Friday’s Guardian article on ‘I refuse to get old’ about how readers strive to keep dementia at bay, on the face of it, seems like a good message. Most cases given focussing on people increasing physical and mental activity, as an active lifestyle is certainly a positive step towards prevention. But these two prevention steps reduce risk by less than B vitamins, omega-3 and reducing sugar and carbs.
The first error is the extent to which dementia can be prevented. The article says by 40%, which is based on the inaccurate Lancet Commission’s Livingston report which, despite being sent all the evidence, doesn’t even mention B vitamins and homocysteine, which is the single most important prevention step. There’s also only one mention of omega-3 from a redundant study so this risk factor is also ignored to arrive at the ‘40% preventable’ figure.
80% of dementia cases could be prevented, not 40%
The latest assessment of how much can be prevented, based on UK Biobank data is “47%–73% of dementia cases could be prevented.” This was published last week in Nature and even this is an underestimate because, while including B vitamins, it excludes the impact of omega-3 and seafood. If that modifiable risk factor were included it is likely that around 80% of dementia cases could be prevented. This would mean that the Guardian is halving the impact of prevention.
The next error is no-one quoted in the article mentions diet, let alone B vitamins or omega-3, except for Professor David Smith. He rightly says: ‘The large leap forward in what we know about preventability has informed his own retirement lifestyle: he walks for half an hour a day, spends at least 15 minutes on an exercise bike, drinks alcohol sparingly, and follows a Mediterranean diet.
Having led a clinical trial into the benefits of B vitamins in people with mild cognitive impairment – a memory-loss condition that increases the chance of those who have it developing dementia – Smith takes 500mcg of vitamin B12 daily and fish oil with Omega 3. Nutrition, he believes, is not given enough prominence when we talk about prevention.’
When we calculated the attributable risk for each risk factor for our online Dementia Risk Index questionnaire each domain scores as follows, adding up to 100%:
B Vitamins 18%
Brain Fats 17%
Glycemic Load 15%
Active Body 15%
Active Mind 10%
Sleep & Calm 10%
Antioxidants 10%
Gut Health 5%
So, the biggest impact you can have on your risk is to supplement B vitamins, especially B12, and omega-3 fish oils, as David Smith does. But the Guardian article then downplays the role of supplements with this statement ‘Alzheimer’s Research UK does not recommend any supplements in particular, but says “there is no harm in people taking a supplement to reduce the risk of deficiency”.
B12 Reference Ranges are wrong
This is not only wrong because brain shrinkage occurs well within the ‘normal’ range of either B12 dietary intake or blood tests, but also ARUK, who largely promotes drug-based solutions, happened to know what they are saying is wrong because they funded, back in 2010, a top level, randomised placebo controlled trial on B vitamins that, virtually stopped cognitive decline and reduced brain shrinkage by 52% – in the group with higher omega 3 , by 73% – that is the most effective disease modifying treatment to date! In fact, David Smith and I have written to ARUK to stop making this inaccurate statement. Here’s why it’s wrong:
The reason so many people are low in B12 is less to do with dietary intake and more due to malabsorption which often becomes worse with age, due to lack of stomach acid secretions which are needed to absorb B12. So relying only of analysing what someone eats (meat, fish, eggs, dairy being the only sources of B12) doesn’t prove sufficiency. Note that David Smith says he supplements 500mcg of B12 daily, while the basic ‘Nutrient Reference Value’ (NRV) that you’ll see on the back of a vitamin supplement is 2.5mcg. So, why does he take two hundred times this amount? Because you cannot rely on your dietary intake to confirm sufficiency. Also, there is growing body of evidence from well designed studies showing that supplements giving nutrients at levels beyond the basic ‘recommended intakes’ delay, eliminate or ameliorate symptoms of dementia.
So, what about blood tests? One UK study reports that 2 in five people over 61 have insufficient levels of B12 to prevent accelerated brain shrinkage. Serum B12 is the ‘standard’ test used by doctors. The UK reference range of above 180pg/ml being sufficient (and the US lower level of 200pg/ml) is out of date and in need of revision. In Europe and Japan anything below 500pg/ml is considered deficient. Accelerated brain shrinkage due to a lack of B12 does happen with B12 levels below 500pg/ml.
In conclusion, while it is good to recommend a physically and intellectually lifestyle, ignoring the need to supplement B vitamins, especially B12, eat fish and supplement omega-3, and cut your intake of carbs and sugar, is not doing anyone any favours.
Food for the Brain is a non-for-profit educational and research charity that offers a freeCognitive Function Testand assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.
By completing theCognitive Function Testyou 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.
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 freeCognitive Function Testand 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.
[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.
[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.
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.
Brain regions
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
Omega 3 fish oil soft gels
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.
Vitamin B Complex
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.
Food for the Brain is a non-for-profit educational and research charity that offers a freeCognitive Function Testand assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.
By completing theCognitive Function Testyou 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.
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).
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
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 freeCognitive Function Testand assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.
By completing theCognitive Function Testyou 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.
[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.
[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.
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.
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.
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]
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.
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.
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://foodforthebrain.jp/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 freeCognitive Function Testand assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.
By completing theCognitive Function Testyou 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.
[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.
[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.
[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.
[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.
