The reason we advocate natural, nutritional, and lifestyle-based approaches to mental health is simple – because they work, and they’re safe.
Unspoken Risks of Psychiatric & Dementia Drugs
The next big challenge is to discover which combination of changes has the most impact. This is what our research is focused on.
From depression to dementia, the typical approach is still, all too often, medication While it’s valid to compare a nutrient or diet to a pharmaceutical – take omega-3s, for example, which have been shown to be as effective as antidepressants – the real concern is how rarely we hear about the risks of psychiatric drugs. For many, by the time those dangers become clear, it’s already too late.
A classic example of this is the well-known increased risk of suicide particularly in young people prescribed antidepressants. Not only did this take more than ten years to ‘come out’, even now, despite on-the-box warnings, many remain unaware of this well-established risk.
A similar situation is emerging with the new anti-amyloid antibody treatments being proposed for dementia sufferers. Reported deaths are often downplayed or not fully disclosed.. In trials of the two drugs Lecanemab and Donanemab, eight deaths were reported. Eight deaths were reported during the trials, which involved 1,785 participants – a rate of one in every 219 – though not all were officially attributed to the drug. That’s quite a risk. But it is also the nature of these deaths, caused by brain bleeding and swelling, that is even more concerning.
Investigative journalist Charles Piller, in his book ‘Doctored’, interviewed the pathologist for the first Lecanemab death who said it was like “her brain exploded”. Another Lecanemab associated death was a 65 year-old woman, who had a blood clot induced stroke and was given a common, often lifesaving intervention (tPA) which went badly wrong. “As soon as they put it in her, it was like her body was on fire,” the woman’s husband told me, he said. “She was screaming, and it took, like, eight people to hold her down. It was horrific. Everybody’s running in and (asking) ‘What the hell is going on?’” His wife was sedated and recovered to intensive care, he said. Soon the woman suffered seizures and was placed on a ventilator. After a few days the family approved disconnecting the device and she died. In his book Piller also reports another case in which a participant ‘died after hideous brain swelling and bleeding, and violent seizures.’
The UK has licensed the use of Lecanemab. The EU has not. The UK has licensed Donanemab, but NICE hasn’t approved it for NHS use.
Safer, Evidence-Based Alternatives
Despite more effective and safer alternatives being available, Alzheimer’s charities continue to advocate for NHS access to these drugs. This raises an important question: why? The combination of homocysteine-lowering B vitamins and omega-3 already has stronger evidence of efficacy – with no adverse effects – and certainly no risk of death (Read Alzheimer’s: Prevention is the Cure for the evidence and the comparison).
We invited Dr Peter Gøtzsche – co-founder of the Cochrane Collaboration, originally established to evaluate health treatments without bias – to speak about the risks of psychiatric drugs and their link to mortality. When the Cochrane Collaboration became corrupted, which he later criticised for being influenced by commercial interests, he founded the Institute for Scientific Freedom.
“Overtreatment with drugs kills many people, and the death rate is increasing. It is therefore strange that we have allowed this long-lasting drug pandemic to continue, and even more so because most of the drug deaths are easily preventable.” he says.
“In 2013, I estimated that our prescription drugs are the third leading cause of death after heart disease and cancer,(1)and in 2015, that psychiatric drugs alone are also the third leading cause of death”.(2)”
Read on to understand how he arrived at the conclusion that psychiatric drugs may be the third leading cause of death.
How many people are killed by psychiatric drugs?
If we want to estimate the death toll of psychiatric drugs, the most reliable source of data comes from placebo-controlled randomised trials. However, we need to consider their limitations.
First, these trials typically last just a few weeks, despite the fact that most patients take psychiatric medications for many years.(3, 4)
Second, polypharmacy – the use of multiple medications – is common in psychiatry, and this significantly increases the risk of mortality.. As an example, the Danish Health Authority has warned that adding a benzodiazepine to a neuroleptic increases mortality by 50-65% (5).
Third, up to half of all deaths go unreported in published clinical trial data.(6) For dementia, published data shows that for every 100 people treated with a newer neuroleptic for ten weeks, one patient dies as a result. (7) This represents a high mortality rate for a pharmaceutical intervention, but FDA data on the same trials show it is double this number, equivalent to two deaths per 100 people over ten weeks. (8) And if we extend the observation period, the death toll becomes even higher. A Finnish study of 70,718 community-dwellers newly diagnosed with Alzheimer’s disease reported that neuroleptics kill 4-5 people per 100 annually, compared to patients who were not treated.(9)
Fourth, the design of psychiatric drug trials is biased. In almost all cases, patients were already in treatment with psychiatric medication before they entered the trial, (1, 2), and some of those randomised to placebo will therefore experience withdrawal effects that will increase their risk of dying, due to withdrawal symptoms such as akathisia. Placebo-controlled trials in schizophrenia cannot be reliably used to assess the effect of neuroleptics on mortality because of the drug withdrawal design. The suicide rate in these unethical trials was 2-5 times higher than the norm. (10,11) Among those enrolled in trials of risperidone, olanzapine, quetiapine, and sertindole, one in every 145 patients died. However, none of these deaths were mentioned in the published scientific literature, and the FDA did not require their inclusion in trial reporting.
Fifth, events occurring after the trial period are often ignored. In Pfizer’s trials of sertraline in adults, the risk ratio for suicides and suicide attempts was 0.52 when follow-up lasted only 24 hours, but increased to 1.47 when follow-up was extended to 30 days — indicating a rise in suicidal events. (12) Furthermore, when researchers reanalysed the FDA trial data on depression drugs and included harms occurring during follow-up, they found that antidepressants were associated with twice the number of suicides in adults compared to placebo (13, 14)
Estimating the True Death Toll of Mental-Health Medications
In 2013, I estimated that, in people aged 65 and above, neuroleptics, benzodiazepines or similar, and antidepressants kill 209,000 people annually in the United States.(2) I used relatively conservative estimates, however, and usage data from Denmark, which is far lower than those in USA. I have therefore updated the analysis based on US usage data, again focusing on older age groups.
For neuroleptics, I used the estimate of 2% mortality from the FDA data.(8)
For benzodiazepines and similar drugs, a matched cohort study showed that the drugs doubled the death rate, although the average age of the patients was only 55.(15) The excess death rate was about 1% per year. In another large, matched cohort study, the appendix to the study report shows that hypnotics quadrupled the death rate (hazard ratio 4.5). The study authors estimated that sleeping pills kill between 320,000 and 507,000 Americans every year. (16) A reasonable estimate of the annual death rate would therefore be 2%.
For SSRIs, a UK cohort study of 60,746 depressed patients older than 65 showed that they led to falls and a 3.6% annual mortality rate among those treated.(17) The study was well-designed, in that the patients were their own control in one of the analyses, which helps control for confounding variables. Nonetheless, the reported death rate is notably high.
Another cohort study, of 136,293 American postmenopausal women (age 50-79) participating in the Women’s Health Initiative study, found that depression drugs were associated with a 32% increase in all-cause mortality after adjustment for confounding factors, which corresponding to an estimated 0.5% annual mortality rate among women treated with SSRIs.(18). The authors noted that the mortality rate was likely underestimated. The authors warned that their results should be interpreted with great caution due to a high risk of exposure misclassification, which would make it more difficult to find an increase in mortality. Further, the patients were much younger than in the UK study, and the death rate increased markedly with age and was 1.4% for those aged 70-79. Finally, the exposed and unexposed women were different for many important risk factors for early death, whereas the people in the UK cohort were their own control.
For these reasons, I decided to use the average of the two estimates, a 2% annual death rate.
These are my results for USA for these three drug groups for people at least 65 years of age (58.2 million; usage is in outpatients only): (19, 20, 21, 22)
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A limitation in these estimates is that you can only die once, and many people receive polypharmacy. It is not clear how we should adjust for this. In the UK cohort study of depressed patients, 9% also took neuroleptics, and 24% took hypnotics/anxiolytics. (17)
On the other hand, the data on death rates come from studies where many patients were also on several psychiatric drugs in the comparison group, so this is not likely to be a major limitation considering also that polypharmacy increases mortality beyond what the individual drugs cause.
Statistics from the Centers for Disease Control and Prevention list these four top causes of death: (23)
COVID-19 deaths are rapidly declining, and many of such deaths are not caused by the virus but merely occurred in people who tested positive for it because the WHO advised that all deaths in people who tested positive should be called COVID deaths.
Young people have a much smaller death risk than the elderly, as they rarely fall and break their hip, which is why I have focused on the elderly. I have tried to be conservative. My estimate misses many drug deaths in those younger than 65 years; it only included three classes of psychiatric drugs; and it did not include hospital deaths.
I therefore do not doubt that psychiatric drugs are the third leading cause of death after heart disease and cancer.
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Learn more and begin your brain upgrade journey today:
Order Alzheimer’s: Prevention is the Cure book here
Contribute to our research and order your accurate, at home, blood tests here.
If you are looking for personalised one to one support, visit the Brain Bio Centre here.
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Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.
By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices. Please support our research by becoming a Friend of Food for the Brain.
References: 1 Gøtzsche PC. Deadly medicines and organised crime: How big pharma has corrupted health care. London: Radcliffe Publishing; 2013.
2 Gøtzsche PC. Deadly psychiatry and organised denial. Copenhagen: People’s Press; 2015.. US News 2016; Sept 27.
2. Gøtzsche PC. Mental health survival kit and withdrawal from psychiatric drugs. Ann Arbor: L H Press; 2022.
3 Gøtzsche PC. Long-term use of antipsychotics and antidepressants is not evidence-based. Int J Risk Saf Med 2020;31:37-42.
4 Gøtzsche PC. Long-term use of benzodiazepines, stimulants and lithium is not evidence-based. Clin Neuropsychiatry 2020;17:281-3.
5 Forbruget af antipsykotika blandt 18-64 årige patienter, med skizofreni, mani eller bipolar affektiv sindslidelse. København: Sundhedsstyrelsen; 2006.
6 Hughes S, Cohen D, Jaggi R. Differences in reporting serious adverse events in industry sponsored clinical trial registries and journal articles on antidepressant and antipsychotic drugs: a cross-sectional study. BMJ Open 2014;4:e005535.
7 Schneider LS, Dagerman KS, Insel P. Risk of death with atypical antipsychotic drug treatment for dementia: meta-analysis of randomized placebo-controlled trials. JAMA 2005;294:1934–43.
8 FDA package insert for Risperdal (risperidone). Accessed 30 May 2022.
9 Koponen M, Taipale H, Lavikainen P, et al. Risk of mortality associated with antipsychotic monotherapy and polypharmacy among community-dwelling persons with Alzheimer’s disease. J Alzheimers Dis 2017;56:107-18.
10 Whitaker R. Lure of riches fuels testing. Boston Globe 1998;Nov 17.
11 Whitaker R. Mad in America: bad science, bad medicine, and the enduring mistreatment of the mentally ill. Cambridge: Perseus Books Group; 2002:page 269.
12 Vanderburg DG, Batzar E, Fogel I, et al. A pooled analysis of suicidality in double-blind, placebo-controlled studies of sertraline in adults. J Clin Psychiatry 2009;70:674-83.
13 Hengartner MP, Plöderl M. Newer-generation antidepressants and suicide risk in randomized controlled trials: a re-analysis of the FDA database. Psychother Psychosom 2019;88:247-8.
14 Hengartner MP, Plöderl M. Reply to the Letter to the Editor: “Newer-Generation Antidepressants and Suicide Risk: Thoughts on Hengartner and Plöderl’s ReAnalysis.” Psychother Psychosom 2019;88:373-4.
15 Weich S, Pearce HL, Croft P, et al. Effect of anxiolytic and hypnotic drug prescriptions on mortality hazards: retrospective cohort study. BMJ 2014;348:g1996.
16 Kripke DF, Langer RD, Kline LE. Hypnotics’ association with mortality or cancer: a matched cohort study. BMJ Open 2012;2:e000850.
17 Coupland C, Dhiman P, Morriss R, et al. Antidepressant use and risk of adverse outcomes in older people: population based cohort study. BMJ 2011;343:d4551.
18 Smoller JW, Allison M, Cochrane BB, et al. Antidepressant use and risk of incident cardiovascular morbidity and mortality among postmenopausal women in the Women’s Health Initiative study. Arch Intern Med 2009;169:2128-39.
Every three seconds, someone in the world develops dementia and the rate is increasing.
Billions of dollars have been spent on the search for a drug that can block the damaging build-up of plaque in the brain that’s thought to be central to the disease. But the results are not impressive and the side effects include bleeding into the brain.
Now, that gloomy picture is being transformed in a remarkable and surprising way. Rather than pinning our hopes on another new, powerful and expensive drug, mounting evidence suggests that such seemingly old-fashioned approaches as changes in diet, lifestyle, and environment, could dramatically reduce the number of Alzheimer’s cases.
An international Alzheimer’s Prevention Expert Teamhas calculated that over 80 per cent of cases could be prevented in this way. A study in Holland last year found that good levels of vitamin D, omega-3 (found in oily fish), and B vitamins reduced the risk of dementia to less than a quarter of the average(1). Other beneficial changes include regular exercise, staying mentally active, and reducing sugar intake. Reducing sugar intake is especially effective, as people with diabetes have twice the risk of cognitive decline.
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The next big challenge is to discover which combination of changes has the most impact. This is what our research is focused on.
That is why we are hosting the Global Alzheimer’s Prevention Day next week and continuing with our research project to discover the hardest hitting combinations of prevention steps. We have already tested over 200,000 participants in the UK.
We are now inviting people around the world to complete a free, online diet and lifestyle questionnaire and a cognitive function test.
The project, led by Oxford University–trained neuroscientist Dr. Tommy Wood, Associate Professor at the University of Washington, aims to test over 20 million people worldwide. This includes one million participants each from the UK, Germany, and Poland; a similar number from the US, Canada, Brazil, and Japan; and 10 million from China, which has the world’s highest prevalence of dementia.
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Dr. Tommy Wood is an Assistant Professor of Pediatrics and Neuroscience at the University of Washington in Seattle.
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In China, the project is supported by the China National Health Association and former Minister of Health, Gao Qiang. “We must popularise prevention,” he says. “With 300 million people over 60, this has to be our focus. Food for the Brain’s initiative is the way forward. It’s something everyone can do, right now, for themselves.” China’s leading prevention expert, Professor Jin-Tai Yu from Fudan University in Shanghai, adds: “It may be possible to prevent up to 80% of dementia cases if all known risk factors are targeted.” He highlights the particular importance of B vitamins, which reduce levels of a toxic amino acid found in the brain called homocysteine. High homocysteine levels can damage both brain cells and blood vessels. (Test your homocysteine levels at home here)
His research, along with findings from Oxford University’s leading prevention expert, Professor David Smith – who has been analysing data from the – has already shown that up to 73% of dementia cases may be preventable, even without factoring in the benefits of B vitamins and omega-3.
“Our research at Oxford found almost nine times less shrinkage in the Alzheimer’s associated areas of the brain in those taking B vitamin supplements, who had raised homocysteine (3), which is common among over 60+ year olds, and in early signs of dementia.” says Professor Smith.
Wu YingPing, President of the China National Health Association, believes it is the combination of diet, nutritional supplementation, and lifestyle that can significantly influence dementia prevention in the ‘silver-haired’ community. “It is education, rather than medication, that we need, and Food for the Brain’s global campaign is something we fully support to help achieve this.”
In the UK, Japan, and Brazil, a task force of over 10,000 doctors is being trained to enrol their patients in the ‘citizen science’ charitable project, which is funded by individuals rather than vested-interest companies.
In the UK, a group of GPs, part of the Public Health Collaboration, have joined the task force to help drive the project to hundreds of thousands of patients across the UK. Former GP and Chair of the Public Health Collaboration, Dr David Jehring, says: “personalised digital health education such as this is the way forward. No drug treatment has yet produced a clinically meaningful effect, without awful adverse effects. We have to face the reality that dementia can only be prevented by tackling that ‘perfect storm’ of 21st-century diet and lifestyle that creates cognitive decline in the first place. It is not likely to be solvable by medication.”
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In the US, Dr Mark Hyman, who is part of our group of prevention experts, is supporting Robert F. Kennedy Jr., the newly appointed Secretary of Health, in the campaign to ‘Make America Healthy Again’, with prevention at its core.
“Our healthcare system is failing because it treats symptoms rather than addressing the root causes of disease. I fully support Robert F. Kennedy Jr.’s commitment to investigating the underlying drivers of chronic illness and ensuring that prevention – not just treatment – is at the core of our national health strategy. The science is clear: food is the most powerful medicine we have to prevent, reverse, and even treat conditions like dementia, autoimmune diseases, and metabolic disorders. If we truly want to make America healthy again, we must shift our focus from managing disease to creating health,” says Dr Hyman
As part of our ‘Going Global’ campaign, we’ve created a shorter, 3-minute version of our Cognitive Function Test – the Alzheimer’s Prevention Check!
Professor Peter Garrard, Director of the Dementia Research Group at St George’s, University of London, says: “It is vital that functional biomarkers such as homocysteine and omega-3 are measured in this research because these can be changed with nutritional interventions and are associated with reducing risk.”
“The purpose of this global campaign is to collect diet, lifestyle, biomarker, and cognitive function data on an unprecedented scale. With this data, we hope to discover which lifestyle changes have the maximum likelihood of preventing cognitive decline early enough to minimise an individual’s dementia risk in the future.” says Dr Tommy Wood, who is leading the research.
Anyone can take part and become a ‘citizen scientist’ by completing our free online Alzheimer’s Prevention Check, which then provides personalised advice on changes you can make to help reduce your future risk.
All data collected is anonymised for research purposes and will be made available to prevention researchers around the world.
Our aim at Food for the Brain is to discover the simplest changes that have the greatest impact on cognitive function in preventing this devastating disease, and then share that information with the public and the public health experts who advise governments around the world.
Fewer than one in a hundred cases of Alzheimer’s is caused by genetics. This means that, potentially, 99% of cases could be preventable.
Order the new book: Alzheimer’s: Prevention is the Cure – A 240-page guide by Patrick Holford, available internationally from 1st May at foodforthebrain.org/apic, and also on Amazon, Kindle, and Audible.
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Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.
By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices. Please support our research by becoming a Friend of Food for the Brain.
References:
1 Roigé-Castellví J, Murphy M, Fernández-Ballart J, Canals J. Moderately elevated preconception fasting plasma total homocysteine is a risk factor for psychological problems in childhood. Public Health Nutr. 2019 Jun;22(9):1615-1623. doi: 10.1017/S1368980018003610. Epub 2019 Jan 14. PMID: 30636652; PMCID: PMC10261079. 2 Kara İS, Peker NA, Dolğun İ, Mertoğlu C. Vitamin B12 Level in Children. J Curr Pediatr. 2023 Aug;21(2):127-134. doi:10.4274/jcp.2023.75688. 3 https://pmc.ncbi.nlm.nih.gov/articles/PMC4440679/
There is no doubt that autism diagnoses, both across the UK and US are escalating at a worrying rate.
A clear illustration of this is the recently published Scottish Schools Census, showing a year by year steady increase in the percentage of Scottish schoolchildren with a diagnosis. Last year, one in 21 schoolchildren had an autism diagnosis, of which one in 14 are boys. This represents a 43-fold increase in 20 years.
As discussed at Food for theBrain’s Smart Kids conference, research is consistently showing that serum homocysteine, which you cantest with us at home here, is a reliable indicator of both folate and B12 status and with each unit increase in homocysteine pre-conceptually, the core symptoms required for an autism diagnosis go up. (1)
The majority of studies show that lack of pre-natal folic acid supplementation or low folate, increase the risk of aspects of neurodivergence. Studies on B12 are less clear however. Further studies are under way which will help determine both the optimal level of folate and B12 and whether they are synergistic, as has been found in Alzheimer’s prevention. Our view is that homocysteine should be measured and high levels lowered with appropriate diet and supplementation.
A recent study of 3,000 EU children reported that one third had B12 levels below 200pg/ml, (2) with deficiency more prevalent in vegan children. Another EU survey reports than only one in ten overweight women supplement folic acid in pregnancy. This is really concerning.
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It’s the total load – not just one thing
The over-arching theme of this excellent conference was that of ‘total load’ and the interaction between predisposing genes and a nutritional deficient diet and/or toxic overload. It stressed the need to think in terms of the ‘total load’ on a child at critical stages of development, starting in pregnancy. A study of 192 twin pairs, published in the Archives of General Psychiatry, concluded that environmental factors were a greater contributor than heritability, contributing 55% of risk (3).
Additionally, there are many gene variations which don’t cause, but do increase the risk of neurodivergence. An example is a methylation gene variant MTHFR677TT, which increases risk for both autism and Alzheimer’s. Healthy methylation requires B vitamins, especially vitamin B12 and folate, found in ‘foliage’ – vegetables and greens. A study in China in the journal ‘Frontiers in Paediatrics’(4), comparing several thousand with or without this gene variation found that having it “… was associated with the increased risk of autism. For those mothers and children who are generally susceptible to autism, prenatal folate and vitamin B12 may reduce the risk that children suffer from autism.” This is just one example of the gene-environment interplay.
The results of a survey by the Autism Research Institute of over 27,000 parents who rated different nutritional interventions they tried, rating whether their child got better or worse, reported some clear winners of diet changes and supplements. The following had 10:1 or better ratings.
Removed milk/dairy 32:1
Removed wheat 30:1
Essential fatty acids 30:1
Removed chocolate 28:1
Removed sugar 27:1
Food allergy treatment 27:1
Feingold diet (no wheat or milk) 26:1
Zinc 24:1
Rotation diet 23;1
Candida diet 20:1
Removed eggs 20:1
Vitamin C 20:1
Vitamin A 16:1
Cod liver oil 14:1
Vitamin B6/magnesium 11:1
Specific carbohydrate diet 10:1
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‘Life-changing’ improvement through dietary changes…
Another parent-reporting survey conducted by the UK charity Thinking Autism in 2014 (5), involving similar dietary guidance, and written up into a report by academics at Queen Mary, University of London in 2016, found that, out of 237 families who reported using various dietary interventions with their children with autism, 170 families reported either ‘life-changing’ or ‘significant’ improvements, while only 12 children were reported as having no noticeable change.
If you are a practitioner and would like a deep dive into theSmart Kids conference, recordings are now available.
If you are a parent or are neurodivergent yourself and would like to hear from clinicians who have considerable experience in helping those with symptoms get better, the Optimising Neurodivergence webinar is now available.
But first, do complete the COGNITION for Smart Kidstest (or the COGNITION testif you are a parent or practitioner) to help both our research and help yourself at the same time.
Here’s an example report.
Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.
By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices. Please support our research by becoming a Friend of Food for the Brain.
References:
1 Roigé-Castellví J, Murphy M, Fernández-Ballart J, Canals J. Moderately elevated preconception fasting plasma total homocysteine is a risk factor for psychological problems in childhood. Public Health Nutr. 2019 Jun;22(9):1615-1623. doi: 10.1017/S1368980018003610. Epub 2019 Jan 14. PMID: 30636652; PMCID: PMC10261079. 2 Kara İS, Peker NA, Dolğun İ, Mertoğlu C. Vitamin B12 Level in Children. J Curr Pediatr. 2023 Aug;21(2):127-134. doi:10.4274/jcp.2023.75688. 3 https://pmc.ncbi.nlm.nih.gov/articles/PMC4440679/ 4 https://pmc.ncbi.nlm.nih.gov/articles/PMC7987783/ 5 https://www.thinkingautism.org.uk/taking-action/resources-and-publications/health-and-service-provision-for-people-with-autism/
What can you do, practically and quickly, to reduce your risk of developing Alzheimer’s?
The International Alzheimer’s Prevention Expert Group, including our founder Patrick Holford, has identified four key areas that could cut your future risk by over 80% – down to less than a quarter – if addressed early.
The four “quick wins”? Increase your vitamin D, omega-3, and B vitamins, and reduce your intake of sugar and refined carbs.
1. Vitamin D: The Sunshine Factor
Vitamin D is primarily made in your skin through sun exposure, particularly at midday in the summer. However, in the winter – especially in the UK and other northern countries – you cannot make enough, so supplementation is essential. A Dutch study found that people with low levels of vitamin D, omega-3s, and B vitamins were over four times more likely to develop dementia¹. Those who supplement with vitamin D have around a third less risk².
Even levels below 62.5 nmol/L (25 ng/mL) increase risk. A French study found that low vitamin D levels tripled Alzheimer’s risk³. The darker your skin, the more sun exposure you need – which makes supplementation all the more vital for many.
2. Omega-3: Feed Your Brain with Fish
Fish is a true brain food – rich in omega-3s, vitamin D, and B12. Eating fish at least once a week reduces Alzheimer’s risk by a third⁴. A recent review confirmed that a daily serving cuts the risk of cognitive decline by 30%⁵.
Omega-3 fats (especially DHA) quite literally build brain cells. The UK Biobank study of over 250,000 people found that those with higher omega-3 levels had a 20% lower risk of dementia⁶. A US study also found that a higher omega-3 index correlated with more white matter in the brain and better cognitive function⁷.
Professor William Harris of the Fatty Acid Research Institute calls it “a safe, simple, cheap and effective tool to forestall Alzheimer’s.”
3. B Vitamins: The Brain Fixers
B6, B12, and folate don’t just support brain function – they’re essential for fixing omega-3s into your brain’s cell membranes. Without them, homocysteine – a toxic amino acid – builds up in your blood. High levels (above 11 μmol/L) are strongly linked to brain shrinkage and Alzheimer’s.
Half of people over 60 in the US have homocysteine levels above 11. The Dutch study found that risk rises even above 8 – a level many people exceed.
As Professor Joshua Miller from Rutgers University says, raised homocysteine is an early warning sign: “a canary in the coal mine.” The good news? It’s easily lowered with a B vitamin supplement – ideally one containing 500 mcg of B12, methylfolate, and B6.
More greens, beans, nuts, and lentils also help. A recent study showed that replacing just one serving of processed meat with nuts or beans (rich in folate) cut dementia risk by 19%⁸.
4. Sugar and Refined Carbs: Silent Brain Saboteurs
The more sugar a person eats – including refined white carbohydrate foods such as bread, pastries, pasta, and rice – the higher their risk of both diabetes and dementia. Fizzy drinks and ultra-processed foods, sweetened with high-fructose corn syrup, are particularly bad for the brain. “The brain needs the most energy of any organ, so it has the most mitochondria to make it. Sugar damages mitochondria,” says Dr Robert Lustig from the University of California, San Francisco.
A study just published this month in Neurology involving 2 million people shows that those with sugar problems (metabolic syndrome) are 24% more likely to develop dementia early¹⁰. Keeping blood glucose levels in the low–normal range is reflected by a low glycosylated haemoglobin (HbA1c), which is the blood test doctors use to diagnose diabetes. Having a lower HbA1c is associated with reduced risk for dementia in several studies⁹. A recent study of 374,021 older men with diabetes found that keeping HbA1c stable over three years cut the risk of dementia by a third¹¹.
Want to know what’s driving your brain risk?
Take our free 3-minute Alzheimer’s Prevention Check atalzheimersprevention.info– or, for the full picture, order the four-in-one home blood test to measure your omega-3 index, vitamin D, homocysteine and HbA1c:foodforthebrain.org/tests
Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.
By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices. Please support our research by becoming a Friend of Food for the Brain.
2 Ghahremani M, et al. Vitamin D supplementation and incident dementia: Effects of sex, APOE, and baseline cognitive status. Alzheimers Dement (Amst). 2023 Mar;15(1):e12404. doi: https://doi.org/10.1002/dad2.12404
3 Feart C, et al. Associations of lower vitamin D concentrations with cognitive decline and long-term risk of dementia and Alzheimer’s disease in older adults. Alzheimers Dement. 2017 Nov;13(11):1207-1216. doi: https://doi.org/10.1016/j.jalz.2017.03.003
4 Beydoun MA, et al. Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis. BMC Public Health. 2014;14:643. doi: https://doi.org/10.1186/1471-2458-14-643
5 Godos J, et al. Fish consumption, cognitive impairment and dementia: an updated dose-response meta-analysis of observational studies. Aging Clin Exp Res. 2024;61:3731–3739. doi: https://doi.org/10.1007/s40520-024-02823-6
6 Sala-Vila A, et al. Plasma Omega-3 Fatty Acids and Risk for Incident Dementia in the UK Biobank Study: A Closer Look. Nutrients. 2023 Nov;15(23):4896.
8 Li Y, et al. Long-term intake of red meat in relation to dementia risk and cognitive function in US adults. Neurology.2025;104(3):e210286. doi: https://doi.org/10.1212/WNL.0000000000210286
9 Luchsinger JA, et al. Hyperinsulinemia and risk of Alzheimer disease. Neurology. 2004;63(7):1187–92. doi:https://doi.org/10.1212/01.WNL.0000140292.04932.04932.87; see also Abbatecola AM, et al. Insulin resistance and executive dysfunction in older persons. J Am Geriatr Soc.2004;52(10):1713–
8. https://doi.org/10.1111/j.1532-5415.2004.52466.x ;see also Xu WL, et al. Uncontrolled diabetes increases the risk of Alzheimer’s disease: a population-based cohort study. Diabetologia. 2009;52(6):1031–
9. doi: 10.1007/s00125-009-1323-x ;see also Hassing LB, et al. Type 2 diabetes mellitus contributes to cognitive decline in old age: a longitudinal population-based study. J Int Neuropsychol Soc. 2004;10(4):599–607. https://doi.org/10.1017/S1355617704104165 ; see also Yaffe K, et al. Glycosylated hemoglobin level and development of mild cognitive impairment or dementia in older women. J Nutr Health Aging. 2006;10(4):293–5. https://pubmed.ncbi.nlm.nih.gov/16886099/ ; see also Roberts RO, et al. Diabetes and elevated hemoglobin A1c levels are associated with brain hypometabolism but not amyloid accumulation. J Nucl Med. 2014;55(5):759–64. https://jnm.snmjournals.org/content/55/5/759
10 Lee JY, Han K, Kim J, Lim JS, Cheon DY, Lee M. Association Between Metabolic Syndrome and Young-Onset Dementia: A Nationwide Population-Based Study. Neurology. 2025 May 27;104(10):e213599. doi: 10.1212/WNL.0000000000213599. Epub 2025 Apr 23. PMID: 40267374.11 Underwood PC, et al. HbA1c time in range and dementia. JAMA Netw Open. 2024;7(8):e2425354. doi: https://doi.org/10.1001/jamanetworkopen.2024.25354
Patrick Holford’s new book claims that almost no one needs to develop Alzheimer’s.
Fewer than 1% of Alzheimer’s cases are genetic, and amyloid deposits – long targeted by new drugs – are neither the cause of the disease nor its cure.
Alzheimer’s is the consequence of a ‘perfect storm’ – a combination of poor diet, unhealthy lifestyle and harmful environmental factors that affect the structure, function or utilisation of the brain, says Patrick Holford, our founder and author of Alzheimer’s: Prevention is the Cure. He says: “Every single known risk factor affects one of these, and it is combinations of these risk factors – which are under our control – that lead to cognitive decline, first experienced as brain fog and forgetfulness”.
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Figure 1 – Structure, Function and Utilisation model of risk factors forcognitive decline
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The book stems from a major global Alzheimer’s prevention project by the charity Food for the Brain, which has assessed the cognitive function of hundreds of thousands of people through a free test, followed by a comprehensive diet and lifestyle questionnaire that calculates their future risk – and shows how to lower it.
“We can detect declining cognitive function from as young as 18. The youngest non-genetic Alzheimer’s diagnosis is just 19,” says Holford, who founded the charity to help prevent Alzheimer’s. “We see a steady decline in cognitive function from the early twenties, with most people starting to show significant cognitive impairment in their seventies and eighties. But this decline cannot only be arrested – it can be reversed with the right diet, supplements and lifestyle choices.”
“Becoming an Alzheimer’s patient is almost always a choice,” says neurologist Dr David Perlmutter, a member of the charity’s Alzheimer’s Prevention Expert Group who also believes that diet and lifestyle, much more than genes, are driving the increase in Alzheimer’s.
“Becoming an Alzheimer’s patient is almost always a choice“
neurologist Dr David Perlmutter
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The book (out today!) explains all the known risk factors we can change – and the extent to which doing so reduces future risk. Particularly important are what Holford calls ‘the four horsemen of the brain health apocalypse’: lack of brain fats, lack of B vitamins, lack of antioxidants, and too much sugar and refined foods. Increasing omega-3 intake from oily fish and supplements cuts risk by about 20%, as does optimising vitamin D levels. Vitamin D is produced in the skin when exposed to sunlight, with some also obtained from oily fish, but supplementation is needed during the winter months. Those who supplement with vitamin D have about one third less risk of developing dementia.
The single biggest–and most easily eliminated–risk factor, is lack of B vitamins, leading to high levels of the toxic amino acid homocysteine. “Homocysteine, if raised above 11 µmol/L, causes brain shrinkage and cognitive decline. If lowered with B vitamins, both shrinkage and decline are arrested. It is the only risk factor for which the evidence is strong enough to say it is causal.” says Holford. “Mine is 7 µmol/L but my wife’s, despite eating the same food, was 15µmol/L – right in the brain-shrinking zone. She now supplements high-dose B12, B6 and folate and her level has dropped to the same as mine. You would never know without testing. We are both in our sixties.” He estimates that half of those over-60 have a homocysteine level above 11, increasing their risk by about one-third.
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Figure 2 – Possible Population Attributable Dementia Risk Reductions (estimates)
The test kit also measures HbA1c, which GPs use to diagnose diabetes. However, the optimal level for Alzheimer’s prevention is lower than the threshold used to diagnose diabetes. Eating less sugar, fewer refined and ultra-processed foods, and reducing total carbohydrate intake also cuts dementia risk by about 20%.
Another big risk reducer is increasing intake of fruits and vegetables rich in antioxidants, and supplementing with vitamin C. Those in the top third of antioxidant intake have half the risk of cognitive decline, according to a study of 2,716 people over age 60 (1). The home-test kit also measures antioxidant status, specifically glutathione levels. Greens and beans are rich sources of the B vitamin folate. A recent study found that swapping one serving of processed meat for a serving of nuts or beans – foods high in folate – was associated with a 19% lower risk of dementia (2).
Getting your diet right is only half the story, says Holford. “Minimising alcohol, not smoking, staying physically active, and having a socially and intellectually stimulating lifestyle are all vital parts of dementia-proofing. So too are getting enough sleep, managing stress, and ensuring good hearing and vision. Cataracts, for example, increase risk, but having cataract surgery significantly lowers it. Women also need to support hormonal health after menopause. Often using ‘natural’ HRT makes a big difference.”
The book is out in the UK, EU today and you can pre-order for USA & Australia too (they will be shipped ot you in 3-5 weeks) .
When you buy a book from us, you’re not just gaining valuable knowledge – you’re supporting a cause. Every penny from your purchase goes directly back into Food for the Brain, helping us advance research and develop life-changing tools to support cognitive health.
Also join us in May for the Alzheimer’s Prevention Day
Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.
By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices. Please support our research by becoming a Friend of Food for the Brain.
As parents or caregivers, nothing matters more than our children’s future. We want them to thrive – mentally, emotionally and physically – and to feel confident and capable in a complex, ever-changing world. Yet when it comes to their brain development, many of us are left wondering: are we doing enough? Are they getting what they need to build healthy, resilient minds?
This is why we’re proud to introduce our groundbreaking Smart Kids Cognitive Function Test. Developed by the team behind the widely respected Adult Cognitive Function Test, this tool is designed to empower parents with the knowledge, insight and practical strategies to support their child’s cognitive and emotional development, right from the start.
Why Early Brain Health Matters
From the moment they’re born, a child’s brain is growing at an extraordinary pace – forming up to a million new neural connections every second. These formative years are a critical window of opportunity, where the right nutrition, environment, and emotional support can set the foundation for a lifetime of strong cognitive function, balanced mood and behavioural wellbeing.
This test doesn’t just measure ‘smarts’ – it helps you understand how your child’s brain is functioning, what might be holding them back, and most importantly, what you can do about it.
What’s Involved?
Tailored for children aged 4 to 17, the test includes three essential elements:
Cognitive Function Assessment. An engaging 15-minute digital test that challenges attention, memory and problem-solving in a fun, interactive way.
Nutrition & Lifestyle Questionnaire. This helps highlight which of the eight key lifestyle areas may be influencing brain health, from sleep and gut health to sugar balance and essential fats.
Strengths & Difficulties Questionnaire. A validated tool assessing emotional and behavioural wellbeing, giving you a fuller picture of how your child is feeling and functioning.
With this holistic insight, you’ll receive tailored guidance and practical steps to help your child move forward – cognitively, emotionally and behaviorally.
What Parents Are Saying
“COGNITION helped me understand why my son was struggling with focus—and what I could do to help. The emails made it so easy to build new habits. We saw a real change.” – Parent of a 9-year-old
“It was like someone had finally put the pieces together. We started with sugar balance and sleep—and within weeks, our daughter’s mood and energy improved.” – Mum of a 13-year-old
A Mission for Change: Your Role as a Pioneer
By joining the first 1,000 families to complete the free Smart Kids Test, you’re helping us shape a healthier, smarter future for the next generation. Together, we can build a new model of prevention and wellbeing that begins not at midlife, but in childhood where it can make the biggest difference.
Have You Taken the Adult Test?
Many parents in our community have already taken the free Adult Cognitive Function Test – designed to help dementia-proof your diet and lifestyle. If you haven’t yet done so, we urge you to take this important step. Your brain matters too, and change is possible at any age.
Also, did you know that you can complete our at home pin prick DRIfT blood test on children over 2 years of age and they are available internationally. So that you can gather more data on what your child needs to thrive.
To Our Dementia Prevention Community
We know that many of you found us through our mission to prevent Alzheimer’s and cognitive decline. This children’s test is a natural extension of that work, because optimising brain health starts young. Helping your child now doesn’t just support their academic success, it lays the foundation for lifelong mental wellbeing.
Take the Smart Kids Cognitive Function Test today – and invest in your child’s brain, their wellbeing, and their future.
Do the adult Cognitive Function Test here if you haven’t done so yet, so you can model what supporting your brain health looks like to your child and family.
Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.
By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices. Please support our research by becoming a Friend of Food for the Brain.
Recently, the Telegraph reported: “Statins can reduce the risk of dementia among those who already have low cholesterol.” The article claimed that those on statins were less likely to develop dementia – even Alzheimer’s – and that low LDL cholesterol was somehow protective.
Frankly, this is dangerous misinformation.
Why? Because it contradicts robust scientific evidence that low cholesterol – particularly below 4 mmol/l – increases the risk for dementia. That’s hardly surprising when you consider that 25% of the cholesterol in your body is in your brain. Cholesterol is a vital component of neuronal membranes – it’s not just blood fat, it’s brain fuel.
And as for statins? There’s no credible evidence that they prevent dementia. Quite the opposite: the evidence points to statins lowering brain-essential cholesterol and raising dementia risk. So I asked cholesterol expert Dr Malcolm Kendrick for his take on the study in question.
His response was blunt but justified: “This study is horseshit. Here’s why…”
Dr Kendrick Key Critiques:
LDL measurement was vague. It’s unclear if they even measured LDL directly- most studies use the Friedewald formula, known to be wildly inaccurate, especially with high triglycerides or low HDL.
Only one measurement. LDL was recorded once at the study’s start – never again. That’s like measuring someone’s blood pressure once and claiming to predict their lifetime stroke risk.
Bizarre cohort overlap. Somehow, 170,174 participants were in both high and low LDL groups? That’s statistically and biologically nonsensical.
Alzheimer’s exclusion unexplained. Those with pre-existing Alzheimer’s were removed, but with no breakdown of their LDL levels – crucial missing data.
Propensity score manipulation. This “retrospective matching” excluded over 350,000 people, distorting the natural associations. Diabetes and hyperlipidaemia were artificially balanced between groups, masking real-world relationships.
Key confounder: statin timing. Participants were only included after being prescribed statins, meaning LDL levels were already artificially lowered. So “low LDL” here is post-drug, not natural. The entire premise collapses.
This study, like too many others published today, exemplifies what Drummond Rennie famously criticised:
“There is no study too fragmented, no hypothesis too trivial, no design too warped, no analysis too self-serving for it to be published.”
So what do we actually know? Here is an extract from Patrick’s new book – Alzheimers: Prevention is the Cure.
Cholesterol and the Brain – The Real Story
Your brain needs cholesterol. Low cholesterol (<4 mmol/l) is a clear risk factor for dementia. One biomarker study found that high homocysteine and low cholesterol were the best predictors of dementia risk【1】.
And what’s a common cause of low cholesterol in the elderly? Statins. These drugs have consistently failed to show benefits in preventing cognitive decline【2】.
This fits what we know genetically. The ApoE gene governs how cholesterol gets into neurons. Those with ApoE4 are less efficient at this – that’s why they’re more prone to cognitive decline.
It’s not high cholesterol itself that’s dangerous – it’s cholesterol mismanagement in the brain.
Yes, very high cholesterol (above 6.5 mmol/l) is statistically linked to increased dementia risk – but modest elevations, particularly with a healthy lifestyle, are not a problem【3】. And even that data is shaky. One meta-analysis of over a million people showed only a 14% increased dementia risk with “high” cholesterol. But the thresholds varied – some studies defined “high” as anything over 6.2 mmol/l【3】.
More importantly, people with higher cholesterol often eat more sugar, processed foods, and trans fats – all factors known to fuel inflammation and oxidative stress in the brain.
The Lancet Commission, which makes the anti-cholesterol case, even acknowledged this diet–dementia link: in a cohort of 94,184 Danes, poor diet predicted both high LDL and dementia risk【4】.
So maybe it’s not the cholesterol – it’s what comes with it.
Statins and the Hope for Vascular Dementia
Originally, statins were hyped for vascular dementia – about 20% of all dementia cases – because of their supposed blood vessel–protective effects. But that theory has fallen flat. A Cochrane review found no benefit from statins for dementia prevention【6】.
And the best independent trial – not funded by drug companies – also found no cardiovascular benefit for statins in older adults【5】.
There’s no data supporting the notion that statins protect the brain. Yet the Lancet Commission listed “high cholesterol” as contributing 7% to dementia risk, which will no doubt spur even more statin prescriptions【4】.
The Optimum Nutrition Perspective
From an optimum nutrition standpoint, we view cholesterol differently.
If your total cholesterol is up to 6.5 mmol/l – but you have high HDL, low triglycerides, low homocysteine, and a healthy diet low in sugar and refined carbs – you’re not at risk. In fact, you’re likely protected.
One recent study showed that higher HDL in midlife predicted significantly lower future dementia risk【7】. Low HDL, not high total cholesterol, is a hallmark of metabolic syndrome – the precursor to diabetes, heart disease, and yes, dementia.
The evidence is clear: cholesterol is essential for brain health. Statins do not prevent dementia – and may contribute to cognitive decline by pushing cholesterol levels too low.
Instead of dumbing down the brain with unnecessary statins, we need to smarten up with nutrients that build brain health: omega-3 fats, phospholipids, B vitamins, and a low-sugar diet.
Doctors prescribing statins as dementia prevention are not only missing the mark – they may be making things worse.
Let’s change the narrative. Let’s put nutrition – not cholesterol fear – at the top of the brain health agenda. Find out more in Patrick’s new book – Alzheimer’s: Prevention is the Cure.
Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.
By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices. Please support our research by becoming a Friend of Food for the Brain.
References
1 Gong, Q., Xie, L., Bi, M., & Yu, L. (2021). A probability formula derived from serum indicators, age, and comorbidities as an early predictor of dementia in elderly Chinese people. Brain and Behavior 11, e2236. https://doi.org/10.1002/brb3.2236
2 Peters, R, Breitner, J, James, S, et al. Dementia risk reduction, why haven’t the pharmacological risk reduction trials worked? An in-depth exploration of seven established risk factors. Alzheimer’s Dement. 2021; 7:e12202. https://doi.org/10.1002/trc2.12202
3 Wee J, Sukudom S, Bhat S, Marklund M, Peiris NJ, Hoyos CM, Patel S, Naismith SL, Dwivedi G, Misra A. The relationship between midlife dyslipidemia and lifetime incidence of dementia: A systematic review and meta-analysis of cohort studies. Alzheimers Dement (Amst). 2023 Mar 8;15(1):e12395. doi: 10.1002/dad2.12395. PMID: 36911359; PMCID: PMC9993469.
4 Kjeldsen EW, Thomassen JQ, Rasmussen KL, Nordestgaard BG, Tybjærg-Hansen A, Frikke-Schmidt R. Adherence to dietary guidelines and risk of dementia: a prospective cohort study of 94 184 individuals. Epidemiol Psychiatr Sci 2022; 31: e71.
5 Han BH, Sutin D, Williamson JD, Davis BR, Piller LB, Pervin H, Pressel SL, Blaum CS; ALLHAT Collaborative Research Group. Effect of Statin Treatment vs Usual Care on Primary Cardiovascular Prevention Among Older Adults: The ALLHAT-LLT Randomized Clinical Trial. JAMA Intern Med. 2017 Jul 1;177(7):955-965. doi: 10.1001/jamainternmed.2017.1442. PMID: 28531241; PMCID: PMC5543335.
6 McGuinness B, Craig D, Bullock R, Passmore P. Statins for the prevention of dementia. Cochrane Database Syst Rev 2016;1: CD003160.
7 Zhang X, Tong T, Chang A, Ang TFA, Tao Q, Auerbach S, Devine S, Qiu WQ, Mez J, Massaro J, Lunetta KL, Au R, Farrer LA. Midlife lipid and glucose levels are associated with Alzheimer’s disease. Alzheimers Dement. 2023 Jan;19(1):181-193. doi: 10.1002/alz.12641. Epub 2022 Mar 23. PMID: 35319157; PMCID: PMC10078665.
With the arrival of spring come brighter days and flowers blooming all around. Sadly, it also marks what feels like yet another season full of sugar, with supermarket shelves overflowing with chocolate eggs, bunnies and other sugary temptations in every shape and size.
But knowing what we now do about how excess sugar impacts brain function (read more about how sugar impacts your brain here), whether you are 4 or 94 years old, the question is: what can you do instead?
We recommend heading into the kitchen to whip up some brain-friendly sweet treats – snacks that not only satisfy your sweet tooth, but also nourish your brain, support appetite control, and feed your gut microbiome.
With the launch of our Smart Kids Programme just weeks away, this recipe is perfect for creating fun and functional treats for the whole family – or even as a healthier option for your garden Easter egg hunt (just wrap them in foil if you’re hiding them for the kids!).
This recipe comes straight from theUpgrade Your Brain App, which includes over 100 delicious, brain-optimised recipes. If you haven’t already, subscribe today for just £30 for the whole year.
Brain-Boosting Highlights Per mini egg (based on 14 per batch, without protein powder or coconut oil)
Low Glycemic Load (GL) & brain-friendly. Naturally sweetened with a little honey or maple syrup, these eggs contain just 2.5g of sugar each – helping to keep blood sugar levels balanced, which is key for maintaining stable mood, focus, and energy. (To reduce the GL you swap in chicory root syrup instead of honey or maple syrup. Use code FFB10 to get 10% off)
Supports the gut–brain axis. As we highlight in the COGNITION Programme and the upcoming Smart Kids initiative, a healthy gut = a healthier brain. Each mini egg delivers around 1.4g of fibre, thanks to oats, almonds, and cacao – feeding your good gut bacteria and reducing inflammation linked to cognitive decline.
Packed with healthy brain fats. With approximately 7g of fat per egg, these treats supply nourishing fats from almond butter (rich in vitamin E and monounsaturated fats) and dark chocolate (a source of flavonoids and magnesium) – both essential for supporting neurotransmitters and building stress resilience.
Optional protein boost. Even without added powder, each egg delivers around 2.5g of protein to help steady energy and mood throughout the day. Protein provides key amino acids – like tryptophan and tyrosine – that your brain uses to make serotonin and dopamine. For a little extra, simply add your favourite clean protein powder to increase the total to around 4g per egg. At any age, regular protein intake is vital for brain performance and emotional stability.
2 tbsp honey or maple syrup (it is also worth buying some low GL chicory root syrup to further reduce sugar intake. Use code FFB10 to save 10% on your order)
2 tbsp good quality cacao powder
2 tbsp oat flour (or ground almonds)
Pinch of salt
Optional: 1 scoop vanilla or chocolate protein powder
Optional: 1 tbsp melted coconut oil (helps texture if mix is too thick)
50g dark chocolate (70%+), melted, for coating
Optional: Crushed nuts, shredded coconut, or freeze-dried raspberries for decoration
Method
In a bowl, mix almond butter, honey, cacao, oat flour, salt, and optional protein powder well until you get a thick but moldable dough.
If it’s too dry, add a teaspoon of water or 1 tbsp melted coconut oil.
Shape into small egg shapes using your hands (about 1 tablespoon – or slightly less per egg). try to work quickly so they don’t get too soft.
Place on a lined tray and chill in the freezer for 15 minutes.
Melt the dark chocolate gently in a bowl over hot water (or microwave in short bursts).
Dip each mini egg in the melted chocolate to coat and place back on the tray.
Optionally, sprinkle with nuts, coconut, or raspberry pieces before the chocolate sets.
Chill until set (about 15 minutes in the fridge).
Store in the fridge for up to a week.
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Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.
By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices. Please support our research by becoming a Friend of Food for the Brain.
If you think that Alzheimer’s or dementia is caused by amyloid plaques in the brain, or tangles of nerves (neurofibrillary tangles) associated with p-tau, you have been successfully fooled. But you would not be alone. There is a vast sleight of hand going on that remarkably continues to hijack research into true causes and potential cures for Alzheimer’s, despite a mountain of clear evidence to the contrary.
Let’s start at the beginning. Some people suffer increasingly severe cognitive decline. This affects about one in ten older people. We call this dementia. Some people with dementia, on scanning their brains, have big gaps in the central part of the brain. This is used to diagnose the form of dementia known as Alzheimer’s disease, due to the clear evidence of ‘pathology’ – something wrong in the brain that amounts to the death of significant amounts of brain cells in critical areas.
So, here we have two clear diagnostic criteria. Firstly, a loss of cognitive function, which is what is tested by the dementia prevention charity, Food for the Brain, with its free, online Cognitive Function Test. Secondly, a loss of actual brain, which is diagnosed by a type of brain scan of the central or medial part of the brain. This scan was first developed based on research at Oxford University, headed by Professor David Smith, who is a member of the Scientific Advisory Board – see foodforthebrain.org/sab.
What Causes Alzheimer’s?
So, then the question is: what causes it? There has never been any evidence (and there is still no evidence), that Alzheimer’s, except for the very rare early-onset types of Alzheimer’s caused by genes, is caused by deposits of amyloid protein or amyloid plaque in the brain. “Over the past 25 years, Alzheimer’s research has suffered a litany of ostensible fraud and other misconduct by world-famous researchers and obscure scientists alike, all trying to ascend in a brutally competitive field,” claims Charles Piller in the New York Times [1], author of the book, Doctored: Fraud, Arrogance, and Tragedy in the Quest to Cure Alzheimer’s.
An example of the ‘doctoring’, reported by Dr Matthew Schrag, professor of neuroscience at Vanderbilt University, in Science in 2022, identified as many as 10 papers on the protein that deserve deeper scrutiny [2]. The report also cited other prominent researchers who have had difficulty replicating results of the studies on the specific proteins. The original research has now been withdrawn.
The reality is that about 30% of older people have plaques in their brains without dementia. About 15% of those with dementia don’t have amyloid plaques [3]. Having amyloid plaques doesn’t cause dementia. Mice whose brains have been molecularly engineered to produce amyloid plaques behave normally. Even a head full of plaques only results in mild memory problems. Many of us have plaques in our brain and remain completely healthy.
What started the amyloid excitement?
Less than 1% of diagnoses of Alzheimer’s are caused by genes. These account for very early onset cases. The genes are Amyloid Protein Precursor (APP) gene and Presenilin (PS1 and PS2). Now these rare dementias can all plausibly be assumed to be caused by amyloid plaque deposition, and to be potentially curable by its removal. However, being so rare, there is little commercial imperative to find out. There is, however, one study in 2019 that tested two different anti- amyloid treatments given to those with this rare early-onset Alzheimer’s. Despite both drugs effectively lowering the amyloid burden, there was no clinical improvement, but a slight worsening for one of these treatments compared to placebo. In addition, one in five had brain swelling [4]. That would be reason enough to give up on the amyloid hypothesis.
The big mistake, however, was the leap of faith assuming that therefore ALL Alzheimer’s, which makes up two thirds of dementias, were also caused by amyloid accumulation and could be so treated with drugs to lower the amyloid burden.
What happens if you ‘treat’ amyloid plaques?
Blocking the enzymes that make amyloid has made people worse, not better, despite lessening the amyloid burden [5]. Vaccinating animals to remove the plaques doesn’t change anything to do with dementia, but it does reduce the amyloid. The anti-amyloid vaccine injections in humans have been equally ineffective (in terms of impacting dementia), despite lowering their amyloid burden.
The pharmaceutical companies running these failed trials have pushed and pushed until they could just about get a ‘significant’ difference in the rate of degeneration of patients versus placebo on assessment questionnaires – just enough to get a medical licence despite being clinically ineffective. Lecanemab was the first to be licensed in the UK, in 2024. The difference in the lecanemab trial between those on the drug and those on placebo was equivalent to less than half a point (0.45) change on an 18 point Clinical Dementia Rating (CDR) scale [6]. According to a British Medical Journal editorial this decrease “fell well short, representing only around a third of what a minimum clinically important difference might look like.” [7]
On another scale, the Alzheimer’s Disease Assessment Scale (ADAS), both those on placebo and drug treatment start to decline rapidly after 15 month (see figure 1 right). The Alzheimer’s Society [8] report this miniscule difference as ‘Lecanemab slowed down the speed at which memory and thinking skills got worse by 27%’.
Figure 1 – Worsening of ADAS cognitive score with lecanemab versus placebo
This was the figure reported in the newspapers, ignoring the fact that, in reality, those on the drug just hit the same rock bottom about 3 months later than those on the placebo and the difference is so small that no-one is likely to notice. No-one got better. They all got worse. Quite a few got adverse effects, with brain bleeding and swelling. More than a quarter had adverse reactions. A few died as a consequence. Is three months of ‘slightly less worse’ worth the suffering of one in four and the death of a few (about one in 500) at vast expense? If such treatment was started before a person was put into care, at best it could mean putting them in a care home three months later, potentially saving £3,000. If treatment were given while in a care home it would mean three months more time in a care home, potentially costing £3,000 more. Either way, at a treatment cost more likely to be in the region of £50,000 per year this is clearly not cost effective for the NHS.
But still, drug regulatory agencies, paid for by the drug industry, dished out licences because the results were ‘statistically significant’- the result of enrolling as many as 1795 people. Larger trials make small positive results look better.
Even so, the UK watchdog NICE said the evidence wasn’t good enough and recommended the National Health Service not to give anti-amyloid treatment – at about £50,000 a patient per year when you factor in the cost of scans needed to check for bleeding and swelling with each injection and medical costs. Despite this you’ll read newspaper headlines such as ‘Alzheimer’s drugs should be prescribed like statins’, as appeared in the Telegraph [9], interviewing Professor Hardy from UCL.
Please also bear in mind that even these bad results are the best that the drug company, who funded and ran their own drug trial could conjure up with questionable methodology. The CDR (Clinical Dementia Rating) is essentially a questionnaire completed by a partner/carer and clinician. If you had vested hope that your loved one might improve on an experimental drug, might you answer slightly more positively?
Also, these trials are meant to be ‘double-blind’ i.e., the patient (and carer/partner) doesn’t know if they are injected with a placebo or drug. But when almost a quarter get severe side-effects just how ‘double-blind’ is it? If you got side-effects, assumed you were on the drug, would the hope of improvement bias your answers?
The truth is it is easy to cheat in trials, or at least massage the results in your favour, and there is a strong motive to do so, if it’s your drug, job and profits at stake. That’s why I trust trials done on drugs or vitamins by independent researchers. These don’t exist for the anti- amyloid drugs and are unlikely to, due to the vast expense of such trials. Independent researcher Sarah Ackley wanted to do a meta-analysis for publication in the British Medical Journal of anti-amyloid drug trials. She identified 34 trials suitable for inclusion in her analysis, but was denied access to the data of 20.[10] In other words, a drug company can run a failed trial, ditch it and move on, only revealing those that show an effect. Out of the 14 trials she was allowed to see the data from their meta-analysis concluded: “Combined results from 14 randomized controlled trials provide evidence that reduction in amyloid levels alone is unlikely to substantially slow cognitive decline within the follow-up period of most typical trials. The results of pooled estimates suggest that use of anti-amyloid drugs is not a viable strategy for the prevention or treatment of Alzheimer’s disease and that other potential targets may merit more attention.”
Pharmacology Professor David Smith from the University of Oxford responded to the British Medical Journal[11] saying “Scientists should seriously question the validity of the basic amyloid hypothesis, as was pointed out more than 10 years ago in relation to earlier trials.[12] These findings should direct our attention to the prevention of Alzheimer’s disease by slowing down the disease process, for which there are many possible approaches. The study also raises an ethical question: is it justifiable to ask patients to undergo yet more trials of anti-amyloid treatments? Moreover, we should all question the morality of the drug companies that declined to give these researchers access to data for 20 of the 34 trials they wanted to study.”
In scientific terms, the poor results of the clinical trials, despite lowering amyloid burden, added to the already existing mountain of evidence, that amyloid deposits don’t cause Alzheimer’s; lowering it doesn’t stop the disease process, doesn’t improve cognitive powers in any meaningful way and doesn’t slow down brain shrinkage. In fact, if anything, it accelerates the main physical measure of brain shrinkage. In the anti-amyloid trial for donanemab, those on the amyloid treatment had considerably more whole brain shrinkage – greater than 20% more than those on the placebo (see graph below).[13]
Figure 2 – Brain shrinkage with donanemab versus placebo
You would think that the whole field would get the message by now; stop funding this dead end and explore other avenues. But there is a lot of investment in the ‘amyloid cascade hypothesis’ that no-one wants to give up. It’s become an unhealthy obsession.
In the US, the Alzheimer’s Association and in the UK the Alzheimer’s Society and Alzheimer’s Research UK, have all supported this line of research and continue to do so. The Alzheimer’s Society, having part funded original research into amyloid with Professor Hardy, consider this their greatest contribution to the field, ‘revolutionising dementia research’.[14] The trouble is, it’s a dead end.
In 2024, there were 164 clinical trials registered assessing 127 drugs, many of which are based on amyloid and p-tau.[15] With several million ‘eligible’ patients, pharma is not going to give up.
Why aren’t other avenues being explored?
It’s partly to do with money. No-one can get research money if they’re not looking at amyloid (or p-tau – more on this in a minute).
In the UK, the Medical Research Council continues to pour good money after bad by making another £20 million available for drug trials.[16] That’s taxpayers’ money backing the wrong horse, despite a lousy track record. In the US, the National Institutes of Health and the National Institutes of Aging spend vast sums pushing in this fruitless direction. Big pharma spends twice as much as the government agencies and the charities, both of which are funded by the taxpayers, probably around $150 billion so far. So, perhaps $250 billion has been spent getting almost nowhere. Sure, we know a lot more about amyloid and p-tau, but are no closer to a ‘cure’.
I remember when, at the G8 Summit in 2013 in London, pharma- funded scientists said, Within ten years we’ll have a cure. Listening to the BBC Radio 4’s Inside Health programme on ‘What’s next for Alzheimer’s’ [17] in November last year, they said the same thing. How can you claim you’ll have a cure when you don’t even know the cause? I predict we’ll be in the same place in ten years if the Alzheimer’s industry doesn’t move on from amyloid and p-tau.
But it gets worse. Despite nothing but evidence to the contrary, based on the completely false notion that ‘Alzheimer’s IS amyloid’, we are being told an amyloid blood test is around the corner. This will tell us nothing useful. It won’t tell us who has Alzheimer’s or who is at risk. So why take the test?
The case for developing a test was made by Professor Hardy in the Telegraph. “My dream is you go the doctor at age 60, have a test, just as you would do for cholesterol. So, it finds you’re at high risk for Alzheimer’s disease, let’s put you on anti-amyloid drugs. Scientifically not difficult.” This may be his pipe dream but, as you have read, no treatment has yet shown a clinically significant effect. A Cognitive Function Test is a better (and free) predictor than an amyloid test, anti- amyloid drugs don’t work and are dangerous. Also, statins don’t work nearly as well as we were led to believe. But the two-step dance of a test that feeds a prescription to healthy people certainly made a lot of money. Over $1 trillion. Statements like this are about sales not science. At best, not that there is evidence to support this, he says that it could
mean going from diagnosis to nursing home in seven years instead of five years. In other words, no-one gets better or stays the same. They would just get worse more slowly.
All this is laid out beautifully in a book by Karl Herrup, Professor of Neurobiology and Investigator at the Alzheimer’s Disease Research Centre at the University of Pittsburgh, called How NOT to study a disease – The Story of Alzheimer’s. If you are questioning what I am saying, please read this book. You can find it in the online bookstore at foodforthebrain.org in the books section.
The medical-pharmaceutical industry is so desperate to find a treatment and make money that it just can’t give up. It reminds me of the story of Mullah Nasrudin, who was looking at the illuminated ground under a lamp post. A passer-by asked, ‘What are you looking for?’ The Mullah said, ‘I dropped a coin.’ The passer-by replied, ‘Did you drop it around here?’ The Mullah said, ‘No, but it’s the only place I can see’.
It’s akin to a campaign to ‘cure’ lemmings when the only cure is for them not to jump off the cliff in the first place. Why spend all that money researching how to give lemmings the medical attention and hospital care as they approach death, when there is a far simpler and less expensive way to help them not need it. Prevention.
A person with dementia will cost the state and family around £100,000 [18]. We can help someone substantially reduce their risk by joining Food for the Brain’s COGNITION programme with a small annual donation. So, for everyone we save from dementia, we could help thousands more.
But let’s be clear. It is true that having lots of amyloid in your brain can increase the PROBABILITY of getting Alzheimer’s in the future, in much the way that being older also increases the probability of getting Alzheimer’s. But it doesn’t cause it. So ‘curing’ amyloid won’t cure the disease.
The same thing is happening with another ‘marker’ in the brain called p-tau, which is associated with having more tangled nerves. Tau is a normal protein that becomes an abnormal, toxic protein called p-tau. The ‘p’ stands for phosphorus or ‘phosphorylated’ because there’s an enzyme that adds on the ‘p’ and another that takes it away. Much like amyloid, having more p-tau increases the PROBABILITY of Alzheimer’s, but does it cause it? Many people have raised levels of p-tau (we all have some) with no problems at all. However, unlike amyloid, there is a threshold such that if you have a lot of p-tau, which means a lot of tangled nerves, this does correlate with the degree of cognitive impairment.
By using the same sleight of hand, £10 million has been put up by the Bill Gates Foundation and people funding Alzheimer’s Research UK, to find the blood test for p-tau (I think they’ve already decided on one called p-tau 217), despite questionable evidence that p-tau causes Alzheimer’s and may just be an artefact of the disease process. In a similar way, tooth decay caused by nutrition and lifestyle deficiencies, such as too much sugar and not brushing your teeth.
No doubt, those with raised p-tau 217 will be told they have ‘pre-clinical dementia’, despite no evidence that they do. Of course, if they had a p-tau lowering drug that actually worked, as in reducing dementia risk, that might be excusable, but they don’t. Those that have blocked the enzymes that cause the accumulation of p-tau have failed. A more relevant question is what causes p-tau to go up? In other words, go to the root of the problem. However, this sleight of hand may be used to sell drugs that don’t work, much like ‘cholesterol’ has been used to sell statins.
My cholesterol is slightly high – I have no disease, no risk factors for heart disease and there is no evidence that lowering my cholesterol will lower my future risk, but still my doctor wants to prescribe me statins. Why? Because GPs are given a calculator called QRisk where you pop in age and cholesterol level and it says ‘prescribe statins’. In any case – two thirds of heart attacks are predicted by high homocysteine – not cholesterol.
P-Tau Delusion
With the failure of amyloid drugs to commercialise much emphasis is being put on p-tau inhibitor drugs. So far there are no good clinical results with several horses in the race.
The only thing I know that does lower p-tau is lowering homocysteine with B vitamins. Homocysteine, a toxic amino acid also found in those with Alzheimer’s and dementia, promotes the enzyme that makes p-tau and blocks the enzyme that clears it from your brain [19], as the diagram overleaf shows.
However, homocysteine, unlike amyloid, is actually causal. That is, lowering homocysteine with B vitamins, stops the accelerated brain shrinkage, stops the cognitive decline and memory loss. That is consistent with a disease-modifying treatment and possibly the only thing, which from the current evidence, could be said to be causal. It is possible that some of its benefit is in lowering p-tau. There’s not enough research yet to say more than that at this point in time.
Figure 3 – How lowering homocysteine inhibits p-tau formation.
Of course, the ‘tauists’ know this and most of the drugs being developed try to do what lowering homocysteine does. Building on a few discoveries that ‘methylene blue’ [20], a methylated colouring, interfered with the formation of p-tau, and that the amino acid cysteine is involved in tau accumulation [21], drugs such as HMTM (Hydromethylthionine mesylate) exploit this bit of chemistry. Lack of B vitamins messes up methylation and homocysteine accumulates, leading to more p-tau formation. (Homocysteine is made from the amino acid methionine, which can also be turned into the amino acid cysteine, then glutathione – see Chapter 6). It is unlikely these drugs will have a substantial clinically significant effect, and much less so than lowering homocysteine. No doubt they will have adverse effects to factor in. But it won’t stop the drive to get such tau accumulation- inhibitor (TAI) drugs to market. Of course, it would be easier to just lower homocysteine with inexpensive and safe B vitamins, but these cannot be patented and hence cannot generate the profit pharma companies are looking for.
If treatment was really being driven by science, everyone would already be shouting about homocysteine lowering B vitamins (see Chapter 6). One senior representative of a pharma company told Professor David Smith, whose research on homocysteine is par excellence, that homocysteine lowering B vitamins would be a ‘multi-billion blockbuster drug if it could be patented’. But therein lies the problem
That doesn’t mean there won’t be other causes. Not everyone who develops Alzheimer’s has high homocysteine levels. There are other natural processes and compounds that can become damaging if they get out of balance. For instance, oxidants and inflammation protect against injury and infection but can damage mitochondria – the so called ‘energy’ factories inside every brain – if levels get too high. The effects of insulin resistance and damaged glucose control are similar.
Diabetes and dementia are strongly linked, the first doubling the risk of the second. [22] In truth, both homocysteine, which is a measure of a vital process called methylation, oxidation, insulin resistance and inflammation all affect the mitochondria. One clue for inflammation being involved relates to the finding that those with rheumatoid arthritis using heavy duty anti-inflammatory drugs have less risk for Alzheimer’s.[23]
These are some of the fruitful avenues that have been explored and show real promise. But they have all largely been ignored because of the unhealthy obsession by Pharma, the Alzheimer’s societies and government funding bodies on amyloid and tau. They will be explored in subsequent chapters.
In Food for the Brain’s model of dementia, glycation, oxidation, methylation and the vital role of brain fats, which actually build the brain, are central. I call them the ‘four horsemen of the mental health apocalypse’. The discovery that the homocysteine lowering B vitamins and omega-3 are co-dependent and together, dramatically slow brain shrinkage and improve cognitive function much better than any amyloid or p-tau treatment to date, is of major importance. Yet, this has been largely ignored by the blinkered Alzheimer’s establishment. So, next time you are asked to donate to Alzheimer’s charities ask them if any of the money is being spent on amyloid or p-tau. If it is, I’d suggest politely declining. If instead they are funding research into oxidation, inflammation, homocysteine, insulin or mitochondrial function, then that’s a much better sign that your money is being put to good use.
Is Alzheimer’s prevention the cure?
However, just focusing on one of these avenues may be misguided. It is based on the current paradigm of medical research – find the thing that is causing the disease, then ‘cure’ that. This assumes there is one cause and therefore one treatment. Of course, this is what you need for a drug to make money.
Let’s take homocysteine as an example. Not everyone who develops dementia or Alzheimer’s has high homocysteine. According to research at the US National Institutes of Health, it accounts for 22% of the risk.[24] Those who do have high homocysteine will reliably develop dementia and lowering it reliably reduces their cognitive decline. So, high homocysteine is a CAUSE, but not the only cause. Insulin resistance leads to diabetes and increases the risk for dementia. So, insulin resistance, driven by too much sugar and refined carbohydrates, is probably a cause, but not the only one. There isn’t enough evidence yet to declare ‘cause’, but the evidence that exists certainly points that way.
There is a different way of thinking and researching called ‘systems-based’ science. Much like the straw that breaks the camel’s back, this approach presumes there are a number of conditions, not just one, that can result in a disease such as Alzheimer’s or dementia. After all, a stroke or head injury can be a cause of cognitive decline, even if you don’t have high homocysteine or blood sugar problems. (It could be that a potential causal mechanism that ties these together is cerebrovascular dysfunction – disturbed blood supply to the brain. High homocysteine, by the way, increases risk of this by 17-fold [25]).
In my book Upgrade Your Brain, which gives all the referenced studies for statements made here, I argue that every known risk factor or biomarker for cognitive decline, dementia or Alzheimer’s affects either the structure, the function or the utilisation of the neuronal network and that it is combinations of these that crank up risk and ultimately brain pathology.
It’s like saying five critical things have to work for your car to move forward and not crash. Tyre pressure good, brakes working, enough gas, oil to lubricate the engine and water to cool it. If any one of these is completely broken, the car stops or crashes. If two are not working well, such as low oil and low water, the car grinds to a halt. If the brakes aren’t working, you crash.
We tend to think this way in nutrition and lifestyle medicine. It’s the combination of insults such as high sugar intake, too many fried foods, lack of vegetables, too much alcohol and smoking, that breaks the camel’s back. That heart attack is the ‘perfect storm’ of several underlying factors.
This systems-based approach isn’t popular in science and very few funders ever put up money to fund this kind of research. Usually, a funder wants to fund one stream of research, possibly a clinical trial of one approach, in the belief that this one factor is the key and a great discovery will be made. The reality is that it is usually combinations of factors that drive risk, with the manifestation of the disease itself being the ‘broken back’. Pollution, for example, is a risk factor for dementia … but not in those with good vitamin B6, folate or B12 status [26], which are the three B vitamins needed for methylation, indicated by lower homocysteine. Methylation is a major mechanism in the body, used to detoxify pollutants and toxins.
This is where Food for the Brain’s approach is unique. By collecting data from people like you who have both taken the Cognitive Function Test and completed the COGNITION questionnaire, and keep doing so, we can look at what drives cognitive function up and down. In other words, what ‘breaks the camel’s back’ or alternatively, makes it ‘strong’. This kind of complex systems-based science has become possible due to big data gathering (such as we are doing), advances in complex statistics, computer power and programming AI algorithms. Our Head of Science, Associate Professor Tommy Wood, is an expert in this kind of approach to neuroscience.
It is, I believe, the future and why we will probably find no single primary cause for Alzheimer’s, and certainly not amyloid or p-tau, but combinations of diet and lifestyle and other factors that create the tipping point that leads to dementia. Then, we will have the means to prevent this tipping point from ever being reached. In other words, we may discover that prevention is the cure.
Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.
By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices. Please support our research by becoming a Friend of Food for the Brain.
3. Herrup K. The case for rejecting the amyloid cascade hypothesis. Nat Neurosci. 2015 Jun;18(6):794–799. doi: https://doi.org/10.1038/nn.4017 (Also see references and full discussion in Chapter 8 of How Not to Study a Disease, K. Herrup, MIT Press. Lopez OL, et al. Association Between β-Amyloid Accumulation and Incident Dementia in Individuals 80 Years or Older Without Dementia. Neurology. 2024 Jan 23;102(2):e207920.)
4. Salloway S, et al. Dominantly Inherited Alzheimer Network–Trials Unit. A trial of gantenerumab or solanezumab in dominantly inherited Alzheimer’s disease. Nat Med. 2021 Jul;27(7):1187–1196. doi: https://doi.org/10.1038/s41591-021-01369-8 Epub 2021 Jun 21.
5. Volloch V, et al. Results of Beta Secretase-Inhibitor Clinical Trials Support Amyloid Precursor Protein-Independent Generation of Beta Amyloid in Sporadic Alzheimer’s Disease. Med Sci (Basel). 2018 Jun 2;6(2):45. doi: https://doi.org/10.3390/medsci6020045
6. van Dyck CH, et al. Lecanemab in Early Alzheimer’s Disease. N Engl J Med. 2023 Jan 5;388(1):9–21. doi: https://doi.org/10.1056/NEJMoa2212948 Epub 2022 Nov 29.
15. Ackley SF, et al. Effect of reductions in amyloid levels on cognitive change in randomized trials: instrumental variable meta-analysis. BMJ. 2021 Feb 25;372:n156. doi: https://doi.org/10.1136/bmj.n156 Erratum in: BMJ. 2022 Aug 30;378:o2094.
10. Smith AD. Anti-amyloid trials raise scientific and ethical questions. BMJ. 2021;372:n805. doi: https://doi.org/10.1136/bmj.n805
12. Sims JR, et al. Donanemab in Early Symptomatic Alzheimer Disease: The TRAILBLAZER-ALZ 2 Randomized Clinical Trial. JAMA. 2023 Aug 8;330(6):512–527. doi: https://doi.org/10.1001/jama.2023.13239
19. Smith AD, Refsum H. Homocysteine, B Vitamins, and Cognitive Impairment. Annu Rev Nutr. 2016 Jul 17;36:211–239. doi: https://doi.org/10.1146/annurev-nutr-071715-050947; see also Li JG, Chu J, Barrero C, Merali S, Pratico D. Homocysteine exacerbates β-amyloid, tau pathology, and cognitive deficit in a mouse model of Alzheimer’s disease with plaques and tangles. Ann Neurol. 2014;75:851–63; doi: https://doi.org/10.1002/ana.24166; see also Shirafuji N, et al. Homocysteine Increases Tau Phosphorylation, Truncation and Oligomerization. Int J Mol Sci.2018 Mar 17;19(3):891. doi: https://doi.org/10.3390/ijms19030891; see also Bossenmeyer-Pourié C, et al. N-homocysteinylation of tau and MAP1 is increased in autopsy specimens of Alzheimer’s disease and vascular dementia. J Pathol. 2019 Jul;248(3):291–303. doi: https://doi.org/10.1002/path.5254 Epub 2019 Mar 19.
20. Wischik CM, et al. Selective inhibition of Alzheimer disease-like tau aggregation by phenothiazines. Proc Natl Acad Sci U S A. 1996 Oct 1;93(20):11213–8. doi: https://doi.org/10.1073/pnas.93.20.1121
21. Al-Hilaly YK, et al. Cysteine-Independent Inhibition of Alzheimer’s Disease-like Paired Helical Filament Assembly by Leuco-Methylthioninium (LMT). J Mol Biol. 2018 Oct 19;430(21):4119–4131. Epub 2018 Aug 16. Doi: https://doi.org/10.1016/j.jmb.2018.08.010
22. Arvanitakis Z, et al. Diabetes mellitus and risk of Alzheimer disease and decline in cognitive function. Arch Neurol.2004 May;61(5):661–666. doi: https://doi.org/10.1001/archneur.61.5.661; see also Yaffe K, et al. Diabetes, impaired fasting glucose, and development of cognitive impairment in older women. Neurology. 2004 Aug 24;63(4):658–663. doi: https://doi.org/10.1212/01.WNL.0000134665.93885.71; see also Tiehuis AM, et al. Diabetes Increases Atrophy and Vascular Lesions on Brain MRI in Patients With Symptomatic Arterial Disease. Stroke. 2008 May;39(5):1600–1603. doi: https://doi.org/10.1161/STROKEAHA.107.502963; see also Samaras K, et al. The impact of glucose disorders on cognition and brain volumes in the elderly: the Sydney Memory and Ageing Study. AGE. 2014;36(2):977–993. doi: https://doi.org/10.1007/s11357-013-9585-3; see also Mortby ME, et al. 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: https://doi.org/10.1371/journal.pone.0073697; see also Crane PK, et al. Glucose levels and risk of dementia. N Engl J Med. 2013 Aug 8;369(6):540–548. doi: https://doi.org/10.1056/NEJMoa1215740; see also Luchsinger JA, et al. Hyperinsulinemia and risk of Alzheimer disease. Neurology. 2004 Oct 12;63(7):1187–1192. doi: https://doi.org/10.1212/01.wnl.0000140292.04932.87; see also Abbatecola AM, et al. Insulin resistance and executive dysfunction in older persons. J Am Geriatr Soc. 2004 Oct;52(10):1713–1718. doi: https://doi.org/10.1111/j.1532-5415.2004.52466.x; see also Ye X, et al. Habitual sugar intake and cognitive function among middle-aged and older Puerto Ricans without diabetes. Br J Nutr. 2011 Nov;106(9):1423–1432. doi: https://doi.org/10.1017/S0007114511001760; see also Power SE, et al. Dietary glycaemic load associated with cognitive performance in elderly subjects. Eur J Nutr.2015 Jun;54(4):557–568. doi: https://doi.org/10.1007/s00394-014-0737-5; see also Seetharaman S, et al. Blood glucose, diet-based glycemic load and cognitive aging among dementia-free older adults. J Gerontol A Biol Sci Med Sci. 2015 Apr;70(4):471–479. doi: https://doi.org/10.1093/gerona/glu135; see also Taylor MK, et al. A high-glycemic diet is associated with cerebral amyloid burden in cognitively normal older adults. Am J Clin Nutr. 2017 Dec;106(6):1463–1470. doi: https://doi.org/10.3945/ajcn.117.162263; see also Gentreau M, et al. High Glycemic Load Is Associated with Cognitive Decline in Apolipoprotein E ε4 Allele Carriers. Nutrients. 2020 Nov 25;12(12):3619. doi: https://doi.org/10.3390/nu12123619
23. Xie W, et al. Association between disease-modifying antirheumatic drugs for rheumatoid arthritis and risk of incident dementia: a systematic review and meta-analysis. RMD Open. 2024 Feb 27;10(1):e004016. doi: https://doi.org/10.1136/rmdopen-2023-004016
24. Beydoun MA, et al. Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis. BMC Public Health. 2014 Jun 24;14:643. doi: https://doi.org/10.1186/1471-2458-14-643
25. Teng Z, et al. Cerebral small vessel disease mediates the association between homocysteine and cognitive function. Front Aging Neurosci. 2022;14:868777. doi: https://doi.org/10.3389/fnagi.2022.868777
26. Chen C, et al. B vitamin intakes modify the association between particulate air pollutants and incidence of all-cause dementia: Findings from the Women’s Health Initiative Memory Study. Alzheimers Dement. 2022 Nov;18(11):2188–2198. doi: https://doi.org/10.1002/alz.12515 Epub 2022 Feb 1.
