New Study: Is Red Meat Bad for Your Brain?

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In a culture where the average plate still leans heavily towards meat – often processed, often excessive – it’s time to reassess the impact of our protein choices not just on our waistlines, but on our brains. A recent study in Neurology (2025) has added fresh weight to decades of evidence linking red and processed meat consumption to an increased risk of dementia and cognitive decline (1). Meanwhile, fish – particularly oily fish – continues to top the charts as the most protective food for your brain (2,3).

So, what does this mean practically for those of us trying to upgrade our brains and reduce our risk of cognitive decline? The answer may be as simple as this: eat more fish and fewer sausages.

Red Meat, Processed Meat and the Rising Risk to Brain Health

A new US cohort study, which followed over 77,000 adults across 30 years, found that:

Processed red meats (bacon, hot dogs, sausages, salami, bologna and other processed meat products) were clearly problematic. Consuming just 0.25 servings per day or more was associated with a 13% higher risk of developing dementia compared with those eating less than 0.1 serving (1).

Unprocessed red meat (e.g. beef or lamb) was linked to a 16% increased risk of subjective cognitive decline – that is people reporting that their memory or mental sharpness was worsening – when consuming more than one serving daily compared to less than half a serving per day. However, the researchers noted that this link did not reach statistical significance for diagnosed dementia overall (1).

More encouragingly, replacing one daily serving of processed red meat with a serving of nuts, lentils, or beans was associated with a 19% lower risk of dementia (1).

These findings are consistent with a large UK Biobank analysis of almost half a million adults, which found that each additional 25 g/day of processed meat (bacon, ham, sausages, meat pies, kebabs, burgers, chicken nuggets) was associated with a 44% higher risk of all-cause dementia and a 52% higher risk of Alzheimer’s disease. In contrast, each 50 g/day of unprocessed red meat was linked to a 19% lower risk of all-cause dementia and a 30% lower risk of Alzheimer’s disease (4).  This reinforces the idea that it is the processing – not necessarily the meat itself – that may be most harmful.

These associations were observed regardless of whether participants carried the APOE ε4 gene variant – further evidence that dietary choices have a significant impact and that Alzheimer’s is ‘not in the genes’. (4).

The Global Pattern

The irrelevance of genetics in these findings is further supported by global evidence. An ecological analysis across 204 countries found that higher national per-capita total meat supply – including both red and white meats – was significantly associated with higher dementia incidence, even after adjusting for ageing, economic development and genetic risk, including APOE ε4 prevalence where available (5). In other words, the meat-dementia link is not confined to particular genetic subgroups but is observable across populations worldwide, suggesting that the way we produce and consume meat may be influencing brain health trends on a global scale. 

What we put on our plate is powerful when it comes to reducing dementia risk – more so than any genetic variations that attract attention in the media.

Why Fish is Brain Food

The answer is not to go hungry, but to swap for something else – and when it comes to brain health, marine foods are your answer.

Unlike red meat, fish – especially oily varieties like salmon, sardines or mackerel – continue to show a strong protective effect.

A comprehensive 2024 meta-analysis found that:

Eating one to two servings of fish per day (roughly 150 g) is associated with a 20% reduced risk of Alzheimer’s disease and up to 30% slower cognitive decline (2).

Another study found that people who ate fish at least once a week had a one-third lower risk of Alzheimer’s compared with those eating fish less than weekly (3).

Why? Omega-3 fats, especially DHA, are critical for brain function and structure. They reduce inflammation, support synaptic plasticity and help clear beta-amyloid – a protein associated with Alzheimer’s disease.

As explained in the COGNITION™ 6-month programme, omega-3 fats from fish oil play a pivotal role in building and repairing the brain, particularly in mid-life, when early signs of cognitive decline can start to emerge.

That’s why we offer omega-3 at-home blood tests – so you can check whether you’re getting enough through your diet or if it’s time to add a supplement. You can test omega-3 on its own here, or as part of our 5-in-1 DRIfT test where you can also check your homocysteine and glutathione status at the same time.

A Simple Swap with Profound Impact

From a cognitive health perspective, the data is now hard to ignore: if you’re regularly eating red or processed meat – especially more than once a day – your brain may be paying the price. But shifting even one of those servings towards fish, eggs or plant-based proteins could make a meaningful difference.

Interestingly, the main culprit in the latest studies was processed meat. This supports a key principle in brain-friendly eating: most natural whole foods – whether meat, fish, fruit, nuts, legumes, wholegrains or dairy – are not the problem. It’s when we distort them into ultra-processed, factory-made food that health is undermined.

This isn’t about becoming vegan or pescatarian. It’s simply more evidence to reduce processed foods and ensure optimal omega-3 intake. 

So next time you’re at the supermarket make a cow happy and buy a fish.

Resources:

Need help knowing what to eat? Get inspired with over 125 brain-friendly recipes in the Upgrade Your Brain Cook App.

Order your omega-3 test today to find out if you are eating enough of these essential fatty acids. You can test omega-3 on its own here, or as part of our 5-in-1 DRIfT test. Available globally.

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:

You J, Zhang L, Zhou Y, et al. Total meat supply and incidence of dementia: an ecological study of 204 countries. Front Public Health. 2025;13:1589936. doi:10.3389/fpubh.2025.1589936.

Li Y, Li Y, Gu X, Liu Y, Dong D, Kang JH, Wang M, Eliassen H, Willett WC, Stampfer MJ, Wang D. Long-Term Intake of Red Meat in Relation to Dementia Risk and Cognitive Function in US Adults. Neurology. 2025;104(3):e210286. doi:10.1212/WNL.0000000000210286.

Godos J, Micek A, Currenti W, Franchi C, Poli A, Battino M, Dolci A, Ricci C, Ungvari Z, Grosso G. Fish consumption, cognitive impairment and dementia: an updated dose-response meta-analysis of observational studies. Aging Clin Exp Res. 2024;36(1):171-182. doi:10.1007/s40520-024-02823-6.

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

Zhang Z, He P, Liu M, et al. Meat consumption and risk of incident dementia: cohort study of UK Biobank participants. Am J Clin Nutr. 2021;113(5):1228-1236. doi:10.1093/ajcn/nqaa343.

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When that mid-morning dip or afternoon slump hits, it’s tempting to reach for a quick fix – something sweet, something carby, something to perk you up. But most conventional snacks don’t fuel your brain – they drain it.

In fact, snacking is one of the easiest ways to sabotage your long-term brain health and memory. Most people wouldn’t eat a plate of sugar at mealtimes (unless they start the day with shop-bought cereal or sweetened yoghurt), yet it’s common to reach for a bar, a biscuit, or something from a petrol station or coffee shop without a second thought.

These everyday choices are a silent driver of brain fog, low mood, memory problems – even dementia. It’s time to upgrade your brain by upgrading your snacks. Below, we share a free Brain Boost Bites recipe and some other smart snack ideas – perfect for long drives, picnics, or busy days on the go.

The Problem with Typical Snacks

The modern snack aisle is a minefield of ultra-processed foods: cereal bars, crisps, flavoured yoghurts, granola bites, and biscuits – many of them marketed as “healthy”. But beneath the surface, they’re often:

High in sugar or refined carbs – causing a rapid blood glucose spike followed by a crash. Many so-called healthy bars contain over 15g of sugar with little fibre, protein, or healthy fat to balance them.
Low in brain-essential nutrients – such as omega-3s, magnesium, or phospholipids.
Full of artificial additives – emulsifiers, preservatives, and even excitotoxins like MSG.
Designed for instant gratification – often with addictive properties rather than sustained energy.

As explained in our Four Horsemen of the Mental Health Apocalypse series (read Part 1 here and Part 2 here), poor glucose control is a key driver of accelerated brain ageing and cognitive decline. A high-sugar snack spikes blood sugar, then causes a crash that reduces brain energy and impairs mental performance. Over time, this rollercoaster leads to insulin resistance, which is strongly linked to cognitive decline and Alzheimer’s disease.

The Smart Snacking Solution

The answer isn’t to stop snacking altogether – it’s to snack smart.

Our in-house chef and lecturer in culinary nutrition and functional health, Kim Close, shares a free recipe below from the Upgrade Your Brain Cook App. It’s packed with brain-supportive nutrients and perfect for keeping your energy and focus steady.

And if you’re not sure what to eat for better brain health, the Cook App includes 120+ recipes (and growing) to guide you meal by meal.

👉 Subscribe to the Cook App – just £30/year

Brain Boost Bites

Refined sugar-free | Fibre-rich | Brain-fat fuelled | Brain Boosting

Other Smart Snack Ideas:

Oatcakes with almond butter or smoked mackerel pâté
Olives 
Square of Dark Chocolate Bar (Recipe in Cook App)
Hummus or nut butter with raw veggie sticks
A boiled egg with cherry tomatoes
A handful of walnuts or pumpkin seeds
A small cup of full-fat Greek yoghurt with blueberries
Chia pudding made with coconut milk (recipe in the app)
2 squares of 85%+ dark chocolate

Snacking wisely is one of the easiest daily upgrades you can make for your brain. And with the right ingredients, it can be delicious too.

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Imagine if a simple, well-researched nutrient protocol could prevent cognitive decline in millions of people worldwide. Imagine further that this protocol has been known for years, supported by multiple clinical trials and global experts, yet systematically ignored by the very institutions meant to protect public health. That is precisely the case when it comes to homocysteine, B vitamins, and dementia.

Last year, the UK-based Lancet Commission on Dementia Prevention, Intervention and Care released its third major report, once again omitting any mention of homocysteine as a modifiable risk factor. This was despite direct submissions of evidence and letters from leading scientists demonstrating that lowering homocysteine with B vitamins can slow brain shrinkage and cognitive decline.

Now, in response to this silence, six of the leading dementia researchers, Professors Joshua Miller (Rutgers), David Smith (Oxford), Helga Refsum (Oslo), Jin-Tai Yu (Fudan), Babak Hooshmand (Karolinska), and Andrew McCaddon (Wrexham), have published a powerful rebuttal in the Journal of Alzheimer’s Disease. Many of these experts serve in the Alzheimer’s Prevention Expert Group (APEG) at Food for the Brain.

They wrote:

“In 2018, we published an ‘International Consensus Statement on Homocysteine and Dementia’ in this journal, in which we concluded that elevated plasma total homocysteine is a modifiable risk factor for the development of cognitive decline, dementia, and Alzheimer’s disease (AD) in older persons. (1)

We further stated that intervention trials in elderly people with cognitive impairment show that homocysteine-lowering treatment with B vitamins markedly slows the rate of both wholeand regional brain atrophy, and also slows cognitive decline. We were therefore puzzled as to why the Lancet Commission on Dementia Prevention, Intervention and Care, failed to discuss the possible role of homocysteine and B vitamins in any of their three reports, including the most recent one.” (2)

A Systematic Omission

The UK-based Lancet Commission on Dementia Prevention is meant to objectively consider the evidence on dementia prevention. Yet each edition, despite being sent the relevant papers, has ignored the evidence concerning homocysteine.

Furthermore, it’s expected to uphold the standards for critical debate which allows for experts to question Published findings. That is exactly what these experts did – yet it declined to publish their letter, instead printing a rebuttal from its own Commission while refusing to let readers see the original letter. (3, 4)

The experts wrote to The Lancet again to respond to the Commission’s letter, but their second letter was also rejected. 

Thatetter has now been published in the leading Alzheimer’s journal where the authors finally have their rightful say. It includes the following:

“We wish to reply to the Commission and continue the debate with the aim of reaching a common view on homocysteine, B vitamins and dementia. This is an important matter of public health.”

In other words, The Lancet published the ‘case for the defence’ for the exclusion of homocysteine without allowing readers to even read the ‘case for the prosecution’. (5)

So, what was The Lancet’s case against B vitamins? It rested on three criticisms – each of which these leading dementia researchers refute with scientific precision in their recent journal paper.

Criticism 1: Misunderstanding Who Benefited in the VITACOG Trial

The Lancet Commission questioned the relevance of the VITACOG trial, arguing that the results “do not show benefits in populations already consuming B vitamins in their food or through supplements.” But this fundamentally misrepresents the study population.

In the VITACOG trial, participants with mild cognitive impairment were given high doses of B6, B12, and folic acid for two years. The result was a 31% reduction in whole brain shrinkage and significantly slower rate of cognitive decline in those with raised homocysteine (6). In participants with levels above 11.3 μmol/L – the median – both cognitive and clinical improvements were observed. Importantly, key Alzheimer’s-related brain regions shrank seven times more slowly in these individuals (7, 8).

The Lancet Commission implied that participants were already supplementing, but that is incorrect. The study excluded anyone taking more than 300 mcg of folic acid, 3 mg of vitamin B6, or 1.5 mcg of vitamin B12 – doses lower  than those found in many common multivitamins. Only 16 to 20 percent were taking low-dose supplements, while the majority were not.. No one was excluded based on their dietary intake of B vitamins.

The experts respond:“The Commission authors’ comment is analogous to expecting additional drug treatment to provide benefits over and above the benefits being obtained in people already taking a high dose of the drug, which is why it puzzles us.”

Criticism 2: No Benefit in the Hong Kong Trial?

The Commission’s response also cited a Hong Kong trial that reported no benefit of B vitamins over two years in people with mild cognitive impairment (MCI) (9). However, this overlooks several important confounders.

Firstly, 22% of participants were taking aspirin, which the study authors themselves found to impair the effect of B vitamins. This interference has since been confirmed in further research (10).

Secondly, the authors of The Lancet response failed to consider another critical factor: omega-3 status. Numerous studies show that B vitamins only deliver cognitive benefits when omega-3 fatty acid levels are sufficient. The Hong Kong study did not measure or control for omega-3 status, which likely explains the lack of consistent benefit over the two-year period.

Thus, the absence of effect in this trial does not disprove the role of B vitamins.  The experts go on to demonstrate in their article the overwhelming body of evidence –  reported by us – that homocysteine-lowering B vitamins do not work optimally in individuals with low omega-3 status.

Criticism 3: No Benefit in the VITAL Trial in Alzheimer’s Patients?

The Lancet authors also referenced the VITAL trial, which reported no overall cognitive benefit from B vitamins in patients already diagnosed with Alzheimer’s disease (11). But again, this conclusion overlooks key details.

In a subgroup analysis, those in the early stages of Alzheimer’s disease did show significant benefit (12). The authors of the VITAL trial themselves highlighted this in their paper, suggesting that earlier intervention is more effective. This finding aligns with multiple other studies showing that B vitamin treatment is most effective in the pre-dementia stages (13).

Furthermore, participants in the VITAL trial began with an average homocysteine level of 9 μmol/L, which is below the threshold (>10–11 μmol/L) associated with brain atrophy.  It is extremely rare to find a group of people with Alzheimer’s disease that start with such a low homocysteine level.  While the B vitamins did reduce homocysteine further to 7μmol/L, there was no overall cognitive benefit observed. But this is akin to giving painkillers to people who are not in pain and then reporting no change in pain levels. At Food for the Brain, we consider a homocysteine level above 10μmol/L as in need of correction with B vitamins.

There are also concerns about conflicts of interest. The lead author, Paul Aisen, is described as “a consultant to the following pharmaceutical companies involved in the development of potential treatments for Alzheimer’s disease”. with more than a dozen firms listed. These companies would certainly favour a trial designed to fail – especially if it were widely publicised.

Additionally, when an anti-amyloid drug trial for lecanemab was published – now licensed in the US and UK – the names of Paul Aisen and Christopher Van Dyck appeared once again as lead authors. In other words, the paid pharmaceutical consultants, responsible for running the drug trial were also tasked with overseeing a trial – designed to fail – on a competing approach: lowering homocysteine with B vitamins. The conflict of interest here is both clear and concerning.

What Does the Evidence Really Say?

You can read the full expert response published in the Journal of Alzheimer’s Disease here. 

Their conclusion is clear:

“We hope that the Lancet Commission will consider the substantial existing evidence of raised homocysteine as an important risk factor for dementia and the possibility of modifying its harm by supplementation with B vitamins.”

They emphasise that the evidence for B vitamin intervention is as strong – or stronger than –  many of the risk factors the Commission did include in its 2024 report. To continue ignoring the proven impact of homocysteine, and the benefits of lowering it through B vitamins is not merely a scientific oversight –  it is a missed opportunity with major implications for medicine and public health.

Remember, prevention is better than cure, and there is so much you can do to protect your brain health

The perfect time to start? Today.

What Can You Do?

Test your homocysteine (and omega-3 status) TODAY –  especially if you’re over 50 or at risk of cognitive decline. At Food for the Brain, we offer an accurate at-home test kit that reliably measures plasma homocysteine reliably. 

You can order your single Homocysteine test here or save money and test both omega-3 index and homocysteine (plus other markers) as part of our DRIfT tests here. International shipping available.

Act on your results –  if your level is above 10 μmol/L, supplementation with vitamin B6 (20 mg), methylfolate (400 µg), and vitamin B12 (500 µg) is recommended.
Read more on supplements and homocysteine here.

Support our mission – become a FRIEND of Food for the Brain! Your donation helps us advance prevention-focused brain health research and education.

As a Friend, you’ll also gain access to:
• Monthly group coaching
• Your personalised brain upgrade programme: COGNITION™

Share the knowledge – public awareness can change public health.
We need a paradigm shift, and it starts with us.

By Patrick Holford

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

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

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

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

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

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

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

Safer, Evidence-Based Alternatives

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

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

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

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

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

How many people are killed by psychiatric drugs?

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

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

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

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

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

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

Estimating the True Death Toll of Mental-Health Medications

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Learn more and begin your brain upgrade journey today:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

by Patrick Holford

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Choline is an often-overlooked but vital nutrient for brain health.

A new study suggests the optimal intake is 400mg, yet there is no Recommended Daily Allowance or widespread promotion of this crucial nutrient. It is also notably low in vegetarian and especially vegan diets.

(We discuss this and more in our COGNITION 6-month brain upgrade programme – available when you become a FRIEND of Food for the Brain.)

A major study published this year found that higher choline intake lowers the risk of dementia, Alzheimer’s, and cognitive decline.

Researchers tracked 125,000 people from the UK Biobank for 12 years and the study was published in the American Journal of Clinical Nutrition. It showed that higher choline intake reduced risk, with the most benefit around 400mg per day.

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Why does it matter?

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

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Also previous studies (2) have found remarkable effects supplementing 480-900mg of choline in pregnancy on promoting ‘smart’ babies with faster reflexes and cognitive processes. It’s important for all ages and a key topic in our Smart Kids & Teens Programme.

What should you do or eat?

Choline is essential for the body, especially the brain, yet it has no Recommended Daily Allowance.

Choline is abundant in eggs, fish, and meat. An egg provides about 120mg, while a 50g serving of beef or salmon contains around 50mg. Beef liver is the richest source, but eggs are the best overall because they contain phosphatidylcholine which is more easily absorbed by the body. Plant-based sources include soy, quinoa, nuts, seeds, beans, and broccoli. A 50g serving of almonds or broccoli provides about 25mg. Phosphatidylcholine, found in lecithin capsules and granules, is an easy supplement option for vegans and vegetarians.

We recommend eating two eggs most days, with a minimum of six per week. Include fish and some meat if you eat it, or soy, quinoa, broccoli, nuts, and seeds if you don’t. Supplementing is likely beneficial, especially for vegetarians. Taking two high-PC lecithin 1,200mg capsules daily provides 250mg of phosphatidylcholine (PC), the form used by the body. These supplements are available at your local health food store.

Remember, your brain is built from what you feed it – and how you use it (as covered in COGNITION). What choline-rich foods can you add to your diet this week?

If you’re unsure what to eat to support your brain or need inspiration, the Cook App is here to help! With over 100 recipes at your fingertips, eating delicious, brain-boosting foods has never been easier—all for just £30 a year.

Actions:

Take the Cognitive Function Test today – our validated online assessment – to find out exactly what you need to focus on.
Become a FRIEND and get access to your 6-month COGNITION programme so you know how to upgrade your brain.

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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.

—Reference list

Reference

Niu YY, Yan HY, Zhong JF, Diao ZQ, Li J, Li CP, Chen LH, Huang WQ, Xu M, Xu ZT, Liang XF, Li ZH, Liu D. Association of dietary choline intake with incidence of dementia, Alzheimer disease, and mild cognitive impairment: a large population-based prospective cohort study. Am J Clin Nutr. 2025 Jan;121(1):5-13. doi: 10.1016/j.ajcnut.2024.11.001. Epub 2024 Nov 7. PMID: 39521435.
Caudill, M. et al, ‘Maternal choline supplementation during the third trimester of pregnancy improves infant information processing speed: a randomized, double-blind, controlled feeding study’ FASEB Journal (Apr 2018); 32(4): 2172-80. doi: 10.1096/fj.201700692RR.

How can we lift our mood and nourish our brain? 

Depression, now the leading cause of disability globally, affects millions. According to the World Health Organization, it represents a significant disease burden, particularly in high-income countries (1). With a staggering 100 million antidepressant prescriptions issued annually—a 70% increase in five years—it’s clear that something is going wrong in our modern western world (1).

Thankfully, nutrition and lifestyle changes provide science-backed ways to boost our mood naturally.

(If you want to know more about how to overcome depression then make sure you watch our webinar ‘Finding your way out of depression’).

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Understanding Depression

Depression manifests through persistent feelings of hopelessness, low energy, disrupted sleep, and even physical changes such as weight loss or gain (2). The root causes can be multifactorial—psychological stress, biochemical imbalances, or nutritional deficiencies.

But here’s the good news: you can take simple, practical steps to nourish your brain, boost serotonin, and improve your mood naturally.

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7 Ways to Boost Mood and Brain Function

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1. Increase Your Omega-3 Fats

Your brain is 60% fat, and omega-3 DHA and EPA are critical for its structure and function. Countries with high fish consumption have lower depression rates. A study from Harvard Medical School found that EPA, specifically, has potent antidepressant effects.

A meta-analysis published in Psychopharmacology Bulletin found that higher omega-3 intake reduces depressive symptoms by 53%. Omega-3 helps build brain cell membranes and boosts serotonin receptor function, which improves mood and cognition.

What to do: Eat oily fish like salmon, sardines, and mackerel at least twice a week or supplement with high-dose omega-3 fish oil. Aim for 1,000–2,000 mg of EPA and DHA combined daily (4, 5, 6).

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2. Optimise Your B Vitamins and Lower Homocysteine

The little-known amino acid, homocysteine, may double your risk for depression if levels are elevated. This toxic by-product accumulates when you’re deficient in B6, B12, and folic acid, impairing brain chemistry. 

Studies by Professor David Smith from Oxford show that lowering homocysteine can dramatically slow brain shrinkage and improve mood. Which is why we now offer at home homocysteine test kits so you can monitor your own level and prevent disease (7,8,9).

What to do: Eat leafy greens, whole grains, and fortified foods. Test your homocysteine and aim for levels below 7 μmol/L. Supplement with a methylated B complex (20 mg B6, 500 μg B12, and 400 μg methylfolate).

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“B vitamins are brain-makers; without them, key neurotransmitters like serotonin can’t be synthesised” – Patrick Holford, Upgrade Your Brain.

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3. Fuel Your Brain with Serotonin Precursors

Serotonin, your “happy hormone”, is made from tryptophan, an amino acid found in protein-rich foods like fish, poultry, beans, and eggs. For some, tryptophan conversion to serotonin is impaired due to poor digestion or low stomach acid, common with age and stress.

Supplementing with 5-HTP can bypass these barriers. Clinical studies show 5-HTP compares favourably with SSRIs in treating depression (10, 11, 12, 13).

What to do: Include tryptophan-rich foods daily and consider a 5-HTP supplement (100–200 mg twice daily). Always consult your doctor if combining with antidepressants.

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4. Balance Your Blood Sugar

Maintaining stable blood sugar levels is essential for mood regulation, as uneven glucose supply to the brain can lead to irritability, fatigue, and depressive symptoms. Diets high in refined carbohydrates and sugar contribute to these fluctuations and are linked to poor mood and an increased risk of depression. A study of 3,456 adults found that individuals consuming diets rich in processed foods had a 58% greater risk of depression, whereas those eating whole foods experienced a 26% reduced risk (14, 14, 16).

 Refined sugars also deplete mood-enhancing nutrients like B vitamins, essential for energy production, and divert chromium, which is vital for glucose regulation. Adopting a low glycaemic load (GL) diet, avoiding caffeine and alcohol, and focusing on whole foods, fruits, and vegetables can help stabilise blood sugar levels and improve mood.

What to do: Follow a Low-GL diet with whole foods, low-GL carbs, and protein at every meal. Avoid sugar, caffeine, and alcohol .

5. Boost Your Vitamin D Levels

The “sunshine vitamin,” vitamin D, is essential for mood regulation. Research shows a 40% lower incidence of depression in those with adequate vitamin D. Alarmingly, over 60% of the UK population is deficient during winter (17, 18, 19, 20).

What to do: Get tested and aim for levels above 75 nmol/L. Supplement with 2,000–3,000 IU daily in winter months.

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6. Include Chromium to Combat Atypical Depression

If you suffer from atypical depression—characterised by weight gain, fatigue, and carbohydrate cravings—you might benefit from chromium. Studies show chromium supplementation can improve mood scores by up to 83% (21, 22, 23).

What to do: Include whole grains and vegetables or supplement with 600 mcg of chromium picolinate daily.

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7. Bring on the Sunshine and Movement

Exercise and sunlight have a direct effect on serotonin levels and mood. Regular exercise boosts brain-derived neurotrophic factor (BDNF), which helps build new brain cells and connections】.

What to do: Aim for 30 minutes of exercise daily and sun exposure for 15 minutes, when safe.

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Key Action Plan

Eat oily fish twice weekly or supplement omega-3s with at least 1,000 mg EPA and DHA.
Test and lower homocysteine with B6, B12, and folic acid supplements.
Try 5-HTP to boost serotonin naturally.
Follow a Low-GL diet to stabilise blood sugar.
Supplement vitamin D during winter. Find out more about dose here.
Add chromium for atypical depression.
Exercise regularly and get sensible sun exposure.

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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

World Health Organization. Depression and Other Common Mental Disorders: Global Health Estimates. WHO; 2017.
Brown G, et al. Social support, self-esteem and depression. Psychol Med. 1986;16(4):813-31.
Hibbeln JR. ‘Fish consumption and major depression’. Lancet, vol 351(9110), pp. 1213 (1998)
M. Peet and R, Stokes, Omega 3 Fatty Acids in the Treatment of Psychiatric Disorders Drugs, vol 65(8), pp. 1051-9 (2005)
S Kraguljac NV, Montori VM, Pavuluri M, Chai HS, Wilson BS, Unal SS (2009) Efficacy of omega-3 Fatty acids in mood disorders – a systematic review and metaanalysis. Psychopharmacology Bulletin 42(3):39-54
Hibbeln JR. Fish consumption and major depression. Lancet. 1998;351(9110):1213.
Coppen A, Bailey J. Folic acid and affective disorders. J Affect Disord. 2000;60(2):121-30.
Taylor MJ, Carney SM, Goodwin GM, Geddes JR. Folate for depressive disorders. Cochrane Database Syst Rev. 2003;(2):CD003390.
Smith AD, Refsum H. Homocysteine, B vitamins, and cognitive impairment. Annu Rev Nutr. 2016;36:211-39.
Poldinger W et al. A comparison of 5-hydroxytryptophan and fluvoxamine. Psychopathology. 1991;24(2):53-81.
E. Turner, Serotoninalacarte: Supplementation with the serotonin precursor 5-hydroxytryptophan.’ Pharmacology&Therapeutics (2005) [article in press].
W. Poldinger et al. A functional-dimensional approach to depression: serotonin deficiency and target syndrome in a comparison of 5-hydroxytryptophan and fluvoxamine, Psychopathology vol 24(2), pp. 53-81 (1991)
Associate editor: K.A. Neve ‘Serotonin a la carte: Supplementation with the serotonin precursor 5-hydroxytryptophan’ ErickH. Turner a,c,d,*, Jennifer M. Loftis a,b,c, AaronD. Blackwell a,b,e Pharmacology & Therapeutics(2005) www.elsevier.com/locate/pharmthera
Akbaraly TN, Brunner EJ, Ferrie JE, et al. Dietary pattern and depressive symptoms in middle age. Br J Psychiatry. 2009;195:408–13.
Benton D, Owens DS, Parker PY. Blood glucose influences memory and mood in an everyday setting. Biol Psychol. 1982;14(1-2):129–35.
Christensen L. Psychological distress and diet – effects of sucrose and caffeine. J Appl Nutr. 1988;40(1):44–50.
Lansdowne AT, Provost SC (1998): Demonstrates that vitamin D3 supplementation enhances mood in healthy subjects during winter.
C. Wilkins et al. (2006): Links vitamin D deficiency to low mood and poorer cognitive performance in older adults.
A. Nanri et al. (2009): Discusses the association between vitamin D levels and depressive symptoms across seasonal changes.
R. Jorde et al. (2008): Shows that vitamin D supplementation alleviates depressive symptoms in overweight and obese individuals
Lifting Depression – The Chromium Connection by Dr Malcolm McLeod (Basic Health Publications):
J. R. Davidson et al, Effectiveness of chromium in atypical depression: a placebo-controlled trial, Biol Psychiatry, vol 53(3), pp. 261-4 (2003)
Docherty, J et al, ‘A Double-Blind, Placebo-Controlled, Exploratory Trial of Chromium Picolinate in Atypical Depression’. Journal of Psychiatric Practice. Vol 11(5), pp. 302-314, (2005)
Holford P. Upgrade Your Brain. HarperCollins; 2024.

By Jerome Burke

Why too much fructose is driving dementia, diabetes and brain fog

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The fruit sugar ‘fructose’ isn’t generally considered a food that’s best avoided. After all, it comes from fruit.

Yet a radical new theory, developed by Richard Johnson, Professor of Nephrology at the University of Colorado, explains how it can trigger various damaging changes in our metabolism that make us more likely to develop chronic conditions such as diabetes, obesity and Alzheimer’s. If doctors better understood this, it could transform the new emphasis on sickness prevention that the government is promising.

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The science of being ‘fructed’

Professor Johnson has produced what is effectively a biochemical wiring diagram of the connections which fructose turns on and off, that are making an increasing number of people sick. Fructose makes up half of white sugar and most of fructose corn syrup which is the main sweetener in fizzy drinks and ultra-processed foods as well as being the main sugar in fruit, particularly fruit juice.

For instance, the amount of fat stored in the liver increases, driving fatty liver disease, while the cell’s mitochondria, which create the body and brain’s energy molecule ATP, become less productive and blood pressure goes up. The result is that you get fatter, with more brain fog and fatigue and feel less inclined to exercise. Fructose is also a major promoter of diabetes.

Meanwhile an anti-ageing process called autophagy, which would normally clear away used up and damaged mitochondria, the cell’s energy factories, to make room for new ones, is disabled. When fructose crosses the blood-brain barrier into the brain, it is one of the factors causing the brain to form the clumps of amyloid protein found in Alzheimer’s, which is the focus of new drug treatments. 

Why on earth does fructose carry out such a blitz on our bodies? Why would the body run a programme that was potentially so lethal?

“It would be wrong to think of fructose as some sort of major toxin, although it becomes neurotoxic in excess,” says Professor Johnson. “Instead, its remarkable range of effects are part of an ancient set of biological programs, which we call the ‘Survival Switch’, that work to prepare animals for hibernation, storing supplies in preparation for times of famine.” This is why fat storage increases and energy drops off producing brain fog. The trouble is we never run out of food or fructose in our modern times.

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Eat your fruit, don’t drink it.

None of this means that we should avoid fruits, which contain only a small amount of fructose that comes with beneficial fibre that feeds our vital gut bacteria, plus various nutrients. Not so for fruit juice, devoid of fibre. A glass of orange juice is the equivalent of three oranges in terms of fructose, but without the fibre. So, eat your fruit, don’t drink it.

But this does explain why too much blood glucose from regularly eating generous amounts of sugar-laden foods and carbohydrates, is so damaging? The liver turns the excess glucose into fructose with all its knock-on effects. Other substances that can accelerate fructose production are alcohol and salt. 

This rise in fructose intake and its presence in processed food makes it all too easy to start piling on the pounds, regardless of how many calories you have cut or how much further you are running.  It’s a connection that very few nutritionists or GPs are aware of. 

A sign of the widespread damage the Survival Switch can cause is that there are low ATP levels in the brains of people with disorders such as obesity, diabetes, fatty liver disease and Alzheimer’s. Understanding this points to new ways to cut the risks of these chronic disorders.  Adenosine triphosphate (ATP) is a molecule that stores and provides energy for cells. It’s a key biomolecule that’s involved in almost all cellular processes.

A simple, but very effective solution, is to run a blood test – HbA1c – the gold standard test GPs use to screen for diabetes. HbA1c is a test that measures your average blood sugar level (glucose) over the past two to three months. A recent study of 374,021 older men with diabetes found that keeping the level of HbA1c stable at an optimal level over a period of three years cut risk of dementia by a third. Similar benefits have been found with patients with pre-diabetes (Prediabetes means that your blood sugars are higher than usual, but not high enough for you to be diagnosed with type 2 diabetes. It also means that you are at high risk of developing type 2 diabetes.) But far lower levels of HbA1c than those used to diagnose diabetes are associated with the first signs of brain shrinkage, which is the hallmark of cognitive decline, even in teenagers.

That is why we offer, as part of our ‘citizen science’ research, an at home pin-prick test of HbA1c, to find out not only who is at risk, but also how to reverse that risk. It also works alongside the  free Cognitive Function Test that calculates your future Dementia Risk Index and suggests various lifestyle and nutrition changes to help reduce it, including a low fructose diet (Find out more about low fructose foods here).   

We also recommend increasing omega-3 intake from oily fish, increasing B vitamins, especially B12, as well as an active lifestyle, as part of COGNITION, our personalised 6-month programme. In this programme we also dive deeper into lowering your ‘glycaemic load’ (GL), which is low in fructose, alongside periods of time of eating in a ‘ketogenic’ way by keeping sugar and carbohydrates to a minimum. The body responds by creating ketones, energy packets that can replace glucose as an energy source for the brain, helping to undo the damage. 

(You get access to COGNITION when you become a FRIEND of Food for the Brain here)

‘Burning ketones can also increase the number and output of the cell’s energy factories, known as mitochondria, which are damaged by fructose,’ says Professor Robert Lustig of the University of California, author of the best-selling book Metabolical and who sits on our Scientific Advisory Board. You can read more in his detailed article here.

Both Professor Johnson and Professor Lustig are also part of the Alzheimer’s Prevention Expert Group who have written to UK dementia prevention authorities to add sugar, and specifically a high fructose diet, to the list of known risk factors.

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The connection to Ozempic…

This low fructose approach also naturally promotes the enzyme GLP-1, targeted by the weight loss drugs Ozempic and Wegovy, but without the side-effects or rebound weight gain. 

Our founder Patrick Holford says: “Today’s typical diet of burgers, carbonated drinks, fruit juice, ice cream, bread, biscuits, cakes and confectionery, plus alcohol and salt, is a dementia time-bomb. Our brains are literally being ‘fructed’. We see the same shrinkage in the same regions of the brain in teenagers with a high sugar intake that are seen in older Alzheimer’s patients. We think of the resulting dementia as type-3 diabetes.”

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Actions

To find out more about low fructose foods visit www.foodforthebrain.org/fructose 
Click here to join our research and test your HbA1c with us
Support our charitable work and research by becoming a FRIEND

Thank you for reading!

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

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

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

References:

Johnson RJ et al. The fructose survival hypothesis for obesity. Philos Trans R Soc Lond B Biol Sci. 2023 Sep 11;378(1885):20220230. doi: 10.1098/rstb.2022.0230
Underwood PC et al HbA1cTime in Range and Dementia JAMA Netw Open. 2024 Aug 1;7(8):e2425354. doi: 10.1001/jamanetworkopen.2024.25354
https://foodforthebrain.org/lancet-commission-letters/ 
Yau PL et al Obesity and metabolic syndrome and structural brain impairments in adolescence. Pediatrics. 2012 Oct;130(4):e856-64. doi: 10.1542/peds.2012-0324

Your Glutathione Index Defines How Your Cells Are Ageing

Nutritional therapists have been measuring red cell glutathione and supplementing glutathione or its precursor N-Acetyl-Cysteine (NAC) for decades. But it’s really hard, and expensive, to measure accurately. Until now.

So how does the Glutathione Index work? 

All of life is a balance between antioxidants and oxidants. That is why we, an oxygen based lifeform, have a finite life. Inside your cells glutathione (GSH) is working every second to stop harmful oxidants from ageing you. The result is spent or oxidised glutathione (GSSG). Our new test – a world first – measures the ratio between fully loaded glutathione (GSH) and oxidised glutathione (GSSG). The Glutathione index (GSH/GSSG) shows you how much antioxidant potential you have and how many metabolic fires you’ve extinguished. This ratio is the difference between mental health and mental illness.

Why does knowing this single marker help with Alzheimer’s, diabetes, schizophrenia, severe autism, depression & more?

Why Does Knowing This Single Marker Help With Alzheimer’s, Diabetes, Schizophrenia, Severe Autism, Depression and More?

The Science

NAC has plenty of evidence to support its use as a promoter of glutathione and mental health, thus reducing the brain’s oxidative stress. The latest 2022 review states:

“N-acetyl-L-cysteine (NAC) is a compound of increasing interest in the treatment of psychiatric disorders. Primarily through its antioxidant, anti-inflammatory, and glutamate modulation activity, NAC has been investigated in the treatment of neurodevelopmental disorders, schizophrenia spectrum disorders, bipolar-related disorders, depressive disorders, anxiety disorders, obsessive compulsive-related disorders, substance-use disorders, neurocognitive disorders, and chronic pain. Currently NAC has the most evidence of having a beneficial effect as an adjuvant agent in the negative symptoms of schizophrenia, severe autism, depression, and obsessive compulsive and related disorders.” (1)

Glutathione and Schizophrenia

Quoting Lorraine Wilder (whose MSc in schizophrenia we funded) “Glutathione (GSH) is an important antioxidant and free radical scavenger that has been found to be decreased in the brains of people with schizophrenia [2, 3]. Although oral GSH supplementation has poor bioavailability [4], N-Acetyl Cysteine (NAC) has been shown to successfully raise plasma glutathione levels in those with schizophrenia [5]”.

Clinical Evidence and Case Studies

In a case study of a 24 year old woman with chronic and worsening paranoid-type schizophrenia that was generally unresponsive to anti-psychotic treatment, the addition of NAC supplementation improved the patient’s symptomatology in seven days. In addition to the schizophrenia-specific symptoms, improvements were observed in spontaneity, social skills and family relations by both the patient and family members. A randomised placebo-controlled trial (RCT) including 42 participants with schizophrenia, who were experiencing an acute phase of symptomatology, were randomly assigned to receive up to 2 g/d of NAC plus up to 6 mg/d of risperidone for 8 weeks as an adjunct intervention. Significant negative symptoms were found in the active treatment group compared to controls but not in positive or general psychopathology [6].

Larger Trials and Longer-Term Findings

Furthermore, a larger RCT of 140 participants observed significant improvements on global symptomatology and general and negative symptoms of schizophrenia in the NAC supplementation (2 g/d; in addition to anti-psychotic medication) group in comparison to the placebo group over a 24-week period, but not positive symptoms [7]. Notably, after a 4-week washout period these beneficial effects diminished, with the exception of clinical severity scores. 

Expert Perspective on Brain Oxidative Stress

According to Dr Chris Palmer, assistant professor at HarvaWhy the Glutathione Index Is the Best Indicator of Brain Oxidative Stress
rd Medical School:

“Glutathione (GSH), the brain’s primary antioxidant, plays a crucial role in maintaining redox balance. Magnetic resonance studies have provided mixed results regarding GSH levels in schizophrenia patients, with some studies indicating decreased levels in chronic schizophrenia, while others found no significant differences. However, these inconsistencies may be due to variations in disease chronicity, age, and symptom severity among study participants. The findings from these studies suggest several potential therapeutic targets for schizophrenia. Addressing mitochondrial dysfunction, redox imbalance, and impaired energy metabolism could lead to more effective treatments. For instance, N-acetylcysteine (NAC), a precursor to GSH, has shown promise in increasing brain GSH levels and improving symptoms in first episode psychosis patients.”

Why the Glutathione Index Is the Best Indicator of Brain Oxidative Stress

The GSH/GSSG ratio reflects the activity of the enzyme glutathione reductase which is responsible for the transformation of GSSG (used, oxidised) to GSH (the reduced or fully loaded form that acts as a radical scavenger). 

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Glutathione Reductase and Dementia

Reductions in glutathione reductase (GR) enzyme levels in patients with dementia are well established. GR levels alone are therefore a fairly good biomarker of dementia. But the mere presence of the enzyme does not guarantee its high activity. GR needs to consume NADP molecules to function properly. The advantage of our test is, therefore, that it shows changes in GR activity not only due to higher/lower GR gene activity but also due to the absence of the reaction cofactor NADP. 

Impaired Glutathione Recycling in Dementia

As shown by Irene Martinez de Toda et al 2019 (8) data, patients with dementia have a reduction in both the enzymes (GR and GP) that recycle glutathione. Thus, in general, it can be said that the glutathione metabolism (recycling) loop in those with dementia ‘spins’ much slower than in healthy patients. As a result, dementia patients have a lower potential to dynamically fight free radicals and will have a worse Glutathione Index.

What Happens When Recycling Slows Down

In patients, the enzyme GR, which is responsible for recycling spent/oxidised glutathione back to fully loaded, slows down, which leads to the accumulation of oxidised glutathione (GSSG) and the depletion and inability to produce GSH. 

Thus, the concentration of GSH decreases while that of GSSG increases. Hence the Glutathione Index gets worse / is lower.

Improving your Glutathione Index

The older a person is the lower their Glutathione Index is likely to be (see figure below)

Improving your Glutathione index is important as higher levels predict better cognitive function according to our preliminary research. (see figure).

Our own laboratory’s study of 8 people given a supplement containing lipoid acid and N-acetyl-Cysteine (NAC) supplements, the precursor for glutathione, show improvement in both the Glutathione Index and Glutazthione. (see figure below)

Studies giving Ubiquinol, the active form of CoQ, also show an improvement in both the Glutathione Index

Developing the Glutathione Index Test

So will you join us and become a part of our Anti-Age Your Brain Campaign? We need Citizen Scientists to order and complete the test so you can start to protect your brain from ageing and so we can research what the ‘perfect number’ is.

Order your Glutathione test here

Thank you for reading!

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

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

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

References

1. Bradlow RCJ, Berk M, Kalivas PW, Back SE, Kanaan RA. The Potential of N-Acetyl-L-Cysteine (NAC) in the Treatment of Psychiatric Disorders. CNS Drugs. 2022 May;36(5):451-482. doi: 10.1007/s40263-022-00907-3. Epub 2022 Mar 22. Erratum in: CNS Drugs. 2022 Apr 28;: PMID: 35316513; PMCID: PMC9095537.

2 Yao JK, Leonard S, Reddy R: Altered glutathione redox state in schizophrenia. Dis Markers 2006, 22(1):83–93.

3 Gawryluk JW, Wang J-F, Andreazza AC, Shao L, Young LT: Decreased levels of glutathione, the major brain antioxidant, in post-mortem prefrontal cortex from patients with psychiatric disorders. Int J Neuropsychopharmacol 2011, 14(01):123–130.

4  Witschi A, Reddy S, Stofer B, Lauterburg B: The systemic availability of oral glutathione. Eur J Clin Pharmacol 1992, 43(6):667–669.

5. Lavoie S, Murray MM, Deppen P, Knyazeva MG, Berk M, Boulat O, Bovet P, Bush AI, Conus P, Copolov D, Fornari E, Meuli R, Solida A, Vianin P, Cuénod M, Buclin T, Do KQ:Glutathione precursor, N-acetyl-cysteine, improves mismatch negativity in schizophrenia patients. Neuropsychopharmacology 2008, 33(9):2187–2199.

6. Farokhnia M, Azarkolah A, Adinehfar F, Khodaie-Ardakani M-R, Hosseini S-M-R, Yekehtaz H, Tabrizi M, Rezaei F, Salehi B, Sadeghi S-M-H, Moghadam M, Gharibi F, Mirshafiee O:, Akhondzadeh S: N-acetylcysteine as an adjunct to risperidone for treatment of negative symptoms in patients with chronic schizophrenia: a randomized, double-blind, placebo-controlled study. Clin Neuropharmacol 2013, 36(6):185–192.

7. Berk M, Copolov D, Dean O, Lu K, Jeavons S, Schapkaitz I, Anderson-Hunt M, Judd F, Katz F, Katz P, Ording-Jespersen S, Little J, Conus P, Cuenod M, Do KQ, Busha AI: N-acetyl cysteine as a glutathione precursor for schizophrenia—a double-blind, randomized, placebo-controlled trial. Biol Psychiatry 2008, 64(5):361–368.

8. Martínez de Toda I, Vida C, Sanz San Miguel L, De la Fuente M. Function, Oxidative, and Inflammatory Stress Parameters in Immune Cells as Predictive Markers of Lifespan throughout Aging. Oxid Med Cell Longev. 2019 Jun 2;2019:4574276. doi: 10.1155/2019/4574276. PMID: 31281577; PMCID: PMC6589234.

9.Tian G, Sawashita J, Kubo H, Nishio SY, Hashimoto S, Suzuki N, Yoshimura H, Tsuruoka M, Wang Y, Liu Y, Luo H, Xu Z, Mori M, Kitano M, Hosoe K, Takeda T, Usami S, Higuchi K. Ubiquinol-10 supplementation activates mitochondria functions to decelerate senescence in senescence-accelerated mice. Antioxid Redox Signal. 2014 Jun 1;20(16):2606-20. doi: 10.1089/ars.2013.5406. Epub 2013 Dec 14. PMID: 24124769; PMCID: PMC4025630.] and glutathione in people with metabolic syndrome

10.Raygan F, Rezavandi Z, Dadkhah Tehrani S, Farrokhian A, Asemi Z. The effects of coenzyme Q10 administration on glucose homeostasis parameters, lipid profiles, biomarkers of inflammation and oxidative stress in patients with metabolic syndrome. Eur J Nutr. 2016 Dec;55(8):2357-2364. doi: 10.1007/s00394-015-1042-7. Epub 2015 Sep 18. PMID: 26385228.)

In a world often filled with daunting health challenges, Alzheimer’s Prevention Day stood out as a beacon of hope and action.

This year was the first launch of this global initiative and we were privileged to witness an incredible turnout: over 10,000 individuals visited our site, driven by a shared determination to tackle Alzheimer’s disease head-on. The day was not just about awareness but about tangible actions that each person can take to safeguard their cognitive health.

One of the highlights was our interactive 3-minute Alzheimer’s Prevention Check, which 8,000 participants eagerly completed. This simple yet impactful test empowers individuals to assess their cognitive health and take proactive steps towards prevention. 

Moreover, the 30-second challenge captured hearts and imaginations alike. We asked people to share on video what they do to help prevent Alzheimer’s each day?

And the answers are astounding!

From paragliding adventures to quirky activities like standing on one’s head or foraging in local forests, participants demonstrated that preventing Alzheimer’s can be both effective and fun.

Watch the rest of the videos here

Ali’s daring paragliding escapade, Zoe’s upside-down yoga prowess, and Nodge’s foraging adventures exemplify the creativity and commitment shown by our community. These actions not only inspire but also remind us that preventing Alzheimer’s is within everyone’s reach, with room for creativity and enjoyment along the way.

Central to the success of Alzheimer’s Prevention Day were the dedicated individuals behind the scenes. We extend heartfelt thanks to Cath and the team for their meticulous editing of inspiring films, and to Alex for crafting a user-friendly website that hosted invaluable resources and engaging content.

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A BIG thank you!

Behind every groundbreaking initiative are the scientists and professors whose expertise and dedication drive progress. Their research forms the backbone of our mission, guiding us towards effective prevention strategies and empowering individuals to make informed choices about their cognitive health.

As we reflect on the triumphs of Alzheimer’s Prevention Day, we invite you to join us in building a repository of inspiring actions. Visit our website to explore videos showcasing innovative ways people are preventing Alzheimer’s, and most importantly, create your own 30-second film. Share your daily practices that promote brain health, from physical activities to dietary choices, and inspire others to do the same.

>> Click here to submit your video and join the challenge

Together, let’s continue to raise awareness, take meaningful action, and pave the way towards a future where Alzheimer’s is preventable. Visit Alzheimer’s Prevention Day website to learn more and get involved today. 

Your actions today can make a difference tomorrow.

Thank you for reading!

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

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

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

Too much sugar shrinks the brain, but it’s so attractive. Why?

We are led by the science here at Food for the Brain, so we know that one of the best things you can do for your brain is to reduce your sugar and support your insulin control. That is why it is one of our key lifestyle domains in the COGNITION programme. 

However, you probably already know too much sugar isn’t great for health but how can we make eating a lower carb and sugar life easier?

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First, let’s recap the science… 

Dr. Robert Lustig, a renowned expert on brain health and a member of our scientific advisory board, highlights the significant role of insulin control and dietary choices in preventing cognitive decline.

Research from Columbia University in 2004 revealed that individuals with high insulin levels, (a primary indicator of metabolic dysfunction), were twice as likely to develop dementia compared to those with healthy insulin levels (1). Furthermore, those with the highest insulin levels exhibited the worst memory retrieval abilities (1). Similarly, an Italian study linked elevated insulin levels to declining mental function (2).

Several studies have established a connection between high sugar consumption and poor cognitive outcomes. For instance, a study among Puerto Ricans found that high sugar intake doubled the risk of cognitive impairment (3), while another U.S. study correlated elevated blood sugar levels with memory loss (4). The detrimental impact of high dietary glycaemic load (GL) on cognitive function has been observed in studies from Ireland and the United States, indicating that high GL diets are strongly associated with Alzheimer’s-related pathological changes (5,6).

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What is Glycaemic load?

Glycaemic load considers both the quality (GI – glycaemic index) and the quantity (carbohydrate content) of the carbohydrates in a food serving. It provides a more accurate picture of how a food will affect blood sugar levels. The formula for calculating glycaemic load is:

GL  = GI x carbohydrate / 100

A high GL diet measured by the total glucose load on the bloodstream, is linked to increased amyloid plaque formation and cognitive decline, particularly in individuals with the ApoE4 gene, which regulates fat metabolism (7). Even individuals with high-normal blood glucose levels experience greater brain shrinkage and cognitive impairment compared to those with lower levels, as shown in long-term studies (8).

Plus, the damage of a high-GL diet can start early in life. Dr. Lustig points out that overweight children on high-GL diets show signs of cognitive decline, and adolescents with metabolic dysfunction from such diets exhibit hippocampal shrinkage and other brain structure changes (9,10).

So it is clear that eating excess sugar or the wrong types of carbohydrates with a high GL is a problem, so what do you eat?

(Wondering if you’re eating too much sugar? Then test, don’t guess with our home HbA1c test – find out more here.)

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What to eat?

There are two options: following a low GL diet or going a step further and adhering to a ketogenic approach (or switching between the two as Patrick highlights in the Hybrid Diet book). For more info on the ketogenic diet click here to find out more

A low GL diet is focused on consuming foods that have a minimal impact on blood sugar. Basically a diet rich in:

Vegetables: Most non-starchy vegetables like spinach, broccoli, and bell peppers.
Fruits: Berries, cherries, grapefruit, and apples.
Legumes: Lentils, chickpeas, and black beans.
Whole Grains: Barley, quinoa, and whole oats.
Fish and meat or tofu/tempeh: unprocessed
Dairy: Plain yoghurt and milk (unsweetened).
Nuts and Seeds: Almonds, walnuts, chia seeds, and flaxseeds.

Whilst eating this way can support your brain health it can also help you sustain energy levels, help with weight loss and improve heart health.

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So how can we make it easier?

At Food for the Brain we have a few ways to help you feed your brain on the right foods:

Complete the Cognitive Function Test and join COGNITION so we can walk you through how to reduce sugar and upgrade your brain over the next few months.
Upgrade Your Brain Cook App – full of low GL recipes and coming soon. Help us by pre ordering today to get brain-loving recipes at your fingertips.
Here is a recipe sample:

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Almond and coconut porridge

Breakfast Serves 2, generously 

TOTAL GLs: 4

Ingredients:

2 tbsp milled flaxseed
2 tbsp coconut flour
2 tbsp whole flaxseed
2 tbsp chia seeds
2 tbsp coconut flakes, toasted in a dry pan
2 tbsp raspberries
2 tbsp blueberries
2 strawberries
8 walnuts, broken up
1 tbsp soft brown sugar alternative (or sweetener of choice)
300ml unsweetened almond milk
1 tbsp chicory root syrup (or sweetener of choice)

Instructions:

Stir everything (except the desiccated coconut, nuts and berries) together in a saucepan and let sit for 10 mins.
Gently heat through until thickened – add a little more milk if needed to get the consistency you like.
Top with the berries, nuts and toasted coconut – add some natural yoghurt if you like.
Drizzle with the chicory syrup 

Cooks Notes

It’s worth seeking out the chicory syrup – very low sugar and also high fibre. 

Nutrition Highlights

Antioxidants: High in antioxidants, particularly vitamins A, C, and E, which help protect cells from damage and support immune function.
Protein: A moderate source of protein, supporting muscle maintenance and repair.
Fibre: Contains a high amount of fibre, aiding in digestion and promoting satiety.

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Other resources

Here are a few other resources to make low sugar easier, 

FATT bars – easy low GL and low carb snacks for on-the-go. Use the code FFTB10 to save 10% and FATT will donate to the charity with every purchase.

Dillon bread – low carb bread and their brand new high fibre, low GL, Chicory Fibre Syrup perfect for adding to porridge and also suitable for diabetics. Use code FFB10 to save 10% and Dillon will donate 10% with every purchase.

Keto Mojo – if you want to take it a step further and follow a ketogenic diet then grab one of their ketone readers to make life easier and to check you are in ketosis. Use code FFB10 to save 10%.

These companies are some of our supporting organisations – find out more here.

Thank you for reading!

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

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

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

References

Abbatecola AM, Paolisso G, Lamponi M, Bandinelli S, Lauretani F, Launer L, Ferrucci L. Insulin resistance and executive dysfunction in older persons. J Am Geriatr Soc. 2004 Oct;52(10):1713-8. doi: 10.1111/j.1532-5415.2004.52466.x. PMID: 15450050.
Abbatecola AM, Paolisso G, Lamponi M, Bandinelli S, Lauretani F, Launer L, Ferrucci L. Insulin resistance and executive dysfunction in older persons. J Am Geriatr Soc. 2004 Oct;52(10):1713-8. doi: 10.1111/j.1532-5415.2004.52466.x. PMID: 15450050.
Ye X, Gao X, Scott T, Tucker KL. Habitual sugar intake and cognitive function among middle-aged and older Puerto Ricans without diabetes. Br J Nutr. 2011 Nov;106(9):1423-32; doi: 10.1017/S0007114511001760. Epub 2011 Jun 1. PMID: 21736803; PMCID: PMC4876724.
Power SE, O’Connor EM, Ross RP, Stanton C, O’Toole PW, Fitzgerald GF, Jeffery IB. Dietary glycaemic load associated with cognitive performance in elderly subjects. Eur J Nutr. 2015 Jun;54(4):557-68. doi: 10.1007/s00394-014-0737-5. Epub 2014 Jul 18. PMID: 25034880.
Seetharaman S, Andel R, McEvoy C, Dahl Aslan AK, Finkel D, Pedersen NL. Blood glucose, diet-based glycemic load and cognitive aging among dementia-free older adults. J Gerontol A Biol Sci Med Sci. 2015 Apr;70(4):471-9. doi: 10.1093/gerona/glu135. Epub 2014 Aug 22. PMID: 25149688; PMCID: PMC4447796.
Taylor MK, Sullivan DK, Swerdlow RH, Vidoni ED, Morris JK, Mahnken JD, Burns JM. A high-glycemic diet is associated with cerebral amyloid burden in cognitively normal older adults. Am J Clin Nutr. 2017 Dec;106(6):1463-1470. doi: 10.3945/ajcn.117.162263. Epub 2017 Oct 25. PMID: 29070566; PMCID: PMC5698843.
Taylor MK, Sullivan DK, Swerdlow RH, Vidoni ED, Morris JK, Mahnken JD, Burns JM. A high-glycemic diet is associated with cerebral amyloid burden in cognitively normal older adults. Am J Clin Nutr. 2017 Dec;106(6):1463-1470. doi: 10.3945/ajcn.117.162263. Epub 2017 Oct 25. PMID: 29070566; PMCID: PMC5698843.
M.E. Mortby 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), vol 8
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Yau PL, Castro MG, Tagani A, Tsui WH, Convit A. Obesity and metabolic syndrome and functional and structural brain impairments in adolescence. Pediatrics. 2012 Oct;130(4)
. doi: 10.1542/peds.2012-0324. Epub 2012 Sep 3. PMID: 22945407; PMCID: PMC3457620.
Lakhan, S.E., Kirchgessner, A. The emerging role of dietary fructose in obesity and cognitive decline. Nutr J 12, 114 (2013).
Loef M, Walach H. Fruit, vegetables and prevention of cognitive decline or dementia: a systematic review of cohort studies. J Nutr Health Aging. 2012 Jul;16(7):626-30. doi: 10.1007/s12603-012-0097-x. PMID: 22836704.