Polyphenol Power. Keep your Brain Young with Antioxidants.

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By Patrick Holford

Life is a balancing act between making energy by combusting glucose or ketones with oxygen, which generates ‘oxidant’ exhaust fumes and dealing with these ‘oxidant fumes’ which harm the body.

Skin goes crinkly, age spots develop all due to oxidation. That’s what makes apples go brown, leaves change colour and iron rust. In the end, we lose, which is why all oxygen-based life forms have a finite life – and why your brain and body do inevitably age.

However, you can not only add years to your life, but also life to your years by improving your intake of antioxidants and polyphenols found in whole foods, fruits, vegetables and herbs and spices. A study in Finland and Sweden compared those with a ‘healthy’ versus ‘unhealthy’ diet in mid-life for future risk of developing Alzheimer’s disease and dementia 14 years later (1). Those who ate the healthiest diet had an 86-90% decreased risk of developing dementia and a 90-92% decreased risk of developing Alzheimer’s disease. Some of the benefit comes from low sugar diets, high in omega-3 and B vitamins and some from foods high in antioxidants and polyphenols which we will focus on here.

Your intake of these versus your intake and generation of oxidants, for example from smoking and pollution, is a major determinant of brain health. An illustration of this is the fact that both smoking and pollution exposure increase risk of cognitive decline and dementia, while vitamin C, which is the antioxidant par excellence, reduces risk.

(This is why we have developed our brand new Glutathione at home blood test – the first of its kind where you can accurately test your antioxidant status from home and support our further research into this important area. You can find out more and pre order the test here )

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Oxidants vs antioxidants – moving the balance in your favour

Smoking increases risk of Alzheimer’s just as much as having low B vitamin or omega-3 status, according to the US National Institute of health’s analysis (2). Smoking is something a person can easily change. Air pollution, for many, is not. It is measured in the amount of particulate matter (PMs) and people living in polluted cities are exposed to more. A study of women living in cities in the US found that those exceeding the ‘safe’ levels (greater than 12 μg/m3) had ‘increased the risks for global cognitive decline and all-cause dementia respectively by 81% and 92%’. (3)

While you may not be able to change where you live, can you mitigate the effects of pollution? The answer is yes – in two ways. Firstly, by increasing your intake of antioxidants and also by improving your B vitamin status since the body detoxifies many toxins, including toxic metals from lead to mercury, by methylation. A similar study to the one above found that residing in locations with PM exposure above the safe level was associated with a higher risk of dementia but only among people with lower intakes of the homocysteine lowering B vitamins (B6, folate, b12) (4). ‘Vitamin C in the diet or taken as supplements might help’ concludes another.(5)

Smokers need at least twice as much vitamin C as non-smokers just to have basic vitamin C levels in their blood (serum). Men do worse than women. Even with an intake of 200mg a day they do not achieve this basic blood level, which is already two to three times the recommended dietary intake and what you’d get in four oranges (6). It is certainly wise for any smoker to supplement vitamin C, perhaps adding 50mg per cigarette – 500mg if you smoke 10 a day, although there is a good case for everyone to supplement 1,000mg a day, or 2,000mg a day if over 50.

Nature always provides a solution to help us with our evolution. It seems obvious to me we need vitamin C to combat excessive pollution.

Vitamin C is a keystone nutrient as far as swinging the antioxidant equation in your favour. It’s made in all living things, from animals to plants, including yeasts and funghi. It’s probably been the essential ‘exhaust recycler’ of all oxygen-based lifeforms. Production is even activated when oxidants are sensed. Animals also make more when stressed or exposed to viruses. Us humans, and all other primates, are one of very few species who can’t make it. The first non-vitamin C making animal to be discovered was the guinea pig. That’s how it became the ‘guinea pig’ for research since, like us, it’s dependent every second of every day on vitamin C from diet. Bats, a few birds and the teleost family of fish have also lost the ability to make vitamin C. 

You’ll see in this figure below and from watching the film above, that vitamin C disarms water-based oxidants, such as smoke, and vitamin E disarms fat-based oxidants such as burnt fat. Then, there are other key antioxidant team players that help to neutralise the reactive oxidants that damage our brain and body.

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Your best bet is probably to both eat a diet with a broad spectrum of antioxidants and also supplement them. The older you are the more you are likely to need. Key antioxidants are:

Vitamin A, C and E – associated with reducing Alzheimer’s risk
Lipoic acid (7) – protects the memory-friendly neurotransmitter acetylcholine and dampens down brain oxidation and inflammation)
Glutathione (8) or N-acetyl Cysteine (NAC)(9) – protects the brain and improves methylation thus having potential in dementia prevention.
Co-enzyme Q10 – protects the mitochondria in the brain from oxidative stress (10)
Resveratrol – resveratrol has antioxidant, anti-inflammatory and neuroprotective properties and prevents hippocampal brain damage. (11)

It doesn’t really make a lot of sense to supplement one without the others.

Individually, their impact on your brain health may be less than when combined. A study of 4,740 Cache County Utah elderly residents found that those supplementing both vitamin E and C cut their risk of developing Alzheimer’s by two thirds. Taking either cut risk by a quarter (12). A recent meta-analysis of all studies on factors that could prevent Alzheimer’s by one of our Scientific Advisory Board members – Professor Jin Tai Yu of Fudan University in Shanghai, China – shows that ‘either a high vitamin E or C intake showed a trend of attenuating risk by about 26%’ making these nutrients ‘grade 1’ top level prevention risk factors (13).

All those listed above – vitamin C, E, glutathione and N-acetyl cysteine, Coenzyme Q10 and resveratrol – work together and are often found in combined antioxidant supplement formulas. There are many other team player ‘cousins’ from B vitamins to minerals such as magnesium, selenium and zinc found respectively in greens, seafood, nuts and seeds.

There are two ways to increase your intake – through food and from supplements. Foods can be measured for their ‘Total Antioxidant Capacity’ or TAC for short. It’s worked out from an equation involving eight key antioxidants from vitamin A, carotenes (think carrots), lycopenes (rich in tomatoes), lutein and zeaxanthine (rich in green vegetables), vitamin E (is nuts and seeds), but most of all vitamin C (rich in berries, broccoli, peppers and other vegetables).

(Click here to read our guidance on supplements)

The higher the TAC score of your diet the lower is your risk of cognitive and memory decline. This was the finding of a recent study of 2,716 people over age 60. The researchers measured the TAC score from their diet, splitting them into the highest to lowest quarter of TAC score, and compared this to a number of memory tests. Those in the highest quarter, eating the most antioxidant-rich foods had half the risk of decreasing memory. The higher the TAC score the better their memory function was. (14)

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Go Rainbow, ‘Mediterranean’ and eat five or more servings of fruit and vegetables a day

So, what do you need to eat and drink to preserve your memory and protect your brain?

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

The trick is to really start thinking of the colours you’re eating and gravitate for the strong colours.

Mustard and turmeric, for example, are strong yellows. Dijon mustard is great – no sugar. But if you like good old-fashioned English mustard go for it. Have a teaspoon every other day.

Add turmeric to almost any steam-fry, curry or soup. 

Bright oranges include butternut squash, sweet potato, carrots – but do buy organic. Translucent mass produced carrots are tasteless and have a higher water content, ie less actual carrot. 

Tomatoes are particularly good for you. Buy seeded, not seedless watermelons. Blend the flesh in a blender, perhaps with some ice. The black husk of the seeds drops to the bottom. The flesh of the seeds, full of essential nutrients, becomes part of this mouth-wateringly refreshing drink. Great for detox. Strawberries are a low GL fruit. Red, yellow, green and orange peppers are all rich in vitamin C.

Anything purple, magenta or blue is brilliant for you. From beetroots (eat them raw, grated into salads) to blueberries, blackberries and raspberries. Strawberries are particularly good. According to a study, part of the Rush Memory and Aging Project at Rush University, Chicago, having a higher intake cut Alzheimer’s risk by a quarter. They are high in both vitamin C and flavanoids, a high level of which were also confirmed to cut risk by a third. (15)

Strong greens are always beneficial – from spinach, kale, Brussels sprouts, broccoli, tender stem, watercress, rocket, asparagus, artichoke, green beans, peas, kohlrabi, and cauliflower (although not green).

Polyphenol power

Some of these foods are particularly rich in ‘polyphenols’ a group of health promoting molecules which also includes flavonoids, sometimes called flavanols.  Blue foods such as blueberries contain another polyphenol called anthocyanins. Tea, the cacao in chocolate, red wine, red onions, olives and all the blueish berries are rich sources of polyphenols. Many of these polyphenol rich foods act as antioxidants but they do much more than this. They improve circulation in the brain, lower blood pressure and dampen down inflammation which lies behind many conditions from depression to dementia. Once again, the principle of what’s good for the heart is good for the brain.

One of the first important studies was carried out in Norway more than a decade ago by Eha Nurk and Helga Refsum and colleagues in Norway. (16)(17) They found that:

Tea – the more you drink the better. The tea benefit has been confirmed more recently in a study in Singapore, with green tea being marginally better than black tea.(18) However, this benefit was not found in a UK Biobank study, which reported tea and coffee drinking to be associated with worsening cognition compared to abstainers. (19)

Chocolate – peaks at 10g, or about 3 pieces – and let’s say dark, 70 or more percent, thus with less sugar, is likely to be better, as sugar is a strong indicator of cognitive decline. If a chocolate is 80% cacao that means almost 20% will be sugar. More recent studies giving cocoa, a rich source of flavanols, have shown improved cognition, possibly by improving circulation.(20) This has been confirmed in a big COSMOS trial involving over 20,000 people given a cacao extract supplement rich in flavanols versus a placebo for five years. (21) The reduction in cardiovascular risk was even greater than that of a Mediterranean diet. For a practical way to include cacao, try our brain-friendly cacao drink with maca and cinnamon.

Wine – consumption reduces risk of cognitive decline up to an intake of 125ml a day, which is a small glass. A thorough study in the British Medical Journal in 2018, which had followed over 9,000 people over 23 years, showed that both abstinence and drinking more than 14 units of alcohol a week, which is equivalent to a medium glass of wine (2.3 units) every day, also increases risk (22). This is consistent with studies showing that a small glass of wine a day decreases risk of cardiovascular disease. Red wine, high in resveratrol is likely to be most beneficial.

All the above are rich in a polyphenol called epicatechin. Jeremy Spencer, an advisor to Food for the Brain, who is Professor of Nutritional Biochemistry and Medicine at the University of Reading, where he specialises in studying the health benefits of polyphenols and other compounds in plants, has shown that these polyphenol rich plants improve blood brain flow in specific regions of the brain that improve attention, decision-making, impulse control and emotion, thus improving overall ‘executive’ function (23). What’s more, the level of flavanols you have in your bloodstream predicts your memory. The biggest impact of increasing flavanols, was seen in the COSMOS study, in those in the lowest third for dietary intake specifically seeing improvement in aspects of memory that link to the hippocampus, that central area of the brain that degenerates in Alzheimer’s (24).

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The Best Fruit and Veg to Eat for Your Brain

Which vegetables pack the biggest punch as far as polyphenols and antioxidants are concerned and are also lower in sugar or low GL?

Taking all these factors into account – the GL, antioxidants and polyphenols these are the dozen best rated fruit and veg. But do not think of this list as finite as more and more research reveals the amazing healing power of nature’s fruits and vegetables.

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The optimal intake for brain protection is 5 to 6 servings of fruit and veg a day. 

Half a plate of a main meal counts as two. A handful of berries would count as one. So, if half your plate for two main meals is vegetables, and you had some berries with your breakfast and another piece of fresh fruit or perhaps some broccoli heads or tenderstem or carrots dipped in hummus as a snack, or half an avocado with some high polyphenol olive oil, you’ve achieved six servings.

The first step is to eat ‘whole’ foods, and especially fresh plant foods with an emphasis on those listed above that are more likely to be high in antioxidants and polyphenols. (Also see the Alzheimers Prevention Diet.) There are some nutrients such as vitamin C for which just eating whole foods doesn’t guarantee you are achieving an optimal intake and are well worth supplementing.

My advice is to supplement 500mg to 1,000mg of vitamin C twice a day and also take an antioxidant formula or antioxidant rich multivitamin containing vitamins A, C, E, lipoic acid, glutathione or NAC, resveratrol and CoQ10.

Summary

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References

Eskelinen MH, Ngandu T, Tuomilehto J, Soininen H, Kivipelto M. Midlife healthy-diet index and late-life dementia and Alzheimer’s disease. Dement Geriatr Cogn Dis Extra. 2011 Jan;1(1):103-12. doi: 10.1159/000327518. Epub 2011 Apr 27. PMID: 22163237; PMCID: PMC3199886.
Beydoun MA, Beydoun HA, Gamaldo AA, Teel A, Zonderman AB, Wang Y. Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis. BMC Public Health. 2014 Jun 24;14:643. doi: 10.1186/1471-2458-14-643. PMID: 24962204; PMCID: PMC4099157.
Cacciottolo M, Wang X, Driscoll I, Woodward N, Saffari A, Reyes J, Serre ML, Vizuete W, Sioutas C, Morgan TE, Gatz M, Chui HC, Shumaker SA, Resnick SM, Espeland MA, Finch CE, Chen JC. Particulate air pollutants, APOE alleles and their contributions to cognitive impairment in older women and to amyloidogenesis in experimental models. Transl Psychiatry. 2017 Jan 31;7(1):e1022. doi: 10.1038/tp.2016.280. PMID: 28140404; PMCID: PMC5299391.
 Chen C, Whitsel EA, Espeland MA, Snetselaar L, Hayden KM, Lamichhane AP, Serre ML, Vizuete W, Kaufman JD, Wang X, Chui HC, D’Alton ME, Chen JC, Kahe K. B vitamin intakes modify the association between particulate air pollutants and incidence of all-cause dementia: Findings from the Women’s Health Initiative Memory Study. Alzheimers Dement. 2022 Nov;18(11):2188-2198. doi: 10.1002/alz.12515. Epub 2022 Feb 1. PMID: 35103387; PMCID: PMC9339592.
 Yu JT, Xu W, Tan CC, Andrieu S, Suckling J, Evangelou E, Pan A, Zhang C, Jia J, Feng L, Kua EH, Wang YJ, Wang HF, Tan MS, Li JQ, Hou XH, Wan Y, Tan L, Mok V, Tan L, Dong Q, Touchon J, Gauthier S, Aisen PS, Vellas B. Evidence-based prevention of Alzheimer’s disease: systematic review and meta-analysis of 243 observational prospective studies and 153 randomised controlled trials. J Neurol Neurosurg Psychiatry. 2020 Nov;91(11):1201-1209. doi: 10.1136/jnnp-2019-321913. Epub 2020 Jul 20. PMID: 32690803; PMCID: PMC7569385.
 Carr AC, Lykkesfeldt J. Factors Affecting the Vitamin C Dose-Concentration Relationship: Implications for Global Vitamin C Dietary Recommendations. Nutrients. 2023 Mar 29;15(7):1657. doi: 10.3390/nu15071657. PMID: 37049497; PMCID: PMC10096887.
 A. Maczurek, et al., ‘Lipoic acid as an anti-inflammatory and neuroprotective treatment for Alzheimer’s disease’, Advance Drug Delivery Review, 2008;60(13-14):1463-70 
 Pocernich CB, Butterfield DA. Elevation of glutathione as a therapeutic strategy in Alzheimer disease. Biochim Biophys Acta. 2012 May;1822(5):625-30. doi: 10.1016/j.bbadis.2011.10.003. Epub 2011 Oct 12. PMID: 22015471; PMCID: PMC3277671.
 Hara Y, McKeehan N, Dacks PA, Fillit HM. Evaluation of the Neuroprotective Potential of N-Acetylcysteine for Prevention and Treatment of Cognitive Aging and Dementia. J Prev Alzheimers Dis. 2017;4(3):201-206. doi: 10.14283/jpad.2017.22. PMID: 29182711.
 Yang X, Zhang Y, Xu H, Luo X, Yu J, Liu J, Chang RC. Neuroprotection of Coenzyme Q10 in Neurodegenerative Diseases. Curr Top Med Chem. 2016;16(8):858-66. doi: 10.2174/1568026615666150827095252. PMID: 26311425.
 Gomes BAQ, Silva JPB, Romeiro CFR, Dos Santos SM, Rodrigues CA, Gonçalves PR, Sakai JT, Mendes PFS, Varela ELP, Monteiro MC. Neuroprotective Mechanisms of Resveratrol in Alzheimer’s Disease: Role of SIRT1. Oxid Med Cell Longev. 2018 Oct 30;2018:8152373. doi: 10.1155/2018/8152373. PMID: 30510627; PMCID: PMC6232815.
 Basambombo LL, Carmichael PH, Côté S, Laurin D. Use of Vitamin E and C Supplements for the Prevention of Cognitive Decline. Ann Pharmacother. 2017 Feb;51(2):118-124. doi: 10.1177/1060028016673072. Epub 2016 Oct 5. PMID: 27708183.
 See reference 5.
 Peng, M., Liu, Y., Jia, X. et al. Dietary Total Antioxidant Capacity and Cognitive Function in Older Adults in the United States: The NHANES 2011–2014. J Nutr Health Aging 27, 479–486 (2023). https://doi.org/10.1007/s12603-023-1934-9
 Agarwal P, Holland TM, Wang Y, Bennett DA, Morris MC. Association of Strawberries and Anthocyanidin Intake with Alzheimer’s Dementia Risk. Nutrients. 2019 Dec 14;11(12):3060. doi: 10.3390/nu11123060. PMID: 31847371; PMCID: PMC6950087.
 Nurk E, Refsum H, Drevon CA, Tell GS, Nygaard HA, Engedal K, Smith AD. Intake of flavonoid-rich wine, tea, and chocolate by elderly men and women is associated with better cognitive test performance. J Nutr. 2009 Jan;139(1):120-7. doi: 10.3945/jn.108.095182. Epub 2008 Dec 3. PMID: 19056649.
 Nurk E, Refsum H, Drevon CA, Tell GS, Nygaard HA, Engedal K, Smith AD. Cognitive performance among the elderly in relation to the intake of plant foods. The Hordaland Health Study. Br J Nutr. 2010 Oct;104(8):1190-201. doi: 10.1017/S0007114510001807. Epub 2010 Jun 16. PMID: 20550741.
 Feng L, Chong MS, Lim WS, Lee TS, Kua EH, Ng TP. Tea for Alzheimer Prevention. J Prev Alzheimers Dis. 2015;2(2):136-141. doi: 10.14283/jpad.2015.57. PMID: 29231231.
 Cornelis MC, Weintraub S, Morris MC. Caffeinated Coffee and Tea Consumption, Genetic Variation and Cognitive Function in the UK Biobank. J Nutr. 2020 Aug 1;150(8):2164-2174. doi: 10.1093/jn/nxaa147. PMID: 32495843; PMCID: PMC7398783.
 Lamport DJ, Pal D, Moutsiana C, Field DT, Williams CM, Spencer JP, Butler LT. The effect of flavanol-rich cocoa on cerebral perfusion in healthy older adults during conscious resting state: a placebo controlled, crossover, acute trial. Psychopharmacology (Berl). 2015 Sep;232(17):3227-34. doi: 10.1007/s00213-015-3972-4. Epub 2015 Jun 7. PMID: 26047963; PMCID: PMC4534492.
 Sesso HD, Manson JE, Aragaki AK, Rist PM, Johnson LG, Friedenberg G, Copeland T, Clar A, Mora S, Moorthy MV, Sarkissian A, Carrick WR, Anderson GL; COSMOS Research Group. Effect of cocoa flavanol supplementation for the prevention of cardiovascular disease events: the COcoa Supplement and Multivitamin Outcomes Study (COSMOS) randomized clinical trial. Am J Clin Nutr. 2022 Jun 7;115(6):1490-1500. doi: 10.1093/ajcn/nqac055. PMID: 35294962; PMCID: PMC9170467.
 Sabia S, Fayosse A, Dumurgier J, Dugravot A, Akbaraly T, Britton A, Kivimäki M, Singh-Manoux A. Alcohol consumption and risk of dementia: 23 year follow-up of Whitehall II cohort study. BMJ. 2018 Aug 1;362:k2927. doi: 10.1136/bmj.k2927. PMID: 30068508; PMCID: PMC6066998.
 See Professor Peremy Spencer’s presentation at the Alzheimer’s is preventable masterclass (2022); also see Spencer JP. The impact of fruit flavonoids on memory and cognition. Br J Nutr. 2010 Oct;104 Suppl 3:S40-7. doi: 10.1017/S0007114510003934. PMID: 20955649.
 Brickman AM, Yeung LK, Alschuler DM, Ottaviani JI, Kuhnle GGC, Sloan RP, Luttmann-Gibson H, Copeland T, Schroeter H, Sesso HD, Manson JE, Wall M, Small SA. Dietary flavanols restore hippocampal-dependent memory in older adults with lower diet quality and lower habitual flavanol consumption. Proc Natl Acad Sci U S A. 2023 Jun 6;120(23):e2216932120. doi: 10.1073/pnas.2216932120. Epub 2023 May 30. PMID: 37252983; PMCID: PMC10265949.

This was the title of a report in the British Medical Journal (1), pointing out that choline is an essential nutrient, much like omega-3 fats, that is vital for health and especially the brain, but not sufficiently supplied in many people’s diets, and especially those who are largely vegan.

While the body can make a little, it does not make enough and thus choline is being reclassified as an essential nutrient with an adequate intake defined as between 400mg and 520mg a day, the latter for pregnant and breast-feeding women. But these levels don’t relate to brain function. They relate to the EFSA allowed claims of “choline is needed for lipids metabolism”, “maintaining healthy liver functioning” and “reduction in homocysteine levels”. You need choline to do the right thing with cholesterol in the liver. 

But even more important is choline’s role in building and maintaining a healthy brain. A pregnant woman’s intake defines the cognitive abilities of their child. Twenty years ago we knew that pregnant rats fed choline half way through their pregnancy have more connections between brain cells, plus improved learning ability and better memory recall. Now we know it’s true for babies. In fact, a lack of choline can lead to a shrinking of a woman’s brain as the foetus robs their brain to build its own – a case of ‘Mummy I shrank your brain’. Babies are born with blood choline levels three times higher than their mother, illustrating how vital this nutrient is for building neuronal connections, which newborn babies do at a rate of up to a million new connections a second! An optimal intake for brain function is likely to be a lot higher than the 400mg recommended for adults.

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

The reason the BMJ says ‘crisis’ is that more people are eating a plant-based diet and shunning eggs, fish and meat, which are the best sources of, not only choline, but also B12. There’s a tiny bit of choline in broccoli and in nuts, but not enough. An egg provides around 120mg, a 50g beef or salmon steak around 50mg. The same amount of almonds or broccoli is about 25mg. Cow’s milk has a little, but a fraction of that found in human milk. Beef liver is the richest source.

Twenty years ago I found the evidence sufficiently compelling to recommend eating an egg a day, three servings of fish and one of meat (or another portion of fish) a week, a handful of nuts, plus daily supplementation of circa 100mg, which is what I do in my ‘brain food’ formula. If you also ate a serving of broccoli a day, you’d be achieving something like 2,100mg a week, or 300mg a day – still short of daily requirements.

If you follow a plant-based diet, getting enough choline requires more attention. Lecithin derived from soya is a particularly concentrated source, while other foods can also contribute. See our guide to vegan sources of choline to learn which foods contain choline and how much you need.

If you want more strategies on what to eat and do to support ad upgrade your brain make sure you complete the Cognitive Function Test below to get your plan of action for improving your brain over the next 6 months.

Reference:

Derbyshire E. ‘Could we be overlooking a potential choline crisis in the United Kingdom?’ BMJ Nutrition, Prevention and Health, 2019; 0:1–4

Phospholipids and Choline: Vegan Sources and How Much You Need

Did you know your brain is largely built from fat? Phospholipids and choline are an important part of that story. Brain-cell membranes are rich in phospholipids, which combine with DHA, the long-chain omega-3 fat particularly important for the brain. Fish and eggs provide both these nutrients, but on a vegan diet you need to think about them separately: where your DHA is coming from, and whether you are getting enough choline to support phospholipid production. The good news is that both can be covered without eating fish or eggs. Here’s how, including the vegan choline sources that genuinely add up.

The DHA problem: plant foods don’t really solve it

Flaxseed, walnuts and chia give you ALA, a plant omega-3, but converting it into the DHA your brain actually needs is remarkably inefficient. The classic human tracer study found women convert around 9% of ALA into EPA at best, men considerably less, and conversion all the way to DHA is lower still, often under 1%.[1] In practice, that means a vegan diet without a direct DHA source usually falls short, whatever the flaxseed packet implies.

The fix is algae oil: it’s the same DHA fish get from eating algae in the first place, just without the fish, and a 2025 study found algae-derived EPA and DHA absorb just as well as fish oil at equivalent doses.[2] For brain health, research suggests that higher intakes may be needed than standard minimum omega-3 recommendations, with studies reporting cognitive benefits at DHA intakes above approximately 580mg a day. A practical target is around 750mg DHA a day, alongside EPA, giving a combined EPA and DHA intake of over 1,000mg a day. If you want to know where you actually stand rather than guess, an Omega-3 Index test measures it directly.

Why does choline matter just as much?

For DHA to become part of a brain-cell membrane, it needs to be incorporated into phospholipids. B vitamins, particularly B12, folate and B6, are involved in the methylation pathways that help make and regulate these phospholipids. Homocysteine gives us a useful window into how well these B-vitamin-dependent pathways are working: when levels are raised, it can be a sign that something in this system needs attention.

Think of DHA as the building material and phospholipids as the structure that puts it in the right place. Having plenty of DHA arriving at the building site is important, but you also need the machinery and materials to build it into the membranes your brain cells depend on.

Several phospholipid types exist (phosphatidyl choline, serine, inositol, ethanolamine), and your body makes some of each, but not enough on its own for optimal brain health. Egg yolk and liver are the richest phospholipid food sources, which is exactly why this needs a separate approach on a vegan diet. That’s why choline is best thought of as semi-essential, and why it’s increasingly treated as a nutrient worth tracking deliberately rather than assuming you’re getting enough.

The evidence for paying attention to choline has only grown stronger. In a large 2025 UK Biobank study of more than 125,000 people followed for almost 12 years, moderate choline intake was associated with a 17–23% lower risk of dementia compared with lower or higher intakes.[3] The relationship was U-shaped, with the lowest risk seen at around 330–354mg a day. Read FFB’s full coverage of that study here .

How much choline do you actually need?

Current EU guidance (EFSA) sets adequate intake at 400mg a day for adults generally, rising to 480mg in pregnancy and 520mg during breastfeeding.[4] There’s no separate UK (SACN) reference value, so this EU figure is what most UK sources, including in our founder Patrick Holford’s own books,

Vegan sources of choline: are you at risk of falling short?

Fish, eggs and organ meats remain the richest sources overall, but the best vegan choline sources are soya (tofu, soya milk), quinoa, nuts and seeds (flaxseed, almonds, peanuts), and cruciferous vegetables: broccoli, cauliflower, Brussels sprouts. Worth noting: serving size matters as much as the food itself. Soya flour looks unimpressive per serving but is one of the most concentrated sources by weight, so it’s worth using where you can (a smoothie or baking flour, for instance) rather than judging foods by the 100g figure alone.

Put together, a full day of vegan eating looks like this:

That adds up to roughly 330mg across the day: a solid base, and still short of the 400mg+ target.

Closing the gap with lecithin

To get from around 330mg through food to 500mg or more, you may want to supplement rather than trying to eat your way there. Lecithin granules and capsules are the most concentrated phosphatidylcholine sources available, and soya is the source almost all vegan phosphatidylcholine supplements are made from (egg-derived lecithin isn’t vegan, so check the label). One tablespoon (7.5g) of standard soya lecithin granules provides roughly 200mg of choline. If you use a high-phosphatidylcholine lecithin (around 18% choline), you need less: around 5g provides a similar amount of choline.

If you’re vegetarian rather than strictly vegan, meeting your choline needs is much easier. Eggs are one of the richest vegetarian sources, providing around 147 mg per large hard-boiled egg, so six eggs a week can make a significant contribution. Non-vegans can also get choline from fish, including varieties that aren’t particularly rich in omega-3.

The bigger picture is not about chasing one nutrient in isolation. Your brain-cell membranes depend on phospholipids, DHA and the B vitamins involved in bringing these systems together. On a vegan diet, all of these can be covered, but DHA and choline deserve particular attention rather than being left to chance.

The principle is simple: give your brain the raw materials it needs to build and maintain healthy cell membranes throughout life.

This information is for educational purposes only and isn’t a substitute for personalised medical advice. If you’re pregnant, breastfeeding, or planning pregnancy, speak to your GP, midwife or a qualified nutrition professional before starting any new supplement.

Related reading:

Phospholipids
New Study: higher choline intake lowers the risk of dementia, Alzheimer’s, & cognitive decline
Choline crisis in the UK?
Brain Health And Vegan Eating: What It Means For Long Term Cognitive Health
How to Keep Building Brain Cells at Any Age

By Patrick Holford

Does what you eat affect your risk for dementia later in life and, if so, what is the best diet to protect your brain and prevent cognitive decline? Many studies have been published with different results ranging from no effect at all, as reported in a study in Sweden[i], to over a 90% reduced risk of Alzheimer’s, as reported in a study in Finland and Sweden which compared those with the a ‘healthy’ versus unhealthy diet in mid-life for future risk of developing Alzheimer’s disease and dementia 14 years later. Those who ate the healthiest diet had an 86-90% decreased risk of developing dementia and a 90-92% decreased risk of developing Alzheimer’s disease.[ii] We have put together a science backed Alzheimer’s Prevention Diet.

Many of these studies are similar in design, by looking at mid-life diet then tracking a group of people over time to see who does or doesn’t develop dementia or its most common type, Alzheimer’s disease. Many also look at some measure of coherence to a ‘Mediterranean’ diet, which usually means eating more fruit, vegetables, legumes, nuts and seeds, as well as more fish, less meat and sometimes some or more wine. Others compare to the standard recommendations for a ‘healthy’ diet made by the country’s authorities. Some foods or drinks could go either way. For example, some studies suggest coffee drinking might reduce risk, yet coffee increases homocysteine levels, which is a strong predictor of risk. Alcohol consumption, especially red wine, may reduce risk in moderation but possibly increase risk in excess.

Another way to answer the question regarding the best anti-dementia diet is to look at studies that have linked specific foods or drinks to risk of cognitive decline then build up the brain-friendly diet from there. These studies can also help define how much of the food or drink is optimal, or too much for those foods or drinks that increase risk.

Protective Foods

One of the first good studies was carried out in Norway more than a decade ago by Eha Nurk and Helga Refsum and colleagues in Norway.[iii] [iv] They found that:

Tea – the more you drink the better. The tea benefit has been confirmed more recently in a study in Singapore, with green tea being marginally better than black tea.[v] However, this benefit was not found in a UK Biobank study, which reported by tea and coffee drinking to be associated with worsening cognition compared to abstainers.[vi]

Chocolate – peaks at 10g, or about 3 pieces – and let’s say dark, 70%+ thus with less sugar is more likely to be better, as sugar is a strong indicator of cognitive decline. More recent studies giving cocoa, a rich source of flavanols, have shown improved cognition, possibly by improving circulation.[vii] For a lower-sugar way to enjoy cacao, try our healthy cacao drink recipe with maca and cinnamon

Wine – consumption reduced risk up to 125g a day, which is a small glass. A study in the British Medical Journal in 2018 showed that while abstinence increased risk by 48% having more than 14 units of alcohol a week, which is equivalent to a medium glass of wine every day, increases risk.[viii]

Grains and potatoes – reached a plateau at 100 to 150g a day, which is one or two servings max. High fibre bread was the most beneficial carb food. White bread increased risk. Fruit and veg – although the more you eat the better, benefits start to plateau at 500g a day, which is about five to six servings a day. Of individual vegetables, carrots, cruciferous vegetables and citrus fruit were the most positive as were mushrooms. A more recent study in the US found that those who ate 1.3 portions of green leafy vegetables a day, compared to less than one a week, had a dramatically slower decline in cognitive function, equivalent to being 11 years younger over a 10-year period. Berries are particularly protective, especially blueberries and strawberries.[ix]

Fish – is the most protective. Nurk’s study found a peak benefit at about 100g a day, which is one to two servings. A study of all studies by National Institutes of Health researcher, Beydoun, reported that eating fish once or more each week reduces risk of Alzheimer’s by a third compared with those who eat fish less than once a week.[x]

Olive oil and nuts – seem to be positive aspects associated with a Mediterranean diet.[xi] One study assigned people to a Mediterranean diet supplemented with either a litre a week of olive oil or 30g of nuts a day which is a small handful, versus a control diet with low fat and reported reduced cognitive decline with the extra olive oil or nuts. [xii]

Protective Diets

Early studies on the Mediterranean style diet reported that high adherence versus low adherence reduced risk of Alzheimer’s by a third.[xiii][xiv] A study which followed 2,000 people over 20 years found that adherence to what they defined as healthy diet which meant ‘modifying the quality of fats, increasing vegetable consumption, and decreasing salt and sugar consumption’ was associated with a halving of dementia risk. With the exception of sugar, no individual food predicted risk significantly.[xv]

But the problem with studies like this is the assumptions. In this case ‘modifying the quality of fats’ means using vegetable oils as opposed to margarine or butter and not eating the visible fat on meat. Vegetable oils is rather vague – it could be olive oil or something like sunflower oil. The assumption is that a low-fat diet might be beneficial, yet a high fat, low carb (HFLC) ketogenic diet appears to be protective.

A study in Holland reported ‘that better diet quality related to larger brain volume, grey matter volume, white matter volume, and hippocampal volume. High intake of vegetables, fruit, whole grains, nuts, dairy, and fish and low intake of sugar-containing beverages were associated with larger brain volumes.’[xvi]

Harmful Foods and Diets

Sugar – be it sucrose (white sugar) or fructose comes out consistently negative. Studies report poorer cognition associated with intake of sugar-sweetened beverages in adults (Ye 2011). This relationship between diet and cognition has also been explored in more recent Food for the Brain research examining dietary patterns and predicted cognitive function.

Animal studies show sucrose and fructose both impair cognition and brain health (Lakhan 2013) (Orr 2014) which is all consistent with the with the fact that diabetes is a risk factor for cognitive decline (see ‘Is Sugar Killing Your Brain’) and supported by recent human studies on blood glucose as a major predictor of Alzheimer’s and dementia later in life.[xvii]

Even so-called ‘high’ levels within the  normal reference range for blood glucose are linked to decreased grey matter in the brain.[xviii]

The most recent and substantial study relates to ultra-processed foods following around 70,000 people over a decade. The more ultra-processed foods eaten the higher was the risk for both dementia, Alzheimer’s and vascular dementia.[xix] Replacing just 10 per cent of ultra-processed food by weight in one’s diet with an equivalent proportion of unprocessed or minimally processed foods was estimated to lower risk of dementia by 19%. So, get off the junk. Choose whole foods only.

What is it about what you eat that could be protective?

The best candidates are foods high in:

Antioxidant vitamins (C and E)
Fruit and vegetables
Flavanols
Vitamin D
Fish and omega-3 fats
Folate and other B vitamins including b12, only found in animal foods
Phospholipids, found in eggs and fish

Apart from the studies above it is certainly logical to include choline rich foods sources, as a source for phospholipids. In animal studies, giving choline slows down Alzheimer’s disease development.[xx]

Also, consuming two tablespoons C-8 oil, a form of medium chain triglyceride, has been shown to enhance cognition in those with mild cognitive impairment and elevate neuronal energy derived from ketones both in those with MCI and Alzheimer’s.[xxi] C8 is rapidly converted into ketones, which can provide an alternative source of energy for the brain. Learn more about how ketones fuel the brain. Given the preponderance of neurons to prefer ketones to glucose for fuel, and the evidence for benefit, such dietary practices such as 18:6 (eating all food within a 6 hour window) or starting the day with a Hybrid Latté, almost carb-free, high in cacao, C8 oil and almonds from carb-free almond milk and almond butter or following a low carb, high fat (LCHF) ketogenic diet, which has been shown to have beneficial for those with Alzheimer’s,[xxii] should be considered.

Although in some respects conjectural calling on all this evidence, especially given the other health-promoting benefits of these foods, the key components of a diet designed to protect brain health and reduce risk of cognitive decline are:

Eat essential fats and phospholipids

Eat an egg a day, or six eggs a week – preferably free-range, organic, and high in omega-3s. Boil, scramble or poach them, but avoid frying.
Eat a tablespoon of seeds and nuts every day – the best seeds are chia, flax, hemp, pumpkin, higher in omega-3. They’re delicious sprinkled on cereal, soups, and salads. The best nuts are walnuts, pecans, and macadamia nuts.  Each are high in omega-3 but all nuts, including almonds, hazelnuts and unsalted peanuts are good sources of protein and minerals.
Eat cold-water, oily carnivorous fish – have a serving of herring, mackerel, salmon or sardines two or three times a week (limit tuna, unless identified as low in mercury, to three times a month). Vegans need to supplement algal omega-3 DHA, as well as choline or lecithin capsules or granules, rich in phosphatidyl choline.
Use cold-pressed olive oil for salad dressings and other cold uses, such as drizzling on vegetables instead of butter. Substitute frying with steam frying with olive oil, coconut oil or butter, e.g. for onions and garlic, then adding a watery sauce such as lemon juice, tamari and water, to ‘steam’, for example, vegetables perhaps with tofu, fish or chicken.

Eat slow-release carbohydrates

Eat wholefoods – whole grains, lentils, beans, nuts, seeds, fresh fruit, and vegetables – and avoid all white, refined and over-processed foods, as well as any food with added sugar.
Snack on fresh fruit, preferably apples, pears and/or berries, especially blueberries.
Eat less gluten. Try brown rice, rye, oats, quinoa, lentils, beans, or chickpeas.
Avoid fruit juices. Eat fresh fruit instead. Occasionally have unsweetened Montmorency cherry juice or blueberry juice (made from unsweetened concentrate).

Eat antioxidant and vitamin-rich foods

Eat half your diet raw or lightly steamed.
Eat two or more servings a day of fresh fruit, including one of berries.
Eat four servings a day of dark green, leafy and root vegetables such as tenderstem broccoli, broccoli, kale, spinach, watercress, carrots, sweet potatoes, Brussels sprouts, green beans, or peppers, as well as mushrooms. Choose organic where possible.
Have a serving a day of beans, lentils, nuts, or seeds – all high in folate, as are peanuts.

Eat enough protein

Have three servings of protein-rich foods a day, if you are a man, and two if you are a woman.
Choose good vegetable protein sources, including beans, lentils, quinoa, tofu, or tempeh (soya) and ‘seed’ vegetables such as peas, broad beans and corn.
If eating animal protein, choose lean meat or preferably fish, organic whenever possible.

New research also suggests that higher consumption of red meat, particularly processed red meat, may be associated with an increased risk of dementia and cognitive decline. Read more about red meat and brain health.

Avoid harmful fats

Minimise your intake of fried or processed food and burnt saturated fat on meat, and cheese. Recent research has also linked higher consumption of red and processed meat with an increased risk of cognitive decline and dementia
Minimise your consumption of deep-fried food. Poach, steam or steam-fry food instead.

Avoid sugar, reduce caffeine, and drink alcohol in moderation

Avoid adding sugar to dishes and avoid foods and drinks with added sugar. Keep your sugar intake to a minimum, sweetening cereal or desserts with fruit.
Avoid or considerably reduce your consumption of caffeinated drinks. Don’t have more than one caffeinated drink a day. Tea is preferable to coffee.
Drink alcoholic drinks infrequently, and preferably red wine, to a maximum of one small glass (125g) a day.
Have up to three slices of dark chocolate, minimum 70% cacao, or drink unsweetened cacao with milk or plant milk.

See how one family put brain-healthy diet and lifestyle changes into practice.

Help support Food for the Brain

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

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

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

References

[i] Glans I, Sonestedt E, Nägga K, Gustavsson AM, González-Padilla E, Borne Y, Stomrud E, Melander O, Nilsson P, Palmqvist S, Hansson O. Association Between Dietary Habits in Midlife With Dementia Incidence Over a 20-Year Period. Neurology. 2022 Oct 12:10.1212/WNL.0000000000201336. doi: 10.1212/WNL.0000000000201336. Epub ahead of print. PMID: 36224029.

[ii] Eskelinen MH, Ngandu T, Tuomilehto J, Soininen H, Kivipelto M. Midlife healthy-diet index and late-life dementia and Alzheimer’s disease. Dement Geriatr Cogn Dis Extra. 2011 Jan;1(1):103-12. doi: 10.1159/000327518. Epub 2011 Apr 27. PMID: 22163237; PMCID: PMC3199886.

[iii] 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.

[iv] Nurk E, Refsum H, Drevon CA, Tell GS, Nygaard HA, Engedal K, Smith AD. Cognitive performance among the elderly in relation to the intake of plant foods. The Hordaland Health Study. Br J Nutr. 2010 Oct;104(8):1190-201. doi: 10.1017/S0007114510001807. Epub 2010 Jun 16. PMID: 20550741.

[v] 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.

[vi] 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.

[vii] Lamport DJ, Pal D, Moutsiana C, Field DT, Williams CM, Spencer JP, Butler LT. The effect of flavanol-rich cocoa on cerebral perfusion in healthy older adults during conscious resting state: a placebo controlled, crossover, acute trial. Psychopharmacology (Berl). 2015 Sep;232(17):3227-34. doi: 10.1007/s00213-015-3972-4. Epub 2015 Jun 7. PMID: 26047963; PMCID: PMC4534492.

[viii] Sabia S, Fayosse A, Dumurgier J, Dugravot A, Akbaraly T, Britton A, Kivimäki M, Singh-Manoux A. Alcohol consumption and risk of dementia: 23 year follow-up of Whitehall II cohort study. BMJ. 2018 Aug 1;362:k2927. doi: 10.1136/bmj.k2927. PMID: 30068508; PMCID: PMC6066998.

[ix]  Devore E et al, ‘Dietary intakes of berries and flavonoids in relation to cognitive decline’, Annals of neurology 2012; 72: 135-43; Agarwal P, Holland TM, Wang Y, Bennett DA, Morris MC. Association of Strawberries and Anthocyanidin Intake with Alzheimer’s Dementia Risk. Nutrients. 2019 Dec 14;11(12):3060. doi: 10.3390/nu11123060. PMID: 31847371; PMCID: PMC6950087

[x] Beydoun MA, Beydoun HA, Gamaldo AA, Teel A, Zonderman AB, Wang Y. Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis. BMC Public Health. 2014 Jun 24;14:643. doi: 10.1186/1471-2458-14-643. PMID: 24962204; PMCID: PMC4099157.

[xi] Román GC, Jackson RE, Reis J, Román AN, Toledo JB, Toledo E. Extra-virgin olive oil for potential prevention of Alzheimer disease. Rev Neurol (Paris). 2019 Dec;175(10):705-723. doi: 10.1016/j.neurol.2019.07.017. Epub 2019 Sep 11. PMID: 31521394.; Salis C, Papageorgiou L, Papakonstantinou E, Hagidimitriou M, Vlachakis D. Olive Oil Polyphenols in Neurodegenerative Pathologies. Adv Exp Med Biol. 2020;1195:77-91. doi: 10.1007/978-3-030-32633-3_12. PMID: 32468462.

[xii] Valls-Pedret C, Sala-Vila A, Serra-Mir M, Corella D, de la Torre R, Martínez-González MÁ, Martínez-Lapiscina EH, Fitó M, Pérez-Heras A, Salas-Salvadó J, Estruch R, Ros E. Mediterranean Diet and Age-Related Cognitive Decline: A Randomized Clinical Trial. JAMA Intern Med. 2015 Jul;175(7):1094-1103. doi: 10.1001/jamainternmed.2015.1668. Erratum in: JAMA Intern Med. 2018 Dec 1;178(12):1731-1732. PMID: 25961184.

[xiii] Singh B, Parsaik AK, Mielke MM, Erwin PJ, Knopman DS, Petersen RC, Roberts RO. Association of mediterranean diet with mild cognitive impairment and Alzheimer’s disease: a systematic review and meta-analysis. J Alzheimers Dis. 2014;39(2):271-82. doi: 10.3233/JAD-130830. PMID: 24164735; PMCID: PMC3946820.

[xiv] Scarmeas N, Stern Y, Tang MX, Mayeux R, Luchsinger JA. Mediterranean diet and risk for Alzheimer’s disease. Ann Neurol. 2006 Jun;59(6):912-21. doi: 10.1002/ana.20854. PMID: 16622828; PMCID: PMC3024594.

[xv] Sindi S, Kåreholt I, Eskelinen M, Hooshmand B, Lehtisalo J, Soininen H, Ngandu T, Kivipelto M. Healthy Dietary Changes in Midlife Are Associated with Reduced Dementia Risk Later in Life. Nutrients. 2018 Nov 3;10(11):1649. doi: 10.3390/nu10111649. PMID: 30400288; PMCID: PMC6265705.

[xvi] Croll PH, Voortman T, Ikram MA, Franco OH, Schoufour JD, Bos D, Vernooij MW. Better diet quality relates to larger brain tissue volumes: The Rotterdam Study. Neurology. 2018 Jun 12;90(24):e2166-e2173. doi: 10.1212/WNL.0000000000005691. Epub 2018 May 16. PMID: 29769374.

[xvii] 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. 2022 Mar 23. doi: 10.1002/alz.12641. Epub ahead of print. PMID: 35319157.

[xviii] Mortby ME, Janke AL, Anstey KJ, Sachdev PS, Cherbuin N. High “normal” blood glucose is associated with decreased brain volume and cognitive performance in the 60s: the PATH through life study. PLoS One. 2013 Sep 4;8(9):e73697. doi: 10.1371/journal.pone.0073697. PMID: 24023897; PMCID: PMC3762736.

[xix] Li H, Li S, Yang H, Zhang Y, Zhang S, Ma Y, Hou Y, Zhang X, Niu K, Borne Y, Wang Y. Association of Ultraprocessed Food Consumption With Risk of Dementia: A Prospective Cohort. Neurology. 2022 Jul 27:10.1212/WNL.0000000000200871. doi: 10.1212/WNL.0000000000200871. Epub ahead of print. PMID: 35896436.

[xx] Velazquez R, Ferreira E, Knowles S, Fux C, Rodin A, Winslow W, Oddo S. Lifelong choline supplementation ameliorates Alzheimer’s disease pathology and associated cognitive deficits by attenuating microglia activation. Aging Cell. 2019 Dec;18(6):e13037. doi: 10.1111/acel.13037. Epub 2019 Sep 27. PMID: 31560162; PMCID: PMC6826123.

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

[xxii] Phillips MCL, Deprez LM, Mortimer GMN, Murtagh DKJ, McCoy S, Mylchreest R, Gilbertson LJ, Clark KM, Simpson PV, McManus EJ, Oh JE, Yadavaraj S, King VM, Pillai A, Romero-Ferrando B, Brinkhuis M, Copeland BM, Samad S, Liao S, Schepel JAC. Randomized crossover trial of a modified ketogenic diet in Alzheimer’s disease. Alzheimers Res Ther. 2021 Feb 23;13(1):51. doi: 10.1186/s13195-021-00783-x. PMID: 33622392; PMCID: PMC7901512.

Brain Fats – Seafood, Omega-3 PUFAs, Phospholipids and Vitamin D

The omega-3 fat, docosahexaenoic acid (DHA) is the most abundant PUFA in the brain, concentrated in the grey matter and, particularly at the synapses.¹ DHA is incorporated into membrane phospholipids, where it affects the properties of the membrane, for example, maintaining membrane fluidity. DHA, along with other omega-3 fats EPA, DPAn-3 and their mediators are involved in a wide variety of processes in the brain, such as making new neurons, synaptic connections and the regulation of inflammation.²

Fish, especially cold-water oily fish, contain high levels of DHA and EPA,  and epidemiological studies consistently suggest that an elevated fish intake is associated with decreased risk of neurodegenerative diseases, such as Alzheimer’s disease.³ Recent estimates suggest that worldwide many populations are currently consuming DHA and EPA at levels well below the recommendations issued by many international authorities (GOED), with and blood levels of EPA and DHA have been estimated to be low to very low for most of the world, which may increase global risk for chronic disease.⁴

This may be especially relevant when fish replaces red meat in the diet. Recent research into red meat and dementia risk found important differences according to both the type and amount of meat consumed.

Interestingly, positive associations have also been found between walnut consumption and cognitive performance.⁵ Walnuts are a source of omega-3 fat, alpha-linolenic acid (ALA) and also a range of antioxidants.

Omega-3 Supplementation and cognitive decline

DHA supplementation appears to show the greatest promise in the early stage before the onset of memory loss symptoms,¹ and at levels at or above 1000 mg per day (Ismail 2015).⁶

A study of healthy 50-75 year olds were given 2,200 mg a day of omega 3 fish oils for six months not only reported significant increase in executive function, one aspect of cognition that is a hallmark of Alzheimer’s, but also beneficial structural changes in white matter integrity and grey matter volume in the brain. The cognitive improvement correlated with blood levels of omega-3 PUFAs.⁷

A randomized, double-blind, placebo-controlled, clinical study, gave 900 mg of DHA a day for 24 weeks and reported an improvement in learning and memory function in those with age-related cognitive decline.⁸ In a further trial by the same research group, giving 2,000 mg a day of DHA or placebo to 402 people with mild to moderate Alzheimer’s disease, therefore further along the disease process, for a period of 18 months found no cognitive improvement.⁹

The effects of omega-3 supplementation may depend on factors including dosage, EPA and DHA content, and an individual’s nutritional status. For practical information about supplement formulations, the research on cognitive health and how products compare, explore our omega-3 supplements for brain health guide.

Phospholipids

Phospholipids, rich in eggs and seafood, are abundant in the brain. They make up the membranes of the different types of cells in the brain. These include Phosphatidylethanolamine (PE) and phosphatidylserine (PS) phosphatidylcholine (PC) and phosphatidylinositol (PI). They become attached to omega-3 DHA. (see film ‘Build Your Brain‘) Phosphatidylethanolamine (PE) and phosphatidylserine (PS) are enriched in DHA, whereas much lower levels are found in phosphatidylcholine (PC) and phosphatidylinositol (PI).³ Attaching DHA to phospholipids is a process that requires methylation, which is dependent on B vitamins.⁹ Interestingly, although DHA is typically found high in PS, levels have been found to be low in PS in post-mortem samples from Alzheimer’s disease patients.¹⁰ PS supplementation may benefit cognition in the elderly,¹¹ but as PS is highly enriched with DHA, it is currently unclear whether the potential beneficial effects of PS on cognition are due to the intact PS or DHA.  Although PC is not highly enriched in DHA, higher plasma concentrations of PC-DHA are associated with reduced risk of dementia and AD,¹² and post mortem samples from AD shows depletion of PC-DHA in grey matter.¹³

Supplementation

A number of trials have investigated the effects of providing multinutrient supplements containing a range of nutritional factors with the aim of supporting phospholipid biosynthesis. Our recent systematic review identified that omega-3 PUFAs and B vitamins as part of these multinutrient formulas confers benefits on cognition in older adults across a range of different types of measures of cognition in older adults.¹⁴ Furthermore, 12-week trial of citicoline has shown cognitive benefits in healthy older adults.¹⁵

Vitamin D

The primary source of vitamin D is exposure to sunlight. Seafood provides the most dietary vitamin D. Vitamin D deficiency increases risk of AD.^161,17,18  Supplements of vitamin D can be derived from animal or fungal sources (mushrooms and yeast). Supplementing 800iu (20mg) a day for 12 months has been shown to improve cognitive function and lessen amyloid protein markers.¹⁹

In a study in France involving 912 elderly patients followed for twelve years, a total of 177 dementia cases (124 AD) occurred: 25(OH)D deficiency was associated with a nearly three-fold increased risk of AD.²⁰

References

1.Dyall, S. C. (2015, 2015-April-21). Long-chain omega-3 fatty acids and the brain: A review of the independent and shared effects of EPA, DPA and DHA [Review]. Frontiers in Aging Neuroscience, 7(52). https://doi.org/10.3389/fnagi.2015.00052

2. Dyall, S. C., Balas, L., Bazan, N. G., Brenna, J. T., Chiang, N., da Costa Souza, F., Dalli, J., Durand, T., Galano, J. M., Lein, P. J., Serhan, C. N., & Taha, A. Y. (2022, Apr). Polyunsaturated fatty acids and fatty acid-derived lipid mediators: Recent advances in the understanding of their biosynthesis, structures, and functions. Prog Lipid Res, 86, 101165. https://doi.org/10.1016/j.plipres.2022.101165

3. Dyall SC, Michael-Titus AT. Neurological benefits of omega-3 fatty acids. Neuromolecular Med. 2008;10(4):219-35. doi: 10.1007/s12017-008-8036-z. Epub 2008 Jun 10. PMID: 18543124.

4. Stark, K. D., Van Elswyk, M. E., Higgins, M. R., Weatherford, C. A., & Salem, N., Jr. (2016, Jul). Global survey of the omega-3 fatty acids, docosahexaenoic acid and eicosapentaenoic acid in the blood stream of healthy adults. Prog Lipid Res, 63, 132-152. https://doi.org/S0163-7827(15)30033-3 [pii]10.1016/j.plipres.2016.05.001 Alzheimers Dement. 2017 Nov;13(11):1207-1216. doi: 10.1016/j.jalz.2017.03.003. Epub 2017 May 16

5. Theodore LE, Kellow NJ, McNeil EA, Close EO, Coad EG, Cardoso BR. Nut Consumption for Cognitive Performance: A Systematic Review. Adv Nutr. 2021 Jun 1;12(3):777-792. doi: 10.1093/advances/nmaa153. PMID: 33330927; PMCID: PMC8166568.

6. Ismail

7. A. Veronica Witte, Lucia Kerti, Henrike M. Hermannstädter, Jochen B. Fiebach, Stephan J. Schreiber, Jan Philipp Schuchardt, Andreas Hahn, Agnes Flöel, Long-Chain Omega-3 Fatty Acids Improve Brain Function and Structure in Older Adults, Cerebral Cortex, Volume 24, Issue 11, November 2014, Pages 3059–3068, https://doi.org/10.1093/cercor/bht163

8. Yurko-Mauro K, McCarthy D, Rom D, et al; Beneficial effects of docosahexaenoic acid on cognition in age-related cognitive decline. Alzheimers Dement. 2010; 6, 456-64

9. Quinn JF, Raman R, Thomas RG, et al; Docosahexaenoic acid supplementation and cognitive decline in Alzheimer disease: a randomized trial. JAMA, 2010; Nov 3;304(17):1903-11.

10. A David Smith, Fredrik Jernerén, Helga Refsum, ω-3 fatty acids and their interactions, The American Journal of Clinical Nutrition, Volume 113, Issue 4, April 2021, Pages 775–778, https://doi.org/10.1093/ajcn/nqab013

11. Cunnane, Stephen & Schneider, Julie & Tangney, Christine & Tremblay-Mercier, Jennifer & Fortier, Mélanie & Bennett, David & Morris, Martha. (2012). Plasma and Brain Fatty Acid Profiles in Mild Cognitive Impairment and Alzheimer’s Disease. Journal of Alzheimer’s disease : JAD. 29. 691-7. 10.3233/JAD-2012-110629.

12. Richter Y, Herzog Y, Lifshitz Y, Hayun R, Zchut S. The effect of soybean-derived phosphatidylserine on cognitive performance in elderly with subjective memory complaints: a pilot study. Clin Interv Aging. 2013;8:557-63. doi: 10.2147/CIA.S40348. Epub 2013 May 21. PMID: 23723695; PMCID: PMC3665496.

13. Schaefer EJ, Bongard V, Beiser AS, Lamon-Fava S, Robins SJ, Au R, Tucker KL, Kyle DJ, Wilson PW, Wolf PA. Plasma phosphatidylcholine docosahexaenoic acid content and risk of dementia and Alzheimer disease: the Framingham Heart Study. Arch Neurol. 2006 Nov;63(11):1545-50. doi: 10.1001/archneur.63.11.1545. PMID: 17101822.

14. Yuki D, Sugiura Y, Zaima N, Akatsu H, Takei S, Yao I, Maesako M, Kinoshita A, Yamamoto T, Kon R, Sugiyama K, Setou M. DHA-PC and PSD-95 decrease after loss of synaptophysin and before neuronal loss in patients with Alzheimer’s disease. Sci Rep. 2014 Nov 20;4:7130. doi: 10.1038/srep07130. PMID: 25410733; PMCID: PMC5382699.

15. Fairbairn, P., Dyall, S. C., & Tsofliou, F. (2022, Apr 27). The Effects of Multi-Nutrient Formulas containing a Combination of Omega-3 Polyunsaturated Fatty Acids and B vitamins on Cognition in the older adult: A Systematic Review and Meta-analysis. Br J Nutr, 1-42. https://doi.org/10.1017/S0007114522001283

16. Nakazaki E, Mah E, Sanoshy K, Citrolo D, Watanabe F. Citicoline and Memory Function in Healthy Older Adults: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial. J Nutr. 2021 Aug 7;151(8):2153-2160. doi: 10.1093/jn/nxab119. PMID: 33978188; PMCID: PMC8349115.

17. Sommer I, Griebler U, Kien C, Auer S, Klerings I, Hammer R, Holzer P, Gartlehner G. Vitamin D deficiency as a risk factor for dementia: a systematic review and meta-analysis. BMC Geriatr. 2017 Jan 13;17(1):16. doi: 10.1186/s12877-016-0405-0. PMID: 28086755; PMCID: PMC5237198;

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

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

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

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

By Robert H. Lustig, MD, MSL

Most people know that refined sugar is not good for you, but what is it about sugar that’s particularly bad for your brain? Why is it essential, not only for brain health and dementia prevention, to reduce your intake of not only sugar but refined carbohydrates in general? (By refined, I mean those whose fiber has been processed away – not ‘whole’ as in vegetables, whole fruit (not juice), beans, and whole grains.

Let’s start at the extreme. What happens if you lived at the North Pole, and ate virtually no carbohydrates, or at least so little as to force your body and brain to switch to a kind of fuel, ketones, produced from fat? This is often called a “very low carb high fat” (LCHF) or “ketogenic” diet. Would you get sick? This is what Vilhjamur Steffanson did, when his Arctic exploration shipwrecked in 1913, and he was forced to live amongst the Inuit for two years. He noted that there was no diabetes, no cancer — and no Alzheimer’s. In 1928, he and his colleague checked themselves into Bellvue hospital, and ate only meat for one year.[1]They were healthier than the researchers who studied them! 

Your brain likes ketones

Ketones are made in the liver from fat – either breaking down your own fat (for example, if you were fasting, eating very little or exercising a lot), or from ingestion of a type of fat containing ‘medium chain triglycerides’ (MCTs). Coconut oil is approximately 54% MCTs and contains all 4 MCTs (C6, C8, C10, C12), but it turns out that one particular kind of MCT, called C8 because it is 8 carbons long, is the best fat for the liver to convert into ketones. For a deeper look at the evidence, read our guide to ketones and brain health.

You may be surprised to know that your brain can run well on glucose (the kind of sugar that is fuel for our cells), but even better on ketones. The reason is that ketones cross into the brain easily, rapidly, and without a biochemical transporter. This is why children with severe epilepsy improve on a ketogenic diet. Watch this short film ‘Fuel your Brain’.

Brain benefits of a low-carb ketogenic diet

In fact, brain cells prefer ketones. In two studies, one on people with Alzheimer’s and the other on those with pre-dementia or mild cognitive impairment, giving 2 tablespoons of C8 oil (called capricin or caprylic acid triglyceride), brain energy derived from ketones went up by 230% and memory and mental acuity improved in those with Minimal Cognitive Impairment (MCI).[2,3]

A ketogenic diet has been shown to reduce schizophrenia symptoms, help reduce shaking in Parkinson’s, and slow down cognitive decline in those with dementia or pre-dementia. In fact, the ketogenic diet has been used to effectively treat childhood epilepsy for over 100 years! There’s a good review on the current status of the ketogenic diet in psychiatry here^.[4]

Ketogenic diets may help in many ways. Firstly, when a person eats too much carbohydrate, sugar, but especially fructose, damages the energy burning factories in cells, called mitochondria, so their ability to produce chemical energy for the neuron is greatly reduced. Switching to burning ketones instead can increase mitochondria number and function. A recent study also shows that a ketogenic diet has a positive effect on the gut microbiome,[5] and this might be one way the diet helps reduce fits in people with epilepsy.[6] Fructose, on the other hand, disrupts the gut microbiome in a negative way.

How sugar damages your brain

But what is it about a ketogenic diet that is good for your brain? Is it the ketones, the lowering of insulin, the type of fat, the elimination of carbohydrate, or specifically the elimination of sugar? We don’t yet know – I ask this question of every Alzheimer’s and metabolic researcher I know, and no one can tell me – just that it works.

There are a few possible mechanisms. First, the more carbs and sugar you eat, the more resistant you become to the hormone insulin. Insulin not only drives glucose into cells (including brain cells), but also sends excess sugar to the liver to turn into fat. When a person becomes insulin resistant, ironically, glucose transport is negatively impacted, reducing brain energy availability. Insulin resistance is a major driver of depression.[7] A ketogenic diet can reverse that. 

Fructose, which comprises half of sucrose (‘white’ or ‘table’ sugar), and half of ‘high-fructose corn syrup’ (added to numerous processed foods), damages our mitochondria, which leads to less brain energy availability. One study showed that fructose reduces liver mitochondrial function, while glucose stimulates it^.[8]  “The most important takeaway of this study is that high fructose in the diet is bad,” said Dr. C. Ronald Kahn from the Joslin Diabetes Center.  “It’s not bad because it’s more calories, but because it has effects on liver metabolism to make it worse at burning fat. As a result, adding fructose to the diet makes the liver store more fat, and this is bad for the liver and bad for whole body metabolism.”

Fructose is the main sugar in most fruits. People then extrapolate, “oh fruit must be bad for you.” Not true. Whole fruit has fibre (both soluble and insoluble); together they slow down glucose and fructose absorption in the GI tract limiting both liver and brain exposure, and they also help feed the gut bacteria (microbiome), so actually you get less fructose entering the bloodstream. Juicing the fruit removes the protective fiber, and juice has been shown to be just as dangerous to metabolism as is soda. So, eat your fruit — don’t drink it!

Carbohydrates and fructose age your brain

There’s another reason why sugar, and especially fructose, is bad for your brain and body. They produce Advanced Glycation Endpoints or AGEs, which damage the brain. These ‘oxidise’ proteins (so does cigarette smoke), rendering them useless , allowing them to aggregate into clumps, and use up valuable antioxidants in your diet such as vitamin C and E.

Fructose acts on your liver to switch your metabolism away from fat burning to fat making and storing, and inhibits an anti-ageing process called ‘autophagy’ which helps clean up and remove damaged mitochondria in order to regenerate new, healthier cells.

Why sweet foods are so addictive

So far we’ve only explored why sugar is bad for your “physical” brain. Knowing this is a good start. But why does your “emotional” brain keep telling you that you want it? Why do people find it so hard to resist, and so many become sugar addicts? The answer is that fructose activates the “reward system” in the brain. It causes dopamine release, the motivational neurotransmitter associated with ‘reward’. Any chemical that does so can be addictive – cocaine, heroin, alcohol, nicotine, or example. The trouble is the more you have, the more your brain ‘down-regulates’, i.e. becomes less responsive to your own natural feel-good dopamine, so you end up needing more sugar to get the hit and, in the end, you get no hit at all but feel thoroughly awful without it. That’s the Law of Diminishing Returns. That’s addiction.

Blood sugar control reduces dementia risk

Keeping blood glucose levels in the low-normal range is reflected by a low blood glycosylated haemoglobin (HbA1C) level, which means ‘sugar-coated red blood cells’. A low HbA1c is good and is a proxy for improved insulin sensitivity, associated with reduced risk for dementia in several studies.[9,10,11,12,13,14] 

A new study also shows that, in 40 year old adults with so-called normal glucose levels but at the higher end of the normal range, have increased their risk of Alzheimer’s by 15% [37]

Type 2 diabetes, the net result of losing blood sugar control, almost doubles the risk for dementia.[15,16] Diabetes is also associated with more rapid brain shrinkage.[17,18] Even people in the upper normal range of blood glucose have increased brain atrophy, impaired cognition, and increased risk of dementia.[19,20]

For instance, one trial measured HbA1c and glucose levels in several thousand elderly people over the course of almost seven years. In that time, slightly more than a quarter of the participants developed dementia, and the bottom line was that rising glucose levels were associated with increased risk of developing the condition, irrespective of whether the participants also had diabetes. Non-diabetics who experienced a modest increase in blood sugar levels had an 18% increased risk of dementia, as compared to those who already had diabetes at the start of the study or developed it within the trial period, who had a 40% increased risk.[21]

Prevention action – how to cut down your sugar load

In practical terms, preventing dementia today means avoiding sugar as much as possible.  If you’re going to eat carbohydrate, eat ‘whole’ carbohydrate foods such as whole vegetables, fruits (not juice), beans, only wholegrain bread (labelled as ‘100% wholegrain’, or pasta in small quantities. 

Starchy carbohydrates such as pasta, rice and potatoes benefit from being cooked and cooled, then eaten cold or re-heated, as some of the carbohydrate is converted into resistant starch – a type of fibre we can’t digest but which has the added benefit of fermenting and feeding our gut bacteria.

Make sure the carbohydrate comes with its inherent fibre. Oat cakes would be better than bread since the fibre in these foods helps ‘slow release’ the sugars. Eating white bread is associated with a poorer cognitive test performance, whereas high fibre bread is associated with better performance.[34] Eating carbohydrate foods with protein, for example brown rice with fish, or porridge oats with seeds, or fruit with nuts, further reduces the glycemic load (GL) of a meal. The best fruits in this respect are low-sugar high-fiber fruits like berries, cherries, and plums.

These kinds of foods are consistent with a Mediterranean diet which has also been shown to reduce risk.[35] Conversely, grapes, raisins, and bananas are high GL. A study in Finland and Sweden compared those with a healthy versus unhealthy diet, including the above criteria, in mid-life for future risk of developing Alzheimer’s disease and dementia 14 years later. Those who ate the healthiest diet had an 88% decreased risk of developing dementia and a 92% decreased risk of developing Alzheimer’s disease.[36] 

The take-home message is, if you are going to eat complex carbohydrates, eat them with fibre, fat and protein.

However, if you want to go one step further, you can switch to eating a ketogenic low-carb, high fat diet. The problem with the ketogenic diet is staying on it – there’s so much carbohydrate out there it’s hard to avoid it. But there are now breath monitors (e.g. Ketoscan, BioSense from ReadOut Health) that can help you stay in ketosis. A good book to help you explore and put into practice either a low carb ketogenic diet or a low GL diet is ‘The Hybrid Diet’ by Patrick Holford & Jerome Burne. And to understand how processed food is your enemy, take a look at my book ‘Metabolical’.

And if you want to know how sugar is impacting your body and brain then you can take one of our at-home, pin-prick, DRIfT blood test so you can know exactly how sugar is impacting your body and also become a part of our vital research into this area.

Become a Citizen Scientist & Join our Research today!

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

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

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

References:

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3. Croteau E, Castellano C-A, Richard MA, Fortier M, Nugent S, Lepage M, et al. Ketogenic Medium Chain Triglycerides Increase Brain Energy Metabolism in Alzheimer’s Disease. Journal of Alzheimer’s disease: JAD [Internet]. 2018;64(2):551–61. Available from: https://pubmed.ncbi.nlm.nih.gov/29914035/

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12. Hassing Lb, Grant Md, Hofer Sm, Pedersen Nl, Nilsson Se, Berg S, et al. Type 2 diabetes mellitus contributes to cognitive decline in old age: A longitudinal population-based study. Journal of the International Neuropsychological Society. 2004 Jul;10(4):599–607.

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14. Roberts RO, Knopman DS, Cha RH, Mielke MM, Pankratz VS, Boeve BF, et al. Diabetes and Elevated Hemoglobin A1c Levels Are Associated with Brain Hypometabolism but Not Amyloid Accumulation. Journal of Nuclear Medicine. 2014 Mar 20;55(5):759–64.

15. Arvanitakis Z, Wilson RS, Bienias JL, Evans DA, Bennett DA. Diabetes mellitus and risk of Alzheimer disease and decline in cognitive function. Arch Neurol. 2004 May;61(5):661-6. doi: 10.1001/archneur.61.5.661. PMID: 15148141.

16. Yaffe K, Blackwell T, Kanaya AM, Davidowitz N, Barrett-Connor E, Krueger K. Diabetes, impaired fasting glucose, and development of cognitive impairment in older women. Neurology [Internet]. 2004 Aug 24 [cited 2022 Mar 16];63(4):658–63. Available from: https://n.neurology.org/content/63/4/658

17. Tiehuis AM, van der Graaf Y, Visseren FL, Vincken KL, Biessels GJ, Appelman APA, et al. Diabetes Increases Atrophy and Vascular Lesions on Brain MRI in Patients With Symptomatic Arterial Disease. Stroke. 2008 May;39(5):1600–3.

18. Samaras K, Lutgers HL, Kochan NA, Crawford JD, Campbell LV, Wen W, et al. The impact of glucose disorders on cognition and brain volumes in the elderly: the Sydney Memory and Ageing Study. AGE [Internet]. 2014 Jan 9 [cited 2022 Aug 5];36(2):977–93. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4039246/

19. Mortby ME, Janke AL, Anstey KJ, Sachdev PS, Cherbuin N. High “normal” blood glucose is associated with decreased brain volume and cognitive performance in the 60s: the PATH through life study. PLoS One. 2013 Sep 4;8(9):e73697. doi: 10.1371/journal.pone.0073697. PMID: 24023897; PMCID: PMC3762736.

20. Crane PK, Walker R, Hubbard RA, Li G, Nathan DM, Zheng H, Haneuse S, Craft S, Montine TJ, Kahn SE, McCormick W, McCurry SM, Bowen JD, Larson EB. Glucose levels and risk of dementia. N Engl J Med. 2013 Aug 8;369(6):540-8. doi: 10.1056/NEJMoa1215740. Erratum in: N Engl J Med. 2013 Oct 10;369(15):1476. PMID: 23924004; PMCID: PMC3955123.

21. Crane PK, Walker R, Hubbard RA, Li G, Nathan DM, Zheng H, Haneuse S, Craft S, Montine TJ, Kahn SE, McCormick W, McCurry SM, Bowen JD, Larson EB. Glucose levels and risk of dementia. N Engl J Med. 2013 Aug 8;369(6):540-8. doi: 10.1056/NEJMoa1215740. Erratum in: N Engl J Med. 2013 Oct 10;369(15):1476. PMID: 23924004; PMCID: PMC3955123.

22. Luchsinger JA, Tang MX, Shea S, Mayeux R. Hyperinsulinemia and risk of Alzheimer disease. Neurology. 2004 Oct 12;63(7):1187-92. doi: 10.1212/01.wnl.0000140292.04932.87. PMID: 15477536.

23. Abbatecola AM, Paolisso G, Lamponi M, Bandinelli S, Lauretani F, Launer L, Ferrucci L. Insulin resistance and executive dysfunction in older persons. J Am Geriatr Soc. 2004 Oct;52(10):1713-8. doi: 10.1111/j.1532-5415.2004.52466.x. PMID: 15450050.

24. Ye X, Gao X, Scott T, Tucker KL. Habitual sugar intake and cognitive function among middle-aged and older Puerto Ricans without diabetes. Br J Nutr. 2011 Nov;106(9):1423-32. doi: 10.1017/S0007114511001760. Epub 2011 Jun 1. PMID: 21736803; PMCID: PMC4876724.

25. Seetharaman S, Andel R, McEvoy C, Dahl Aslan AK, Finkel D, Pedersen NL. Blood glucose, diet-based glycemic load and cognitive aging among dementia-free older adults. J Gerontol A Biol Sci Med Sci. 2015 Apr;70(4):471-9. doi: 10.1093/gerona/glu135. Epub 2014 Aug 22. PMID: 25149688; PMCID: PMC4447796.

26. Power SE, O’Connor EM, Ross RP, Stanton C, O’Toole PW, Fitzgerald GF, Jeffery IB. Dietary glycaemic load associated with cognitive performance in elderly subjects. Eur J Nutr. 2015 Jun;54(4):557-68. doi: 10.1007/s00394-014-0737-5. Epub 2014 Jul 18. PMID: 25034880.

27. Taylor MK, Sullivan DK, Swerdlow RH, Vidoni ED, Morris JK, Mahnken JD, Burns JM. A high-glycemic diet is associated with cerebral amyloid burden in cognitively normal older adults. Am J Clin Nutr. 2017 Dec;106(6):1463-1470. doi: 10.3945/ajcn.117.162263. Epub 2017 Oct 25. PMID: 29070566; PMCID: PMC5698843.

28. Taylor MK, Sullivan DK, Swerdlow RH, Vidoni ED, Morris JK, Mahnken JD, Burns JM. A high-glycemic diet is associated with cerebral amyloid burden in cognitively normal older adults. Am J Clin Nutr. 2017 Dec;106(6):1463-1470. doi: 10.3945/ajcn.117.162263. Epub 2017 Oct 25. PMID: 29070566; PMCID: PMC5698843.

29. Gentreau M, Raymond M, Chuy V, Samieri C, Féart C, Berticat C, Artero S. High Glycemic Load Is Associated with Cognitive Decline in Apolipoprotein E ε4 Allele Carriers. Nutrients. 2020 Nov 25;12(12):3619. doi: 10.3390/nu12123619. PMID: 33255701; PMCID: PMC7761247.

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31. Lakhan, S.E., Kirchgessner, A. The emerging role of dietary fructose in obesity and cognitive decline. Nutr J 12, 114 (2013). https://doi.org/10.1186/1475-2891-12-114

32. Yau PL, Castro MG, Tagani A, Tsui WH, Convit A. Obesity and metabolic syndrome and functional and structural brain impairments in adolescence. Pediatrics. 2012 Oct;130(4):e856-64. doi: 10.1542/peds.2012-0324. Epub 2012 Sep 3. PMID: 22945407; PMCID: PMC3457620.

33. Mangone A, Yates KF, Sweat V, Joseph A, Convit A. Cognitive functions among predominantly minority urban adolescents with metabolic syndrome. Appl Neuropsychol Child. 2018 Apr-Jun;7(2):157-163. doi: 10.1080/21622965.2017.1284662. Epub 2017 Feb 22. PMID: 28631969.

34. Loef M, Walach H. Fruit, vegetables and prevention of cognitive decline or dementia: a systematic review of cohort studies. J Nutr Health Aging. 2012 Jul;16(7):626-30. doi: 10.1007/s12603-012-0097-x. PMID: 22836704.

35. Martínez-Lapiscina EH, Clavero P, Toledo E, Estruch R, Salas-Salvadó J, San Julián B, Sanchez-Tainta A, Ros E, Valls-Pedret C, Martinez-Gonzalez MÁ. Mediterranean diet improves cognition: the PREDIMED-NAVARRA randomised trial. J Neurol Neurosurg Psychiatry. 2013 Dec;84(12):1318-25. doi: 10.1136/jnnp-2012-304792. Epub 2013 May 13. PMID: 23670794.

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March is caffeine awareness month. Coffee is one of the commonest forms in which caffeine is consumed daily. In the UK alone, it is estimated that nearly 100 million cups of coffee are consumed per day. Despite coffee’s popularity, there remains much conflicting scientific evidence regarding the benefits and potential downsides of drinking coffee, and the impact of caffeine on brain health.

Caffeine is a psychoactive substance, which may increase alertness and arousal, and therefore enhance cognitive performance. Long term coffee consumption across the lifespan has been associated with a decreased risk of developing Alzheimer’s disease and Parkinson’s disease. These findings may be explained by some of the phytochemicals present in coffee, which may exert protective effects. 

Coffee has been indicated to modulate dopamine-mediated responses related to cognition and movement, which may have some preventative and ameliorative effects in Parkinson’s disease.  In Alzheimer’s, coffee has been suggested to decrease the accumulation of beta-amyloid, a key marker of Alzheimer’s, when >2 cups per day were consumed. However, positive results with respect to coffee and Alzheimer’s risk reduction specifically have not been observed consistently across studies, and therefore further research is merited. Additionally, caffeine consumption may disrupt sleep, depending on the time of day that it is consumed. This could theoretically increase risk of Alzheimer’s disease development long term as sleep is essential for the functioning of the glymphatic system, which is involved in beta amyloid clearance. 

Daily consumption of caffeine over 600 mg could have a detrimental impact on the heart-brain axis, via increasing serum homocysteine and cholesterol levels. Furthermore, higher intakes of caffeine have also been suggested to increase anxiety, restlessness and cause gastrointestinal disturbances. 

Caffeine increases levels of dopamine, a neurotransmitter, involved in experiencing pleasure, and also involved in the biology of addiction. Addiction to coffee, and therefore caffeine, is prevalent, and can manifest with a variety of withdrawal symptoms, including headaches, tiredness and irritability. Coffee should therefore be enjoyed in moderation, at no more than 200 mg in one sitting (around 2½ cups of coffee) or 400 mg overall daily (which equates to 5 cups of coffee). 

Current NHS guidelines suggest that no more than 200mg of caffeine should be consumed daily during pregnancy. Notably, the British Medical Journal has recently challenged this view based on findings from observational studies, which suggest that caffeine should be avoided completely whilst trying to conceive and during pregnancy, as it may increase incidences of miscarriage, stillbirth and adverse pregnancy outcomes. 

In conclusion, individuals should moderate their consumption of coffee, and caffeine. If sensitive to the effects of caffeine, trying to become pregnant, or pregnant, individuals should consider caffeine free alternatives to coffee. A further caveat specifically for pregnancy is that some caffeine free herbal teas should only be consumed in small amounts, and some must be avoided completely, in pregnancy, and the advice of a midwife or physician should be sought if needed. 

Our latest blog explores specific nutrients and dietary patterns that are most supportive of female brain health across the lifespan.

Premenstruation

The age at which periods begin varies from female to female. Therefore it is highly beneficial to establish a varied diet from an early age, with a wide range of colourful vegetables and fruits, nuts, seeds, pulses and essential fats from nutritious sources such as oily fish and unprocessed olive and coconut oils. This will help to set the foundations for key nutrients, which will support female hormone health, as well as brain and overall health, across the lifespan.  

Menstruation

Periods normally begin between the ages of 10-16, although they can begin at a younger age, due to genetic and environmental factors. Periods onset may also be delayed to a later age in individuals who have a family history of late-onset periods, are doing large amounts of exercise, experience stress, are underweight, or have an eating disorder or health condition affecting the ovaries. 

Some key nutrients for menstruating women include:

Iron

The average blood loss experienced across a period is estimated to be between 3-5 tbsps of blood, and iron loss may occur at varying degrees depending on heaviness of the period blood flow. It is therefore imperative to ensure iron levels are maintained across a woman’s lifespan. Females with iron deficiency may manifest with symptoms such as pale skin, low energy, failure to thrive, reduced appetite and behavioural and emotional issues. 

Females with iron deficiency may also have higher risk of developing depression and anxiety, because deficiency of iron causes altered levels of serotonin and dopamine. Serotonin and dopamine are two neurotransmitters involved in mood regulation. Furthermore, iron deficiency results in alteration to balances of the neurotransmitters glutamate and GABA, which have an excitatory and calming effect on the nervous system, respectively. Iron status should be monitored and supported through nutrition and, if required, supplementation throughout a woman’s menstrual life. 

Fats 

Consuming fats is essential for female hormone health. Oestrogen and progesterone, hormones involved in the female reproductive system, are synthesised from cholesterol. There has been a focus in the last few decades on cholesterol levels that are too high. However, it is equally important, but perhaps less discussed, to ensure that cholesterol levels do not become too low, as this can impact on female hormone balance. Female adolescents following low fat diets, or diagnosed with an eating disorder, are particularly at risk of experiencing hormonal imbalance, for this reason.  

Women should ensure they are consuming monounsaturated fats, such as avocado and olive oil, and polyunsaturated fats, such as omega-3. Research has demonstrated that omega-3 is involved in modulating mood, memory and cognition. The role of omega-3 in supporting the gut-brain axis is also an important consideration. Omega-3 fats are essential for increasing and maintaining levels of beneficial bacteria in the gut microbiome. Some strains of beneficial gut bacteria are involved in the synthesis of neurotransmitters such as serotonin, dopamine and GABA, which are all involved in modulating mood. This provides one possible explanatory mechanism for why omega-3 may be supportive of mental well being during a woman’s cycle, as low serotonin and dopamine levels have been suggested to be associated with some symptoms of PMS and PMDD. Furthermore, in a recent study women with PMS who were administered omega-3 fatty acids were observed to experience fewer symptoms long term.

Omega-3 fats, in the forms of EPA and DHA, are found in oily fish such as salmon and mackerel, as well as in algae. They are also found in walnuts and flaxseeds, in the form of ALA. However, it should be noted that the body has to convert ALA into DHA and EPA, forms the brain can utilise more readily. This conversion process is not particularly efficient, but recent research has suggested that this conversion pathway can be enhanced by curcumin, which is found in turmeric. Although these findings hold promise for the potential role of curcumin, and possibly other polyphenols, in supporting ALA conversion, further research is required to explore these findings in humans.

Zinc

An emerging area of research is the role of zinc in supporting women’s hormone health. A recent randomised double blinded control trial indicated that women with PMS who were administered zinc sulphate were observed to experience significant improvement to PMS symptom severity and improvement to quality of life. These findings were further supported in a 2020 study on female university students. An additional study demonstrated that zinc supplementation had a significant impact on reducing physical and psychological symptoms of PMS, as well as increasing levels of BDNF (brain derived neurotrophic factor), a key molecule in the brain involved in learning and memory, and reducing oxidative stress, a major trigger for inflammatory processes.

Menopause

Menopause is a normal part of a woman’s natural ageing process. It normally occurs between the ages of 45-55. However, premature menopause affects 1 in 100 women, and may occur due to genetic and environmental factors, including early menarche and heavy alcohol consumption throughout life.

Role of Oestrogen and Homocysteine in Women’s Increased Risk of Cognitive Decline Postmenopausally

The nutrition research and strategies discussed above are of merit to continue throughout menopause due to their role in supporting female hormone health, as well as the gut-brain-axis. A key consideration for menopause and brain health is that women’s risk of developing Alzheimer’s disease increases. One hypothesis is that changes in levels of oestrogen and subsequent impact on the brain’s bioenergetic system may decrease metabolic activity and increase deposit of a key marker of Alzheimer’s disease, beta-amyloid.  Recent research has also indicated that levels of homocysteine, a marker involved in neurological diseases such as Alzheimer’s disease, rise in response to a fall in oestrogen levels during the menopause.

For a deeper look at what happens in the brain as oestrogen, progesterone and testosterone change, read our guide to how female hormones shape brain health.

B Vitamins, Omega-3 and Zinc 

Research has indicated that increasing levels of folate and B12, as well as omega-3, may help to reduce levels of homocysteine. This can be done through increasing consumption of green leafy vegetables (folate), chicken and fish (B12) and oily fish (omega-3), as well as through supplementation of these nutrients (particularly B12 and omega-3 if vegetarian or vegan). Furthermore, recent research has highlighted the key role of zinc in significantly reducing concentrations of homocysteine. This may be due to its synergistic relationship with folate and B12. 

Mediterranean Diet

Following the Mediterranean diet, which involves consuming extra-virgin olive oil, vegetables, fruits, legumes, pulses, nuts and oily fish, may be particularly supportive during menopause. The European Menopause and Andropause Society has also recently proposed the Mediterranean diet as an appropriate dietary pattern post-menopause, as it may help to reduce cognitive decline, cardiovascular and metabolic diseases, which are both risk factors for Alzheimer’s disease. An additional food of note, which can be incorporated into a Mediterranean diet, is flaxseed, which has been specifically shown to support women during and post menopause. This is possibly due to flaxseed’s omega-3 content (ALA), as well as lignan content, which may help to modulate oestrogen levels. 

Manganese

An area of emerging research is manganese levels and menopause. A recent study  indicated that alterations in blood levels of manganese occur before and during menopause. Manganese is a micronutrient required for insulin secretion and blood glucose balance, as well as modulating the body’s endogenous antioxidant systems and thereby reducing oxidative stress, as well as the homeostasis of neurotransmitters such as dopamine, glutamate, and GABA. Further research is required to explore the full mechanisms through which manganese is involved in the menopause, and how altered levels may impact on female brain health.

Notably, many women opt during this stage of life to take hormone replacement therapies (HRT). A recent study published in the British Medical Journal has demonstrated that some types of HRT may increase risk of developing Alzheimer’s disease when used long term. Individuals should consult their doctor before beginning HRT, particularly raising any concerns if they have a family history of Alzheimer’s disease, or exhibiting symptoms of cognitive decline. 

Disclaimer: Always consult your doctor or a qualified healthcare practitioner if you are experiencing any symptoms that concern you, such as unexpected period cessation, heavy blood loss, mood swings or memory loss. Also always consult a qualified healthcare practitioner before beginning any new supplement regimen.

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.

MIND Diet vs Mediterranean Diet: Which Is Better for Brain Health?

If you search for the “best diet for brain health,” you’ll almost always come across the same two names: the Mediterranean diet and the MIND diet. In this article, we’ll explore the MIND Diet vs Mediterranean Diet debate to see how the two really compare. But after a decade of advances in nutritional neuroscience, perhaps that’s no longer the most useful question to ask.

When it comes to diets backed by the strongest evidence for brain or overall health, two consistently stand out: the Mediterranean diet and the MIND diet. Both have genuine scientific credibility. The Mediterranean diet has decades of research behind it, originally focused on cardiovascular health before later demonstrating important cognitive benefits, including a landmark trial showing improved cognitive performance in those following it [1]. The MIND diet was developed later, specifically to reduce cognitive decline by combining elements of the Mediterranean and DASH diets. One of the first large studies, involving almost 1,000 older adults, found that greater adherence was associated with significantly slower cognitive decline [2].

Both are excellent dietary patterns and are backed by a good and growing body of scientific evidence. If you are already eating this way, you are doing something positive for your brain.

But here is the question we can forget to ask.

What if the real opportunity is not choosing between these diets, but building on them?

This is not another article arguing that one diet is superior to the other. The more interesting question is whether either reflects everything we now know about protecting brain health and preventing dementia.

Neither diet was designed around the full body of evidence we have today. They were developed using the best available science at the time, and our understanding of dementia has advanced considerably since then. That does not make either diet wrong. It simply means they have provided an excellent foundation rather than the finished picture.

This is what we are interested in. Rather than forcing people into a specific dietary silo, we want to build on the various dietary strategies with newer evidence from nutritional neuroscience, biomarker research, and lifestyle medicine that has emerged over the past decade.

Before comparing the Mediterranean and MIND diets, it’s worth recognising that they have far more in common than they have differences. A comprehensive review published in 2019 found evidence supporting the Mediterranean, DASH, and MIND diets for better cognitive health [8], reflecting their shared emphasis on vegetables, whole grains, legumes, nuts, and minimally processed foods.

Mediterranean Diet vs MIND Diet: A Detailed Comparison

Although the DASH diet is often included in these comparisons, it largely serves as one of the foundations of the MIND diet rather than a separate competitor. For that reason, the real comparison today is usually between the broader Mediterranean dietary pattern and the more brain-focused MIND diet.

Does the MIND Diet or Mediterranean Diet Offer Greater Brain Protection?

Based on the evidence, probably not.

One of the largest clinical trials to test the MIND diet followed participants for three years, comparing it with another healthy, calorie-reduced diet [4]. Both groups improved, but neither clearly outperformed the other. Rather than suggesting one dietary pattern is superior, the study reminds us that there are many ways to eat well and that healthy diets can have far more in common than they have differences.

The Mediterranean and MIND diets remain two of the best-researched dietary patterns for healthy ageing and brain health. Both are associated with better cognitive outcomes than a typical Western diet, and both provide an excellent foundation for most people.

The real opportunity in the MIND Diet vs Mediterranean Diet debate lies not in choosing between them, but in building on their shared strengths using what we have learned over the last decade.

Two people can follow exactly the same diet and have very different omega-3 levels, homocysteine levels, blood sugar control, and ultimately, different risks of cognitive decline.

Today, we can go beyond general dietary advice. Instead of simply recommending fish, we can assess omega-3 status. Instead of assuming a diet rich in leafy greens provides enough B vitamins, we can measure homocysteine. Instead of relying on diet alone to judge metabolic health, we can monitor HbA1c to identify early insulin resistance. The future of brain health is not choosing between dietary patterns. It is combining healthy eating with objective measures of what your brain actually needs.

A healthy diet does not guarantee optimal nutrition

Both the Mediterranean and MIND diets encourage leafy green vegetables, and with good reason. They are rich in folate, one of the B vitamins needed to help regulate homocysteine, a naturally occurring compound that becomes one of the clearest modifiable risk factors for brain shrinkage and cognitive decline when levels are elevated.

However, following these diets does not guarantee healthy homocysteine levels. Age, genetics, digestion, certain medications, and nutrient absorption all influence homocysteine, meaning two people eating the same diet can have very different results.

This highlights an important principle. Eating whole, unprocessed foods is an excellent and essential starting point, but it cannot tell you whether your nutritional status is optimal. In a randomised controlled trial, B vitamin supplementation slowed brain atrophy in people with elevated homocysteine [5], demonstrating that identifying and correcting nutritional deficiencies can make a measurable difference.

The story becomes even more interesting when we look at omega-3. Research suggests these nutrients work together rather than independently. In one study, B vitamins only slowed brain atrophy in people who already had adequate omega-3 status [6]. Another found the reverse: omega-3 supplementation only improved cognitive outcomes in people with low homocysteine, suggesting adequate B vitamin status is necessary for the brain to fully benefit from omega-3 [7] (read more overview of the interaction between omega-3, B vitamins, and brain health). Elevated homocysteine, which often reflects inadequate functional B vitamin status, is itself an established risk factor for cognitive decline.

The message is not that either diet is lacking. Rather, it is that nutrients interact in complex ways that no dietary pattern alone can predict. You cannot accurately know whether your omega-3 status or homocysteine levels are optimal simply by looking at what’s on your plate.

This is why you need a more personalised approach. Alongside encouraging healthy dietary patterns such as the Mediterranean or MIND diet, or even ketogenic or low-carb diets, we also believe in measuring key biomarkers, including homocysteine and omega-3 status, through the DRIfT® test. By combining dietary advice with specific biomarkers, or through tools like the Cognitive Function Test, it becomes possible to understand what your brain actually needs, rather than relying on assumptions.

Blood sugar matters too

Another thing to reflect on is that neither the Mediterranean nor the MIND diet was designed around blood sugar control as its primary goal. Compared with a typical Western diet, both are a major improvement. Their emphasis on vegetables, legumes, healthy fats, and minimally processed foods naturally supports steadier blood sugar than diets high in refined carbohydrates and ultra-processed foods.

However, neither diet asks an important question: how much carbohydrate is right for you?

Carbohydrate tolerance varies considerably between individuals. Someone who exercises regularly and is metabolically healthy may thrive on a Mediterranean-style pattern. Someone with insulin resistance or pre-diabetes may benefit from a lower-carbohydrate approach, even if the carbohydrates they eat come from healthy sources. Reflecting this, some clinicians are now using lower-carbohydrate and ketogenic diets therapeutically for selected neurological and mental health conditions.

The point is not that everyone should follow a lower-carbohydrate diet. It is that good metabolic health is consistently associated with better cognitive health, and no single dietary pattern is right for everyone. Healthy eating provides the foundation, but measuring markers such as HbA1c allows dietary advice to become far more personalised and useful for prevention.

Why diet alone is not enough for brain health?

Food is one of the most powerful tools we have to support brain health, but it is only one part of the picture.

Research consistently shows that regular physical activity, restorative sleep, social connection, and cognitive stimulation all influence the risk of cognitive decline. No dietary pattern can account for these factors on its own. This is why our COGNITION framework brings together the evidence across multiple areas of brain health, recognising that it is the combination of nutrition, lifestyle, and key health markers, rather than any single intervention, that has the greatest influence on long-term cognitive resilience.

Rather than searching for the single “best” diet, we believe it is more helpful to combine evidence-based nutrition with an understanding of your own biomarkers and lifestyle. This allows recommendations to be tailored to the individual, rather than the dietary label.

MIND diet vs Mediterranean diet: the question that matters more than which diet is best

Instead of asking whether the Mediterranean or MIND diet is better, perhaps the more useful question is:

How many proven brain health habits are part of your routine?

You might eat a Mediterranean diet yet still have elevated homocysteine, low omega-3 status, raised HbA1c, or poor sleep, all of which can influence long-term brain health. Diet is one important lever, but it is not the whole system.

To help people understand their own brain health more completely, we developed the Cognitive Function Test™ alongside the DRIfT® at-home blood test. Together, they assess key biomarkers, lifestyle, and established risk factors, helping identify where the greatest opportunities for improvement lie. They are not diagnostic tools, but they can provide a far clearer picture of your brain health than diet alone ever could.

The Mediterranean and MIND diets remain among the best-researched dietary patterns for healthy ageing and cognitive health. Both also share many principles with the DASH diet, reinforcing that healthy dietary patterns have far more in common than they have differences. But protecting your brain is about more than blindly following a dietary pattern, or worse, getting locked into dietary dogma. It is about understanding your own biology, identifying the risk factors you can change, and taking action before problems develop.

The future of brain health is not choosing the “perfect” diet. It is combining the best of nutritional science with personalised testing and evidence-based lifestyle changes, giving every person the opportunity to understand what their brain needs to stay healthy for decades to come.

Ready to understand your own brain health?

Healthy eating is a great place to start, but understanding your own risk factors allows you to make more informed decisions.

This article is intended for general information only and does not constitute medical advice. It is not a substitute for consultation with a qualified healthcare professional, and anyone with concerns about their cognitive health should seek individual guidance.