By Patrick Holford
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:
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.
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.
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】.
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 the Upgrade 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.
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Ingredients (makes about 12-16 mini eggs)
Method
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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.
By Patrick Holford
This is taken from Patrick Holford’s NEW book – Alzheimer’s: Prevention is the Cure which you can pre-order here today!
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.
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.
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.
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%’.
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]
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.
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.
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.
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.
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.
References:
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.
7. Walsh S, et al. Lecanemab for Alzheimer’s disease. BMJ. 2022;379:o3010. doi: https://doi.org/10.1136/bmj.o3010
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
11. Smith AD. Why are drug trials in Alzheimer’s disease failing? Lancet. 2010;376:1466. doi: https://doi.org/10.1016/S0140-6736(10)61994-0
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
14. Cummings J, et al. Alzheimer’s disease drug development pipeline: 2024. Alzheimers Dement (N Y). 2024 Apr 24;10(2):e12465. Dutch. doi: https://doi.org/10.1002/trc2.12465
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.
By Patrick Holford
In 1965, UK paediatrician Dr Richard Smithells discovered that children with low folate were at significantly higher risk of neural tube defects, then commonly referred to as spina bifida.
It took more than 25 years for his research to be taken seriously.
It wasn’t until the late 1980s that the Medical Research Council agreed to fund a study, the results of which were published in 1990. In 1991 the UK government told all women who were pregnant or planning pregnancy, to supplement 400 mcg of folic acid.
Folic acid reduces risk by supporting the process of methylation, which can be assessed through homocysteine levels. The process of methylation is vital for neuronal development and it depends not only on folate, but also on vitamins B6 and B12. Nine in ten obese women in the EU fail to achieve basic guidelines for folic acid supplementation in early and pre-pregnancy which would help to prevent such tragic neurodevelopmental problems (1).
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More than half of all children, and probably their parents, are deficient in B12. Accelerated brain shrinkage occurs below 500 pg/ml, as established by Professor David Smith’s research at Oxford University more than a decade ago. This is why several countries, such as Japan, set the ‘normal’ range for serum B12 as being above 500 pg/ml. Despite clear evidence to the contrary over the past decade, both UK and US health authorities have failed to correct the wrongful reference range for vitamin B12, set at less than half this, namely 180pg/ml (2).
A recent study of 3,000 EU children reported that the median level was 347 pg/ml and one third were below 200 pg/ml (3). This means that at least half of the children had levels associated with accelerated brain atrophy. This deficiency is especially prevalent in vegan children.
Poor methylation, identified by raised homocysteine, isn’t just an established risk factor or biomarker for neural tube defects. It is also a biomarker for autism, poor cognition in children, epilepsy, congenital heart defects, reduced birth weight and size, pregnancy complications, miscarriages, bipolar disorder, depression and schizophrenia (4). Methylation is required to ‘marry’ omega-3 DHA to phospholipids such as phosphatidylcholine, to form neuronal membranes essential for brain communication. Without healthy, fully functional neuronal membranes, cognition becomes ‘disconnected’.
The Bristol Avon study of 11,875 pregnant women showed a clear relationship between the amount of seafood consumed by a pregnant woman and their child’s development. The less seafood consumed, the worse the child’s social behaviour, fine motor skills, communication, social development, and verbal IQ (5).
At the Chelsea and Westminster campus of Imperial College London, Professor Michael Crawford’s team at the Institute of Brain Chemistry and Human Nutrition, has identified which mothers are likely to have neurodevelopmentally impaired infants based on their blood level of a type of oleic acid, which is produced as a substitute when insufficient omega-3 DHA is available to build the foetal brain (6). DHA is not only critical for brain development, but also essential for optimal visual function.
Insufficient choline, a primary constituent of phospholipids, during pregnancy is strongly linked to poor cognition. Women given choline in the last trimester have infants with faster speed of processing information and memory between four and thirteen months of age (7). The protective intake, 400mg per day, has also been shown to cut the risk of cognitive decline, dementia and Alzheimer’s by about 20% (8). So, lack of folate, B12, omega-3 fats and possibly choline are all extremely common and all strongly linked to many aspects of neurodivergence, including autism.
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The culturally ‘acceptable’ view is that neurodivergence can’t be ‘treated’ – that the challenging symptoms experienced by those classified as neurodivergent or autistic (for example, cognitive and communication problems, anxiety and depression) can never be improved, despite clear evidence to the contrary. It is believed by some that autism, since it sometimes occurs within families, might be largely ‘in the genes’, as it was for Alzheimer’s. But families share environments, including habits from diet, smoking and drinking. We now know that genes cause less than one in a hundred cases of Alzheimer’s (9). Also, the gene hypothesis cannot adequately explain the dramatic rise in autism diagnoses in recent decades nor does it accept the simple fact that genes can only exert their effects across our biology – which is directly affected by nutrition.
That is not to say that genes don’t play a part in neurodivergence. There are several known genetic polymorphisms that do increase risk of neurodivergence such as a key methylation gene polymorphism, MTHFR677TT, which means that a person is less good at methylation, and needs more B vitamins. If present in the mother or child it almost doubles the risk of autism. A recent meta-analysis concludes, “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.” (10) This is the same gene polymorphism that increases risk of Alzheimer’s disease.
Associate Professor Murphy’s research in Spain found that those women who had a homocysteine level above 9 mcmol/l, which is not uncommon (ideal is below 7), strongly predicted neurodivergent problems in their children at 4 months and again at 6 years of age, including an increased risk of autism, with children more likely to suffer from anxiety, depression, social problems and aggressive behaviour (11).
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Neurodivergence, including conditions such as autism, is a broad and evolving concept, which currently encompasses so many children. There are many potential contributors including gut-brain problems, neuro-inflammation, nutritional deficiencies, toxic excesses, microbe infections including mould, food and other allergies, smartphone overuse, psychological and social issues, as well as genes. Every child needs a full assessment of these potential contributory factors. Individual assessment is required, with nutrition being one of the key factors to address.
As Dr Rona Tutt, OBE, past President of the National Association of Head Teachers, an expert in special needs and on the board of Trustees says:
“People come in assorted shapes and sizes with brains that are unique. A significant minority who are neurodivergent, need to be recognised, valued and supported, so they can maximise their strengths and overcome their challenges. We need to understand what is driving this increase in neurodivergence and how to best support and optimise a child’s potential.”
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Our goal in launching COGNITION for Smart Kids & Teens is to empower children and their parents to be the best they can be. Children are our future, yet the current system is already struggling, with one in six children identified as having special educational needs. We can no longer ignore the clear and growing body of evidence linking neurodivergence to widespread deficiencies in B vitamins and omega-3 fats – key drivers of impaired methylation. Addressing these foundational nutritional gaps must be the starting point for effective intervention. Ignoring or opposing this imperative is no different from what happened to Dr Smithell’s research on folic acid and neural tube defects. Initially, they said it wasn’t true and wasn’t important. Twenty five years later, to the cost of many thousands of children, it was finally recognised as both true and very important.
I hope we do not have to wait as long for the role of nutrition in neurodivergence to be taken seriously.
What we are campaigning for is widespread social awareness, along with governmental acceptance. The purpose of COGNITION for Smart Kids & Teens is to give parents a direct way to assess their children and identify simple and doable ways to help them reach their full potential for health and happiness.
Visit foodforthebrain.org/smartkids to find out more about the campaign, which launches on April 24th with both a conference for health professionals and a public webinar for parents. This coincides with the launch of the free on-line COGNITION for Smart Kids and Teens – an assessment with personalised advice on how to help children reach their full potential.
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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 https://www.cdc.gov/mmwr/volumes/72/ss/ss7202a1.htm?s_cid=ss7202a1_w
2 https://researchbriefings.files.parliament.uk/documents/POST-PN-0612/POST-PN-0612.pdf; see also Russell G, Stapley S, Newlove-Delgado T, Salmon A, White R, Warren F, Pearson A, Ford T. Time trends in autism diagnosis over 20 years: a UK population-based cohort study. J Child Psychol Psychiatry. 2022 Jun;63(6):674-682. doi: 10.1111/jcpp.13505
3 https://www.gov.scot/publications/pupil-census-supplementary-statistics/
4 https://www.health-ni.gov.uk/news/publication-prevalence-autism-including-aspergers-syndrome-school-age-children-northern-ireland-a nnual-report-2023
5 D’Adamo C et al., Reversal of Autism Symptoms among Dizygotic Twins through a Personalized Lifestyle and Environmental Modification Approach: A Case Report and Review of the Literature. J Pers Med. 2024 Jun 15;14(6):641. doi: 10.3390/jpm14060641
6 Survey conducted in collaboration with the charity Thinking Autism. The full survey results will be shown at the Smart Kids conference, April 24th 20025.
7 https://www.nhs.uk/conditions/autism/autism-and-everyday-life/treatments-that-are-not-recommended-for-autism/
8 https://www.nice.org.uk/guidance/cg142/chapter/Recommendations#interventions-for-autism-2
9 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; see also Murphy MM, Fernandez-Ballart JD, Molloy AM, Canals J. Moderately elevated maternal homocysteine at preconception is inversely associated with cognitive performance in children 4 months and 6 years after birth. Matern Child Nutr 2017;13,e12289 . doi: 10.1111/mcn.12289
10 Hasler M, Fideli ÜS, Susi A, Hisle-Gorman E. Examining the relationship between autism spectrum disorder and neural tube defects. Congenit Anom (Kyoto). 2023 Jul;63(4):100-108. doi: 10.1111/cga.12516. Epub 2023 Apr 18. PMID: 37073427.11 Smith AD, Refsum H. Homocysteine – from disease biomarker to disease prevention. J Intern Med. 2021 Oct;290(4):826-854. doi: 10.1111/joim.13279
By Patrick Holford
Something concerning is happening to our children – an increasing number are experiencing psychological and behavioural challenges, often diagnosed as autism.
These challenges range from reduced eye contact and language delays to social difficulties, cognitive struggles, emotional meltdowns, aggression, and in some cases, depression. But what is driving this surge?
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While mainstream medicine largely attributes autism to genetics, explaining the rise as improved diagnostic recognition, a growing body of independent researchers and clinicians in the US and UK suggests otherwise. The rapid increase in cases across multiple countries cannot be solely explained by genetics, as genes do not change so quickly. In the US, autism rates have skyrocketed from 2 in 10,000 to 1 in 36 over 50 years. In the UK, official government data estimates 1 in 62 children are classified as autistic; an eightfold increase in 20 years. Meanwhile, school census data from Scotland and Northern Ireland report even higher rates, with 1 in 20 children diagnosed. These numbers strongly indicate that environmental factors, including diet, play a key role. This also suggests that proactive steps could help reduce risk.
That is why we are launching COGNITION for Smart Kids &Teens in April with the online ‘Smart Kids’ conference. We are bringing together leading experts to examine ways to prevent and potentially mitigate the impact of autism through environmental and nutritional interventions. In addition, we also have our ‘Optimising Neurodivergence public webinar for parents, caregivers or any non-practitioners who want to learn how to support our children to reach their full potential.
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Dr. Chris D’Adamo, Assistant Professor at the University of Maryland School of Medicine and Director of the Centre for Integrative Medicine, has been at the forefront of research into environmental influences on autism. His recent paper, published in Personalized Medicine, estimates a 300% rise in autism cases since 2000. The study also documents a case where early intervention reversed autism symptoms by addressing modifiable lifestyle and environmental factors.
The case involved twin toddler girls exhibiting classic autistic traits;limited communication, repetitive behaviours, resistance to change and severe gastrointestinal issues. Under a comprehensive programme, led by a team of physicians, they implemented tailored interventions focused on diet, environment and lifestyle. The results were striking; within months, both girls showed dramatic improvements. Their autism severity scores dropped significantly, with one twin’s score reducing from 76 to 32 and the other from 43 to just 4. (Read more on this case here)
In the UK, Dr. Lorene Amet, a functional nutritionist and founder of The Lauriston Centre, has been applying similar integrative approaches. She has worked with hundreds of families, with remarkable success. A survey conducted with the charity Thinking Autism, assessed 220 children who followed her recommendations. 169 families reported either ‘life-changing’ or ‘very beneficial’ improvements, while only 11 children saw no noticeable change.
Yet, despite such promising results, the NHS maintains that autism has no cure and advises against interventions such as vitamins, minerals, and dietary modifications. The NICE guidelines currently offer no targeted nutritional strategies for autism management, leaving many parents with limited options.
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Another key topic at the Smart Kids Conference is prevention; reducing the likelihood of autism before birth. Research led by Associate Professor Michelle Murphy of the Universitat Rovira I Virgili in Spain, has revealed a crucial link between B vitamin deficiencies in early pregnancy and a child’s likelihood of developing autism-related traits. Her studies show that children of mothers who were low in B vitamins before conception were significantly more likely to display withdrawn behaviour, anxiety, depression or aggression by age six.
The connection between maternal nutrition and neurological development is well established. For decades, pregnant women have been advised to take folic acid to prevent neural tube defects; a policy delayed by 25 years, resulting in hundreds of thousands of avoidable birth defects. Children with autism are six times more likely to have neural tube defects, further linking B vitamin deficiencies to neurodevelopmental issues.
This aligns with earlier research from Oxford University’s Professor David Smith, one of our scientific advisors. His work demonstrated that B vitamins lower homocysteine, a toxic amino acid linked to autism, depression, cognitive impairments in children and Alzheimer’s in adults. Professor Murphy’s research further suggests that even mildly elevated homocysteine levels before pregnancy strongly predict neurodivergent traits in children. This underscores the importance of nutritional screening and intervention before conception.
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We are inviting parents to take part in a free online assessment of their child’s cognitive, emotional, and behavioural function, alongside a diet and lifestyle questionnaire to help optimise brain health. Parents can also access a home test kit for homocysteine levels, providing valuable insight into potential nutritional deficiencies that may affect brain function.
The Smart Kids conference will provide further guidance on evidence-based interventions, bringing together researchers, clinicians, and parents seeking practical solutions to support children’s cognitive development.
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“People come in assorted shapes and sizes, with brains that are unique,” says Dr Rona Tutt, OBE, a trustee of Food for the Brain and past President of the National Association of Head Teachers. “A significant minority who are neurodivergent need to be recognised, valued, and supported to maximise their strengths and overcome challenges. Understanding the factors driving the rise in neurodivergence is key to ensuring the best outcomes for future generations.”
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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 https://www.cdc.gov/mmwr/volumes/72/ss/ss7202a1.htm?s_cid=ss7202a1_w
2 https://researchbriefings.files.parliament.uk/documents/POST-PN-0612/POST-PN-0612.pdf; see also Russell G, Stapley S, Newlove-Delgado T, Salmon A, White R, Warren F, Pearson A, Ford T. Time trends in autism diagnosis over 20 years: a UK population-based cohort study. J Child Psychol Psychiatry. 2022 Jun;63(6):674-682. doi: 10.1111/jcpp.13505
3 https://www.gov.scot/publications/pupil-census-supplementary-statistics/
4 https://www.health-ni.gov.uk/news/publication-prevalence-autism-including-aspergers-syndrome-school-age-children-northern-ireland-a nnual-report-2023
5 D’Adamo C et al., Reversal of Autism Symptoms among Dizygotic Twins through a Personalized Lifestyle and Environmental Modification Approach: A Case Report and Review of the Literature. J Pers Med. 2024 Jun 15;14(6):641. doi: 10.3390/jpm14060641
6 Survey conducted in collaboration with the charity Thinking Autism. The full survey results will be shown at the Smart Kids conference, April 24th 20025.
7 https://www.nhs.uk/conditions/autism/autism-and-everyday-life/treatments-that-are-not-recommended-for-autism/
8 https://www.nice.org.uk/guidance/cg142/chapter/Recommendations#interventions-for-autism-2
9 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; see also Murphy MM, Fernandez-Ballart JD, Molloy AM, Canals J. Moderately elevated maternal homocysteine at preconception is inversely associated with cognitive performance in children 4 months and 6 years after birth. Matern Child Nutr 2017;13,e12289 . doi: 10.1111/mcn.12289
10 Hasler M, Fideli ÜS, Susi A, Hisle-Gorman E. Examining the relationship between autism spectrum disorder and neural tube defects. Congenit Anom (Kyoto). 2023 Jul;63(4):100-108. doi: 10.1111/cga.12516. Epub 2023 Apr 18. PMID: 37073427.11 Smith AD, Refsum H. Homocysteine – from disease biomarker to disease prevention. J Intern Med. 2021 Oct;290(4):826-854. doi: 10.1111/joim.13279
by Patrick Holford
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Neurodivergence refers to differences in mental or neurological function from what is considered typical. This concept encompasses conditions such as autism spectrum disorder (ASD), ADHD, Tourette’s syndrome, dyspraxia, synaesthesia, dyscalculia, Down syndrome, epilepsy, and chronic mental health conditions like bipolar disorder, OCD, borderline personality disorder, anxiety, and depression. The overlap of traits in ASD and ADHD has led to the term AuDHD, recognising their frequent co-occurrence [1].
The term ‘neurodiversity’ refers to the natural variations in how human brains function, emphasising that every individual is unique [2]. While some neurodivergent individuals face challenges in communication, information processing, and social integration, others exhibit remarkable creativity and intelligence. The former president of the National Association of Head Teachers, Dr Rona Tutt, highlights that neurodevelopmental disorders often co-occur, challenging outdated beliefs that conditions exist in isolation [3].
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While genetics may contribute to neurodivergence, environmental factors play a significant role. The rise in neurodevelopmental diagnoses cannot be solely attributed to better awareness and diagnosis . Factors such as air pollution, processed food consumption, chemical exposure, and modern technology use are increasingly considered potential contributors [3]. Many characteristics of neurodivergence appear within families, often assumed to be genetic. However, shared environmental influences—nutritional deficiencies, exposure to toxins, and psychosocial stressors—may drive this heritability rather than genes alone [3].
The increase in neurodevelopmental diagnoses is particularly striking in children. In the US, one in six children is classified as neurodivergent, and autism diagnoses have risen fourfold in two decades [1]. A practical measure of this shift is the number of children classified as having special educational needs (SEN). These classifications are often made reluctantly by parents and educators, underscoring the genuine increase in neurodivergence rather than mere overdiagnosis.
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Nutrition plays a crucial role in cognitive development and mental health. Dr Carl Pfeiffer, a pioneering physician, identified zinc deficiency and pyroluria as biological imbalances linked to sensory overload and neurodevelopmental difficulties [4].
Nutrient deficiencies can contribute to key symptoms of ASD and ADHD. The following table is adapted from data provided by the US Centers for Disease Control and Prevention (CDC) on common ASD characteristics and their potential nutritional correlations. Research has linked the following deficiencies to common neurodivergent traits:
| Common Neurodivergent Traits | Associated Nutrient Deficiencies |
| Avoids eye contact | Vitamin A, Omega-3 DHA |
| Delayed language skills | Omega-3 DHA, Hcy/B vitamins, vitamin A |
| Delayed movement skills | Omega-3 DHA, Hcy/B vitamins, vitamin A |
| Delayed cognitive or learning skills | Omega-3 DHA, Hcy/B vitamins, vitamin A |
| Hyperactive, impulsive, and/or inattentive behaviour | Omega-3 DHA, Hcy/B vitamins, dysglycemia (sugar), additives eg MSG) |
| Epilepsy or seizure disorder | Omega-3 DHA, Hcy/B vitamins, dysglycemia (sugar), magnesium |
| Unusual eating and sleeping habits | Food intolerance, sugar, magnesium, zinc, tryptophan |
| Gastrointestinal issues (for example, constipation) | Food intolerance (e.g., coeliacs), gut dysbiosis, zinc |
| Unusual mood or emotional reactions | Omega-3 DHA, Hcy/B vitamins, dysglycemia (sugar), additives eg MSG), food intolerance, iron |
| Anxiety, stress, or excessive worry | Omega-3 DHA, Hcy/B vitamins, dysglycemia (sugar), vitamin C |
| Lack of fear or more fear than expected | Omega-3 DHA, Hcy/B vitamins, dysglycemia (sugar), vitamin C |
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The foundation of brain health is laid during pregnancy. By birth, 70% of brain cells are already formed, making prenatal and early childhood nutrition crucial [5]. Deficiencies during this period can have long-term consequences.
For example, studies have shown:
Given the strong link between nutrition and brain function, proactive dietary changes can support neurodevelopment and alleviate symptoms of neurodivergence. Key recommendations include:
It is also important to note that the DRIfT test can be administered to any child over the age of two. Also note you can do the DRIfT test on any child over 2 years old. Find out more about the DRIfT test here
While some neurodevelopmental conditions may not be entirely preventable, improving prenatal and childhood nutrition can help reduce risks and alleviate symptoms. The rising prevalence of neurodivergence suggests an urgent need to address environmental and dietary factors [10]. Rather than normalising suboptimal brain development, prioritising nutrition and early intervention can improve outcomes for neurodivergent individuals.
By fostering a deeper understanding of how environmental and nutritional factors influence neurodivergence, we can better support individuals in reaching their full potential while reducing unnecessary suffering.
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How to get involved:
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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.Centers for Disease Control and Prevention (CDC). Autism Data. Available at: https://www.cdc.gov/autism/data-research/?CDC_AAref_Val=https://www.cdc.gov/ncbddd/autism/data.html
2. Psychology Today. “What Is Neurodiversity?”. Available at: https://www.psychologytoday.com/gb/basics/neurodiversity
3. Tutt, R. Neurodiversity insights. Trustee and Scientific Advisor, Food for the Brain.
4. Pfeiffer, C. Nutritional insights. Pfeiffer Treatment Center.
5. McNulty, H., et al. (2019). Effect of continued folic acid supplementation beyond the first trimester of pregnancy on cognitive performance in the child: a follow-up study from a randomized controlled trial (FASSTT Offspring Trial). BMC Medicine, 17(1), 196. doi:10.1186/s12916-019-1432-4.
6. Hibbeln, J.R., et al. (2007). Maternal seafood consumption in pregnancy and neurodevelopmental outcomes in childhood (ALSPAC study). Lancet, 369(9561), 578–585. doi:10.1016/S0140-6736(07)60277-3.
7. Liu, Z. (2021). The Impact of Vitamin A on Cognitive Functions. Behavioral Neurology, 2021:5417497. doi:10.1155/2021/5417497.
8. Veena, S.R., et al. (2010). Higher maternal plasma folate but not vitamin B-12 concentrations during pregnancy are associated with better cognitive function scores in 9- to 10-year-old children in South India. Journal of Nutrition, 140(5), 1014–1022. doi:10.3945/jn.109.118075.
9. Roigé-Castellví, J., Murphy, M., Fernández-Ballart, J., & Canals, J. (2019). Moderately elevated preconception fasting plasma total homocysteine is a risk factor for psychological problems in childhood. Public Health Nutrition, 22(9), 1615–1623. doi:10.1017/S1368980018003610.
10. Kranz, S., Jones, N.R.V., & Monsivais, P. (2017). Intake Levels of Fish in the UK Paediatric Population. Nutrients, 9(4), 392. doi:10.3390/nu9040392.
by Cath Verner
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A landmark study from the Centre for Healthy Brain Ageing (CHeBA) at the University of New South Wales (Sydney, Australia) has provided compelling evidence that targeted diet and lifestyle changes can improve cognitive function in older adults.
Or put simply, what we teach and promote at Food for the Brain works when it comes to promoting brain health.
Raising awareness and providing tools to support the critical role of diet and lifestyle in long-term cognitive health is both essential and part of the solution.
This recent study affirms our approach: sustained step-by-step adjustments to diet, exercise, sleep, and social engagement significantly reduces the risk of dementia as well as maintaining – and even enhancing – cognitive function.
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The CHeBA study recruited over 6000 adults aged 55 to 77, dividing them into two groups, one participating in an online lifestyle intervention programme and the other serving as a control group.
While both groups showed some cognitive improvements, those in the intervention group experienced significantly greater gains, demonstrating the added value of a structured, multi-domain approach.
Professor Brodaty, one of the study’s research team, stated:
“Participants aged 55-65 showed greater improvement than those aged 66-77, suggesting that prevention programmes should start earlier.”
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Unlike traditional approaches that focus on just one or two factors, the COGNITION® Programme, which you get access to when you become a FRIEND of Food for the Brain, is similarly built on eight interwoven pillars—including diet, physical exercise, sleep, social involvement, and even the gut microbiome—to provide a comprehensive brain health plan.
The study’s ‘Maintain Your Brain’ trial further supports this, showing that targeting multiple lifestyle domains simultaneously – including physical activity, nutrition, brain training, and mental well-being – leads to greater cognitive benefits, rather than focusing on a single risk factor.
And, as we always say, the earlier you start, the better!
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In line with this study, we focus on 8 key domains that influence brain health. These areas provide strategies to help individuals reduce their risk of cognitive decline and support long-term brain health:
Domain 1: Low Glycemic Load (GL) Diet – Managing blood sugar levels is crucial for brain function. High-sugar diets contribute to inflammation and insulin resistance, impairing cognitive performance. A low-GL diet helps stabilise energy levels and protects brain cells from damage
Domain 2: B Vitamins & Homocysteine Levels – High homocysteine levels, a by-product of metabolism, are linked to cognitive decline. Ensuring adequate B vitamins (B6, B12, and folate) supports brain function and lowers homocysteine levels.
Domain 3: Brain-Boosting Fats – Healthy fats like omega-3s (found in fish, flaxseeds, and walnuts) are essential for brain cell structure and function. They help reduce inflammation, enhance memory, and support cognition.
Domain 4: Antioxidants & Polyphenols – Free radicals damage brain cells, but antioxidants (from colourful fruits, vegetables, green tea, and dark chocolate) help combat oxidative stress and keep your brain young.
Domain 5: Healthy Gut & Microbiome – The gut-brain connection is vital for mental clarity and mood. A diverse microbiome (supported by fibre-rich foods, fermented foods, and probiotics) can reduce inflammation and improve neurotransmitter function, supporting memory and mental health.
Domain 6: Active Body (Exercise & Movement) – Regular physical activity boosts blood flow to the brain, supports neuroplasticity, and reduces the risk of dementia. Both aerobic exercise (like walking and cycling) and strength training play a role in maintaining cognitive health.
Domain 7: Active Mind – The brain thrives on challenge! Lifelong learning, problem-solving activities, and hobbies stimulate new neural connections and help build cognitive resilience.
Domain 8: Sleep & Stress Resilience Management – Poor sleep and chronic stress are major contributors to cognitive decline. Deep, restorative sleep allows the brain to clear toxins, while mindfulness, relaxation techniques, and breathing exercises help reduce stress hormones that damage brain cells.
We know that these 8 domains can help you protect your brain and prevent cognitive decline – but most of us need support, accountability, motivation and structure to be able to implement the necessary changes consistently.
That is why the COGNITION® Programme exists.
It’s designed to make implementing the above easier and simpler, one step at a time. By providing tailored advice and guidance on all eight areas, the programme offers tangible, practical steps that members can take to enhance brain function, reduce dementia risk, and improve overall cognitive well-being.
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As a research charity with a stellar scientific advisory board, we care about excellent research being carried out.
Yet the most important thing is that ‘the science’ helps to transform lives, families and communities. Citizen science in action!
Here is what can happen when you join COGNITION. One participant told us:
“I have taken the CFT for at least seven years now and find it very worthwhile.
By monitoring sensibly what I eat, as you advise and exercising within my limitations, I have found that despite being 84, my results have improved.”
This experience is echoed by another participant who found benefit in making small, sustainable lifestyle changes every day:
“I’ve taken on board your recommendations and I’ve increased my vitamin B intake and started doing puzzle books every day to keep my brain active in different ways from before. I also do more exercise and yoga daily. I love the fact that I can make these small changes myself and hopefully reduce my chances of getting dementia.”
Another participant shared how working with Food for the Brain and starting with the COGNITION® Programme was a wake-up call that led to lasting changes:
“Since starting with Food for the Brain, I’ve completely reshaped my lifestyle. I now attend a weekly Pilates class, work on my allotment, swim regularly, and take longer evening walks. I’ve also cut down on alcohol and meat, increased my vitamin B intake, and started doing daily puzzles to challenge my brain in new ways. My sleep has improved and I feel more energetic with fewer foggy days.”
These testimonials show how small, targeted lifestyle changes can significantly enhance cognitive resilience and well-being. The COGNITION® Programme equips individuals with the necessary tools to take charge of their brain health, which leads to improved cognitive test scores, better mental clarity, and a greater sense of control over their future.
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As a non-profit charity we aim to make resources affordable and accessible to all, while covering essential staff and research costs. Membership of the 8-domain COGNITION® Programme is just £50 per year or £5 per month, ensuring that everyone can benefit from the programme.
You get access to the programme when you become a FRIEND of Food for the Brain.
Members receive:
How it works:
*You do not need to be a FRIEND to do this test – you can access it for free here.
Start today!
Your brain health is in your hands.
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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.
By Patrick Holford
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At the end of 2024, as part of Food for the brain international expansion, I was honoured to attend and speak at a conference creating a task force to ‘popularise prevention’ in the ‘silver-haired’ economy. I’d like to share excerpts from the speech given by China’s Former Minister of Health, Gao Qiang.
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“Dear esteemed leaders, distinguished guests, and fellow advocates for the development of the silver economy. I am delighted to join you here in Nanjing to discuss the topic of high-quality development in the silver economy. In his earlier presentation, Mr Ai Bo, the General Manager of Xiangjia Group, categorised the living conditions of elderly individuals into four stages: early ageing, active ageing, semi-active ageing, and disabled ageing. I fully agree with Mr Ai’s perspective and commend his boldness, as a young entrepreneur, to invest in the silver industry. However, I have one small suggestion: the living conditions of elderly individuals should not be defined solely by age but rather by their actual health status. Take myself as an example—while my age has technically surpassed the “active” stage, I still feel full of energy”.
Earlier, Patrick Holford also mentioned five criteria for optimal health, which align closely with the “Five Forces” standard I previously proposed for active seniors: physical strength, energy, intelligence, financial resources, and charisma. Physical and mental strength pertain to health, financial resources reflect economic stability, and charisma is the comprehensive result of personal influence. The above represents my personal understanding of health standards for the elderly population.
This year, the State Council issued a key directive on the development of the Silver Economy. This is not the first time relevant Chinese authorities have introduced the concept. In 2021, the 14th Five-Year Plan for the Development of the Ageing Industry officially highlighted the importance of developing the silver economy.
China’s neighbour, Japan, as the country with the most serious ageing population in the world, and one of the first countries to enter an ageing society, proposed the concept of the silver economy as early as the 1970s. In 2008, the European Union also introduced and actively promoted the development of the silver economy. It is not an exaggeration to say that the Silver Economy is the most important issue at this stage in Asia and even globally. It is closely related to the duration and extent of a country’s ageing population. The more severe the ageing process, the more prominent the role of developing the silver economy. And now, the time for the development of the Silver Economy is just right.
A person with health does not necessarily have everything, but when health is lost, everything else is inevitably lost. This is especially true for the elderly, whose demand for health is even stronger. The decline in physical strength and energy is a natural process, and we cannot resist ageing, nor can we stop it. What we can do is slow it down, as this is an inevitable part of human development. The goal is to minimise illness in old age, prevent serious diseases, and promote long-term health and longevity. This represents the highest pursuit of health. Professor Chen Xiaobing’s interpretation of health is correct in the first part—‘health benefits longevity.’ However, I don’t entirely agree with the second part: ‘longevity does not necessarily mean health.’ Longevity without health is meaningless
I was impressed by Mr Holford’s closing remarks, where he stated that Western health maintenance mainly relies on medicine, but he hopes that in China, the primary means of maintaining health would focus on prevention—avoiding illness or preventing serious disease. Having recognised this, we must work even harder to implement and integrate this into all aspects of our work, especially in meeting the basic needs of the elderly—such as clothing, food, housing, transportation, and daily necessities.
I have conducted a systematic analysis on this, and the core lies in food and daily necessities. We have long passed the stage of food insecurity, and severe malnutrition resulting in physical damage is no longer a common issue. The focus now is on balance, even controlling nutritional excess and reducing obesity. Ensuring that the elderly eat nutritionally and beneficially is our primary goal. Achieving this requires collaborative research from multiple experts. Solely relying on doctors is not enough, as their advice is often limited to six simple words: ‘less salt, less oil, less sugar.’ But does reducing salt, oil, and sugar guarantee health? The answer is ‘no’; a balanced and reasonable diet is essential. Traditional Chinese medicine emphasises the idea that food and medicine come from the same source. In my discussions with related experts, I often stress that the concept of medicinal food is not enough on its own; it needs specific plans to support it. What kind of diet is beneficial for enhancing specific aspects of health? What kind of diet can enhance preventive effects? Only by addressing these questions can families across the country incorporate these dietary combinations and structures into their daily cooking.
Most people are familiar with healthy living, but its scientific basis is not always well understood.Among the five major tasks within the five key elements of building a Healthy China, the primary task is to promote healthy living. This is a prerequisite for preventing various functional diseases and maintaining long-term health. However, whether this goal has been initiated, implemented, and started to produce benefits remains uncertain. Practitioners in relevant fields, including enterprises involved in the silver economy, need to promptly correct misconceptions—medications are not the primary means of promoting the widespread adoption of healthy living. What plays a larger role are nutritional supplements, health products, and adjunctive treatments.
Mastering these techniques would support health, prevent disease, and promote long-term well-being. ‘Daily necessities’ is the most promising area for development. It includes not just daily living products but also health supplements, entertainment products, and age-friendly items, among others.
In conclusion, I hope that the Silver Economy will become a new focal point in China’s economic development, not only serving the elderly population in China but also contributing to the global silver population, showcasing China’s wisdom and spirit of dedication to the world, bringing blessings to all.”
Speech by China’s Former Minister of Health, Gao Qiang.
Patrick Holford with President of the China National Health Association, Wu YingPing (to the left) , former Vice Minister of Health, Zhang Fenglou, and former Minister of Health, Gao Qiang (to the right)
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Wouldn’t it be refreshing if our health ministers were talking and thinking in this way?
We are on the brink of shifting from a drug-focused model to one centered on true prevention through optimal nutrition It is an exciting time.
Will you join us in our mission of making prevention the primary focus?
This paradigm shift first needs to start in your own body and home, so here is how you can begin
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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.
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Attention-deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD) and other neurodevelopmental disorders, all classified as ‘neurodivergent’, have rocketed in both the UK and USA.
One in six children is classified as neurodivergent or in need of special education and and one in 36 is diagnosed as autistic – a fourfold increase in 20 years.
This cannot be explained away by genetics or better diagnosis.
On April 24th, we are hosting a multi-disciplinary team of global experts – coming together for a virtual conference in London to explore what optimum nutrition and lifestyle choices are needed for smart, happy and healthy children and teens and what is driving this escalation of cognitive and behavioural problems.
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The conference starts at the beginning – with pregnancy. Professor Michelle Murphy from the University of Madrid has found that the B vitamin status in the first trimester of pregnancy, measured with a homocysteine blood test, predicts problems, specifically withdrawn behaviour, anxiety or depression, social problems and aggressive behaviour in the child at age 6. Folate is one of these vital B vitamins and nine out of ten obese women in the EU fail to meet basic guidelines for folic acid supplementation to prevent neurodevelopmental problems.
At the Chelsea and Westminster campus of Imperial College London, Professor Michael Crawford’s team at the Institute of Brain Chemistry and Human Nutrition, based at the Chelsea and Westminster campus of Imperial College London, is discussing the importance of marine food in the maternal diet., They have identified which mothers are likely to have neurodevelopmentally impaired infants based on their blood fat levels,, with omega-3 DHA, found in oily fish, being a critical brain-building nutrient.
Professor Julia Rucklidge, Director of New Zealand’s Mental Health and Nutrition Research Lab at the University of Canterbury, will present evidence for the essential role of multivitamins and minerals both during pregnancy and in improving children’s mental health.
This kind of research is also helping to identify what the optimal intake of nutrients is to optimise children’s potential. Dr Alex Richardson from Oxford University is presenting her evidence for helping children with ADHD-like symptoms and paediatric endocrinologist Professor Robert Lustig from the University of California San Francisco is pioneering research showing the dangers of high-fructose diets. “Teenagers with blood sugar problems are showing early signs of the same kind of cognitive decline and shrinkage of the hippocampus that are seen in Alzheimer’s.” The youngest non-genetic Alzheimer’s diagnosis is age 19.
Two clinicians, assistant professor Dr Chris D’Adamo from the University of Maryland in the US and Dr Lorene Amet from France, will be presenting cases of children diagnosed with autism who no longer are diagnosable as such and discussing nutritional and other interventions that are helping autistic children lessen troubling symptoms. “We have over 200 cases of autistic children who have benefitted. The majority have shown significant improvements but not all respond.” Says Dr Amet.
Dr Tommy Wood, Associate Professor of Pediatrics and Neuroscience at the University of Washington, will address the role of an active lifestyle, backed up by a presentation on the dangers of early smartphone use by Dr Jonathan Haidt, author of the New York Times best-seller ‘The Anxious Generation’. “The changes in diet, less active lifestyles and early smart phone use have created a perfect storm, negatively impacting a child’s healthy brain development. These are issues we have to address urgently for the sake of our children”, says Dr Tommy Wood, who heads research at the foodforthebrain.org, the charity hosting the conference.
The conference is opened by Dr Rona Tutt, OBE, past president of the National Association of Head Teachers and an expert in special needs. “People come in assorted shapes and sizes with brains that are unique. A significant minority who are neurodivergent, need to be recognised, valued and supported, so they can maximise their strengths and overcome their challenges. We need to understand what is driving this increase in neurodivergence and how to best support and optimise a child’s potential”, she says.
The conference, which is tailored for nutritionists, doctors, teachers, and health professionals, is also open to interested parents.
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We also have a webinar for everyone (parents, carers etc), where we will dive deeper into the topic of optimising neurodivergence. Find out more about the webinar here.
The conference coincides with the launch of COGNITION for Smart Kids & Teens, which offers a free online assessment to all parents and teenagers as part of a global research project aimed at optimising children’s intellectual and emotional development.
Please visit foodforthebrain.org/smartkids to find out more.
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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 Loperfido, F., Sottotetti, F., Bianco, I. et al. Folic acid supplementation in European women of reproductive age and during pregnancy with excessive weight: a systematic review. Reprod Health 22, 13 (2025). https://doi.org/10.1186/s12978-025-01953-y
4 J. Jianping et al. ‘A 19-Year-Old Adolescent with probable Alzheimer’s Disease’ Journal of Alzheimer’s Disease 1 Jan 2023: 915-922
