Parkinson’s affects 120,000 people in the UK, both young and old.

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Parkinson’s affects 120,000 people in the UK, both young and old.

A recent review from the NCBI in the US (1) on Parkinson’s disease begins with the following:

‘Parkinson’s disease (PD) is a common neurodegenerative disease for which there is no treatment modifying the course of the disorder and no reliable biomarkers for early diagnosis. (2)  In just 26 years, the number of PD patients around the world has more than doubled. (3) A relatively conservative prediction model shows that it is expected that there will be 12 million PD patients in the world by 2050.’ 

Thus, early detection and timely intervention of PD appear to be particularly important.

Thanks to the pioneering work of Dr Geoffrey Leader and Lucille Leader, a doctor and nutritionist living in London, we now know that the right nutritional intervention can effectively support the symptoms of Parkinson’s disease.

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Parkinson’s and Dopamine

Dopamine is a neurotransmitter (chemical messenger) found within the brain. It has a variety of influences on brain function including playing a role in regulation. (Fig 1) [4]  

There is little doubt that dopamine deficiency is the major cause of the symptoms of Parkinson’s, and most drug therapy aims to improve the body’s ability to make dopamine from L-dopa. But, why do some people develop this impaired ability to make this key neurotransmitter?

There are many answers to this question.

In some cases the neurons that produce dopamine don’t work properly, sometimes because they lack the raw materials, or the enzymes that turn on the building blocks, amino acids.  (Amino acids are commonly known as the building blocks of protein. There are 20 standard amino acids from which almost all proteins are made.) The neurons can die off or be damaged, for example by oxidants, or by environmental toxins such as pesticides and herbicides.

Interestingly, researchers at the University of Miami have found levels of these chemicals to be higher in the brains of Parkinson’s sufferers.[5] The incidence of Parkinson’s is notably higher in rural areas where a lot of crop spraying takes place, and some pesticide combinations have shown a clear geographical correlation with incidences of the disease.[6,7] 

Deficiency of nutrients such as folate which is critical during pregnancy for the development of a baby’s brain and nerves and also essential for brain and nerve function, play a part, making these dopamine-producing brain cells more susceptible to damage.[8]

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The Homocysteine Connection

The balance of neurotransmitters, including dopamine, is controlled to a large extent by the process of methylation. (Methylation is what occurs when the body takes one substance and turns it into another, so that it can be detoxified and excreted from the liver.)

Most people with Parkinson’s have raised homocysteine levels. [9] Homocysteine is an amino acid found in the blood. Elevated levels of homocysteine have been associated with narrowing and hardening of the arteries and an increased level indicates disrupted methylation patterns. The latest review [10] states that “Homocysteine is linked with the occurrence and progression of Parkinson’s. This review briefly discussed the structure of Hcy, the metabolism of Hcy, and the mechanism of HHcy in PD. There are many disputes about the relationship between HHcy and PD which remain to be investigated. It also remains to be examined whether homocysteine is a causative agent or marker of damage.” Additionally,treatment with L-dopa medication tends to raise homocysteine levels.[11] 

Either way, testing for homocysteine and supplementing homocysteine-lowering nutrients accordingly would be a recommendation. Buy your test kit here.

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Parkinsons & Nutrition

In addition to faulty methylation, sometimes there is a problem in how the body detoxifies, a job primarily done by the liver, leaving neurons unprotected.[12] Then there are other factors such as prolonged stress and the likelihood of genetic predispositions. Geoffrey and Lucille Leader figured that each of these pieces of the jigsaw puzzle could be made a lot better if sufferers followed a targeted optimum nutrition programme. They started to test patients with Parkinson’s disease and found that literally 100 percent of them had nutritional deficiencies based on tests that measure what is going on within cells. They also found that many were deficient in stomach acid and digestive enzymes. Digestive enzymes break down carbohydrates, fats and proteins into their smallest components, allowing them to be absorbed by the body. Examples of deficient digestive enzymes might look like poor digestion, and increased intestinal permeability, leading to faulty absorption of nutrients. 

Intestinal permeability is easily tested by drinking a solution that shouldn’t pass through the gut wall, and then measuring urinary levels. Using such a test, people with Parkinson’s disease may often show an increase in gut permeability or evidence of malabsorption. While there is no conclusive evidence yet that Parkinson’s disease is caused by nutrient deficiencies, the Leaders have found that correcting these deficiencies often helps. 

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Brain Toxins, Oxidants and the Liver

All this faulty digestion and absorption places extra stress on the liver, the detoxification capital of the body. Since the brain’s neurons can’t protect themselves from toxins, they depend on the liver. A simple example of this is alcohol – once you drink more than your liver can detoxify, you get drunk, which is what happens when brain cells are exposed to this toxin. In excess, you lose muscular control and movements, including speech, slow down.

Problems with liver detoxification are often a hallmark of Parkinson’s patients.

One of the liver’s best detox allies are the sulphur-containing amino acids, which have the ability to mop up undesirable toxins in a process called sulphation. Researchers have reported faulty sulphation in patients with Parkinson’s, which can be helped by supplementing cysteine, methionine and molybdenum. These can help rid the body of protein breakdown products, strengthen teeth and may help reduce the risk of tooth decay [13] . 

Avoiding wine, coffee, certain cheeses and chocolate, all known inhibitors of sulphation [12] and eating foods rich in glucosinolates, such as broccoli, brussel sprouts, cabbage, cauliflower and kale, also help the liver to detoxify. 

The greatest toxins of all are oxidants, or ‘free-radicals’. Giving antioxidants helps to prevent free radical damage to brain cells and slows the progression of the disease.

In a 7-year pilot study, 21 patients with early Parkinson’s were given 3,000mg of vitamin C and 3,200iu of vitamin E daily. The need for drug therapy was delayed up to two to three years compared to those who did not receive the antioxidants.[14] 

Along with its negative effect on neurons, Parkinson’s also damages function in the mitochondria, which are the energy factories in our cells where energy conversion takes place. One of the most critical antioxidants for protecting mitochondria is coenzyme Q10 (CoQ10). The older you are, the more likely you are to be deficient. 

These nutrients are some but by no means all of the allies that can support liver function, thereby preventing brain damage from toxins.. Dr Jeffrey Bland from Gig Harbor, Washington, an expert in liver detoxification, has also found tremendous improvement by supporting liver function with nutritional supplementation, increasing the effectiveness of drugs, reducing symptoms and boosting energy levels in those suffering from the early stages of Parkinson’s in studies.[15] 

As detoxification may be compromised in Parkinson’s Disease, as is demonstrated by tests and clinical experience, personal clinical experience demonstrates that it is best to clean up the diet very gradually and recommend nutrients which support detoxification pathways.

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Personalised Nutrition Works Best

The Leaders have found the best approach involves a tailor-made nutritional programme of diet and supplements and have found that this may often reduce symptoms and make drugs more effective, thus optimising dosage. 

They recommend appropriate supplements based on patients’ biochemical individuality, including vitamins, minerals, essential fats, amino acids, antioxidants, phospholipids and brain-friendly herbs, providing that there are no contraindications for the administration of any herbs or nutrients for daily use, or in preparation or recovery from surgery. 

As with so many mental health problems, controlling blood sugar and checking and correcting food allergies or intolerances can make a big difference. The most common allergy-provoking foods are the gluten grains (especially wheat, but also rye, oats, barley and spelt) and dairy products. Managing stress is also important because we respond to stress by producing the stress hormones noradrenalin and adrenalin, which are made from dopamine. This is why the symptoms of Parkinson’s often get worse when the sufferer is stressed.

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Working with Medication: What to Eat

The right diet is very important in tackling every piece of the jigsaw of Parkinson’s. Movement problems can get worse when dense proteins are eaten too close to the times of taking L-dopa medication.[16] This is because L-dopa competes with the amino acids for absorption at the receptor sites in the intestine and at the blood-brain barrier, so less gets through.

To make best use of the L-dopa, protein-rich foods containing the other amino acids should not be eaten at the same time as taking L-dopa medication, according to the following guidelines:

 L-dopa medication and diet – what to eat when*

L-dopa is affected by protein-containing foods which contain significant amounts of the amino acids: tyrosine, phenylalanine, valine, leucine, isoleucine, tryptophan, methionine and histidine. Foods which contain these amino acids include eggs, fish, meat, poultry, dairy produce (not butter), pulses, green peas, spinach, sago, soy, couscous, bulgar, coconut, avocado, asparagus and gluten-containing grains (oats, rye, wheat, barley, spelt).

Take L-dopa medication. Wait ONE HOUR or until the drug takes effect before eating any of the foods listed above.
After eating any of the foods listed above, wait TWO HOURS, if possible, before taking L-dopa medication again if it is needed.

*This dietary protocol has been developed and proven helpful by Dr Geoffrey and Lucille Leader and is reproduced with their kind permission.  (Their book, Parkinson’s Disease Optimising ON-OFF Periods during L-dopa Therapy www.denorpress.com) provides all the monitoring forms for patients and medical professions in order to assess more precise timing and dosage of administration – diet and metabolic pathways also presented.

Some people are more susceptible to this dose-dependent side-effect than others, and few react at a dose of 10mg, which is commonly given for Parkinson’s.[15]

While being careful to avoid these foods around medication, it is important to get enough protein from foods at other times. Good whole proteins include fish and eggs. Many people choose to have their meal containing concentrated protein at night. This is because they do not need as much help with movement control at night as during the day when their L-dopa medication is necessary to see them through all their activities. Some people leave out L-dopa completely after the protein meal. Otherwise, it is best to follow the time protocol for taking L-dopa with a protein-rich meal, as above.

It is also important to have a well-balanced diet throughout the day including fruits and vegetables, gluten-free wholegrains and plenty of fluids. A common problem in Parkinson’s is constipation. Having a diet rich in fruits and vegetables and drinking plenty of water throughout the day makes a big difference, as can a few prunes, figs or dried apricots between meals with water. There are also special fibres, such as glucomannan, which help relieve constipation.

What to do:

Attend our ‘Optimising Parkinson’s’ Webinar – sign up here 
See a nutritional therapist or doctor who can assess you for nutritional deficiencies, digestive problems and liver function.
Pursue a tailor-made nutritional strategy, including a specific diet regime that maximises the effects of any medication.
Have your homocysteine levels checked and supplement homocysteine-lowering nutrients accordingly – buy your homocysteine at home blood test here.
Avoid environmental toxins and eat organic when possible.

Thank you for reading!

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

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

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

REFERENCES:

1 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10848096/pdf/CNS-30-e14420.pdf]

2 Surguchov A. In: Peplow PV, Martinez B, Gennarelli TA, eds. Neurodegenerative Diseases Biomarkers: Towards Translating Research to ClinicalPractice. Springer US; 2022:155-180.

3 GBD 2016 Neurology Collaborators. Global, regional, and national burden of neurological disorders, 1990–2016: a systematic anal- ysis for the global burden of disease study 2016. Lancet Neurol. 2019;18:459-480. doi:10.1016/S1474-4422(18)30499-X

4 V.L. Davidson and D.B. Sittman, Biochemistry: The National Medical Series for Independent Study, Harawl Publishing (1994), pp.477-8

5. L. Fleming et al., ‘Parkinsons’ disease and brain levels of organochlorine pesticides’, Ann Neurol, Vol 36(1), 1994, pp.100-3

6. M. Thiruchevlvam et al., ‘The Nigrostriatal Dopaminergic System as a preferential target of repeated exposures to combined paraquat and maneb: implications for Parkinson’s Disease’, Journal of Neuroscience, Vol 20(24), 2000, pp.9207-14 and J. Corell et al., ‘The risk of Parkinson’s disease with exposure to pesticides, farming, well water and rural living’, Neurology, Vol 67, 1998, pp.1210-18

7. L. Leader, Parkinson’s Disease – The Way Forward, Denor Press (2000), p.77

8. W. Duan et al., ‘Dietary folate deficiency and elevated homocysteine levels endanger dopaminergic neurons in models of Parkinson’s Disease’, J Neurochemistry, vol 80, 2002, pp.101-10

9. Zhou L. Homocysteine and Parkinson’s disease. CNS Neurosci Ther. 2024 Feb;30(2):e14420. doi: 10.1111/cns.14420. Epub 2023 Aug 29. PMID: 37641911; PMCID: PMC10848096; see also

10. Zhou L. Homocysteine and Parkinson’s disease. CNS Neurosci Ther. 2024 Feb;30(2):e14420. doi: 10.1111/cns.14420. Epub 2023 Aug 29. PMID: 37641911; PMCID: PMC10848096; see also

S. Hassin-Baer et al., ‘Plasma homocysteine levels and Parkinson’s disease: Disease progression, carotid intima-media thickness and neuropsychiatric complications’, Clin Neuropharmacol, Vol 29(6), 2006, pp. 305-11

11.R.B. Postuma et al., ‘Vitamins and entacapone in levodopa-induced hyperhomocysteinemia: A randomized controlled study’, Neurology, Vol 66(12), 2006, pp. 1941-3

12. L. M. de Lau et al., ‘Dietary folate, vitamin B12, and vitamin B6 and the risk of Parkinson’s disease’, Neurology, Vol 67(2), 2006, pp. 315-8

13. G.B. Steventon et al., ‘Plasma cysteine and sulphate levels in patients with motor neurone, Parkinson’s and Alzheimer’s Disease’, Neurosci Letts, Vol 110, 1990, pp.216-20

14. S. Fahn, ‘A pilot trial of high dose alpha-tocopherol and ascorbate in early Parkinson’s Disease’, Ann Neurol, Vol 32(S), 1992, pp.128-32

15. J.S. Bland and J.A. Bralley, ‘Nutritional upregulation of hepatic detoxification enzymes’, J Applied Nutrition, Vol 4, 1992, pp.3-15

16. R.B. D’Agostino et al., ‘Plasma homocysteine as a risk factor for dementia and Alzheimer’s disease’, N Engl J Med, Vol 346(7), 2002, pp. 476-83

If you ask the man on the street what’s driving Alzheimer’s, they’ll probably say it’s in the genes or that it is just what happens when you age. 

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Now, neither of these statements are strictly true. 

Alzheimer’s is a largely preventable disease. 

The big question though is WHAT exactly needs to be done and HOW do we do this?

This is why Patrick recently interviewed two experts in these areas who are also members of our Scientific Advisory Board:

Dr. Tommy Wood is an Assistant Professor of Pediatrics and Neuroscience at the University of Washington in Seattle. His research program focuses on factors associated with brain health and function across the lifespan. He received his undergraduate degree in Natural Sciences from Cambridge in 2007, a Medical Degree from Oxford in 2011, and a PhD from the University of Oslo in 2017. Alongside his academic training, Tommy has provided Performance Consulting for Olympians and world champions in a dozen different sports. He is a founding trustee of the British Society of Lifestyle Medicine and associate editor for the journal Lifestyle Medicine.

Dr Kristina Curtis is an Expert in Digital Behaviour Change Interventions (DBCIs). She has a multidisciplinary background spanning across industry, research, teaching, training and consultancy. Her primary research interests are in the development and evaluation of mHealth (mobile health) interventions, in particular how the convergence of behavioural science and UX design promotes effective engagement.

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(Want to learn more about the Citizen Science Research Team? Click here to find out more)

Interview:

Diagnosis & the difference between Alzheimer’s, dementia and mixed dementia.

Patrick Holford (PH)

My guests today are tackling the two fundamental questions. 

Firstly, what are the positive and negative behaviours, diet lifestyle and environment that both either drive dementia or prevent it?
And then the big question is, how do you encourage people to change those behaviours? 

So we have a system Professor, Tommy Wood from the University of Washington about the ‘what’.  Then to Dr. Kristina Curtis, a behavioural scientist and honorary lecturer at the University College London who heads the applied behaviour change team about how to affect behaviour change. 

Now, your background in relation to the brain is broad I see, from your time at Cambridge and Oxford University then Norway and now as assistant professor of Paediatrics and Neuroscience at the University of Washington. I believe you’ve also brain-trained Formula One drivers. Tell us about your background and how you became involved in this challenge to prevent Alzheimer’s.

Tommy Wood (TW)

I essentially fell into neuroscience initially, around 20 years ago when I was an undergraduate at Cambridge. I spent a summer in the neonates neuroscience lab looking at brain injury in babies. This is still partly what I do 20 years later.  

In between, I then went to medical school where I trained as a doctor and I also developed a lot of interest in other neurodegenerative conditions. For instance, I spent a lot of time looking at a systems approach to multiple sclerosis because my step brother was diagnosed with multiple sclerosis when he was a similar age to me in his mid 20s.  

Then, as I worked through my PhD in my early formal academic career as a professor, I worked increasingly with athletes as a performance consultant. So anything related to their cognitive and physical performance which could be sleep, diet and other stresses that they are frequently exposed to.  So, as this story of my career comes together, I work with brain injury at the beginning of life, then as I work with athletes, I do more around concussions and traumatic brain injury. And then you think, well, there were all these factors that start early in life, probably even before you’re born, that create this trajectory of how your brain functions. And that continues as you get older. So then, that makes me think about, how do we intervene at any life stage to ensure that we have cognitive function that lasts as long as possible, ideally preventing significant cognitive decline and dementia in old age. Then you start to see that these same risk factors are important at every stage so that you can start to build this idea of what the brain needs, and then you can figure out how you might want to intervene. 

PH 

I was just interviewing Professor Michael Crawford, age 93, and using some sort of quantum physics, he’s worked out how the photons that hit our eye turn into the image that we actually see. And I remember at the same age of 93, filming Linus Pauling on his theory of lipoprotein A. So I’ve witnessed people well into their 90s as sharp as a razor.

But before that, a little bit of background, what is the difference between Alzheimer’s and dementia overall, and we also hear about vascular dementia?

TW  

Dementia is essentially a catch-all diagnosis for when an individual has reached a point of cognitive decline where they are no longer able to perform regular daily tasks or usually look after themselves. So it’s a clinical diagnosis based on overall cognitive functioning. 

Then you might ask, Well, what’s causing this dementia in an individual and then we we have the sub categories, so Alzheimer’s dementia, which, if you asked Alzheimer himself, apparently he was unsure whether they should all be classified as the same thing, but that’s a sort of semantic argument.

But what we would call Alzheimer’s clinically makes up maybe 60 to 80% of dementia. Vascular dementia, which is more directly focused on blood supply to the brain, makes up something like 5 to 10%. Then there are other dementias that have very special effects on very specific parts of the brain but overall, their effect on broad cognitive function eventually ends up in a similar place. 

So with Alzheimer’s, dementia is often thought to be this continuous, gradual decline in function. Whereas with vascular dementia, what is often thought to happen is you have these very small strokes that happen throughout the brain. And each time that happens, you lose a portion of function, so you have more of this step change over time. However, in reality, there tends to be lots of overlap between say vascular and Alzheimer’s dementia, because blood supply to the brain is also important, for Alzheimer’s and sometimes it can be difficult to differentiate between the two. 

PH

And how is Alzheimer’s diagnosed as you know, in that form of dementia?

Usually, it’s going to involve some cognitive function tests. So there are lots of standardised tests like the MACA, MMSE appeal  – you may have heard of these. But there’s a whole range of tests that you’re usually going to do in person with a neurologist or an old age psychiatrist and part of it is going to be a diagnosis of exclusion. So you want to make sure that somebody doesn’t have something else going on, like a very significant vitamin deficiency or other things that can be significant like depression as they can look like significant cognitive decline or dementia, but they aren’t necessarily the same thing. So part of it is going to be excluding these other causes. Then you will probably do some brain scans and look at how the brain looks either on a CT scan or an MRI and then that, in conjunction with cognitive function, and some part of the medical history is going to tell you this is likely Alzheimer’s dementia. Often, we hear of someone being diagnosed with mixed dementia. 

PH

Is that mainly part Alzheimers, part vascular? 

TW

Yes, that’s the most common combination, but if you think about Lewy body dementia, or Frontotemporal dementia, these can also occur in different combinations in different people. But usually, because of the overlap in terms of the risk factors, Alzheimer’s with some vascular component is relatively common. 

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Preventing Alzheimer’s

PH

Now, if a person could change all their circumstances, and we’re sort of talking from early life as well, – their diet, their lifestyle, the environment that they’re born into, and their education, to what extent could we say that Alzheimer’s is a preventable disease?

TW  

It depends on how you want to try and tackle the question. But if you can change everything about an individual’s circumstances other than their genetics, then the vast majority is preventable. Depending on who you ask, some will say that it’s maybe 40 to 50%. Others will say that it’s up to maybe 70 to 80%. In some populations around the world, usually hunter-gatherer or indigenous populations, dementia is almost entirely unheard of. So it’s definitely possible that there are some combinations of environment and genetics where dementia just doesn’t occur and in that scenario, it is entirely preventable. 

PH

Now, do these same prevention steps, which obviously we’re going to go into, also prevent vascular dementia? And if so, if we put Alzheimer’s and vascular and a chunk of mixed dementia together, are we talking about 80% of dementia for example, being potentially 80% preventable?

TW  

Yes. So, as I mentioned briefly earlier, there’s a lot of overlap between the risk factors for vascular dementia. And those are also related to cardiovascular disease risk factors. So things that affect your body’s ability to move blood to the places that you want it to move to, the health of your blood vessels. There is a lot of overlap between those risk factors or things that affect negatively and those are risk factors for Alzheimer’s disease.

In fact, cardiovascular disease and poor vascular health are risk factors for Alzheimer’s dementia more directly. So if we think about the upper end of the subcategories of dementia that, 80% is Alzheimer’s disease, 10% is vascular dementia, which based on estimates could be up to 90% then yes, up to 90% of dementia is probably at least 70 ish to 80 ish percent preventable.

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How important a role do genes play?

PH

It’s often said that early onset Alzheimer’s, which is defined as before the age of 65, is that small genetic part, but a study that came out earlier this year questioned that. It was on the basis of data from the UK Biobank and it actually said that many of the same factors that are driving dementia or Alzheimer’s later in life are also present in those who develop a diagnosis before 65. So that sort of de-emphasises the genes to some extent. 

Is this true, that early onset is much the same phenomena that we’re looking at.

TW  

Yes and no. 

So traditionally, early onset Alzheimer’s, is thought to be almost entirely genetic, and driven by single significant, high penetrance genetic mutations that result in early cognitive decline. In Alzheimer’s dementia, which is thought to be more similar to what Alzheimer himself was describing when he first described the disease, it was thought to be maybe five to 10% of dementia. Now, as Alzheimer’s diseases become more prevalent,  it’s maybe around 1% of cases. However, I certainly know clinicians who have patients who have one of these mutations in a presenilin gene, or the amyloid precursor protein gene and by attending to lifestyle factors, they managed to maintain good cognitive function late into life. So even if you have some of these mutations, which are thought to almost definitely lead to Alzheimer’s disease, there does seem to be an interaction with lifestyle and other health related factors. 

Then, at the same time, we’re seeing earlier diagnosis of non-monogenic Alzheimer’s disease, which is what this paper you described, was talking about. And that’s probably because the health of the population is declining, such that we’re seeing pre-diabetes earlier, we’re seeing people that are less physically active, maybe they’re less cognitively stimulated.  All these other risk factors are adding up and they’re affecting our brains earlier in life. So now there’s more of a mix, in early onset Alzheimer’s disease, as those risk factors become prevalent earlier in life. 

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Diagnosed with Alzihemrs at age 19?  A growing tsunami of cognitive decline 

PH

I saw a report from China, of a man aged 19 diagnosed with Alzheimer’s, it said it was non-genetic, so presumably, they tested and there wasn’t the Apoe gene or the pre Senlin gene, I can’t confirm that. But can it really happen that fast, this cognitive decline that we are seeing that is so prevalent?

TW  

If you think about cognitive function as a trajectory, over time, there are three or four different components to that. 

So first of all, as you get older, cognitive function generally peaks on average, towards the end of your formal period of education. So if that education extends into university or maybe a graduate degree, then that’s going to peak sometime in your 20s or early 30s. But if you don’t even complete secondary school or high school, then it’s going to peak much earlier, and it’s going to have a much lower peak. After the peak, then you have a period of decline, and the speed of that decline depends on a number of factors, the majority of them related to ongoing stimulus to the brain as well as a whole host of health-related and nutritional factors, as you know very well. So there’s certainly a possibility where if you had a low peak of cognitive function, and that may even be based on something like maternal nutrition and epigenetics related to the health of your parents, so you had a low peak, and you have poor overall health, you’d have a more rapid decline. It’s certainly possible that this could happen very early in life, though, thankfully, at least right now, that’s very rare.

PH  

Yeah, we’ve seen the youngest with type two adult onset diabetes age three, so quite extraordinary. 

So is Alzheimer’s, just the tip of the iceberg of a growing tsunami of cognitive decline that is likely to start happening earlier?

TW  

Yes and no.

I say no, because having had lots of conversations, including with one of your close colleagues and mentors, David Smith. When you look at the specific prevalence of Alzheimer’s disease, it has not increased over time. And in fact, in some populations, it’s decreased.  It’s probably decreased a little bit more in men, because we focus very heavily on cardiovascular disease risk factors, which are more important in men in terms of causes of death.

And that has come with some improvement in terms of age-specific incidence of Alzheimer’s disease, when the reason why Alzheimer’s disease is becoming more prevalent, and it’s going to double or triple in the next few decades, is because we’re living longer. So there’s a combination of we’re living longer, and in general, our health is declining. 

So you could say, there’s this oncoming wave of Alzheimer’s disease, and that is expected. But we know that if we target specific risk factors, that doesn’t have to be the case. So I don’t think it’s all bad news.

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(Donations solely fund our research – please donate to fund our Citizen Science)

Our Citizen Science Research Team

PH  

Now, you’re the principal investigator at Food for the Brain heading, the research and the science there. So what does that involve? 

What’s your goal as a principal investigator?

TW  

One of the most important tools that we have when we’re looking at diseases or specific functions or health of the population are our population datasets, and there are lots of these. 

Governments around the world organise them, there’s Haynes in the US, there’s the UK Biobank in the UK that people have heard of, and you collect lots of data from lots of people, and at that kind of scale, you can start to maybe pick up relationships that you couldn’t otherwise. 

When we think about the risk factors for cognitive decline, and dementia, specifically, none of the datasets that exist so far are really designed to focus on that. So one of the most important ideas is to collect data, specifically related to risk factors for Alzheimer’s, dementia, and hopefully those that are modifiable. So it’s kind of a citizen science idea, right?  We’re going to people who are interested in this or maybe interested in this for their loved ones.  They are providing their data and part of it is to help understand their own risk, but then allowing us to look at a wide variety of risk factors. 

There are over a hundred questions in a questionnaire that look at different risk factors and we have the cognitive function test and blood tests. So then, when you have very large datasets like this, we can start to look for complex interactions between risk factors, and we can figure out which risk factors are most important. These are things that still need to be done as it pertains to most Alzheimer’s disease. I think, hopefully, Food for the Brain is going to be in a good position to help people understand that.

Figuring out the perfect food and lifestyle combo – what matters more!

PH

So what’s your ultimate goal from this data set – to find the sort of perfect diet lifestyle combo?

TW 

I think that there are two main things. In reality, I think that we know what is going to be best for most people.  If we look across all the evidence, we probably know that already we can have a good guess of what you should aim for.

When you say, here are the 50 things you need to fix to improve your brain health. There’s just an overwhelming amount of information – you don’t know where to start, what should I do? 

First, what’s most important to me, what’s most impactful? So figuring out which factors an individual should focus on first, which gives the biggest bang for their buck is what’s going to be a big, big part of this. Then the million dollar question is how do you actually change a person’s often highly entrenched behaviour, especially if we want to reach hundreds of 1000s across a digital platform?

PH 

So Dr. Kristina Curtis, welcome. 

You’re a behaviour change expert and an associate of UCLA Centre of Behaviour Change and founder of Applied Behaviour Change, which focuses on digital health programmes to help prevent and manage chronic conditions. 

Can you explain a bit about your background and the reason you are interested and involved in this Alzheimer’s prevention project? 

Khristina Curtis KC

After my psychology degree, I had a few years out working in industry because I hadn’t found the area of psychology that I wanted to specialise in. And so this led me to return to studies to specialise in health psychology, which is all about health behaviours. And then immediately afterwards, I then started a PhD, which really culminated my experience back then, which was web to technology, with my academic knowledge of health psychology at the Institute of Digital Healthcare at Warwick University.  

My PhD was really focused on how we would embed behaviour change models into mobile health apps and digital health interventions. And really, I feel passionate about preventing chronic conditions and particularly Alzheimer’s disease, as there are a lot of misconceptions about it. And we’ve talked a lot about them today. And in terms of many people think it’s a symptom of ageing, and largely down to our genes. Whereas, as we’ve heard, we can do a lot to reduce our risk by adopting healthier habits. 

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How do we implement these ‘risk-reducing’ behaviours and habits?

PH

And what are you doing in the cognition project at Food for the Brain? What’s your game plan? 

KC

Let’s talk about the kinds of preventative behaviours. 

For example, increasing physical activity, eating a healthier diet, social interaction, brain training, might all help to reduce our risk of developing things like Alzheimer’s and dementia. One of the issues here is that actually sustaining these long term changes and making them long term habits is extremely challenging. 

There is quite a good evidence base on which behaviour change techniques work but we’re still really in the early stages of understanding how to implement these techniques in a way that engages different groups of people. There is strong evidence which suggests that we should have a tailored approach.

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We are a small but mighty team and charity running on donation alone – please donate to our continued research here.

Also, you can learn more about our Citizen Science Research Team here.

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Thank you for reading!

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

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

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

Everyone knows that Alzheimer’s and cognitive decline are preventable IF you can find out who is at risk. 

While those selling anti-amyloid or p’tau drugs will exaggerate the importance of blood testing for amyloid or p’tau, which are damaged proteins found in the brains of people with Alzheimer’s, so far lowering these markers hasn’t worked. In other words, they are a marker, but not a cause.

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So, what is a biomarker that predicts risk? 

And therefore what biomarkers, if corrected, reduce risk?

To date, there are four:

Homocysteine, a toxic amino acid, which goes up when your intake of B vitamins (B6, B12, folate, as well as zinc) is low. If you then lower homocysteine with B vitamins, it stops the brain shrinkage associated with Alzheimer’s and improves cognitive function. Brain shrinkage stops below 10 mcmol/l, and that’s what you’re aiming for. So that’s both ‘biomarker’ and ‘causal’ ticked.

At Food for the Brain, we are offering the first accurate at home, pinprick test for homocysteine that is both painless and accurate.

Omega-3 index is another. This is the % of your red blood cell membranes that are omega-3 EPA and DHA. The higher your % (ideally above 8) the better your cognition. Low levels also predict risk. So that’s also two boxes ticked. 

Vitamin D is another. Low levels predict risk and supplementing it reduces risk. Again, two boxes ticked but we don’t really know how it does this.

Combining these three to make a ‘nutritional index’ shows that the better you score, the lower a person’s future risk of dementia is.

HBA1c is another. This is a measure of your blood sugar resilience. It measures the spikes in your blood sugar that then damage red blood cells. Below 5.4% (or 37 mmol/mol) is the idea.

We divide your scores across four levels – worst is RED, then ORANGE, then YELLOW, then GREEN, which is what you’re shooting for. 

That’s what our DRIfT test measures – all four as a Dementia Risk Index functional Test.

This chart shows you why these four measures are so essential. 

What about antioxidants?

But you might have noticed there’s no ‘antioxidant’ measure.

Well, actually there is. It’s the body’s most important antioxidant called glutathione. Think of it like the body’s fire department with glutathione being the water. Every time there’s an oxidant fire, glutathione rushes in to put the fire out. The water, then, turns into steam. Glutathione is called GSH. It’s not bad as a measure of ‘antioxidant potential’. That’s why most functional medicine doctors measure red blood cell glutathione. But what if it all gets used up? It becomes oxidised or spent, much like the water putting out a fire turns into steam. This is called oxidised glutathione or GSSG. Think of the fully loaded glutathione (GSH) as cold water. It’s going to protect you much better from inflammation than spent (oxidised) glutathione (GSSH), a highl level of which means you’ve been trying to put out a lot of inflammatory fires in your brain and body. Neuro-inflammation is a key driver of brain degeneration and dementia, as well as ageing in general, which is why this is important to know.

We’ve been researching the ratio that is your GSH/GSSG. If you’ve got lots of fully loaded glutathione, and very little oxidised/spent glutathione, your GSH/GSSG ratio or index is high. That’s good news. If you’ve got very little fully loaded glutathione and lots of oxidised glutathione then you’re ‘oxidising’ –  which is an aspect of ageing that we want to prevent.

We want to be able to research this and test your Glutathione Index. This is exactly what we are working on right now with the hope of releasing another ‘world first’ home test kit for your Glutathione Index soon. This kind of research is funded by you, as a Friend of Food for the Brain.

An example would be a person who smokes a lot, lives in a polluted environment, eats no fresh veg, berries, herbs and spices. Their Glutathione Index will be low and their body and brain will likely be ageing faster. If you did smoke but also ate well and took vitamin C daily, (they say you need 50mg of vitamin C for each cigarette) would that mitigate the effect? 

Would you join our research, support our charitable work and upgrade your own brain by ordering one of our DRIftT tests?

If you’ve also done the Cognitive Function Test and Dementia Risk Index questionnaire (which we strongly recommend) that’s even better because we can see how you score in the ANTIOXIDANT domain and in future, how that will correlate with your Glutathione Index (which is coming soon).

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Thank you for reading!

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

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

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

by Patrick Holford

This is the headline from the New York Times exposing a proposal from an ‘Alzheimer’s Working Group’ that we should all have an amyloid blood test to then be prescribed anti-amyloid drugs. This is a similar strategy to statins which are given to anyone with ‘high cholesterol’ despite no evidence of heart disease and limited benefit from taking the statins, except in the drug companies own trials. Their representatives also reduced the ‘acceptable’ blood test level in a process known as ‘diagnostic creep’.

The working group, many of whose members, say the NYT, are ‘employed by companies developing drugs and diagnostics’ is chaired by Dr Clifford R. Jack Jr., an Alzheimer’s researcher at the Mayo Clinic.  “Someone who has biomarker evidence of amyloid in the brain has the disease, whether they’re symptomatic or not,” said Dr Jack. “The pathology exists for years before symptom onset,” he added. “That’s the science. It’s irrefutable.”

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But wait…

Let’s back up here a minute.

Amyloid has never been proven to be a cause of Alzheimer’s. 

In fact, the repeated failure of anti-amyloid drugs that do successfully lower amyloid to deliver any meaningful clinical effect has proven, time and time again, that raised amyloid is not the cause of Alzheimer’s. It is, I believe, an effect, an artefact. Not all who develop Alzheimer’s have raised amyloid but most do. But the fact that it is present doesn’t mean removing it with anti-amyloid drugs will ‘cure’ the disease. The real pathology of Alzheimer’s is both a reduction in cognitive function and brain shrinkage.

The last drug trial reported that those on the drugs had 20% more brain shrinkage than those on the placebo. In other words the pathology got worse, not better. We reported this because it was in the published research paper but no newspaper coverage mentioned it. (Perhaps journalists only read the press release, not the study itself).  This was finally reported in the Telegraph two weeks ago: ‘‘Breakthrough’ Alzheimer’s drugs can shrink the brain, scientists warn’.

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The risk-to-benefit ratio is terrible

According to Dutch researchers, 10 percent of cognitively normal 50 year-olds would test amyloid positive, as would almost 16 percent of 60-year-olds and 23 percent of 70-year-olds. Most of those individuals would never develop dementia. But, if this scenario were to roll out, they would be prescribed the anti-amyloid drug treatment at an estimated £40,000 a year. Given that there were seven deaths of participants in the last two anti-amyloid drug trials, reported by ourselves and the Telegraph, and over a third of patients got potentially fatal brain bleeding or swelling, that’s a hell of a downside for something that isn’t likely to deliver any benefit. 

“Anti-amyloid trials raise scientific and ethical questions.” Writes Professor David Smith in the British Medical Journal (1). “Ackley and colleagues found that lowering brain β-amyloid levels in Alzheimer’s disease had no significant effect on cognition in 14 clinical trials on a total of 4,596 patients. 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.”.

“These findings” he says  “should direct our attention to the prevention of Alzheimer’s disease by slowing down the disease process, for which there are many possible approaches.”

Professor David Smith is one of the many scientific advisors instrumental in shaping our prevention policy which goes like this:

Test actual cognitive function, which is known to show changes up to 40 years before a diagnosis. That’s the Cognitive Function Test which you can do here.
As part of this assessment, you will complete a questionnaire covering all known risk factors. That’s the Dementia Risk Index which follows the Cognitive Function Test.
Then measure actual blood markers of things that predict risk – homocysteine, omega-3 index, HbA1c for sugar control, and vitamin D. That’s the DRIfT test, available here.
Then advise the individual on how to reduce their risk by targeting the risk factors that they can change, which, in turn, bring down the biomarkers in the DRIfT test.

There are no downsides, only benefits, with this kind of prevention approach. 

There is only one problem – prevention is not profitable.

Thank you for reading!

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

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

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

References

1 http://dx.doi.org/10.1136/bmj.n805

On April 24^th we are gathering experts from around the world to present at our Upgrade Your Brain Conference to explore solutions for the escalating incidence of mental health problems, described as a ‘global brain health emergency’ by the European Federation of Neuroscience Societies. 

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In the last three years, The Children’s Society report that the likelihood of a young person having a mental health issue has increased by 50 per cent. 

One in six children aged 5-16 are now likely to have a mental health problem. 

Antidepressant prescriptions are close to 100 million in the last year representing a 70% increase in the past five years. 

Mental illness is now costing health services more than cancer and heart disease.

So we have joined forces with the Nutrition Collective to bring together some world-class experts so that we all learn how to protect and upgrade our brains.

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The Experts

Professor Michael Crawford from Imperial College’s Institute of Brain Chemistry and Human Nutrition, who discovered the essentiality of omega-3 DHA for brain function; 
Professor Bill Harris, leading US omega-3 researcher; 
Sugar expert, Professor Robert Lustig; 
Neurologist Dr David Perlmutter; 
Neuroscientist Assistant Professor Tommy Wood from the University of Washington, expert in active lifestyle; 
Metabolic psychiatrist Dr Georgia Ede, whose speciality is low-carb keto diets; 
Professor Julia Rucklidge on children’s mental health and nutrition;
Dr Sabine Donnai, presenting on fixing a leaky blood-brain barrier for dementia prevention;
Harvard psychiatrist Uma Naidoo on the mood food connection; 
Dr Victoria Sampson on the oral and gut microbiome and brain connection.

This virtual conference focuses both on the latest science and solutions, and is focused on giving practitioners practical advice from leading clinicians. 

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The Mission

Our mission at Food for the Brain is to stem the rising tide of mental illness in children and adults. 

The growth in mental illness is not sustainable.

In some poorer areas one in two women are now on antidepressants.

Close to a million in the UK have dementia.

On the current trend, by 2080, one in three children will have severe neurodevelopment impairment with major functional and communication deficits.

These children are our future. 

It is literally our humanity that is at stake. 

We need a united and progressive understanding of what’s driving this brain drain to enable the right solutions.

We need governments to wake up to the reality of this cerebral tsunami otherwise we are heading for an idiocracy. 

The global Upgrade Your Brain conference brings all the pieces together with an unparalleled team of experts. 

All healthcare practitioners, and anyone in mental health and education, need to be there. 

Further information:

The Nutrition Collective: The ground-breaking educational platform for Healthcare Professionals. The Nutrition Collective is a leading educational community for Healthcare Professionals bringing a wealth of knowledge and the latest research on a broad range of healthcare and wellbeing topics, including brain and mental health. We offer cutting-edge education to professionals in the form of webinars, seminars, in-person and virtual conferences and events, led by world class experts. Healing chronic disease with insights from the leaders in nutrition.
See https://www.childrenssociety.org.uk/good-childhood for their report
The European Society of Neuroscientists represent 22,000 neuroscientists across 31 countries

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Thank you for reading!

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

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

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

Brain size is shrinking, IQ is falling, mental health problems are rising. 

A recent EU report has declared a ‘global brain health emergency’. 

One in six children are neurodivergent, many with autism or ADHD. 

While one in four over 80 have pre-dementia – memory decline is happening for many in their 30’s. 

One in four adults are on anti-depressants, sleeping pills or tranquillisers. 

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What is going wrong and how do we recover?

After 45 years of research Patrick Holford, our founder and CEO, has the answers and has written them all down in his brand new book Upgrade Your Brain!

This book, coming out on April 25th 2024, will be your guide on how to reclaim your brain. This coincides with our national Upgrade Your Brain campaign, where we will not only focus on Alzheimer’s prevention but also on supporting wider brain and mental issues.

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No matter your age or stage you CAN upgrade your brain and we are here to help you.

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In the book you will learn how to :

Improve your mood and get a good night’s sleep 
Deprogram anxiety and build stress resilience
Free your brain from addiction (including sugar, alcohol and coffee)
Recover your memory and rebuild the brain’s connections
Build healthy young brains to prevent neurodivergence

You will be able to preorder the book soon but there is also a live seminar book tour where you can see Patrick live and receive a signed copy. There is also an Upgrade Your Brain Conference for health professionals who want to hear from world-class speakers like Dr David Perlmutter, Professors Robert Lustig, Michael Crawford, William Harris and Tommy Wood, who heads our research team – and more.

The book will be available for preorder soon.

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Thank you for reading!

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

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

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

By Patrick Holford

In recent years the number of children diagnosed with learning, behavioural and mental health problems has escalated. Attention-deficit hyperactivity disorder (ADHD), autistic spectrum disorder (ASD) and other neurodevelopmental disorders, all classifying children as ‘neurodivergent’, as opposed to ‘neurotypical’, have rocketed in both the UK and USA.

Over the past decade there has also been a steady increase in young people with now four in ten reporting persistent feelings of sadness or hopelessness and almost a quarter (22%) reporting contemplating suicide. (1) 

‘Now, one in six children in the USA are classified as neurodivergent and one in 36 as autistic – a fourfold increase in 20 years,’(2) says paediatric Professor Alessio Fasano from Massachusetts General Hospital for Children, Harvard Medical School.

Rising numbers are being reported in the UK. According to Dr Rona Tutt, OBE, past president of the National Association of Headteachers, ‘There has been a dramatic increase in the number of people being diagnosed with ASD. Although some of this is due to a broader definition of autism, as well as better diagnosis, it raises the question of whether it may also be the result of environmental changes, which have also been dramatic.’ Some UK schools are reporting as many as one in four children having problems.

For clarification, the University of Washington defines a ‘neurodivergent’ person as ‘a person on the autism spectrum or, more generally, someone whose brain processes information in a way that is not typical of most individuals. These people may have learning disabilities, attention deficit and anxiety disorders, obsessive-compulsive disorder, and Tourette’s syndrome. Through a neurodiversity lens, such conditions reflect different ways of being that are all normal human experiences. Although “neurodiversity” is usually used to describe a group of neurodivergent individuals, it also refers to all of humankind, because everyone has a unique way of processing information.’

For those with neurodivergent traits that cause individuals immense difficulty, the question is, why do they occur in some and not others, and can they be prevented?

(Want to learn more about Autism & Neurodivergence in children? Click here to watch our 3-hour Masterclass here with 5 experts in the field.)

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Making healthy babies

Autistic spectrum disorder has often been positioned as being genetically linked. However, since the genes cannot have changed this rapidly, this suggests the influence of environmental factors, of which diet and maternal nutrition are big contributors.

Brain development starts from conception

Brain development is influenced from the moment of conception. That is why a mother’s nutrition before conception is so critical.

Nothing can be built without healthy methylation, which means a low homocysteine level. Raised homocysteine is a well-known predictor of miscarriage and pregnancy problems, which is why I recommend no woman attempts pregnancy until her homocysteine level is below 7mcmol/l. While we have learned that a homocysteine level above 11 means increased brain shrinkage, even a homocysteine level of above 9 during pregnancy predicts more problems, specifically withdrawn behaviour, anxiety, depression, social problems and aggressive behaviour in the child at the age of six. (3)

That’s why building a healthy child’s brain starts with ensuring mothers-to-be are optimally healthy.

(Find out your Homocysteine levels with our accurate, at home blood test here)

We already know that pioneering researcher Professor Michael Crawford can predict which babies are going to be born preterm with a greater risk of having developmental problems from the fats in the pregnant woman’s blood. But the most convincing evidence comes from a study of 11,875 pregnant women which 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 and social development, and verbal IQ. (4)

Also, a lack of vitamin A during pregnancy can affect brain development and lead to long-term or even permanent impairment in the learning process, memory formation, and cognitive function. (5)

Supplementing mothers-to-be with folic acid (400 µg/day) during the second and third trimesters of pregnancy is associated with better cognition in their children at the age of three and better word reasoning and IQ (verbal and performance) at seven. (6)

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Nourishing infants with optimum nutrition

Once a baby is born, 75 percent of all the energy derived from breastmilk goes to build the brain, as brain development continues at the mind-boggling rate of something like 1 million connections a minute. Babies use ketones to power their early brain development, but they also need the raw materials – essential fats, phospholipids and vitamins. Without sufficient omega-3, vitamin A, D and B vitamins, especially folate and B12, as well as minerals such as iodine, magnesium, iron and zinc, the brain cannot develop optimally.

This means that a breastfeeding mother must, at least, supplement omega-3 fish oils, but many other nutrients are also necessary. Without sufficient nutrients, not only do brain cells not make the connections, but the production and flow of neurotransmitters doesn’t happen optimally.

Low vitamin D status in both the mother and newborn baby increases the likelihood of the child developing ASD by 54 per cent. (7)

Bruce Ames, Emeritus Professor of Biochemistry and Molecular Biology at the University of California, thinks that ‘serotonin synthesis, release, and function in the brain are modulated by vitamin D and the two marine omega-3 fatty acids, eicosapentaenoic acid, EPA, and docosahexaenoic acid, DHA’. He says, ‘Insufficient levels of vitamin D, EPA, or DHA, in combination with genetic factors and at key periods during development, would lead to dysfunctional serotonin activation and function and may be one underlying mechanism that contributes to neuropsychiatric disorders and depression in children.’(8)

We know that a mother’s folate intake predicts the child’s performance in cognitive tests at the age of nine to ten (9) and the higher a baby’s B-vitamin status, the higher their cognitive function at the age of 25. (10)

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Nourishing the growing child

In the UK, fewer than 5 percent of children achieve the basic dietary recommendations for omega-3 and fish. (11) Lower DHA concentrations are associated with poorer reading ability, poorer memory, oppositional behaviour and emotional instability. (12) Several studies have shown increased aggression in those with low omega-3 DHA and EPA, and giving more omega-3 reduces aggression. (13)

Fish and omega-3 are associated with better cognition in children. 

A study of 541 Chinese schoolchildren found that fish consumption predicted sleep quality and that those who ate the most fish had the highest IQ, 4.8 points higher than those who ate none. Improved sleep quality, linked to fish intake, was correlated with IQ. (14)

A study in Northern Ireland found that half of schoolchildren were deficient in vitamin D, with a level below 50 nmol/l (I recommend above 75 nmol/l). Another found that low vitamin D levels in childhood were related to behaviour problems in adolescence. (15)

Is it any wonder so many children are neurodivergent?

Another nutrient that is rich in marine food is vitamin A. Cod liver oil is a rich source of vitamin A, vitamin D and omega-3 fats. Vitamin A is vital for proper black and white vision and the proper functioning of the retina in the eye, hence its name, retinol, and the idea of eating carrots to see in the dark. Dr Mary Megson, a paediatrician in the USA, identified a particular genetic weakness in several children on the spectrum which would affect their ability to use vitamin A. She associates this with children who won’t look you in the eye because they see better on the periphery of their visual field. (16) Giving a source of retinol such as cod liver oil improves eye coordination and vision, helping those with autism who don’t make eye contact.

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Think zinc and magnesium

My teacher, Dr Carl Pfeiffer, was the first to put zinc on the map for mental health, in the 1970s, thanks to a girl called Lisa.

Lisa was mentally unwell, but her parents had learned how to keep her sane: oysters. If she had a couple of oysters a day, her mind calmed down.

Dr Pfeiffer worked out it was zinc. Zinc is essential for cellular growth and repair, and thus found in all seeds, nuts, beans and lentils, as well as eggs, meat and fish, but nothing beats oysters. Zinc is one of the most essential minerals in pregnancy, along with iron, and babies and children, due to their rapid growth, need more.

Bear in mind that vegetarian sources of zinc, such as nuts and seeds, also contain phytates, which inhibit zinc’s absorption, so those on an exclusively plant-based diet might need more.

The basic calculation for our zinc needs to support growth is 7.5mg a day. (An oyster gives 5.5mg.) But is that really the minimum? What’s the optimum? The Nutrient Reference Value is 10mg. Many children fail to achieve this.

Few have explored what zinc intake is needed for optimal mental health. Researchers in North Dakota gave 200 schoolchildren in the 7th grade zinc supplements and found that those taking 20mg of zinc a day, as opposed to those taking 10mg (the RDA) or a placebo, had faster and more accurate memories and better attention spans within three months.(17) The girls, also, behaved better.

Children with ADHD tend to have lower levels of zinc, chromium and magnesium. 

Some have low levels of copper, according to research in New Zealand. (18)

One study of ADHD children found higher levels of copper. (19) Copper, the main source of which is copper water pipes, and zinc compete, so if zinc is low the body’s copper levels tend to rise. It was the copper-to-zinc ratio that was especially high in neurodivergent versus neurotypical children and predicted the degree of ADHD.(20)

The same applies to schizophrenia, with some of those diagnosed having low zinc levels (21) and higher copper levels (22) Copper is likely to be higher in softer water areas and in newer houses with copper pipes. Blue staining in baths or sinks is an indication of a high copper level in the water. Both zinc and magnesium levels tend to be lower in those with depression.

Magnesium, a commonly deficient mineral, is calming. Zinc deficiency is linked to disperceptions both in eating disorders and schizophrenia, as well as depression and anxiety. Both zinc and magnesium are critical co-factor nutrients, activating enzymes that make the all-important brain fats such as DHA and EPA, as well as neurotransmitters, from the food we eat.

Checking a child’s zinc, chromium and magnesium status, which can be done with a hair or blood sample, is a standard practice in nutritional therapy, but not routine in mainstream medicine. Red cell magnesium levels and serum zinc are perhaps more reliable, but hair is less invasive in children. A small study found lower hair levels of chromium in those with ADHD.(23) 

Nuts and seeds are high in all three nutrients, and correcting deficiencies with diet and/or supplementation is a must for neurodivergent children. Greens and other vegetables are rich in magnesium. A placebo-controlled trial giving ADHD children magnesium together with vitamin D for eight weeks showed a major reduction in emotional, conduct and peer problems and improved socialisation compared with children given a placebo.(24)

A Polish study from 1997 which examined the magnesium status of 116 children with ADHD found that magnesium deficiency occurred far more frequently in them than in healthy children (95 per cent of the children with ADHD were deficient), and also noted a correlation between the levels of magnesium in the body and severity of symptoms. The children were divided into two groups, one supplemented with 200mg of magnesium a day for six months and the other receiving no supplements. The magnesium status of the group receiving supplements improved and their hyperactivity was significantly reduced, while hyperactive behaviour worsened in the control group.(25)

Andrew’s story is a classic example of how effective magnesium can be in helping restless, hyperactive children:

When he was three years old, Andrew’s sleep-deprived parents brought him to our Brain Bio Centre. He was hyperactive and seemed never to sleep. Not surprisingly, he was grumpy most of the time.

We recommended that his parents give him 65mg of magnesium daily in a pleasant-tasting powder added to a drink before bed. Two weeks later, his mum phoned to say that he was sleeping right through every night and had been transformed into a delightful child during the day too.

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The four drivers of ADHD

Optimum nutrition has a big role to play in helping neurodivergent children. 

Multi-nutrient trials have shown improvements in irritability, hyperactivity and self-harm.(26) Raised homocysteine and low B12 or folate are associated with greater risk of developing ASD and worse symptoms,(27) creating methylation abnormalities that could explain many of the symptoms (28). Supplementing homocysteine-lowering B vitamins makes symptoms better. (29)

Conditions like ADHD may be the result of either:

a high-GL diet, with too much sugar
a lack of essential omega-3 fats
a lack of critical nutrients such as B vitamins, zinc and magnesium
unidentified food intolerances.

Adolescents with blood sugar problems and diagnosed with metabolic syndrome, already show the same kind of cognitive deficiencies and hippocampal brain shrinkage found in adults with pre-dementia. (164)

That’s how important it is to stop children developing a sweet tooth.

Studies by Dr Alex Richardson from the University of Oxford, giving children with ADHD these vital brain fats, have shown an improvement in learning and the behavioural problems that define ADHD. (30) Her book They Are What You Feed Them, based on a lifetime of research, explains how diet affects children’s behaviour and learning.

Over in New Zealand, Professor Julia Rucklidge tested the effects of giving children aged 7 to 12 who had been diagnosed with ADHD a high-strength comprehensive multivitamin and mineral supplement, including plenty of B vitamins (B6 23mg, folate 267mcg, B12 300mcg, magnesium 200mg, zinc 16mg). A total of 47 children were given the supplement and 46 a placebo. At the end of the 10-week trial, almost four times more children (32 per cent versus 9 per cent) had shown a clinically meaningful improvement in their attention. Also, based on a clinician’s assessment and parent and teacher reports, those on micro-nutrients showed greater improvements in emotional regulation, aggression and general functioning compared to those on the placebo. (31)

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Autism and the gut

Many children on the spectrum complain of gut problems. Some, though certainly not all, respond well to gluten and casein-free diets (32) My strong advice is to test a child for IgG-based food intolerance before embarking on a restrictive diet.

But it’s not just milk and wheat that can be a problem, nor do food intolerances only affect those with ASD.

Michael, a five-year-old we saw at the Brain Bio Centre, used to be so hyperactive that he could only go to school on a part-time basis.

He was unable to concentrate on anything, was disruptive in class and also found it difficult to socialize with other children. After taking a YorkTest 113 food intolerance test, Michael discovered he was intolerant to a range of foods, mainly dairy, wheat, oranges, carrots, soya, chicken and pork.

Staff at Michael’s school were amazed by the changes in his behaviour just one week after making the dietary changes. He could sit still and calmly draw pictures and went back to school on a full-time basis.

Putting all these pieces together, US researchers ran a 12-month study of a comprehensive nutritional and dietary intervention, enrolling 67 children and adults with autism spectrum disorder (ASD) aged 3–58 years and using 50 non-sibling neurotypical controls of similar age and gender. Treatment began with a comprehensive vitamin/mineral supplement, and additional treatments were added sequentially, including essential fatty acids, Epsom salts baths, carnitine, digestive enzymes and a healthy, gluten-free, casein-free, soy-free (HGCSF) diet. There was a major improvement in both autistic symptoms and non-verbal intellectual ability (non-verbal IQ) in the treatment group compared to the non-treatment group, with a gain of 7 IQ points. This is equivalent to what we found in the first vitamin IQ study back in 1987, when adolescents put on a B-vitamin-rich multivitamin had a 7-point increase in IQ compared to those on a placebo over seven months. (33)

Parents in the ASD study reported that the vitamin/mineral supplements, essential fatty acids and HGCSF diet were the most beneficial. (34)

I did a similar thing in a south London school for the BBC. They had challenged me to change the behaviour of disruptive kids in a week.

Of the 30 children, aged six to seven, the teacher said 10, roughly a third, were disruptive or had learning or behaviour problems. The worst was Reece. He couldn’t sit still or pay attention and was constantly getting into trouble.

I enrolled Reece’s mother and the other parents in a one-week experiment in which they’d give their children no sweets or food with added sugar, additives or colourings, a drink containing vitamins and minerals, and try to eat more fish, fruit, vegetables, nuts and seeds. To measure change, the teacher asked the children to write a story on the day before we started and then again one week later. You can see the change in one week in Reece’s stories below.

In the following month, his reading and writing age went up by a year. Now able to sit still and concentrate, he went from close to the bottom of the class to close to the top. His parents noticed he was worse after eating Monster Munch, which contains monosodium glutamate. Some children are particularly sensitive to this flavour enhancer.

Reece’s handwriting before and after ‘optimum nutrition’

Dr Alessio Fasano, who is also both Professor of Paediatrics at Harvard Medical School and Professor of Nutrition at Harvard’s Chan School of Public Health, thinks something is going wrong in the gut, with many ASD children reporting gut problems, including diarrhoea, constipation, belching and excessive flatulence and dysbiosis indicated by an abnormal pattern of gut bacteria. (35)

His findings support a connection between metabolism, gastrointestinal physiology and complex behavioural traits. This has been confirmed by a small trial ‘cleansing’ the gut with an antibiotic, then giving ‘healthy’ faecal transplants to 18 children with ASD. (36) This resulted in significant improvements in constipation, diarrhoea, indigestion and abdominal pain, as well as behavioural ASD symptoms. The improvements persisted eight weeks after treatment.

In some children, wheat and milk may contribute to these symptoms. Professor Fasano’s research finds that neurodivergent children show high levels of zonulin, which can lead to leaky gut. (37) The gluten in wheat makes the zonulin levels go up.

ASD children have also been found to have opioid-like wheat and milk proteins in their urine, making these foods especially ‘addictive’. This was the discovery of researchers at the Autism Research Unit at the University of Sunderland, headed by Paul Shattock, now known as ESPA Research. They developed successful strategies for helping children with autism known as the Sunderland Protocol. (38)

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Summary

In summary, to build healthy young brains and help prevent neurodivergence, including ADHD and autism, it is important for mothers-to-be, pregnant women and breastfeeding mothers and their children to:

limit or avoid foods with added sugar and follow a low-GL diet
avoid chemical colouring and flavour additives such as MSG
optimize omega-3 intake, as phospholipids, from seafood and eggs, and supplement omega-3 DHA and EPA
optimize vitamins A and D, with sufficient sun exposure to encourage good body stores of vitamin D
ensure healthy methylation with B vitamins, especially vitamin B12 in vegans and those on a largely plant-based diet
check for food intolerances, including gluten, if digestive symptoms are present.

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Thank you for reading!

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

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

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

References

1 van Os J, Guloksuz S. Population Salutogenesis—The Future of Psychiatry? JAMA Psychiatry. Published online December 20, 2023. doi:10.1001/jamapsychiatry.2023.4582

2. https://www.cdc.gov/ncbddd/autism/data.html

3 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. 

4. Hibbeln JR, Davis JM,] Steer C, Emmett P, Rogers I, Williams C, Golding J. Maternal seafood consumption in pregnancy and neurodevelopmental outcomes in childhood (ALSPAC study): an observational cohort study. Lancet. 2007 Feb 17;369(9561):578-85. doi: 10.1016/S0140-6736(07)60277-3. PMID: 17307104.

5. Z.Liu Behav Neurol. 2021 Dec 7;2021:5417497

6. McNulty H, Rollins M, Cassidy T, Caffrey A, Marshall B, Dornan J, McLaughlin M, McNulty BA, Ward M, Strain JJ, Molloy AM, Lees-Murdock DJ, Walsh CP, Pentieva K. 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 Med. 2019 Oct 31;17(1):196. doi: 10.1186/s12916-019-1432-4. PMID: 31672132; PMCID: PMC6823954.

7. Wang Z, Ding R, Wang J. The Association between Vitamin D Status and Autism Spectrum Disorder (ASD): A Systematic Review and Meta-Analysis. Nutrients. 2020 Dec 29;13(1):86. doi: 10.3390/nu13010086. PMID: 33383952; PMCID: PMC7824115.

8. Patrick RP, Ames BN. Vitamin D and the omega-3 fatty acids control serotonin synthesis and action, part 2: relevance for ADHD, bipolar disorder, schizophrenia, and impulsive behavior. FASEB J. 2015 Jun;29(6):2207-22. doi: 10.1096/fj.14-268342. Epub 2015 Feb 24. PMID: 25713056.

9. Veena SR, Krishnaveni GV, Srinivasan K, Wills AK, Muthayya S, Kurpad AV, Yajnik CS, Fall CH. 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. J Nutr. 2010 May;140(5):1014-22. doi: 10.3945/jn.109.118075. Epub 2010 Mar 24. PMID: 20335637; PMCID: PMC3672847.

10. Qin B, Xun P, Jacobs DR Jr, Zhu N, Daviglus ML, Reis JP, Steffen LM, Van Horn L, Sidney S, He K. Intake of niacin, folate, vitamin B-6, and vitamin B-12 through young adulthood and cognitive function in midlife: the Coronary Artery Risk Development in Young Adults (CARDIA) study. Am J Clin Nutr. 2017 Oct;106(4):1032-1040. doi: 10.3945/ajcn.117.157834. Epub 2017 Aug 2. PMID: 28768650; PMCID: PMC5611785.

11. Kranz, S., Jones, N.R.V., Monsivais, P., Intake Levels of Fish in the UK Paediatric Population. Nutrients 2017, 9, 392. https://doi.org/10.3390/nu9040392

12. Montgomery P, Burton JR, Sewell RP, Spreckelsen TF, Richardson AJ. Low blood long chain omega-3 fatty acids in UK children are associated with poor cognitive performance and behavior: a cross-sectional analysis from the DOLAB study. PLoS One. 2013 Jun 24;8(6):e66697. doi: 10.1371/journal.pone.0066697. Erratum in: PLoS One. 2013;8(9). doi:10.1371/annotation/26c6b13f-b83a-4a3f-978a-c09d8ccf1ae2. PMID: 23826114; PMCID: PMC3691187.

13. Raine A, Ang RP, Choy O, Hibbeln JR, Ho RM, Lim CG, Lim-Ashworth NSJ, Ling S, Liu JCJ, Ooi YP, Tan YR, Fung DSS. Omega-3 (ω-3) and social skills interventions for reactive aggression and childhood externalizing behavior problems: a randomized, stratified, double-blind, placebo-controlled, factorial trial. Psychol Med. 2019 Jan;49(2):335-344. doi: 10.1017/S0033291718000983. Epub 2018 May 10. PMID: 29743128; see also Choy O, Raine A. Omega-3 Supplementation as a Dietary Intervention to Reduce Aggressive and Antisocial Behavior. Curr Psychiatry Rep. 2018 Apr 5;20(5):32. doi: 10.1007/s11920-018-0894-y. PMID: 29623453; see also Gow RV, Hibbeln JR. Omega-3 fatty acid and nutrient deficits in adverse neurodevelopment and childhood behaviors. Child Adolesc Psychiatr Clin N Am. 2014 Jul;23(3):555-90. doi: 10.1016/j.chc.2014.02.002. Epub 2014 May 27. PMID: 24975625; PMCID: PMC4175558.

14. Liu, J., Cui, Y., Li, L. et al. The mediating role of sleep in the fish consumption – cognitive functioning relationship: a cohort study. Sci Rep 7, 17961 (2017). https://doi.org/10.1038/s41598-017-17520-w

15. Sonia L Robinson, Constanza Marín, Henry Oliveros, Mercedes Mora-Plazas, Betsy Lozoff, Eduardo Villamor, Vitamin D Deficiency in Middle Childhood Is Related to Behavior Problems in Adolescence, The Journal of Nutrition, Volume 150, Issue 1, 2020, pp.140–148, ISSN 0022-3166, https://doi.org/10.1093/jn/nxz185.

16. Megson MN. Is autism a G-alpha protein defect reversible with natural vitamin A? Med Hypotheses. 2000 Jun;54(6):979-83. doi: 10.1054/mehy.1999.0999. PMID: 10867750.

17. Zinc Affects Cognition and Psychosocial Function of Middle-School Children, April 2005, The FASEB Journal Conference: Experimental Biology

18. Rucklidge JJ, Eggleston MJF, Darling KA, Stevens AJ, Kennedy MA, Frampton CM. Can we predict treatment response in children with ADHD to a vitamin-mineral supplement? An investigation into pre-treatment nutrient serum levels, MTHFR status, clinical correlates and demographic variables. Prog Neuropsychopharmacol Biol Psychiatry. 2019 Mar 8;89:181–192. doi: 10.1016/j.pnpbp.2018.09.007. Epub 2018 Sep 12. PMID: 30217770.

19. This has not been observed in New Zealand; see: https://pubmed.ncbi.nlm.nih.gov/30217770/.

20. Skalny AV, Mazaletskaya AL, Ajsuvakova OP, Bjørklund G, Skalnaya MG, Chao JC, Chernova LN, Shakieva RA, Kopylov PY, Skalny AA, Tinkov AA. Serum zinc, copper, zinc-to-copper ratio, and other essential elements and minerals in children with attention deficit/hyperactivity disorder (ADHD). J Trace Elem Med Biol. 2020 Mar;58:126445. doi: 10.1016/j.jtemb.2019.126445. Epub 2019 Dec 6. PMID: 31869738.

21. Joe P, Petrilli M, Malaspina D, Weissman J. Zinc in schizophrenia: A meta-analysis. Gen Hosp Psychiatry. 2018 Jul-Aug;53:19-24. doi: 10.1016/j.genhosppsych.2018.04.004. Epub 2018 Apr 27. PMID: 29727763.

22. Vidović B, Dorđević B, Milovanović S, Škrivanj S, Pavlović Z, Stefanović A, Kotur-Stevuljević J. Selenium, zinc, and copper plasma levels in patients with schizophrenia: relationship with metabolic risk factors. Biol Trace Elem Res. 2013 Dec;156(1-3):22-8. doi: 10.1007/s12011-013-9842-1. Epub 2013 Oct 24. PMID: 24150923.

23. Perham JC, Shaikh NI, Lee A, Darling KA, Rucklidge JJ. Toward ‘element balance’ in ADHD: an exploratory case control study employing hair analysis. Nutr Neurosci. 2022 Jan;25(1):11-21. doi: 10.1080/1028415X.2019.1707395. Epub 2020 Jan 3. PMID: 31900097.

24. Hemamy M, Pahlavani N, Amanollahi A, Islam SMS, McVicar J, Askari G, Malekahmadi M. The effect of vitamin D and magnesium supplementation on the mental health status of attention-deficit hyperactive children: a randomized controlled trial. BMC Pediatr. 2021 Apr 17;21(1):178. doi: 10.1186/s12887-021-02631-1. Erratum in: BMC Pediatr. 2021 May 12;21(1):230. PMID: 33865361; PMCID: PMC8052751.

25. B. Starobrat-Hermelin and T. Kozielec, ‘The effects of magnesium physiological supplementation on hyperactivity in children with attention deficit hyperactivity disorder (ADHD): Positive response to magnesium oral loading test’, Magnes Res, Vol 10(2), 1997, pp. 149-56

26. Mehl-Madrona L. Journal of Alternative and Complementary Medicine 2017 , 23(7), 526–533.

27. Li B, Xu Y, Pang D, Zhao Q, Zhang L, Li M, Li W, Duan G, Zhu C. Interrelation between homocysteine metabolism and the development of autism spectrum disorder in children. Front Mol Neurosci. 2022 Aug 15;15:947513. doi: 10.3389/fnmol.2022.947513. PMID: 36046711; PMCID: PMC9421079.

28. Antonio Belardo, Federica Gevi, Lello Zolla, The concomitant lower concentrations of vitamins B6, B9 and B12 may cause methylation deficiency in autistic children, The Journal of Nutritional Biochemistry, Volume 70, 2019, Pages 38-46, ISSN 0955-2863, https://doi.org/10.1016/j.jnutbio.2019.04.004; see also James SJ, Melnyk S, Fuchs G, Reid T, Jernigan S, Pavliv O, Hubanks A, Gaylor DW. Efficacy of methylcobalamin and folinic acid treatment on glutathione redox status in children with autism. Am J Clin Nutr. 2009 Jan;89(1):425-30. doi: 10.3945/ajcn.2008.26615. Epub 2008 Dec 3. PMID: 19056591; PMCID: PMC2647708.

29. Rossignol DA, Frye RE. The Effectiveness of Cobalamin (B12) Treatment for Autism Spectrum Disorder: A Systematic Review and Meta-Analysis. J Pers Med. 2021 Aug 11;11(8):784. doi: 10.3390/jpm11080784. PMID: 34442428; PMCID: PMC8400809; see also ref xx below; Adams JB, Audhya T, Geis E, Gehn E, Fimbres V, Pollard EL, Mitchell J, Ingram J, Hellmers R, Laake D, Matthews JS, Li K, Naviaux JC, Naviaux RK, Adams RL, Coleman DM, Quig DW. Comprehensive Nutritional and Dietary Intervention for Autism Spectrum Disorder-A Randomized, Controlled 12-Month Trial. Nutrients. 2018 Mar 17;10(3):369. doi: 10.3390/nu10030369. PMID: 29562612; PMCID: PMC5872787; see also James SJ, Melnyk S, Fuchs G, Reid T, Jernigan S, Pavliv O, Hubanks A, Gaylor DW. Efficacy of methylcobalamin and folinic acid treatment on glutathione redox status in children with autism. Am J Clin Nutr. 2009 Jan;89(1):425-30. doi: 10.3945/ajcn.2008.26615. Epub 2008 Dec 3. PMID: 19056591; PMCID: PMC2647708.

30. Yau PL, Castro MG, Tagani A, Tsui WH, Convit A. Obesity and metabolic syndrome and functional and structural brain impairments in adolescence. Pediatrics. 2012 Oct;130(4): e856–64. doi: 10.1542/peds.2012-0324. Epub 2012 Sep 3. PMID: 22945407; PMCID: PMC3457620; see also Mangone A, Yates KF, Sweat V, Joseph A, Convit A. Cognitive functions among predominantly minority urban adolescents with metabolic syndrome. Appl Neuropsychol Child. 2018 Apr-Jun;7(2):157-163. doi: 10.1080/21622965.2017.1284662. Epub 2017 Feb 22. PMID: 28631969

31. Richardson AJ. Review: ω-3 fatty acids produce a small improvement in ADHD symptoms in children compared with placebo. Evid Based Ment Health. 2012 May;15(2):46. doi: 10.1136/ebmental-2011-100523. Epub 2012 Feb 18. PMID: 22345102.

32. Rucklidge JJ, Eggleston MJF, Johnstone JM, Darling K, Frampton CM. Vitamin-mineral treatment improves aggression and emotional regulation in children with ADHD: a fully blinded, randomized, placebo-controlled trial. J Child Psychol Psychiatry. 2018 Mar;59(3):232-246. doi: 10.1111/jcpp.12817. Epub 2017 Oct 2. PMID: 28967099; PMCID: PMC7779340.

33. Piwowarczyk A, Horvath A, Łukasik J, Pisula E, Szajewska H. Gluten- and casein-free diet and autism spectrum disorders in children: a systematic review. Eur J Nutr. 2018 Mar;57(2):433-440. doi: 10.1007/s00394-017-1483-2. Epub 2017 Jun 13. PMID: 28612113.

34. Benton D, Roberts G. Effect of vitamin and mineral supplementation on intelligence of a sample of schoolchildren. Lancet. 1988 Jan 23;1(8578):140-3. doi: 10.1016/s0140-6736(88)92720-1. PMID: 2892988.

35. Adams JB, Audhya T, Geis E, Gehn E, Fimbres V, Pollard EL, Mitchell J, Ingram J, Hellmers R, Laake D, Matthews JS, Li K, Naviaux JC, Naviaux RK, Adams RL, Coleman DM, Quig DW. Comprehensive Nutritional and Dietary Intervention for Autism Spectrum Disorder-A Randomized, Controlled 12-Month Trial. Nutrients. 2018 Mar 17;10(3):369. doi: 10.3390/nu10030369. PMID: 29562612; PMCID: PMC5872787.

36. Needham BD, Adame MD, Serena G, Rose DR, Preston GM, Conrad MC, Campbell AS, Donabedian DH, Fasano A, Ashwood P, Mazmanian SK. Plasma and Fecal Metabolite Profiles in Autism Spectrum Disorder. Biol Psychiatry. 2021 Mar 1;89(5):451-462. doi: 10.1016/j.biopsych.2020.09.025. Epub 2020 Oct 10. PMID: 33342544; PMCID: PMC7867605.

37. Kang DW, Adams JB, Gregory AC, Borody T, Chittick L, Fasano A, Khoruts A, Geis E, Maldonado J, McDonough-Means S, Pollard EL, Roux S, Sadowsky MJ, Lipson KS, Sullivan MB, Caporaso JG, Krajmalnik-Brown R. Microbiota Transfer Therapy alters gut ecosystem and improves gastrointestinal and autism symptoms: an open-label study. Microbiome. 2017 Jan 23;5(1):10. doi: 10.1186/s40168-016-0225-7. PMID: 28122648; PMCID: PMC5264285.

38. Asbjornsdottir, Birna, et al. “Zonulin-dependent intestinal permeability in children diagnosed with mental disorders: a systematic review and meta-analysis.” Nutrients 12.7 (2020): 1982.

This week CNN ran a story about a dementia prevention clinic in the US, run by neurologist Professor Richard Isaacson, who used our Cognitive Function Test in his prevention study at Cornell University.

—

The basic concept, much like what Food for the Brain is doing online, is that people get screened with blood tests, complete a cognitive function test and are assessed for diet and lifestyle factors that increase future risk. The article highlights nutrition, insulin resistance, genetic, behavioural and lifestyle risk factors along with the ability to track your progress with new ‘experimental blood tests’.

What’s the difference between this and what Food for the Brain is offering? 

This screening would set you back at least $2000 compared to Food for the Brain’s, with the DRIfT blood test, costing closer to £200.

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Brain Blood Tests that Predict Risk

In Alzheimer’s there are increases in Amyloid and p-tau. That’s not in dispute. Despite all the hype, the anti-amyloid drugs such as Lecanemab, featured in last week’s Panorama programme, have produced what is widely regarded as a clinically insignificant benefit with very high risk of adverse effects, including a small risk of death. Five people died as a consequence of the drug treatment in the last two trials, which is approximately one in 500. The British Medical Journal editorial concluded  ‘No clinically meaningful effect. 30% get brain bleeding or swelling. Two trial deaths under investigation.’ 

The ‘just’ statistically significant benefit, which got the drug its licence, was several times less than that reported in a comparative trial of omega-3 in those with low homocysteine (sufficient B vitamins) and the rate of brain shrinkage actually increased by 20% compared to a 73% reduction in a trial of homocysteine lowering B vitamins in those with sufficient omega-3 DHA in their blood (read more about that here.)

So, yes, test amyloid but no – there is not sufficient evidence that lowering it with anti-amyloid drugs is going to realistically make much difference.

The trouble with the anti-amyloid monthly injection (which costs circa £20,000 a year) is that each injection will need to be followed by an expensive brain scan precisely because of the risk of brain bleeding and swelling, experienced by a third in trials. That’s also why the BBC reported that Alzheimer’s Research UK has warned that the NHS is ‘not ready’ for new Alzheimer’s drugs Lecanemab and Donanemab. It’s not prepared for such a treatment rollout due to the benefit it delivers versus the cost of on going assessment. Together with the medical costs it will probably cost closer to £50,000 per year per person. 

While in contrast, £50,000 would fund 1,000 people follow our COGNITION programme for a year.

—

All eyes on p-tau lowering drugs…

With the failure of the amyloid hypothesis, all eyes are on p-tau lowering drugs. 

Yet none have worked. 

But, much like cholesterol for heart disease, the media messaging will be to test p-tau rather than prescribe a drug. The irony here is that a lack of B vitamins, or rather raised homocysteine (which you can test here), is well established to increase p-tau so the simplest way to stop the formation of p-tau, and neurofibrillary tangles, and keep your brain healthy, is to keep your plasma homocysteine level below 10mcmol/l. In addition, the fact that there is no solid evidence that lowering levels of p-tau or amyloid protein prevents dementia or slow down progression is why these are called ‘‘experimental blood tests” in the CNN coverage.

We have combined four tests (omega-3 index, vitamin D, HBA1c for sugar balance, homocysteine for B vitamins) that each have clear evidence that

a) good levels correlate with less risk
b) bringing blood test levels into the optimal range reduces risk. 

So we are ahead in that respect. This is the 4-in-1 DRIfT test which calculates a biological Dementia Risk Index. 

We want you to take this test, not only for your benefit but also, when we have enough results of tests and retests, together with FREE Cognitive Function Test results we can research the correlation to find out how your DRIfT score predicts cognitive function. 

Genetic Fears

The other issues raised are around genes that predict Alzheimer’s risk. 

There’s quite some confusion here which, if misunderstood, creates unnecessary fear. ‘Causative’ genes (APP and Presenelin) are very rare – less than 1 in 100. The Panorama programme included a younger person with this gene. Much more common is having the ApoE4 gene, which one in seven people have. This doesn’t cause Alzheimer’s. Technically, it increases risk by 4 to 6% but all the changes we recommend to your diet mitigate even this increased risk. That is why, in studies where people ate better or took the right supplements, there was no difference in the outcome of the individuals with or without the ApoE4 gene variant.

The bottom line is that almost no-one needs to develop dementia if they follow ‘optimum nutrition’ advice – diet, supplements and lifestyle and that is what we are here to do.

Food for the Brain is making prevention a reality.

Join us in our mission, research and reclaim your brain this year. The first things you want to do are:

Complete the FREE Cognitive Function Test. This is an online, validated assessment of your current cognitive function and your dementia risk. Over 400k have completed this test and upgraded their brain in the process.
Order your DRIfT test. These accurate, at-home blood tests are the perfect way to improve your brain health and reduce your risk.

Thank you for reading!

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

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

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

Omega 3 supplements are becoming more popular and rightly so as another recent UK BioBank study (1) reported that there was a 30% less risk of dementia in those with higher omega-3 status in their blood.

Another study (2), found a 49% reduced risk for dementia in those with the highest omega-3 DHA level (top fifth) in their red blood cells versus the lowest (bottom fifth). Oily fish and fish oil supplements contain two kinds of omega-3 fat called DHA and EPA. DHA is the main fat found in brain cells of all animals.

What’s more your omega-3 index predicts both your brain size and cognitive abilities according to this study (3) from Loma Linda University, featured in the Blue Zones film,  so you might want to check you’re above 8%.

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The benefits go beyond preventing dementia.

A person’s omega-3 index, which is a composite score of both EPA and DHA bound into red blood cell membranes, predicts both the risk for depression (4) and, and poorer reading ability, lower IQ, worse memory, difficulty sleeping, aggression and emotional instability in children – hallmarks of ADHD (5) .

It also predicts risks for heart disease (6) and developmental problems in babies from measures taken in women both before and during pregnancy. Pregnant women with a higher omega-3 index have a much lower risk of having a baby with developmental problems, according to research at Imperial College London from the Institute of Brain Chemistry at the Chelsea & Westminster Hospital campus.

The missing piece…

You may read this and immediately order yourself some quality omega-3 supplements and eat some smoked salmon for lunch, but there is a missing piece.

Omega-3 fats can only become useful or active through the process of methylation. 

This new study (7) concludes that the combination of B vitamins and fatty acids improved cognitive function. This is because in methylation DHA attaches to a phospholipid and thereby enables it to be incorporated into the neuronal membrane of the brain. The process of methylation is totally dependent on vitamins B6, B12 and folate.

So you need both the high omega-3 status (over 8%) and you need the B vitamins to incorporate the DHA fatty acid into the brain. You know you are doing methylation properly if your homocysteine is below 11mcmol/L. In a big Omega-3 study people with early-stage dementia were given 2.3 grams (think two big fish oil tablets) a day but only those with lower homocysteine levels benefitted.

Having a raised homocysteine, above 11mcmol/L, is extremely common. In the US about 40% of people over 60 years old have higher levels. Often this is due to poor absorption of vitamin B12 and requires high-dose supplementation to normalise homocysteine. (Read more about homocysteine here)

That’s why it’s important to check both your homocysteine level and your omega-3 index.

You need to test your status for both in order to truly protect and reclaim your brain. 

This is why we have launched our new at-home, 4 in 1, pinprick DRIfT blood test to easily check your Omega-3 index, homocysteine, Vitamin D and HbA1c (the best measure for glucose control). These four risk markers, measured in the DRIfT test, are thought to account for over half the modifiable risk for Alzheimer’s disease and dementia. Having an active lifestyle, both physically, socially and intellectually further reduces risk substantially. (We will help you assess your risk through our free Cognitive Function Test and then tell you exactly what you need to do to protect your brain!)

We launched DRIFT as part of our global prevention study and research so when you order your test you will not only help upgrade your brain but become a Citizen Scientist and be a part of our research into optimising brain health for all ages.

 An accurate and easy way to check your brain health and know exactly what to supplement and do to look after your brain.

To join our  join the global prevention study:

Be the first to order the DRIfT Test here.
Then take the free online Cognitive Function Test

Thank you for reading!

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

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

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

References

1  Sala-Vila, A.; Tintle, N.; Westra, J.; Harris, W.S. Plasma Omega-3 Fatty Acids and Risk for Incident Dementia in the UK Biobank Study: A Closer Look. Nutrients 2023, 15,4896. https://doi.org/10.3390/ nu15234896

2  Sala-Vila, A.; Satizabal, C.L.; Tintle, N.; Melo van Lent, D.; Vasan, R.S.; Beiser, A.S.; Seshadri, S.; Harris, W.S. Red Blood Cell DHA Is Inversely Associated with Risk of Incident Alzheimer’s Disease and All-Cause Dementia: Framingham Offspring Study. Nutrients 2022, 14, 2408. https://doi.org/10.3390/ nu14122408

3 Loong S, Barnes S, Gatto NM, Chowdhury S, Lee GJ. Omega-3 Fatty Acids, Cognition, and Brain Volume in Older Adults. Brain Sci. 2023 Sep 2;13(9):1278. doi: 10.3390/brainsci13091278. PMID: 37759879; PMCID: PMC10526215.

4 Yonezawa K, Kusumoto Y, Kanchi N, Kinoshita H, Kanegae S, Yamaguchi N, Ozawa H. Recent trends in mental illness and omega-3 fatty acids. J Neural Transm (Vienna). 2020 Nov;127(11):1491-1499. doi: 10.1007/s00702-020-02212-z. Epub 2020 May 25. PMID: 32451632.

5 Montgomery P, Burton JR, Sewell RP, Spreckelsen TF, Richardson AJ. Low blood long chain omega-3 fatty acids in UK children are associated with poor cognitive performance and behavior: a cross-sectional analysis from the DOLAB study. PLoS One. 2013 Jun 24;8(6):e66697. doi: 10.1371/journal.pone.0066697. Erratum in: PLoS One. 2013;8(9).doi:10.1371/annotation/26c6b13f-b83a-4a3f-978a-c09d8ccf1ae2. PMID: 23826114; PMCID: PMC3691187; see also Raine A, Ang RP, Choy O, Hibbeln JR, Ho RM, Lim CG, Lim-Ashworth NSJ, Ling S, Liu JCJ, Ooi YP, Tan YR, Fung DSS. Omega-3 (ω-3) and social skills interventions for reactive aggression and childhood externalizing behavior problems: a randomized, stratified, double-blind, placebo-controlled, factorial trial. Psychol Med. 2019 Jan;49(2):335-344. Doi 10.1007/s11920-018-0894-y. PMID: 29623453. ; see also Liu, J., Cui, Y., Li, L. et al. The mediating role of sleep in the fish consumption – cognitive functioning relationship: a cohort study. Sci Rep 7, 17961 (2017). https://doi.org/10.1038/s41598-017-17520-w

6 Gutierrez L, Folch A, Rojas M, Cantero JL, Atienza M, Folch J, Camins A, Ruiz A, Papandreou C, Bulló M. Effects of Nutrition on Cognitive Function in Adults with or without Cognitive Impairment: A Systematic Review of Randomized Controlled Clinical Trials. Nutrients. 2021 Oct 22;13(11):3728. doi: 10.3390/nu13113728. PMID: 34835984; PMCID: PMC8621754.

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

 By Patrick Holford

Alzheimer’s is a preventable, but not reversible disease.

Less than one in a hundred cases are directly caused by genes. Prevention is entirely possible if you can identify who is at risk early enough and encourage the right diet and lifestyle changes. 

This is why we have designed our new pinprick blood test which not only aims to predict your future risk for dementia but tells you how to reduce it. We now have a limited number available on pre-order as part of a global prevention research study aiming to involve a million people worldwide. 

This much-awaited home-test kit measures your blood sugar, vitamin D, omega-3 and B vitamin status which account for more than half the modifiable risk for dementia. The results show how a person can reduce their risk with specific diet changes.

“By tracking a person’s blood sugar, vitamin B, D and omega-3 status against changes in cognitive function over time, in addition to lifestyle factors such as sleep and physical activity, we can learn what really helps prevent cognitive decline.” says Dr Wood, Assistant Professor at the University of Washington and the principal investigator for the prevention project.

We have already tested over 410,000 people with our free Cognitive Function Test, and hope to enrol a million people, to make this the largest Citizen Science global prevention initiative. 

Subtle changes in cognition occur at least 30 years before a diagnosis, which is why we screen people online with a free Cognitive Function Test. And four simple blood tests are not only predictive but can help a person to understand how to drive down that risk. We call them the four horsemen of the mental health apocalypse because they also drive depression and ADHD. The incidence of both of these are on the increase. 

(Read more about the four horsemen of the mental health apocalypse here and here).

The four tests, called DRIfT (the Dementia Risk Index functional Test) is carried out using a simple home-test kit and a single pinprick of blood, adding further predictive capability, and helping guide the individual to make diet changes to reduce future risk.

—

Why these four markers?

Blood sugar (HbA1c) – Even raised blood sugar levels from age 35, but within ‘reference’ ranges, predict a 15 per cent increased risk of Alzheimer’s disease 35 years later, according to research by Boston University School of Medicine (1). This confirms other research from the University of Washington showing an 18% increased risk with raised sugar levels in older people seven years later and a 40% increased risk in those with diabetes (2). Even better than your blood sugar level, which varies across the day, is a long-term measure of blood sugar, called HbA1c, used to predict diabetes, which is what this test measures.

B vitamins (Homocysteine) – Low levels of B12, found in animal products, and folate, found in greens, raise blood levels of homocysteine. Raised homocysteine is considered a top marker for dementia risk, and is a causative driver of the disease process (3). Studies lowering homocysteine with B vitamins have more than halved the rate of age-related brain shrinkage. A Swedish study, started in 1968, found that those in the top third of homocysteine scores in their 40’s had double the risk for Alzheimer’s almost 35 years later (4). When homocysteine goes up memory gets worse and when it goes down memory gets better, according to a six-year study in Norway  (5). 

About half of all people over 60 have homocysteine levels above 11mcmol/l  (6), which is the level associated with increased brain shrinkage. A study in Italy found that those with a homocysteine above 15mcmol/l have five times the risk of developing Alzheimer’s, compared to those with a level below 10 (7). 

Last year, a study in China showed that raised homocysteine increases risk of cognitive decline by ten times (8). Homocysteine is easily lowered by supplementing vitamin B6, B12 and folate but at levels higher than achievable from diet because many older people do not absorb B12 well. 

Oxford University’s health economist Dr Apostolos Tsiachristas estimates “Screening for homocysteine in people over 60 in the UK and treating those with raised levels with B vitamins could save the UK economy approximately £60 million per year.”

Omega-3 – Increased intake of omega-3, either from diet or supplements and having a higher omega-3 blood level, is associated with cutting risk for dementia by a fifth (20%), according to a study of 48 studies involving over 100,000 people (9). 

Supplementing fish oils (10) cuts risk of dementia by 9%, according to research from the UK Bio Bank. Being in the top third for omega-3 blood levels, compared to the lowest third, reduced the rate of brain shrinkage in a year by more than two-thirds in those given B vitamins with mild cognitive impairment (11). 

The omega-3 index, which is what the DRIfT test measures, predicts both brain size and cognitive function (12). This Oxford University research establishes that the brain needs both sufficient B vitamins and omega-3 to stay healthy.

Vitamin D – Having a higher vitamin D above 75nmol/l (25 ng/ml) cuts risk for Alzheimer’s and dementia by a third (13).  In turn, those with a vitamin D level below 50nmol/l, increase their risk for Alzheimer’s and dementia by a third (14). 

Six out of 10 adults in the UK (15) and three out of 10 in the US (16) have a vitamin D level below this. Taking vitamin D supplements may help ward off dementia, according to a 2023 study involving over twelve thousand dementia-free 70+ year olds in the US. Those taking vitamin D supplements had 40% lower incidence of dementia during a ten-year period. Vitamin D is essential to supplement during winter months.

These four risk factors, measured in the DRIfT test, are thought to account for over half the modifiable risk for Alzheimer’s disease and dementia. Having an active lifestyle, both physically, socially and intellectually further reduces risk substantially. 

To join our  join the global prevention study:

Be the first to order the DRIfT Test here.
Then take the free online Cognitive Function Test

Thank you for reading!

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

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

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

References

¹ 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.

² P.K. Crane et al., ‘Glucose levels and risk of dementia’, New England Journal of Medicine (2013), vol 369(6):540–548.

³ Smith AD, Refsum H, Bottiglieri T, Fenech M, Hooshmand B, McCaddon A, Miller JW, Rosenberg IH, Obeid R. Homocysteine and Dementia: An International Consensus Statement. J Alzheimers Dis. 2018;62(2):561-570. doi: 10.3233/JAD-171042. PMID: 29480200; PMCID: PMC5836397.

⁴ Zylberstein DE, Lissner L, Bjorkelund C, Mehlig K, Thelle DS, Gustafson D, Ostling S, Waern M, Guo X, Skoog I (2011) Midlife homocysteine and late-life dementia in women. A prospective population study. Neurobiol Aging 32, 380-386

⁵ Nurk E, Refsum H, Tell GS, Engedal K, Vollset SE, Ueland PM, Nygaard HA, Smith AD (2005) Plasma total homocysteine and memory in the elderly: The Hordaland Homocysteine study. Ann Neurol 58, 847-857. 

⁶ Pfeiffer CM, Osterloh JD, Kennedy-Stephenson J, Picciano MF, Yetley EA, Rader JI, Johnson CL. Trends in circulating concentrations of total homocysteine among US adolescents and adults: findings from the 1991-1994 and 1999-2004 National Health and Nutrition Examination Surveys. Clin Chem. 2008 May;54(5):801-13. doi: 10.1373/clinchem.2007.100214. Epub 2008 Mar 28. PMID: 18375482.

⁷ Ravaglia G, Forti P, Maioli F, Martelli M, Servadei L, Brunetti N, Porcellini E, Licastro F (2005) Homocysteine and folate as risk factors for dementia and Alzheimer disease. Am J Clin Nutr 82, 636-643.

⁸ Teng Z, Feng J, Liu R, Ji Y, Xu J, Jiang X, Chen H, Dong Y, Meng N, Xiao Y, Xie X and Lv P (2022) Cerebral small vessel disease mediates the association between homocysteine and cognitive function. Front. Aging Neurosci. 14:868777. doi: 10.3389/fnagi.2022.868777 

⁹ Wei BZ, Li L, Dong CW, Tan CC; Alzheimer’s Disease Neuroimaging Initiative; Xu W. The Relationship of Omega-3 Fatty Acids with Dementia and Cognitive Decline: Evidence from Perspective Cohort Studies of Supplementation, Dietary Intake, and Blood Markers. Am J Clin Nutr. 2023 Apr 5:S0002-9165(23)46320-4. doi: 10.1016/j.ajcnut.2023.04.001. Epub ahead of print. PMID: 37028557.

¹0 Huang Y, Deng Y, Zhang P, Lin J, Guo D, Yang L, Liu D, Xu B, Huang C and Zhang H (2022) Associations of fish oil supplementation with incident dementia: Evidence from the UK Biobank cohort study.Front. Neurosci. 16:910977.doi: 10.3389/fnins.2022.910977 

¹1 Jernerén F, Elshorbagy AK, Oulhaj A, Smith SM, Refsum H, Smith AD. Brain atrophy in cognitively impaired elderly: the importance of long-chain ω-3 fatty acids and B vitamin status in a randomized controlled trial. Am J Clin Nutr. 2015 Jul;102(1):215-21. doi: 10.3945/ajcn.114.103283. Epub 2015 Apr 15. PMID: 25877495.

¹² Loong, S.; Barnes, S.; Gatto, N.M.; Chowdhury, S.; Lee, G.J. Omega-3 Fatty Acids, Cognition, and Brain Volume in Older Adults. Brain Sci.2023,13,1278. https://doi.org/ 10.3390/brainsci13091278

¹³ https://foodforthebrain.org/the-role-of-vitamin-d-in-reducing-risk-of-alzheimers-diseasewilliam-b-grant-ph-d/

¹⁴ Chai et al. BMC Neurology (2019) 19:284 https://doi.org/10.1186/s12883-019-1500-6 

¹⁵ Calame W, Street L, Hulshof T. Vitamin D Serum Levels in the UK Population, including a Mathematical Approach to Evaluate the Impact of Vitamin D Fortified Ready-to-Eat Breakfast Cereals: Application of the NDNS Database. Nutrients. 2020 Jun 23;12(6):1868. doi: 10.3390/nu12061868. PMID: 32585847; PMCID: PMC7353432.

¹⁶ Liu X, Baylin A, Levy PD. Vitamin D deficiency and insufficiency among US adults: prevalence, predictors and clinical implications. Br J Nutr. 2018 Apr;119(8):928-936. doi: 10.1017/S0007114518000491. PMID: 29644951.

¹⁷ https://foodforthebrain.org/what-is-the-scientific-basis-of-the-cft-dri-cog-nition/