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]

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).

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] 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.

Avoid harmful fats

Minimise your intake of fried or processed food and burnt saturated fat on meat, and cheese.
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.

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.

By Patrick Holford

Why Dementia rates are higher in the west

In some countries, for example India and China, that proportion appears to be less than half that occurring in Britain. When people in one country suffer much more from a disease than people of a similar age in another country, this is a sure sign that the difference has something to do with diet, lifestyle or other environmental factors – or genetic variance. We can rule out genetic differences as the major factor, particularly because Chinese and Indian people who emigrate to Britain soon acquire a similar risk for developing dementia. In any event only one in a hundred cases of Alzheimer’s is caused by genes.²

How many people get diagnosed with dementia?

A decline in memory and concentration is not the same thing as a diagnosis of dementia or probable Alzheimer’s, although it does mean your chances of developing these conditions are higher. Every year roughly 10 million people are diagnosed with dementia – that is one person every 3 seconds³ . Currently, around 900,000 people in the UK have dementia.⁴ By 2050 this will be over 1.53 million. Globally over 50 million have dementia. By 2050 this is expected to increase to 152 million.⁵

Two in three people diagnosed with dementia will end up diagnosed with probable Alzheimer’s, while 17 per cent will be given a diagnosis of vascular dementia, caused by constricted blood flow to the brain due to blocked arteries, and 10% will be given a ‘mixed’ diagnosis, which is usually part Alzheimer’s, part vascular dementia. But the risk factors, and prevention treatments, for Alzheimer’s and vascular dementia are the same. So, combined, well over 80% of all dementia diagnoses should be preventable.

What is dementia?

There are other forms, such as dementia with Lewy bodies, fronto-temporal dementia and dementia caused by a stroke, a bleed in the brain or a brain tumour. But as Alzheimer’s is the most widespread, let’s look at it in depth.

Dementia – including Alzheimer’s – is an insidious condition. In the early stages, sufferers have increasing symptoms of absentmindedness, low mood and an inability to learn new things. Judgement, and their ability to function intellectually and socially, begin to go awry. The person may repeatedly forget to turn off the iron, or may not recall which medicines they took in the morning. They may start to show mild personality changes, such as a lack of spontaneity or a sense of apathy and a tendency to withdraw from social interactions.

Later on, there will be a loss of logic and memory, disorientation and poor coordination. Speech deteriorates and paranoia may appear. At this point, a diagnosis of probable Alzheimer’s disease may be given. Why ‘probable’? Because Alzheimer’s is properly diagnosed, not simply by symptoms, but by the presence of a specific kind of degeneration in a specific part of the brain – and this is difficult to see without the aid of expensive scans.

How was Alzheimer’s discovered?

The German neuropathologist Alois Alzheimer discovered this characteristic degeneration in the brain back in 1906. Using a technique known as silver stain, he examined the brain cells of a woman who died prematurely at 55 with signs of dementia, and found a tangled mess of proteins and clusters of degenerating nerve endings, called neurofibrillary tangles. This condition is associated with a gradual dying-off of neurons and poor communication between neurons. There is also often a build-up of something called beta-amyloid plaque, a protein-like substance that shouldn’t be there.

Since that time, research into Alzheimer’s has continued apace. Largely thanks to the pioneering work of Professor David Smith and colleagues in the University of Oxford’s pharmacology department, we now know that Alzheimer’s is a specific disease process, not just a random, gradual decline in brain cells, and that it originates in a particular brain region. Their Optima (Oxford Project to Investigate Memory and Ageing) study has been running since 1988 and has proved, among other things, that the damage leading to Alzheimer’s begins in a central part of the brain known as the medial temporal lobe.^6-7

Pinpointing the problem area

The medial temporal lobe is vital for both mood and memory. Even though this lobe accounts for only 2 per cent of the brain’s total area, it is essential for the processing of everything we sense, feel or think.

Precisely because it’s in the middle of the head, it’s a difficult region to scan. This is also where there are more neurofibrillary tangles and beta-amyloid plaques – the hallmarks of Alzheimer’s. These indicate damage and chaos to the normal network of neurons and their connections.

Since information is passed from and to the medial temporal lobe from other parts of the brain, as this area becomes more damaged, fewer signals are sent to other parts of the brain. These then also start to decline, becoming more and more disconnected, with ever-decreasing blood flow. The beginning of damage is estimated to occur as early as 40 years before a person is diagnosed with dementia. That is why it is important to start your prevention plan young.

So far we’ve talked about the spread of damage seen in Alzheimer’s, starting with the medial temporal lobe, and radiating out to other areas of the brain, which are in effect starved of signals, much as a muscle atrophies through lack of use. Other indicators of Alzheimer’s are neurofibrillary tangles (p’tau), the lack of blood flow in the brain, and the presence of beta-amyloid plaques. There is also the presence of high levels of homocysteine in the blood.

Exactly which of these factors ‘causes’ Alzheimer’s, or kickstarts the process of damage, is the subject of much debate and ongoing research.

Clues to curbing the epidemic

At the other end of the spectrum, scientists have been looking for ways to prevent Alzheimer’s disease, and are conducting more and more studies revealing the specific dietary and lifestyle factors that greatly increase or decrease risk. Around half of the risk can be prevented.⁸For example, having a high intake of omega-3 fats and B vitamins appears to reduce risk, while consuming a lot of sugar increases the risk. The National Institutes of Health attributes 22% of Alzheimer’s to high homocysteine and 22% to low omega-3/seafood consumption.⁹ What’s more people with pre-dementia with good omega-3 status, given extra B vitamins have a 73% less brain shrinkage than those on placebo.¹⁰

Somewhere in the middle, scientists are discovering how changes in diet could cause changes in the brain. An example of this is the discovery of an enzyme that both regulates insulin – the key hormone for keeping your blood sugar in balance – and beta-amyloid.  There are, however, many other ways, and growing evidence, that sugar and high carb diet driven by eating junk food damages the brain.

The most exciting discovery is the role of B vitamins and how too little can lead to increases in homocysteine in the blood. Since neither beta-amyloid nor those neurofibrillary tangles can be measured before its too late, the discovery that levels of a simple chemical in your blood could be the best predictor of all is the most welcome news – and it should, in our opinion, have revolutionised the early diagnosis and preventative treatment of those most likely to develop Alzheimer’s. There is good evidence that homocysteine, a measure of faulty methylation, is a primary driver of Alzheimer’s for a number of reasons:

Giving people with raised homocysteine and pre-dementia (mild cognitive impairment or MCI) extra homocysteine lowering B vitamins has been shown to reduce the rate of shrinkage of the medial temporal regions by nine fold.
Amyloid blocking drugs have little to marginal effects on the actual disease. A meta-analysis of these drugs that did effectively lower amyloid found virtual no significant cognitive benefit from doing so.¹¹ Measures of Clinical Dementia Ratings show that both homocysteine-lowering B vitamins and Omega-3 fish oil supplements surpass anti-amyloid drugs. (See our newsletter)
The formation of neurofibrillary tangles, associated with p-tau proteins, could be a consequence of faulty methylation (eg raised homocysteine). When p-tau is high so is homocysteine. There are three known ways whereby raised homocysteine would raise p-tau.
Homocysteine is found in the regions of brain damage and is capable itself of causing brain damage.
A raised homocysteine increases the risk of cerebral vascular dysfunction by a remarkable 17 times.¹¹
Every study that has effectively lowered homocysteine in people at risk, eg with MCI or mild Alzheimer’s, has shown benefit, except in the later stages of the disease which may just be too late.

An International Consensus Statement in 2018 concluded that moderately raised plasma total homocysteine (>11mcmol/L), found in half of those over age 70 ¹², is a main cause of age-related cognitive decline and dementia.¹³ Two major meta-analyses of hundreds of studies conclude that raised homocysteine is one of the best evidenced risk factors for AD and accounts for around a fifth of all risk ¹⁴, ¹⁵.

The key to prevention is to understand the contributing factors and to do something about them as soon as possible. Right now, because the thought of Alzheimer’s is so terrifying, most people avoid even seeing their doctor and are usually diagnosed only in the late stages, usually reported by a relative who has found their partner becoming unmanageable. That’s why it is critical to look for the earliest possible signs of cognitive decline, then there’s time to reverse the trend.

The Cognitive Function Test

The Food for the Brain Foundation offer an excellent free online Cognitive Function test and a simple Dementia Risk Index questionnaire which also works out your risk factors and which simple changes will have the most effect. Do please do this yourself and encourage everyone you know over 50 to do the test as well. Prevention, in this case, is the only likely ‘cure’ for this terrible disease.

For more on Alzheimer’s see our article on Preventing Alzheimer’s Disease

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

Rowe J., Kahn R., ‘Human ageing: usual and successful’, Science, 237 (4811): 143-9 (1987).
 Bekris, L et al., ‘Genetics of Alzheimer disease’ Journal of Geriatric Psychiatry and Neurology 2010, 23(4) 213-227).
Smith A.D., ‘Homocysteine, B vitamins and cognitive deficit in the elderly’, American Journal of Clinical Nutrition, 75:785-6 (2002).
https://www.alzheimers.org.uk/about-us/policy-and-influencing/dementia-scale-impact-numbers
World Alzheimer Report. (2018). Available online at: https://www.alzint.org/resource/world-alzheimer-report-2018
Bradley K.M. et al., ‘Cerebral perfusion SPET correlated with Braak pathological stage in Alzheimer’s disease’, Brain, 125:1772-81 (2002); see alsp Jobst K.A. et al., ‘Detection in life of confirmed Alzheimer’s disease using a simple measurement of medial temporal lobe atrophy by computed tomography’, Lancet, 340:1179-83 (1992).
Jobst K.A. et al., ‘Association of atrophy of the medial temporal lobe with reduced blood flow in the posterior parietotemporal cortex in patients with a clinical and pathological diagnosis of Alzheimer’s disease’, J Neurol  Neurosurg Psychiat, 55:190-4 (1992); see also Jobst K.A. et al., ‘Rapidly progressing atrophy of medial temporal lobe in Alzheimer’s disease’, Lancet, 343:829-30 (1994).
Smith,D., Jaffe,K. ‘Dementia (Including Alzheimer’s Disease)can be Prevented: Statement Supported by International Experts’ Journal of Alzheimer’s Disease 38 (2014) 699–703
M. Beydoun et al, ‘Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis BMC Public Health 2014, 14:64 [http://www.biomedcentral.com/1471-2458/14/643]
Jernerén F, Elshorbagy AK, Oulhaj A, Smith SM, Refsum H, Smith AD. Brain atrophy in cognitively impaired elderly: the importance of long-chain ω-3 fatty acids and B vitamin status in a randomized controlled trial. American Journal of Clinical Nutrition. 2015;102:215-21.
Teng Z, Feng J, Liu R, Ji Y, Xu J, Jiang X, Chen H, Dong Y, Meng N, Xiao Y, Xie X, Lv P. Cerebral small vessel disease mediates the association between homocysteine and cognitive function. Front Aging Neurosci. 2022 Jul 15;14:868777. doi: 10.3389/fnagi.2022.868777. PMID: 35912072; PMCID: PMC9335204.
Smith AD Effect of reductions in amyloid levels on cognitive change in randomized trials: instrumental variable meta-analysis BMJ 2021;372:n156
Smith AD, Smith SM, de Jager CA, Whitbread P, Johnston C, Agacinski G, et al. Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment. A randomized controlled trial. PLoS ONE. 2010; 5: e12244.
Smith AD, Refsum H, Bottiglieri T, Fenech M, Hooshmand B, McCaddon A, et al. Homocysteine and dementia: An international consensus statement. J Alzheimers Dis. 2018; 62: 561-70
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; 14: 643.
Yu JT, Xu W, Tan CC, Andrieu S, Suckling J, Evangelou E, et al. 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; 91: 1201-9

By Patrick Holford

A global conference of leading world experts in dementia prevention has today identified four easy ways that could reduce risk of dementia by half and eight that could cut your risk by two thirds. 

The research was shared, for the first time, at the Alzheimer’s Prevention Conference, organised by the charitable foundation Food for the Brain. 

The new research showed that there are four easy ways to cut your risk of dementia in half:

1. Supplementing omega-3 fish oils

According to a new study of almost half a million participants of the UK’s Biobank supplementing fish oils cuts dementia risk.^[i] This new research was presented at the conference by China’s leading dementia prevention expert from Shanghai’s Fudan University, Professor Jin-Tai Yu, “Our current research, using data from the UK Bio Bank, shows that having a higher blood levels of omega-3, and supplementing fish oils, is associated with less risk of dementia.”

Other studies reported by Dr Simon Dyall, clinical neuroscientist at the University of Roehampton, showed that a higher intake of fish was associated with cutting risk of Alzheimer’s disease by a third.^[ii] “Half your brain is fat, and a type of omega- 3 called DHA has a very important role in the communication between brain cells.” said Dyall.

2. B Vitamins

According to Professor Yu, another very promising prevention treatment is B vitamins.^[i] “Lowering blood homocysteine levels, an established indicator of Alzheimer’s risk, with B vitamins is a most promising treatment.” Raised homocysteine is found in one in two people over 70.

In a trial at Oxford University by Professor David Smith, who was presenting at the conference, giving high dose B vitamins versus placebos, resulted in 52% less brain shrinkage and little further memory loss.^[ii]

Combining omega-3 and vitamin B. The discovery of the synergistic role of omega-3 led the Oxford Professor to reanalyse blood samples taken at the start of the trial for omega-3. They found that those with low omega-3 DHA blood levels, one of the main nutrients found in fish and fish oil supplements, had no benefit from the B vitamins, while those with high omega-3 DHA had 73% less shrinkage and almost nine times less shrinkage of the Alzheimer’s related areas of the brain.^[iii]

Furthermore, another study in Sweden, that had given omega-3 fish oil supplements, reanalysed their results and found those with good B vitamin status substantially reduced their dementia risk.^[iv]

A third study in the US, called ‘B proof’, that had given B vitamins with marginal improvements, reanalysed their results and found that those with higher omega-3 levels also had a much greater improvement.^[i]

“Research shows that you get impressive results if you give omega-3 and B vitamins together rather than on their own.” Says Professor Smith. 

While US National Institutes of Health researchers attributed 22% to lack of seafood or omega-3 and another 22% to the B vitamin factor they also attributed 32% of risk to inactive lifestyle.^[ii]

3. Exercise

“For many people the worst thing they can do for their brain is to retire”

Keeping your brain active. Another expert at the conference, Tommy Wood, Assistant Professor at the University of Washington, showed that your muscle mass predicts brain volume. “Exercise, especially resistance exercise, is important because it makes the brain do things that keep it healthy, such as growth and repair.” he says. “When they aren’t stimulated, the health of brain tissues deteriorates, with a knock-on effect on memory and thinking.”

And it’s not just physical exercise that does this, we also benefit from the mental exercise involved in activities like solving puzzles or learning a new language. “For many people the worst thing they can do for their brain is to retire”, says Wood. “They lose much of the stimulation that kept it healthy.” 

4. Sugar

“Sugar levels at age 35 predict Alzheimer’s risk later in life”

While it has long been known that diabetics have a much higher risk for dementia, a recent study at Boston University School of Medicine, found that higher blood sugar levels at age 35, but still in the ‘normal’ non-diabetic range, predict Alzheimer’s later in life.^[i] Talking at the conference Professor Robert Lustig, from the University of California, said, ”A high level of sugar and insulin in the blood – linked with a high carbohydrate diet – is definitely a driver for Alzheimer’s.” 

The conference, hosted by the UK charity foodforthebrain.org, identified eight domains of risk, in other words, four more actions you can take to reduce your risk of dementia: eating antioxidants from fruit and veg; having a healthy gut; sleeping well; and controlling stress. 

Targeting all eight risk factors earlier in life may reduce risk by two thirds. 

But how do you know what your risk is and what and how to change to reduce your risk? That’s what the charity, the Food for the Brain Foundation has been working on for a decade. On their website, foodforthebrain.org, you can do a free Cognitive Function Test. Almost 380,000 people have taken the test and, according to research by NHS and University College London researchers, 88% find it useful. You then complete a questionnaire that works out your future dementia risk index. It also tells you exactly what’s driving your risk up and what to do about it. By downloading the COGNITION app you can tack your progress, get advice on how to reduce your risk further, and get support to help you dementia-proof your diet and lifestyle.

Do the test now and reduce your risk!

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 bybecoming a Friend of Food for the Brain.

References:

^[1] Yu JT et al, Circulating polyunsaturated fatty acids, fish oil supplementation, and risk of incident dementia: a prospective cohort study of 440,750 participants, BMC medicine (pending publication)

^[2] Wu S, Ding Y, Wu F, Li R, Hou J, Mao P. Omega-3 fatty acids intake and risks of dementia and Alzheimer’s disease: a meta-analysis. Neurosci Biobehav Rev. 2015 Jan;48:1-9. doi: 10.1016/j.neubiorev.2014.11.008. Epub 2014 Nov 21. PMID: 25446949.

^[3] 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.

^[4] Smith, A.D. et al., ‘Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment: a randomized controlled trial’, Public Library of Science ONE, 5(9) (2010)

^[5] Jernerén F, Elshorbagy AK, Oulhaj A, Smith SM, Refsum H, Smith AD (2015). Brain atrophy in cognitively impaired elderly: the importance of long-chain ω-3 fatty acids and B vitamin status in a randomized controlled trial. Am J Clin Nutr. 2015 Jul;102(1):215-21

^[6] Jernerén F, Cederholm T, Refsum H, Smith AD, Turner C, Palmblad J, Eriksdotter M, Hjorth E, Faxen-Irving G, Wahlund LO, Schultzberg M, Basun H, Freund-Levi Y. Homocysteine Status Modifies the Treatment Effect of Omega-3 Fatty Acids on Cognition in a Randomized Clinical Trial in Mild to Moderate Alzheimer’s Disease: The OmegAD Study. J Alzheimers Dis. 2019;69(1):189-197. doi: 10.3233/JAD-181148. PMID: 30958356.

^[7] van Soest, A.P.M., van de Rest, O., Witkamp, R.F. et al. DHA status influences effects of B-vitamin supplementation on cognitive ageing: a post-hoc analysis of the B-proof trial. Eur J Nutr (2022). https://doi.org/10.1007/s00394-022-02924-w

^[8] 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.

^[9] 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 . doi: 10.1002/alz.12641. Epub ahead of print. PMID: 35319157.

Date: 15th November 2022 
Time: 6:30pm to 7:30pm

How to help children focus, stay engaged and accelerate learning with a clear mind and good mood. Dr Alex Richardson is a world-renowned researcher, educator, speaker and published author; and Founder Director of the UK-based charity, Food and Behaviour (FAB) Research.

In this webinar you will learn:

How to optimise your child’s focus and attention
Support emotional stability
Build brain connections

Live Q&A with Dr Alex Richardson

Live viewers will be able to participate in a 15 minute Live Q&A with Dr Alex Richardson. You can submit your questions in advance or during the webinar to be answered at the end.

Your Recording to Watch at Your Leisure

All ticket holders will receive a recording of the webinar the following day, so you can watch again or for the first time if you are unable to attend on the day.

Tickets

Tickets are £10.00.

Please purchase your tickets here:

About Dr Alex Richardson, Founder Director @Food and Behaviour (FAB) Research

Alex is internationally known for her pioneering research into the role of nutrition (especially dietary fats) on brain development and function, and its implications for ADHD and related conditions affecting behaviour, learning and mood. Her academic publications include experimental, epidemiological, genetic and brain imaging studies; the first controlled treatment trials investigating effects of omega-3 (and omega-6) fatty acids in ADHD, dyslexia, dyspraxia and related conditions; and the earliest case reports of potential benefits from similar nutritional interventions for depression and schizophrenia. Alex is also a highly experienced teacher and speaker for public and professional as well as academic audiences, and a frequent contributor for the media. Her book for parents and professionals – ‘They Are What You Feed Them’ – is dedicated to FAB Research, the charity she founded to raise awareness of the links between diet and mental health, wellbeing and performance.

Online Event

By Patrick Holford

After 40 failed trials for drugs injecting anti-amyloid antibodies (AAAs) one, Lecanemab^[i], has finally shown a modest benefit on cognitive function in those with early-stage Alzheimer’s. But they come with a terrible cost – adverse effects that include brain swelling and haemorrage which occurred in one in five trial participants.. When a similar drug, Aducanumab, was conditionally approved by the US FDA last year, despite nine out of ten of their experts voting against it, many resigned in protest^[ii]. Yet the pressure on pharma to get an amyloid drug to market, having spent over $42 billion^[iii], is immense.

Let’s consider the alternative 

Prevention with simple, doable changes to diet, lifestyle and supplementation with B vitamins and omega-3 fish oils.

The two most relevant measures of success of any treatment are reduction in the rate of brain shrinkage and a reduction in clinical dementia symptoms which lead to a diagnosis.

In relation to brain shrinkage the best AAAs have achieved is 2% less brain shrinkage. In a landmark trial by Professor David Smith and colleagues at the University of Oxford, B vitamin supplements, given to those with pre-dementia (mild cognitive impairment) have achieved a reduction in the rate of brain shrinkage of 52%, up to 73% in those with sufficient omega-3.^[i] This effect was shown in those with raised blood levels of homocysteine, a marker for B vitamin status that is raised in approximately half of pre-dementia patients and many more with Alzheimer’s. We now know that B vitamins need omega-3 to make the biggest difference, and vice versa.^[ii]

Figure 1. Reduction in brain shrinkage B vitamins and omega 3 vs AAAs. Sources: Jernerén F, Elshorbagy AK, Oulhaj A, et al. Am J Clin Nutr. 2015 Jul;102(1):215-21;  Schwarz AJ, Sundell KL, Charil A, et al. Alzheimers Dement (N Y). 2019 Jul 30;5:328-337; Smith AD, Smith SM, de Jager CA, et al. PLoS One. 2010;5(9):e12244.

Clinical Dementia Rating (CDR) with B vitamins and Omega 3’s

What about actual clinical improvement, called Clinical Dementia Rating (CDR), which is what counts for the person concerned? A CDR score of zero means no clinically significant cognitive impairment. In the Oxford trial on B vitamins  65% of participants on B vitamins with higher omega-DHA status ended the 2 year trial with a clinical dementia rating of zero compared with 25% receiving placebo.^[i] It was more than twice as effective as the recent drug. In a Swedish omega-3 trial those with sufficient B vitamin status, also had a marked reduction in clinical dementia rating, which was reduced by 1.5 points compared with placebo after 6 month’s treatment with omega-3.^[ii] The improvement in clinical dementia rating reported for Lecanemab, which was a modest 0.45 point reduction. This was marginally better than a 0.39 difference for Aducanumab, compared to placebo.^[iii] [iv] In other words, no AAA drug has even reduced  a CDR score by 1 point but both B vitamins and omega-3 have.

Figure 2. Comparison of Clinical Dementia Rating (CDR) reduction between synergistic B vitamin/Omega-3 supplementation and two AAA drugs. Sources: Oulhaj A, Jernerén F, Refsum H, et al. J Alzheimers Dis. 2016;50(2):547-57; Eisai press release; Tampi RR, Forester BP, Agronin M. Drugs Context. 2021 Oct 4;10:2021-7-3; Jernerén F, Cederholm T, Refsum H, et al. J Alzheimers Dis. 2019;69(1):189-197.

A trial in Holland, called B-proof, which had shown no significant effects overall in those supplementing B vitamins, recently reported that those with higher Omega-3 levels had a significant improvement in cognitive function. A French^[i] and Chinese study^[ii] reported a similar finding – the combination of B vitamins and omega-3 shows clear improvements in cognitive function – better than achieved by AAA drugs, without adverse effects.

So, on all three counts – brain shrinkage, cognitive function and clinical dementia rating – B vitamins plus omega-3 – wins out at a fraction of the cost since nutrients cannot be patented which is the requirement for the scale of profitability required by pharma.

Blood Sugar Levels and their impact

But, there’s two other points to make. Firstly, B vitamin and omega-3 status are but two of eight known actions that reduce risk or improve these critical criteria. Others are sugar, antioxidant rich fruit and veg, vitamin D, exercise, cognitive stimulation, gut health, sleep and stress.^[i] Having a high blood sugar level from age 35 predicts Alzheimer’s risk.^[ii] Being diabetic or having high insulin levels, which is a consequence of eating too many refined sugar and carbs, doubles risk.^[iii] Having a high carb intake is associated with increasing amyloid plaques in the brain – so why not tackle the upstream cause? One study reported that “Those who ate the healthiest diet had an 88% decreased risk of developing dementia and a 92% decreased risk of developing Alzheimer’s disease.”^[iv] Increasing lean muscle mass with resistance exercise is associated with better cognitive function and brain volume.^[v] The charity foodforthebrain.org have a free, validated online Cognitive Function Test, followed by a Dementia Risk Index questionnaire, that not only measures your cognitive function, but also shows you exactly what your risk is and how to reduce it by targeting your ‘weakest links’ in these eight known prevention steps.

Then, there’s the issue of side-effects. For each of these prevention steps there are none. Or rather, there are plenty – less risk for diabetes, heart disease, arthritis, premature ageing, better energy, sleep and weight control to name a few.

For the AAA drugs the side-effects are potentially devasting. Since one in five can be expected to experience brain swelling and microbleeds, regular brain scans will be necessary to monitor for these frequent complications. Is it right to expose an older person with cognitive decline to this scale of risk and medical intervention for such a modest benefit? The annual cost of treatment is expected to be above $10,000 but that doesn’t include the cost of medical monitoring or the cost of treatment when things go wrong. The cost benefit equation just doesn’t add up.

Early Intervention

Writing in the Financial Times last year Professor Smith says “ Your editorial is correct in saying ‘A resurrection of the amyloid approach must not divert resources and attention away from other ways to tackle dementia, which are in earlier stages of research and might give better results.’ These alternative approaches include identifying and then treating modifiable risk factors for dementia, of which about a dozen are already known. These account for about half of the cases of Alzheimer’s disease .” The high price proposed for the drug is disturbing, especially when a very much cheaper alternative treatment is available: high-doses of B vitamins and omega-3 from seafood or supplements. He estimates that early intervention , targeting all the prevention steps recommended by the Food for the Brain Foundation could cut a person’s risk by two thirds. 

For more details on Alzheimer’s prevention visit: https://smartkidsandteens.foodforthebrain.org/preventing-alzheimers-disease/

Alzheimer’s Is Preventable – LEARN more now

WE currently have 2 events on sale so that you can take a deep dive on this topic:
⭐️ MASTERCLASS – 4 hour conference with world leading experts on Alzheimer’s – Practitioner level. Book tickets here: https://smartkidsandteens.foodforthebrain.org/aipmasterclass/

🧠 Upgrade Your Brain – 8 steps to reduce your Alzheimer’s risk with with Patrick Holford – A condensed version of the masterclass that is 90 minutes long and aimed at the general public. Book your tickets here: https://www.eventbrite.co.uk/e/upgrade-your-brain-tickets-415953948457

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:

^[1] Oulhaj A, Jernerén F, Refsum H, Smith AD, de Jager CA. Omega-3 Fatty Acid Status Enhances the Prevention of Cognitive Decline by B Vitamins in Mild Cognitive Impairment. J Alzheimers Dis. 2016;50(2):547-57. doi: 10.3233/JAD-150777. PMID: 26757190; PMCID: PMC4927899.

^[2]  Jernerén F, Cederholm T, Refsum H, Smith AD, Turner C, Palmblad J, Eriksdotter M, Hjorth E, Faxen-Irving G, Wahlund LO, Schultzberg M, Basun H, Freund-Levi Y. Homocysteine Status Modifies the Treatment Effect of Omega-3 Fatty Acids on Cognition in a Randomized Clinical Trial in Mild to Moderate Alzheimer’s Disease: The OmegAD Study. J Alzheimers Dis. 2019;69(1):189-197. doi: 10.3233/JAD-181148. PMID: 30958356.

^[3] Cummings JL, Goldman DP, Simmons-Stern NR, Ponton E. The costs of developing treatments for Alzheimer’s disease: A retrospective exploration. Alzheimers Dement. 2022 Mar;18(3):469-477. doi: 10.1002/alz.12450. Epub 2021 Sep 28. PMID: 34581499; PMCID: PMC8940715.

^[4] Jernerén F, Elshorbagy AK, Oulhaj A, Smith SM, Refsum H, Smith AD (2015). Brain atrophy in cognitively impaired elderly: the importance of long-chain ω-3 fatty acids and B vitamin status in a randomized controlled trial. Am J Clin Nutr. 2015 Jul;102(1):215-21

^[5] https://smartkidsandteens.foodforthebrain.org/campaigns/alzheimers-prevention/omega-3-and-b-vitamins/

^[6] Oulhaj A, Jernerén F, Refsum H, Smith AD, de Jager CA. Omega-3 Fatty Acid Status Enhances the Prevention of Cognitive Decline by B Vitamins in Mild Cognitive Impairment. J Alzheimers Dis. 2016;50(2):547-57. doi: 10.3233/JAD-150777. PMID: 26757190; PMCID: PMC4927899.

^[7] Jernerén F, Cederholm T, Refsum H, Smith AD, Turner C, Palmblad J, Eriksdotter M, Hjorth E, Faxen-Irving G, Wahlund LO, Schultzberg M, Basun H, Freund-Levi Y. Homocysteine Status Modifies the Treatment Effect of Omega-3 Fatty Acids on Cognition in a Randomized Clinical Trial in Mild to Moderate Alzheimer’s Disease: The OmegAD Study. J Alzheimers Dis. 2019;69(1):189-197. doi: 10.3233/JAD-181148. PMID: 30958356.

^[8] https://www.fiercepharma.com/pharma/eisai-and-biogen-need-meet-cms-halfway-after-lecanemabs-alzheimers-clinical-trial-win

^[9] Awaiting actual Lecanemab, trial – see press release ref 1 above

^[10] Maltais M, de Souto Barreto P, Bowman GL, Smith AD, Cantet C, Andrieu S, Rolland Y. Omega-3 Supplementation for the Prevention of Cognitive Decline in Older Adults: Does It Depend on Homocysteine Levels? J Nutr Health Aging. 2022;26(6):615-620. doi: 10.1007/s12603-022-1809-5. PMID: 35718871.

^[11] Li M, Li W, Gao Y, Chen Y, Bai D, Weng J, Du Y, Ma F, Wang X, Liu H, Huang G. Effect of folic acid combined with docosahexaenoic acid intervention on mild cognitive impairment in elderly: a randomized double-blind, placebo-controlled trial. Eur J Nutr. 2021 Jun;60(4):1795-1808. doi: 10.1007/s00394-020-02373-3. Epub 2020 Aug 28. PMID: 32856190.

^[12] https://smartkidsandteens.foodforthebrain.org/8-ways-to-upgrade-your-brain/

^[13] 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.

^[14] https://smartkidsandteens.foodforthebrain.org/is-sugar-killing-your-brain/

^[15] 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.

^[16] https://smartkidsandteens.foodforthebrain.org/exercise-and-keep-physically-active/

By Patrick Holford

What makes us humans so different to other apes is our larger brain, especially the cortex. It is three times larger than a chimpanzee. How did this happen? How did Homo Sapiens evolve our level of intelligence despite sharing almost the same genes? 

The brain’s origin, for all species, is from the ocean. It had to be as that is where life began. Millions of years ago the rudimentary eye cell, dinoflagellate, which is a type or marine phytoplankton, used a specific fat – the omega-3 fat docosahexanoic acid (DHA) – to convert solar photon energy into the first nerve impulse or twitch – a twitch towards food. That is the origin of the nervous system and brain.

Back in the ‘80’s, when zoologist Professor Michael Crawford analysed the types of fat in different animal’s organs and muscles they varied according to their dietary environment, except the brain. He discovered that the brain is always rich in DHA. The more DHA the brighter the animal, with the sea mammals and us humans having exceptionally high levels.

Recently it has been proven that DHA (docosahexanoic acid) has a unique structure involving six double bonds, arranged in a horseshoe shape, which actually makes it a semi-conductor with unique electrical properties. Its close cousins, ALA (alpha linolenic acid) in chia or flax, and EPA (eicosapentanoic acid) don’t have this potential. It’s all about DHA. While some EPA converts into DHA less than 1 per cent of ALA in plant-based sources of omega-3 such as chia seeds converts to DHA, the richest source of which is marine-based food from rivers and the sea.

Over 6 million years ago our hominid ancestors split from other apes (chimps, gorillas and bonobos), culminating in Homo Sapiens around 100,000 years ago. It clearly wasn’t genes that made us different. We share 98.5% of the same genome. It had to be the environment our ancestors exploited. During this time brain size steadily increased up to 1.45kg 10,000 years ago, roughly three times the size of a chimpanzee, at 384g.

Homo Aquaticus

We have over twenty profound anatomical, physiological and biochemical differences apart from our vastly different psychological advancement as in intelligence and language. More than anything, it is this, illustrated by our brain size, that makes us different. But, before looking closely at the circumstances, and diet, that almost certainly drove our gain in brain size and intelligence, let’s take a look at the fundamental differences we have. These have been so clearly delineated in an excellent book, The Waterside Ape, by Peter Rhys-Evans, and ear, nose and throat surgeon. He explores why we:

Stand upright
Have (virtually) no body hair
Have a layer of sub-cutaneous fat
A waxy, waterproof layer, the vernix, at birth
A diving reflex at birth, meaning we are able to swim before we can walk, and hold our breath underwater
A descended larynx, a precursor of being able to have complex language/speaking
Enlarged sinus cavities
A nose shape that is good for keeping the water out while swimming
Ears that actually form a protective boney protusion in those who spend a lot of time diving
Different kidneys, in how they filter salt and water 
Manual dexterity
Crinkly fingers when in water for a few minutes

Of course, the story we’ve all been told is that we came out of the trees, into the savannah and stood upright for better hunting. Anyone who has been on safari will know that a) you don’t stand a chance catching anything by standing upright – you crawl; and b) all the good hunters can sprint much faster than man (lion 80kph, leopard 60kph, cheetah 100kph, man under 30kph) precisely because four legs are better than two. But, can you explain any one of these other changes, let alone our increase in intelligence, by moving from the trees into the savannah for hunting? If so, how did we suddenly develop manual dexterity, tools and spears overnight to even survive? Also, why do certain ‘sea nomad’ tribes exist, such as the Moken and Bajou, who can hold their breath for up to 10 minutes under water, spending up to five hours a day in the sea, giving birth in the sea? Their spleen is adapted to oxygenate tissue, as it is in dolphins, to enable long dives. Where did that evolutionary adaptation come from?

The only logical explanation that I have encountered, which eloquently fits all these adaptations, in that our hominid ancestors exploited the waterside – wetlands, swamplands, rivers, estuaries and coasts. In the process of so doing, became upright, and started to eat a diet high in marine foods, providing the essential nutrients for brain development, that is omega-3 DHA, phospholipids, plus vitamin B12, iodine, and all those other essential elements from magnesium to selenium. From this perspective let’s briefly examine all the changes listed above, between us and other apes:

Stand upright – better for wading in water, so gradually our anatomy adapts but, even so, we are prone to the problems of uprightness, eg hips and knees because it is  anatomically inferior to walk on all fours, with better weight distribution.
Have (virtually) no body hair and a layer of sub-cutaneous fat – consistent with semi-aquatic mammals better for floating and insulation
A waxy, waterproof layer, the vernix, at birth – found in no land mammals, only other semi-aquatic mammals such as seals and chemically identical
A diving reflex at birth, meaning we are able to swim before we can walk, and hold our breath underwater
A descended larynx, a precursor of being able to have complex language/speaking – being upright, and diving, could have led to this vital adaptation. This, by the way, only occurs after a year or so, before which a baby’s language cannot develop the complexity of sounds and voice control only we have
Enlarged sinus cavities, which help to keep the head above water, but still have drainage holes in the ‘wrong’ place, eg good if on all fours but bad if upright, which is why we are prone to sinus problems.
A nose shape that is good for keeping the water out while swimming
Ears that actually form a protective boney protusion in those who spend a lot of time diving
Manual dexterity – if we were wading, and swimming, not walking on all fours, we have ‘free’ hands. Opening shells would develop manual dexterity.
Crinkly fingers when in water for a few minutes – perfect for catching fish.

Part of the idea of the ‘savannah’ theory is that food became scarce with climate changes so we switched to hunting. But the water’s edge was, until recently, abundant with easily accessible food. Even 200 years ago, in 1706, Daniel Dafoe wrote this regarding the Firth of Forth. “Off the Pentland Firth the sea was one third water and two thirds fish; the operation of taking them could hardly be call’d fishing, for they did little more than dip for them into the water and take them up.” Our estuaries were packed with mussels, oysters and crabs.

Historically, wherever early man is found so too is evidence of seafood consumption, with remains of shells, fish bones etc. from Pinnacle Point in South Africa, where early remains are found together with sea shells, to Wales. When a 40,000 year old Homo sapiens was found in the Gower peninsular DNA evidence showed that a quarter of their diet was seafood.

A marine food diet high in critical brain building nutrients, especially DHA, phospholipids and B12, is the best explanation for our cerebral expansion. “Docosahexaenoic acid (DHA), the omega-3 fatty acid that is found in large amounts in seafood, boosts brain growth in mammals. That is why a dolphin has a much bigger brain than a zebra, though they have roughly the same body sizes. The dolphin has a diet rich in DHA. The crucial point is that without a high DHA diet from seafood we could not have developed our big brains. We got smart from eating fish and living in water.” says Crawford.

The dry weight of the brain in 60 per cent fat and DHA makes up over 90 per cent of the structural fat of neurons (brain and nerve cells). The intelligent membrane that makes up all neurons is composed of phosphorylated DHA – that is DHA attached to phospholipids. The most abundant phospholipid is phosphatidyl choline, found predominantly in fish, eggs and organ meats. These are bound together by a process called methylation, itself dependent on vitamins B12, folate and B6. While folate and B6 is found in both plant foods and seafood, B12 is only found in foods of animal origin, and is especially high in all marine foods.

The evidence that exists suggests we were eating a diet rich in marine food, as well as  plant foods along the water’s edge, enjoying the ‘fruité del mare’. We would have eaten much more than we do today – at least double the calories. Today’s convenience world has dramatically reduced the calories we need to expend hunting and gathering food, travelling and staying warm.

The idea that we were eating twice as much and at least a quarter from marine foods makes sense of what we know about the optimal intake of both omega-3 fats rich in DHA, phospholipids and vitamin B12, lack of which are the main drivers of today’s endemic dementia. This would be equivalent to at least half our diet today needing to be from marine foods rich in fats.

Optimal amounts of omega-3 from seafood is estimated at 2 grams a day by Joseph Hibbeln at the US National Institute’s of Health, while choline is estimated at 400mg to 800mg. An optimal intake of B12 is probably 10mcg. None of these can easily be achieved even by eating seven servings of oily fish a day. (Choline is rich in all fish, but DHA is only rich in oily fish, fish roe and liver.)

In the chart below the last column combines EPA and DHA and shows the amount provided in an 85g serving. None provide 2,000mg, although they do get close, suggesting that we would have needed to eat at least a serving of fish or seafood a day, if not more. 

Brain size remains reasonably constant from 100,000 to 10,000 years ago, then starts to shrink, perhaps coinciding with the birth of agriculture and diets based more on meat, milk and plants than marine foods. Today, average brain size is 1.35kg. 

The evolution of intelligence and self-awareness

Apart from brain size and, more pertinently, brain to body size ratio, what sets us apart from other animals is self-awareness. Animals have the equivalent of thoughts and feelings but humans are relatively unique in being able to witness one’s own thoughts and feelings, that is self- awareness. This is not an easy thing to measure, but some other mammals, notably dolphins, gorillas and chimpanzees, also have a degree of self-awareness. Other contenders for higher cognition include octopuses and elephants, all large brained creatures. However, it isn’t just size that counts. In essence, there are three evolutions of the brain. First, the reptilian brain located on the brain stem, which programmes basic survival needs. Then there’s the mammalian brain, with more cognitive and emotive functions (think dog), then the neo-cortex, associated with higher cognition. But, while elephants have larger brains they have smaller neo-cortexes. It’s the neo-cortex that starts to grow in our hominid ancestors.

An indication of an advancing intelligence could be supposed from the earliest evidence of ancient rock art, as well as use of complex tools and adornments.  The earliest rock art is found in South Africa, dating back 77,000 years ago, and in Western Europe about 37,000 years ago, and possibly in Australasia (Sulawesi) around that time.

The richest concentration of ancient rock art over 6,000 years ago, however, is found in sub-Saharan Africa, the Nile Valley and Red Sea hills, then a green belt with vast lakes, rivers and wetlands, hence abundant marine foods, which lasted until about 3,500 years ago when much of Egypt is becoming a desert. Whether the drying up of the Sahara was linked to the Younger Dryas (see below), a change in the Earth’s tilt or over grazing is a subject of debate.^[i]

Meanwhile, groups of our early ancestors who had left Africa, living in Europe as far west as Ireland, north as Scandinavia, East as China and Australia, were also struck by cataclysmic weather changes. In Europe the Magdalenian culture, with advanced stonework, exists from 17,000 years ago, coinciding with the end of the Ice Age, until 12,000 years ago, coinciding with the Younger Dryas, a period of extreme cooling which lasted for circa 1,000 years, possibly triggered by a meteor shower^[i]. One theory has ancestors migrating south, towards warmer climates with available water, possibly carrying with them the sticky grains they had previously gathered, and may have planted them in moist soil as a means to survive, thus giving birth to the agricultural age whereby mankind moves away from a hunter gatherer lifestyle towards an agricultural lifestyle. This also makes sense as these two pockets of humanity, in Mesopotamia (now Iraq), between the Tigris and Euphrates river, and Egypt, becoming more densely populated with the need for stored food, supplied by grains and domesticating animals. This stable food supply would have allowed expansion of these populations. (There is another evolutionary hotspot in Asia and China^[i].)

Early Enlightenment

The likely existence of an ‘enlightened’ culture, Atlantis, is eluded to in the writings of Plato, possibly existing around the fertile region of the then much smaller Black Sea, which is thought to have flooded across the Bosphorus peninsular when the Mediterranean sea levels rose to a critical mass, dated back to around 7,000 years ago. This may also be the origin of the Flood myth, which occurs in ancient Sumerian lore dating back 5,000 years and later Hebrew lore.

Thus we have this triangle between the Black Sea to the North, Egypt to the South, and Mesopotamia to the East, all with evidence of evolved culture, including monotheism. The Sumerian culture appears over 6,000 years ago in the fertile crescent of Mesopotamia. Later, circa 2,500 years ago, we have the enlightened Zoroastra in Mesopotamia forming the Parsi culture in what is now Iran. Also,The Aryan-(Dru)Vedic culture, sometimes located east of the Black sea, migrated into the Indus valley in northern India as the main influence of the now Hindu culture, and the start of the Greek culture, considered to be the origin of our Western culture. The earliest hint of a Druidic culture dates back to this time. One stream of ancient druidic lore talks of a cataclysmic event, stones pouring from the sky, raising the possibility that early stone structures and barrows were built effectively as ‘bomb shelters’.^[i] While the meaning of the word ‘dru’ is associated with oak (those who meet by the oak) and truth, it also may also mean worshippers of the red Sun (du rua). Sun and fire worship is shared by the early Egyptians (Ra), (dru)vedic culture (Agni and Surya), Zoroastrian culture(Mithra) and even Sumerian culture (Utu). The use of fire started much earlier, with it’s discovery a million years ago, and widespread use from 500,000 years ago, which expanded humanity’s ability to derive energy from previously indigestible carbohydrates, as evidenced in the DNA with the emergence of multiple variations in carbohydrate- digesting amylase enzymes. This is also linked to an expansion in brain size.^[ii]

Is Homo Sapiens devolving?

Globally, there is an increase in mental illness which is fast becoming the biggest health threat, according to the World Health Organisation. There is also evidence that our brain size has reduced by 10 per cent, from 1.45kg 10,000 years ago^[1] to an average now of 1.35kg, coinciding with a more land-based food supply. According to Scandinavian research, our IQ is also falling by 7 per cent a generation. Global rates of depression and dementia, suicide and stress-related disorders of anxiety and insomnia are escalating. One in six children in the UK are classified with ‘special educational needs’ (SEN). Suicide, globally, has become the most cause of violent deaths, ahead of all wars and murders. In the UK 790 people a day, nine double decker buses worth, are diagnosed with dementia. Global incidence will top 100 million this decade, already costing over 1% of GDP.

On the assumption that our brains still require at least the same supply of nutrients that our semi-aquatic ancestors were able to eat during the period of maximum brain evolution – although one could argue that the digital age has put more stress on our brain function, hence we might even need more nutrients – and the fact that we are simply not achieving anything like the same intake of the brain’s essential fats, phospholipids and micronutrients, is it any wonder that mental health is in sharp decline? With a growing population and declining available seafood, coupled with contamination with heavy metals, PCBs and micro-plastic particles, matters are likely to get much worse.

High sugar intake, in animals, has been shown to lead to shrinking of the brain’s hippocampal region. This is where the nucleus accumbens, the seat of the brain’s dopamine-based ‘reward’ system, stimulated by sugar, caffeine and tech addiction, (especially that based on variable rewards such as the ‘like’ button) resides. Marketeers have learnt how to create addiction to their products by stimulating the reward system, selling short-term pleasure, the dopamine-based feeling, in the guise of happiness. The happy hour, the happy meal, happiness in a bottle etc. Over-stimulation of the reward system ultimately leads to dopamine depletion and brain cell death, coupled with a decline in serotonin, the tryptamine associated with happiness, connection, love, empathy and other essential qualities of a harmonious society – and the very qualities that make us human.

We are therefore witnessing the devolution of the brain, the decline and fall of mental health and harmonious society, a situation that is likely to get worse as population expands, unless we rapidly find a way to optimally nourish the brain.

Building Healthy Brains

The emphasis in human nutrition has, for too long, been on the body. With more protein, meat and dairy products, we have grown taller, but not smarter. As director of the Institute of Brain Chemistry at the Chelsea and Westminster Hospital, Professor Michael Crawford has been able to accurate predict which pregnant women are most likely to have pre-term babies, with an increased risk of cognitive delay or impairment. This is based on determining the supply, by analysing the pregnant woman’s blood, of DHA. In its absence levels of a surrogate fat, oleic acid, rises to fulfil the requirement of the neonatal brain, when DHA is in short supply. It is, however, an inadequate substitute and thus cognitive development is impaired. Babies born of mothers with low blood DHA levels, compared to those supplementing DHA, have smaller brains.^[2]

According to Crawford, with a growing population and shrinking fish supply, we must develop marine agriculture on a massive scale to survive and protect the brain. In the same way that man moved from hunter gatherer on the land to peasant farmer, we too must move from hunter gatherer in the oceans to marine farmer. In Japan he has been instrumental to the creation of artificial reefs in the estuaries to attract back the marine food web, from mussels to crustaceans, and fish, as well as farming seaweed on a massive scale. By processing seaweed it is possible to create DHA, the critical brain fat that is crucially lacking in a plant-based diet. As Crawford says “We now face a world in which sources of DHA – our fish stocks – are threatened. That has crucial consequences for our species. Without plentiful DHA, we face a future of increased mental illness and intellectual deterioration. We need to face up to that urgently.”

At the other end of the lifecycle, more and more older people are slipping into dementia, which is a preventable but not reversible condition. At the University of Oxford, Professor David Smith has shown that inadequate omega-3 fats (DHA and EPA) and B vitamins, especially vitamin B12, are the principle drivers of cognitive decline. Yet, by providing these nutrients to those with pre-dementia, further memory decline and brain shrinkage can be arrested. B12 is only found in animal foods and is especially rich in seafood. A plant-based diet alone does not provide sufficient DHA, B12 or phospholipids require for optimal brain development.

Therefore, it is vital that the needs for optimal brain function are put at the top of the health agenda to prevent the decline of our mental health and potentially the fall of Homo Sapiens. Without our fully functioning brains humanity will neither have the insight nor cooperation to face and resolve the challenges we face with a growing population, reducing food supply, increasing pollution, climate changes and ever-increasing energy demands.

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

^[1] https://www.astrobio.net/news-exclusive/how-earths-orbital-shift-shaped-the-sahara/; see also https://phys.org/news/2019-01-sahara-swung-lush-conditions-years.html; see also https://www.ncdc.noaa.gov/abrupt-climate-change/End%20of%20the%20African%20Humid%20Period

^[2] https://en.wikipedia.org/wiki/Younger_Dryas_impact_hypothesis

^[3] https://www.nature.com/news/how-china-is-rewriting-the-book-on-human-origins-1.20231

^[4] https://www.youtube.com/watch?v=t9Zjd0TIHsY

^[5] K. Hardy et al., ‘The importance of dietary carbohydrate in human evolution’, Quarterly Review of Biology(2015), vol 90(3):251–268.

^[6] https://www.discovermagazine.com/planet-earth/the-human-brain-has-been-getting-smaller-since-the-stone-age

^[7] Randomized controlled trial of brain specific fatty acid supplementation in pregnant women increases brain volumes on MRI scans of their newborn infants.

Ogundipe E, Tusor N, Wang Y, Johnson MR, Edwards AD, Crawford MA.

Prostaglandins Leukot Essent Fatty Acids. 2018 Nov;138:6-13. doi: 10.1016/j.plefa.2018.09.001. Epub 2018 Sep 21.

PMID:

30392581

How much thought do you give to your brain? Probably not much when everything is going well. But the actions we take throughout life can have a big impact not only on our brain health as we age, but also how we feel now, including how we cope with stress, deal with set-backs and enjoy life to the fullest.

Despite its diminutive size, your brain steals roughly 25% of your body’s energy. Like a performance car, it is highly dependent on the fuel you feed it as well as how well you sleep, your level of physical exercise, and the extent to which you keep your mind active throughout life.

We decided to research why brain health matters regardless of age and life stage, and created a brand new resource on our website. Read below for a snapshot of some key findings. 

Please note that the life stages we have come up with are intended as signposts only and a way to organise information. We recognise the potential for overlap across life stages as well as individual diversity of experiences. 

Pregnancy

The first 1,000 days of life, including 280 days of prenatal life, are a crucial stage of baby brain growth and development. Recent scientific evidence has identified that parental health and nutrition status at the time of conception and throughout pregnancy plays an important role in brain development. 

Although rapidly growing foetal brains exhibit greater ability to adapt and change than adult brains, they are still vulnerable to injury. Optimising nutrition during pregnancy is one way of several to support foetal brain development. All nutrients are essential to neuroplasticity, but studies have highlighted the particular importance of glucose, fats, protein, iron, zinc, iodine, copper, folate and choline. Read more

Infancy

Infancy (0-3 years) is a time of rapid transition, growth and change. From the moment a child is born it should have all the brain cells that it will ever need (around 100 billion cells), although new brain cells can still be created into adulthood. Synapses, which facilitate the brain’s ability to send and receive information, are formed far quicker during these first three years of life compared to other stages of growth.

Within the first year of life, the cerebellum, involved with memory and movement, can triple in size to account for all the visual and physical experiences the infant encounters. Moreover, within the first three years of life the weight of the brain triples, as it undergoes profound growth. During these first three years of intense neurobiological growth, ketones (water-soluble molecules produced from fatty acids), are an infant’s primary fuel in the developing brain. 

At this stage of life, vitamins A, C and D, omega-3 and omega-6, iron, folic acid, B12, iodine, copper, choline and zinc are important nutrients for development. Read more 

Childhood

Childhood (4-11 years) is an important period of brain maturation, involving the shaping of cognitive function and resilience across the lifespan. Malnutrition amongst children is a worldwide issue. This encompasses two types of undernutrition: those in developing nations, where food scarcity has led to malnutrition and adverse health outcomes; and prevalence of obesity in developed nations, where abundance of high sugar, salt and fat processed foods at low prices has led to increased incidences of weight gain, reduced consumption of vegetables, fruit and other wholefoods, and therefore increased vitamin and mineral deficiency. 

Childhood is a critical period of learning and memory. Nutrients that support this include omega-3, magnesium, vitamin D, zinc. Sleep, physical exercise, and fussy eating are additional factors that can influence a child’s neurological development. Read more

Teenager

Adolescence is a time of transition, change and increasing independence. During this important period of development, a healthy, varied diet is important to support learning and growth. Additionally, due to increased autonomy, it is essential that young people are educated and empowered regarding food choices and positive lifestyle habits. 

Adolescence is also a time of increased susceptibility to mental health problems, and a lifestage where mental illnesses such as depression, anxiety, eating disorders, substance abuse disorders and psychosis may begin to develop. Moreover, schizophrenia and personality disorders may also begin to develop during adolescence. Globally, 1 in 7 10-19 year olds develop a mental health condition, and suicide is the fourth leading cause of death in 15-19 year olds. Key risk factors for the development of mental health conditions during adolescence include stress, the influence of media, lower socioeconomic status, and violence and abuse in the home. 

Supporting health and wellbeing during adolescence is vitally important. Protective nutrients and dietary strategies include eating three healthy meals a day, exercising regularly, sleeping well, supporting bone health and promoting iron, B vitamin, omega-3 and vitamin D status. Read more

Young Adult

Young adulthood (18-30 years) is a life stage full of transition and change, characterised by increasing independence and autonomy typically. The brain continues to develop until the mid to late twenties, particularly areas responsible for reasoning and decision making, as well as emotional regulation. 

Most mental health conditions emerge and are diagnosed during late adolescence. In fact, 75% of all mental illness diagnoses occur by age 24. During early adulthood, anxiety and depression remain prevalent and personality disorders may also be diagnosed. Early intervention in the form of psychological support, with nutrition as an adjunct, is crucial. 

Research has identified a close link between the gut microbiome and mood/mood disorders. Fibre and probiotics help regulate the gut microbiota, which in turn helps produce neurotransmitters such as serotonin and GABA which influence mood. Read more

Middle Age

This life stage (30-50 years) is often characterised by progressions in careers and settling down. This may be accompanied by greater stress, which can influence neurological health. Building stress resilience through diet, sleep and adequate relaxation becomes key. 

Many of the social, physical and psychological experiences of early life and young adulthood influence this life stage. For example, individuals who foster positive, meaningful relationships during their early adulthood have been observed to have better psychological outcomes during midlife. 

Menopause normally occurs between the ages of 45-55, but premature menopause can affect 1 in 100 women. Decades of research supports a role for oestrogen in brain health. This hormone can function to produce energy within multiple brain regions involved in cognitive function. It is widely understood that oestrogen levels significantly decline when entering menopause, having a potentially negative impact on memory and cognition. Research has revealed the supportive role of diet and lifestyle factors through this period of transition, helping to attenuate the effects of menopause. 

Midlife adults are generally less physically active and more at risk of unhealthy ageing related to sedentary lifestyle choices. Physical activity has positive effects not only on body composition but also mental health, sleep and menopause symptoms. ​​Read more

Older Adult

Older adults (50-70 years old) are at increased risk of cognitive decline compared to their younger counterparts. Risk factors include cardiovascular disease, which has been correlated with increased incidence of cognitive decline and dementia, including Alzheimer’s disease. This intrinsic link between the heart and brain is further evidenced by how cardiac dysfunction has been identified as a predictor for cerebrovascular events. Coronary heart disease specifically has been associated with lower scores on cognitive function tests.

Novel nutritional and psychological approaches are constantly being explored to optimise brain health during the ageing process. Following a Mediterranean diet is supported by in-depth evidence demonstrating its benefits on cognitive health. This diet includes high intake of fats from fish and olive oil, and antioxidants from the consumption of fruit and vegetables.

Newer research has also highlighted the MIND diet, which recommends daily consumption of whole grains, fruits, vegetables, nuts and berries, and weekly consumption of beans, poultry and fish. Limited consumption of processed foods, meat, dairy and added sugars are suggested. Based on findings from a recent systematic review, researchers concluded that the MIND diet is superior to numerous other plant-rich diets for improving cognitive function and may possibly be associated with improved brain health in older adults. 

Social interaction also becomes incrementally more important for health and wellbeing with age. Elderly people report improved self esteem and health and wellbeing outcomes when experiencing belonging in friendships, compared to those who reported loneliness and isolation. Finding ways to increase social interaction, via meeting up with friends for coffee, activities or hobbies are all ways to increase social interaction. Read more

Senior

This life stage is characterised by a slower pace of life for many people. It can be a time of great fulfilment, spending time with loved ones and having more time to pursue passions. However, it can also be a time of increased illness, loneliness and memory loss, as demonstrated in dementia.

Some individuals may be more at risk of developing memory loss and cognitive impairment. The APOE4 gene variation has been one of the most studied genetic risk factors with relation to Alzheimer’s disease. Telomeres, the protective ends of chromosomes, have also been observed to be shorter in individuals with the APOE4 gene variant. Telomeres shorten across the life span and are associated with the natural ageing process, but this can be accelerated due to oxidative stress caused by chronic stress, alcohol consumption and poor diet. Importantly, only 1 in a 100 cases of Alzheimer’s is caused by genes. Much of the risk comes from diet and lifestyle factors that we can change, highlighting the importance of prioritising brain health across the lifespan. 

Maintaining physical exercise, increasing social interaction and eating well via the Mediterranean or MIND diet become important considerations at this stage of life. Read more

Final thoughts
Tracking cognitive function at all stages of life empowers you to optimise your brain health for the long-term. Take our free Cognitive Function Test here for personalised feedback on how your cognitive function is performing and ways to improve it.

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

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

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.

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 upi can take one of our at-home, pin-prick, HbA1c (sugar) blood test so you can know exactly how sugar is impacting your body and also become apart of our vital research into this area.

Become a Citizen Scientist & Join our Sugar 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.

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The mouth is a hub of activity, housing around 50–100 billion bacteria from 200 different bacterial species. The role of these resident bacteria in the mouth, also known as the oral microbiome, is an emerging area of research. Alterations in the oral microbiome may occur as a result of factors including consuming high amounts of sugar, smoking tobacco and experiencing chronic stress. Drinking large amounts of alcohol can also negatively impact the oral microbiome. Disruptions to the oral microbiome can lead to gut dysbiosis, which has been associated with increased permeability of the Blood Brain Barrier (BBB). 

Findings to date suggest that the oral microbiome, via interactions with the gut and brain (a network called the oral-gut-brain axis), may be a key consideration for brain health, and multiple associated conditions. This post will focus on three key areas where there is present research: autism, Down’s syndrome, and Alzheimer’s disease. 

Autism

Individuals with autism have been indicated to have alterations in their oral microbiome, as well as gut dysbiosis and related disruptions to the gut-brain axis. A study investigating the oral microbiome indicated that children with autism have a higher incidence of gastrointestinal disturbance and food allergies. Moreover, children with autism were observed to have a disruption to the ratio of Firmicutes: Bacteroidetes bacteria, in favour of Firmicutes. Balance of the Firmicutes: Bacteroidetes ratio is key for integrity of the gut, and disruptions to this ratio are indicative of gut dysbiosis.  

Moreover, two specific groups of bacteria, Brucella and Enterococcus faecalis were observed to be elevated in autistic children, whilst Flavobacterium sp. levels were demonstrated to be decreased. Research has suggested that individuals with autism have a higher risk of developing Alzheimer’s disease earlier in life. One potential mechanism for this could be due to alterations to the Firmicutes: Bacterodetes ratio.

Firmicutes and Bacteroidetes both utilise amyloids in the gut as structural material. Recognition of amyloids may become impaired by increased synthesis of inflammatory T cells by the innate immune system, as the result of intestinal permeability. Translocation of amyloids across the BBB has been hypothesised to be associated with enhanced Aβ deposit in the brain, although this requires further research.

Down’s Syndrome

Individuals with Down’s syndrome have been demonstrated to be more susceptible to periodontitis, or gum disease. One potential explanation for these findings could be due to alterations in oral microbiome composition. One study observed that individuals with Down’s syndrome have higher levels of Streptococcus mutans in their saliva. A further study observed increased levels of the pathogenic bacterial strains Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis.  Individuals with Down’s syndrome have an increased risk of developing Alzheimer’s disease later in life, with 50% of individuals >60 years of age meeting diagnostic criteria for dementia. One hypothesised mechanism for this is because of altered expression of inflammation and immune system modulating genes in periodontitis.

Alzheimer’s Disease

Individuals with Alzheimer’s disease have been observed to have higher levels of the oral bacteria, Treponema, in the brain. Moreover, disruptions to the oral-gut-brain axis has been associated with increased accumulation of beta amyloid and Tau, two key markers of Alzheimer’s disease.

Supporting the Oral-Gut-Brain Axis 

Supporting the oral-gut-brain axis is an area of research that is undeveloped, however, it seems logical that many of the measures employed for supporting gut and brain health would also be salient. 

Increase Fibre & Polyphenols

Consuming a wide array of colourful vegetables, fruits, herbs and spices is a great way of increasing prebiotic fibres, which help to support gut health via increasing production of SCFAs (short chain fatty acids), and polyphenols, plant compounds that have antioxidant properties and have been demonstrated to support the oral-gut-brain axis. 

Increase Omega-3 Fats

Omega-3 fats exert anti-inflammatory effects in the body, whilst increasing microbiome diversity via balancing the Firmicutes: Bacteroidetes ratio, which is essential for gut health and gut barrier integrity. Additionally, increased levels of omega-3 have been associated with reduced incidence of periodontitis. Ways to increase omega-3 include increasing consumption of oily fish such as salmon, mackerel and sardines, and also flaxseeds, walnuts and algae. 

Increase Fermented, Probiotic Foods

Probiotics have been associated with improved oral health due to decreased presence of pathogenic bacteria in the mouth. Examples of probiotic foods include fermented foods such as kimchi, kombucha, kefir, sauerkraut and sourdough bread.