan H, Campbell MJ, Newell-Price J, Darzy K, Merke DP, Arlt W, Ross RJ. Modified-release hydrocortisone to provide circadian cortisol profiles. J Clin Endocrinol Metab. 2009 May;94(5):1548-54. doi: 10.1210/jc.2008-2380. Epub 2009 Feb 17. PMID: 19223520; PMCID: PMC2684472. https://pubmed.ncbi.nlm.nih.gov/19223520/   

(10) Xuan Wang, Hao Ma, Qi Sun, Jun Li, Yoriko Heianza, Rob M Van Dam, Frank B Hu, Eric Rimm, JoAnn E Manson, Lu Qi, Coffee drinking timing and mortality in US adults, European Heart Journal, 2025;, ehae871, https://doi.org/10.1093/eurheartj/ehae871 

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

(12) Feng L, Chong MS, Lim WS, Lee TS, Kua EH, Ng TP. Tea for Alzheimer Prevention. J Prev Alzheimers Dis. 2015;2(2):136-141. doi: 10.14283/jpad.2015.57. PMID: 29231231. https://pubmed.ncbi.nlm.nih.gov/29231231/ 

(13) Cornelis MC, Weintraub S, Morris MC. Caffeinated Coffee and Tea Consumption, Genetic Variation and Cognitive Function in the UK Biobank. J Nutr. 2020 Aug 1;150(8):2164-2174. doi: 10.1093/jn/nxaa147. PMID: 32495843; PMCID: PMC7398783.  https://pmc.ncbi.nlm.nih.gov/articles/PMC7398783/

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Homocysteine may not be a household word, but at Food for the Brain, we want it to become one!

It is arguably one of the most important blood biomarkers for your brain and overall health, predicting the risk of over 100 diseases, from cardiovascular issues to cognitive decline, depression, and developmental disorders in children (1,2,3). For many years it was difficult to obtain accurate testing privately or at home – which is why we developed a new, accurate at-home pin-prick test that is one of our most popular options.

The reason we think this is such a good biomarker to track and research is that whilst high homocysteine is linked to increased risk of over 100 diseases – it can be quick and easy to lower!

Learn more about homocysteine and why it matters in the video below:

What level should you be aiming for?

Based on Patrick Holford’s research in his book Upgrade Your Brain, the recommended homocysteine levels are:

Ideal/Optimal Level: Below 7.5 µmol/L –  This is especially important for women preparing for pregnancy, as higher levels are linked to increased risk of chromosomal damage and developmental problems in children.

Treatment Threshold: Above 10 µmol/L  – Anyone with a homocysteine level above this should be treated with B vitamins to reduce brain shrinkage and risk of dementia.

Warning Level: Above 11 µmol/L – Associated with increased brain shrinkage and elevated risk for Alzheimer’s and cardiovascular disease.

Ideally, with regular testing, you should maintain homocysteine levels well below 10 µmol/L to support optimal brain health and reduce the risk of neurodegenerative conditions.

Here are eight proven ways to bring your homocysteine levels into the optimal range and keep your brain firing on all cylinders:

1. Supplement Smart: The B Vitamin Trio (and Friends)

The fastest way to reduce homocysteine is through targeted supplementation. The ‘magic trio’ is vitamin B6 (20mg), B12 (500µg as methylcobalamin), and methylfolate (400µg). A major paper has shown that supplementing these B vitamins not only lowers homocysteine, but also slows brain shrinkage and cognitive decline in people with mild cognitive impairment. Add trimethylglycine (TMG), zinc, and N-acetyl cysteine (NAC) for additional support, particularly in older adults with memory concerns. These nutrients work synergistically to support methylation and brain function. (1) Get our supplement guidelines here.

2. Eat for B12: Fish, Eggs, Dairy and Meat

Vitamin B12 is primarily found in animal-derived foods. Aim to eat oily fish three times a week, eggs most days, and small amounts of organic meat or dairy (if tolerated). Pescatarians thrive here. For vegans, the focus should be on fortified foods and sources such as shiitake mushrooms. However, supplementation and regular testing are strongly recommended to ensure optimal levels. Poor B12 absorption – particularly in older adults or those taking proton pump inhibitors – is a common risk factor for elevated homocysteine and brain shrinkage (1,2).

3. Load Your Plate with Greens and Beans

Folate is critical for methylation. Aim for seven servings of fruit and vegetables ​​a day. Prioritise leafy greens, broccoli, lentils, chickpeas, and asparagus. These naturally support homocysteine metabolism and keep your methylation processes running smoothly (1).

4. Move Your Body

Regular physical activity helps lower homocysteine. Studies show that consistent aerobic or resistance exercise can reduce levels, improve circulation, and support metabolic health. Aim for at least 30 minutes of brisk walking, cycling, or swimming five times a week to complement your nutritional strategy (3).

5. Cut Back on Coffee – Especially Excessive Intake

Drinking more than two cups of coffee a day can raise homocysteine levels. While low to moderate coffee intake may  offer  some antioxidant benefits, high intake (six or more cups a day) has been linked to elevated homocysteine levels and an increased risk of dementia (4).

6. Mind Your Alcohol

Keep it light. Up to seven small glasses (125ml) of red wine or two pints of beer per week is the maximum. Excess alcohol increases homocysteine levels and impairs nutrient absorption – particularly of B vitamins (1).

7. Manage Stress and Prioritise Quality Sleep

Chronic stress may indirectly raise homocysteine by increasing inflammation and depleting vitamin B6 – both linked to higher mortality and accelerated cellular ageing (5).Make stress reduction a priority. Meditation, yoga, deep breathing, regular exercise, and talking therapies are all effective. Equally important is prioritising restorative sleep. The brain clears toxins and resets during deep sleep – both are vital for healthy methylation. Learn more about sleep and your brain here.

8. Test, Don’t Guess – Know Your Level

You can’t manage what you don’t measure. Have your homocysteine levels tested.. We now offer at-home pinprick tests, which also contribute to our ongoing research. Don’t be surprised if your levels are higher than expected. Forty per cent of people over 60 have homocysteine levels above 11 µmol/L. As we age, our ability to absorb vitamin B12 declines (3).

Homocysteine is a key indicator for cognitive and overall health. As we can see, with a few dietary tweaks, lifestyle upgrades, and targeted nutrients, you can lower your homocysteine, support methylation, and quite literally upgrade your brain!

Start today:

Join our research and test your homocysteine level today. Purchase a single homocysteine test here or get it as part of the DRIfT 5 in 1 test, which also measures your antioxidant status (another world first in accurate home testing), omega-3, vitamin D and HbA1c.
Read more in the Upgrade Your Brain book – This fully referenced guide offers practical strategies to improve your brain health – including how to lower homocysteine through diet, lifestyle, and supplementation.
Support our charitable work by becoming a FRIEND. From just £5 a month, you can help fund vital research and public education. Become a FRIEND today

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 Smith AD, Refsum H. Homocysteine – from disease biomarker to disease prevention. J Intern Med. 2021 Oct;290(4):826-854.

2 Vogiatzoglou A, Refsum H, Johnston C, et al. Vitamin B12 status and rate of brain volume loss. Neurology. 2008 Sep 9;71(11):826-32.

3 Vincze G, et al. Physical activity and plasma homocysteine in the elderly: the Rotterdam Study. Am J Clin Nutr. 2011;93(5):1025–31.

4 Grubben MJAL, et al. Unfiltered coffee increases plasma homocysteine concentrations in healthy volunteers: a randomized trial. Am J Clin Nutr. 2000;71(2):480–4.

5 Pusceddu I, et al. Subclinical inflammation, telomere shortening, homocysteine, vitamin B6, and mortality: the Ludwigshafen Risk and Cardiovascular Health Study. Eur J Nutr. 2020;59:1399–411.

By Patrick Holford

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Most people think forgetfulness and failing memory only begin in later life. But what if you found out that cognitive decline actually begins much earlier – around the age of 18 – and that what you do when you’re young can dementia-proof yourself for when you’re older?

This is the latest discovery from Food for the Brain’s research! Now that hundreds of thousands of participants have completed the Cognitive Function Test, we are starting to extract these world first findings.  Although the test was designed to identify those at risk for dementia later in life, the extraordinary finding is that cognitive function declines, on average, year by year from the age of 18.

The results involving 172,098 people who took the free test between 2011 and 2024 show that there is a steady decline, on average, with a sharp drop-off after the age of 80. 

In one alarming case that underscores the need to promote prevention as early as possible, researchers in South China recently diagnosed probable Alzheimer’s disease in a 19-year-old male – the youngest ever recorded – highlighting the fact that dementia, while rare in youth, is not exclusively a condition of old age (1).  This makes early prevention not only relevant but essential.

This isn’t a message of fear.  It’s one of hope and empowerment, emphasising that it’s never too early to start supporting your brain health. (This is why we created the Smart Kids & Teens COGNITION Programme.) Cognitive slippage doesn’t happen to everyone – it’s possible to maintain or even improve brain function with optimal nutrition and lifestyle habits. Food for the Brain’s research also found that those whose Dementia Risk Index is in the top quarter, in ‘the green’- are not expected to come close to the zone of cognitive decline before age 100. A person’s Dementia Risk Index is calculated from completing the COGNITION diet and lifestyle questionnaire that follows the free Cognitive Function Test.

The five most impactful prevention steps are: 

Sufficient intake of B vitamins
Omega-3 from seafood and supplements
More vegetables and fruit, and less sugar and refined carbohydrates
More exercise
Less alcohol 

See the Alzheimer’s Modifiable Risk Factor chart below:

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Understanding that decline can start early in life means you can take steps now – whether you’re 18 or 80 – to protect your brain. This is also where our Citizen Scientist FRIEND community plays a vital role! Whether you’re a parent, grandparent, teacher, coach, youth worker, mentor, or simply someone who cares about young people, you can help the next generation build lifelong resilience – by becoming a FRIEND of Food for the Brain, accessing your personalised six-month Brain Upgrade Programme and encouraging as many as possible to take the free Cognitive Function Test to become ‘dementia-proof’.

How to ‘Dementia-Proof’ Yourself

We describe someone as ‘dementia-proof’ when the projection of their Cognitive Function Test results suggest they will remain in the healthy ‘green zone’ (optimal cognitive health) beyond the age of 100, as shown in the graph above.

Food for the Brain is helping thousands  of people achieve this dementia-proof status through our COGNITION programme, which identifies a person’s ‘quick wins’ and supports behaviour change with personalised, interactive emails and live group health coaching. For some, this means going to bed earlier for more sleep. For others, it might mean avoiding foods with added sugar, cutting back on alcohol or getting outdoors to exercise. For many it means optimising intake of B vitamins, omega-3, vitamin D, and antioxidants.
(Do you know what your levels of these important brain-protecting nutrients are? If not, make sure you order our accurate  at-home pinprick DRIfT test, another way to support our research and upgrade your brain.)

Start Young to Prevent Cognitive Decline

Brain fog, poor concentration, low mood, or forgetfulness aren’t just part of “being busy” or “getting older.” These can be early signs that your brain isn’t getting what it needs.  Better sleep, nutrition, regular activity, and lower stress levels all help preserve cognitive function as you age.  

Investing in your brain health early means:

Sharper focus and concentration for study, work, and everyday life
Greater emotional resilience, reducing anxiety and improving your mood
Improved memory and creativity, helping you perform optimally in all areas of life
More energy and better sleep, to improve the way you feel and function every day

When you support your brain health, you support every other aspect of your health too!h. Be it that outer glow on the skin, more balanced hormones, or improved gut health, all of it starts with brain health. It’s never too late, and it’s never too early – it is only important to make a start!

Whether you’re a teenager, a student in your 20s, raising a family in your 40s, or retired in your 70s, your brain is changing every day – and the good news is that it can respond positively to lifestyle changes at any age.

Remember: there is so much you can do to help to prevent Alzheimer’s and optimise your brain health – whatever your age.

Ready to take control of your brain’s future?

Use our Smart Kids programme if you have kids/grandchildren
Complete the Cognitive Function Test today – it’s quick, free, and potentially life-changing. ( Encourage anyone you know over the age of 18 to do it too!)

Order your at-home DRIfT pinprick blood test to contribute to our research and discover your unique levels of essential brain-supporting nutrients.

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We are one of the few charities focused on independent research and education around prevention – join our mission today and become a FRIEND.  

As a FRIEND, you’ll receive:

Access to your 6-month personalised Brain Upgrade Journey

Entry to our Education Hub

Monthly live group health coaching

Further reading: This idea is echoed in the work of Associate Professor Tommy Wood, Head of Research at Food for the Brain, in his article Use it or Lose it: Why an Active Lifestyle is a Brain Essential.

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. Jia J, Zhang Y, Shi Y, Yin X, Wang S, Li Y, Zhao T, Liu W, Zhou A, Jia L.  A 19-Year-Old Adolescent with Probable Alzheimer’s Disease.  J Alzheimers Dis.  2023;91(3):915-922.  doi: 10.3233/JAD-221065.  Erratum in: J Alzheimers Dis.  2023;92(4):1501-1502.  doi: 10.3233/JAD-239001.  PMID: 36565128.

By Patrick Holford

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

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

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

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

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

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

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

Safer, Evidence-Based Alternatives

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

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

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

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

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

How many people are killed by psychiatric drugs?

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

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

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

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

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

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

Estimating the True Death Toll of Mental-Health Medications

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Learn more and begin your brain upgrade journey today:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Every three seconds, someone in the world develops dementia and the rate is increasing.

Billions of dollars have been spent on the search for a drug that can block the damaging build-up of plaque in the brain that’s thought to be central to the disease. But the results are not impressive and the side effects include bleeding into the brain. 

Now, that gloomy picture is being transformed in a remarkable and surprising way. Rather than pinning our hopes on another new, powerful and expensive drug, mounting evidence suggests that such seemingly old-fashioned approaches as changes in diet, lifestyle, and environment, could dramatically reduce the number of Alzheimer’s cases.

An international Alzheimer’s Prevention Expert Team has calculated that over 80 per cent of cases could be prevented in this way. A study in Holland last year found that good levels of vitamin D, omega-3 (found in oily fish), and B vitamins reduced the risk of dementia to less than a quarter of the average(1). Other beneficial changes include regular exercise, staying mentally active, and reducing sugar intake. Reducing sugar intake is especially effective, as people with diabetes have twice the risk of cognitive decline. 

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

That is why we are hosting the Global Alzheimer’s Prevention Day next week and continuing with our research project to discover the hardest hitting combinations of prevention steps. We have already tested over 200,000 participants in the UK.

We are now inviting people around the world to complete a free, online diet and lifestyle questionnaire and a cognitive function test. 

The project, led by Oxford University–trained neuroscientist Dr. Tommy Wood, Associate Professor at the University of Washington, aims to test over 20 million people worldwide. This includes one million participants each from the UK, Germany, and Poland; a similar number from the US, Canada, Brazil, and Japan; and 10 million from China, which has the world’s highest prevalence of dementia.

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In China, the project is supported by the China National Health Association and former Minister of Health, Gao Qiang. “We must popularise prevention,” he says. “With 300 million people over 60, this has to be our focus. Food for the Brain’s initiative is the way forward. It’s something everyone can do, right now, for themselves.”
China’s leading prevention expert, Professor Jin-Tai Yu from Fudan University in Shanghai, adds: “It may be possible to prevent up to 80% of dementia cases if all known risk factors are targeted.” He highlights the particular importance of B vitamins, which reduce levels of a toxic amino acid found in the brain called homocysteine. High homocysteine levels can damage both brain cells and blood vessels. (Test your homocysteine levels at home here)

His research, along with findings from Oxford University’s leading prevention expert, Professor David Smith – who has been analysing data from the – has already shown that up to 73% of dementia cases may be preventable, even without factoring in the benefits of B vitamins and omega-3.

“Our research at Oxford found almost nine times less shrinkage in the Alzheimer’s associated areas of the brain in those taking B vitamin supplements, who had raised homocysteine (3), which is common among over 60+ year olds, and in early signs of dementia.” says Professor Smith. 

Wu YingPing, President of the China National Health Association, believes it is the combination of diet, nutritional supplementation, and lifestyle that can significantly influence dementia prevention in the ‘silver-haired’ community. “It is education, rather than medication, that we need, and Food for the Brain’s global campaign is something we fully support to help achieve this.”

In the UK, Japan, and Brazil, a task force of over 10,000 doctors is being trained to enrol their patients in the ‘citizen science’ charitable project, which is funded by individuals rather than vested-interest companies.

In the UK, a group of GPs, part of the Public Health Collaboration, have joined the task force to help drive the project to hundreds of thousands of patients across the UK. Former GP and Chair of the Public Health Collaboration, Dr David Jehring, says: “personalised digital health education such as this is the way forward. No drug treatment has yet produced a clinically meaningful effect, without awful adverse effects. We have to face the reality that dementia can only be prevented by tackling that ‘perfect storm’ of 21st-century diet and lifestyle that creates cognitive decline in the first place. It is not likely to be solvable by medication.”

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In the US, Dr Mark Hyman, who is part of our group of prevention experts, is supporting Robert F. Kennedy Jr., the newly appointed Secretary of Health, in the campaign to ‘Make America Healthy Again’, with prevention at its core.

“Our healthcare system is failing because it treats symptoms rather than addressing the root causes of disease. I fully support Robert F. Kennedy Jr.’s commitment to investigating the underlying drivers of chronic illness and ensuring that prevention – not just treatment – is at the core of our national health strategy. The science is clear: food is the most powerful medicine we have to prevent, reverse, and even treat conditions like dementia, autoimmune diseases, and metabolic disorders. If we truly want to make America healthy again, we must shift our focus from managing disease to creating health,” says Dr Hyman

As part of our ‘Going Global’ campaign, we’ve created a shorter, 3-minute version of our Cognitive Function Test – the Alzheimer’s Prevention Check!

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Get personalised insight into your brain health in just a few minutes. Take the 3-minute brain test here.

Professor Peter Garrard, Director of the Dementia Research Group at St George’s, University of London, says: “It is vital that functional biomarkers such as homocysteine and omega-3 are measured in this research because these can be changed with nutritional interventions and are associated with reducing risk.”

“The purpose of this global campaign is to collect diet, lifestyle, biomarker, and cognitive function data on an unprecedented scale. With this data, we hope to discover which lifestyle changes have the maximum likelihood of preventing cognitive decline early enough to minimise an individual’s dementia risk in the future.” says Dr Tommy Wood, who is leading the research.

Anyone can take part and become a ‘citizen scientist’ by completing our free online Alzheimer’s Prevention Check, which then provides personalised advice on changes you can make to help reduce your future risk.

All data collected is anonymised for research purposes and will be made available to prevention researchers around the world.

Our aim at Food for the Brain is to discover the simplest changes that have the greatest impact on cognitive function in preventing this devastating disease, and then share that information with the public and the public health experts who advise governments around the world.

Fewer than one in a hundred cases of Alzheimer’s is caused by genetics. This means that, potentially, 99% of cases could be preventable.

Actions You Can Take:

Take the comprehensive Cognitive Function Test here
Join us for the international Alzheimer’s Prevention Day here – happening 20th May 2025
Order the new book: Alzheimer’s: Prevention is the Cure – A 240-page guide by Patrick Holford, available internationally from 1st May at foodforthebrain.org/apic, and also on Amazon, Kindle, and Audible.

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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 Roigé-Castellví J, Murphy M, Fernández-Ballart J, Canals J. Moderately elevated preconception fasting plasma total homocysteine is a risk factor for psychological problems in childhood. Public Health Nutr. 2019 Jun;22(9):1615-1623. doi: 10.1017/S1368980018003610. Epub 2019 Jan 14. PMID: 30636652; PMCID: PMC10261079.
2 Kara İS, Peker NA, Dolğun İ, Mertoğlu C. Vitamin B12 Level in Children. J Curr Pediatr. 2023 Aug;21(2):127-134. doi:10.4274/jcp.2023.75688.
3 https://pmc.ncbi.nlm.nih.gov/articles/PMC4440679/

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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.

As parents or caregivers, nothing matters more than our children’s future. We want them to thrive – mentally, emotionally and physically – and to feel confident and capable in a complex, ever-changing world. Yet when it comes to their brain development, many of us are left wondering: are we doing enough? Are they getting what they need to build healthy, resilient minds?

This is why we’re proud to introduce our groundbreaking Smart Kids Cognitive Function Test. Developed by the team behind the widely respected Adult Cognitive Function Test, this tool is designed to empower parents with the knowledge, insight and practical strategies to support their child’s cognitive and emotional development, right from the start.

Why Early Brain Health Matters

From the moment they’re born, a child’s brain is growing at an extraordinary pace – forming up to a million new neural connections every second. These formative years are a critical window of opportunity, where the right nutrition, environment, and emotional support can set the foundation for a lifetime of strong cognitive function, balanced mood and behavioural wellbeing.

This test doesn’t just measure ‘smarts’ – it helps you understand how your child’s brain is functioning, what might be holding them back, and most importantly, what you can do about it.

What’s Involved?

Tailored for children aged 4 to 17, the test includes three essential elements:

Cognitive Function Assessment. An engaging 15-minute digital test that challenges attention, memory and problem-solving in a fun, interactive way.
Nutrition & Lifestyle Questionnaire. This helps highlight which of the eight key lifestyle areas may be influencing brain health, from sleep and gut health to sugar balance and essential fats.
Strengths & Difficulties Questionnaire. A validated tool assessing emotional and behavioural wellbeing, giving you a fuller picture of how your child is feeling and functioning.

With this holistic insight, you’ll receive tailored guidance and practical steps to help your child move forward – cognitively, emotionally and behaviorally.

 What Parents Are Saying

“COGNITION helped me understand why my son was struggling with focus—and what I could do to help. The emails made it so easy to build new habits. We saw a real change.”
– Parent of a 9-year-old

“It was like someone had finally put the pieces together. We started with sugar balance and sleep—and within weeks, our daughter’s mood and energy improved.”
– Mum of a 13-year-old

A Mission for Change: Your Role as a Pioneer

By joining the first 1,000 families to complete the free Smart Kids Test, you’re helping us shape a healthier, smarter future for the next generation. Together, we can build a new model of prevention and wellbeing that begins not at midlife, but in childhood where it can make the biggest difference.

Have You Taken the Adult Test?

Many parents in our community have already taken the free Adult Cognitive Function Test – designed to help dementia-proof your diet and lifestyle. If you haven’t yet done so, we urge you to take this important step. Your brain matters too, and change is possible at any age.

Also, did you know that you can complete our at home pin prick DRIfT blood test on children over 2 years of age and they are available internationally. So that you can gather more data on what your child needs to thrive.

To Our Dementia Prevention Community

We know that many of you found us through our mission to prevent Alzheimer’s and cognitive decline. This children’s test is a natural extension of that work, because optimising brain health starts young. Helping your child now doesn’t just support their academic success, it lays the foundation for lifelong mental wellbeing.

Take the Smart Kids Cognitive Function Test today – and invest in your child’s brain, their wellbeing, and their future. 

Because every child deserves the chance to shine.

Actions:

Take the Smart Kids test here
Find out more about our at home pin prick blood test here – suitable from age 2+

Do the adult Cognitive Function Test here if you haven’t done so yet, so you can model what supporting your brain health looks like to your child and family.

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.

SAD (or seasonal affective disorder) is a sub-form of major depression or bipolar, according to the Diagnostic and Statistical Manual of Mental Disorders, which most commonly occurs during the darker and colder autumn and winter months. Key identified risk factors include: a family history of the disorder, and living at northern latitudes. Specifically women, people with darker skin tones and individuals between the ages of 18 to 30 years of age are most at risk of developing the disorder. In order to have a diagnosis of SAD, the condition must be observed to improve outside of the colder seasons. Depending on the latitude, SAD has a prevalence of 1.9 – 9%. Individuals with lower levels of the metabolism regulating hormone adiponectin have also been observed to be at higher risk of developing SAD.

Nutrition and SAD

Vitamin D has been hypothesised to play a key role in SAD development due to reduced sunlight in northern latitudes during colder months. Additionally, it has been observed that there is a correlation between blood levels of Vitamin D and symptoms of depression, due to reduced levels of the neurotransmitters serotonin and dopamine. Vitamin D has also been hypothesised as being involved in circadian rhythm, which is affected by seasonal changes. However, supplementation of Vitamin D in SAD has yielded mixed results, and further studies are needed in this area.

Practical Interventions for Supporting Individuals with SAD

Due to the prevalence of Vitamin D in depressive conditions, the lack of sunlight during the winter months and the hypothesised role of Vitamin D deficiency in the development of SAD, increasing Vitamin D exposure is potentially of merit. This may be done through the following:

• Consuming foods which are natural sources of Vitamin D, such as oily fish including salmon and mackerel, egg yolks and organic milk and cheese
• Increasing exposure to sunlight in the winter months by being outside, particularly engaging in physical activities and spending time in nature 
• Supplementation of Vitamin D3. The RDA in the UK for Vitamin D is 10 micrograms (µg) or 400 IU. However, some individuals may benefit from supplementing higher levels of this vitamin, particularly if they have a higher BMI, a diagnosed mental health condition or darker skin pigmentation. Baseline levels of Vitamin D as established via blood test, calcium intake, genetics, oestrogen use, dietary fat content and composition, as well as co-existing diseases and medication use may also impact on Vitamin D requirements*.

*Note: before beginning any new supplement regimen, always consult your physician and a qualified nutrition practitioner.