Attention-Deficit Hyperactivity Disorder (ADHD) is not just an issue to address with our children. Many adults are finding themselves diagnosed with this brain disorder and conventional medicinal support is limited.

Why are we struggling to focus and concentrate OR focus on one specific task at a cost to our health, relationships and other essential life activities (known as hyperfocus)? 

We can see how this, if not managed, can be problematic for children and the impact it can have on their learning and confidence but what if you are an adult who has recently realised that your brain works and struggles differently to those around you? (If you are interested in supporting your child’s brain and development we have our Smart Kids programme coming soon)

The incidence of neurodevelopmental disorders like Attention-Deficit Hyperactivity Disorder (ADHD) and Autism Spectrum Disorder (ASD) has surged in recent years and both are classified as neurodivergent conditions (along with other conditions like learning disabilities, attention-deficit and anxiety disorders, obsessive-compulsive disorder and Tourette’s syndrome).

In the UK and the USA, the rise in diagnoses has been significant, prompting questions about underlying causes and potential solutions. While there may be a familial aspect, we know ‘it is not in the genes’. So, why are we facing this attention deficit disaster?

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The Attention Deficit Disaster in Adults

ADHD is not confined to childhood; many adults continue to experience its symptoms, which can significantly impact their personal and professional lives. Also, many parents discover this about themselves as they go through the process of getting their child diagnosed. 

Common symptoms of adult ADHD include:

Inattention: difficulty sustaining attention during tasks, making careless mistakes, not listening when spoken to directly, and being easily distracted (1,2).
Hyperfocus: paradoxically, some adults with ADHD can become intensely focused on tasks they find stimulating or rewarding, often to the exclusion of other activities (3).
Disorganisation: chronic issues with organising tasks and activities, often leading to missed deadlines and forgotten appointments (4).
Time Management Problems: struggling to manage time effectively, leading to procrastination and difficulty completing tasks (5).
Impulsivity: making hasty decisions without considering the long-term consequences, interrupting others, and difficulty waiting for their turn (6).
Emotional Dysregulation: experiencing intense emotions, such as frustration or anger, and difficulty managing stress (7,8).

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It looks different for men and women…

ADHD can present differently in men and women, which often leads to underdiagnosis or misdiagnosis in women. Here are some key differences:

Inattention vs. Hyperactivity: women are more likely to exhibit inattentive symptoms, such as disorganisation, forgetfulness, and difficulty focusing. In contrast, men often display more hyperactive and impulsive behaviours, like restlessness and acting without thinking (9,10).
Emotional Symptoms: women with ADHD may experience higher levels of emotional dysregulation, including mood swings, anxiety, and depression. Men are more likely to exhibit externalising behaviours, such as aggression and conduct problems (11,12).
Coping Mechanisms: women tend to develop coping strategies that mask their symptoms, such as becoming perfectionists or overworking to compensate for their inattentiveness. This can delay diagnosis and treatment (13).
Social Consequences: women with ADHD often face significant social consequences, including challenges in maintaining relationships and social isolation. Men, however, may struggle more with academic and behavioural issues in school settings (14,15).

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Start at the very beginning of brain development…

The adult brain begins at conception, making maternal nutrition crucial. 

As well as avoiding alcohol and smoking during pregnancy we know from a study of 11,875 pregnant women there is 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. (16) 

In addition, a lack of vitamin A during pregnancy, another nutrient rich in seafood, can affect brain development and lead to long-term or even permanent impairment in the learning process, memory formation, and cognitive function. (17) 

Plus, there is folic acid. A mother’s folate intake predicts the child’s performance in cognitive tests at the age of nine to ten (18) and the higher a baby’s B-vitamin status, the higher their cognitive function at the age of 25. (19) Supplementing mothers-to-be with folic acid (400mcg/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.(20) 

Nothing can be built properly in the brain without healthy methylation and methylation requires folate (which is reflected by 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 7 mcmol/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. (21) 

So looking back to your childhood development might help you to understand your adult brain. How well nourished was it? Did you get adequate folate, vitamin A and consume seafoods as a child?

Our hope is some of the deficit in brain function can be recovered by providing all brain-dependent nutrients at an optimal level and see what happens. 

What would happen if you started to eat more fish and seafood? Here is some of the science:

Lower DHA concentrations are associated with poorer reading ability, poorer memory, oppositional behaviour and emotional instability. (22)
Several studies have shown increased aggression in those with low omega-3 DHA and EPA, and giving more omega-3 reduces aggression.(23) 
Improved IQ and sleep quality: 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. (24) 

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Other Essential Nutrients for Brain Health

The brain needs nourishing, especially in childhood as it is growing and developing rapidly, but also as adults.

Here are some of the essential nutrients you may want to focus on to optimise your brain:

Vitamin A: can affect brain development and lead to long-term or even permanent impairment in the learning process, memory formation, and cognitive function. (17)

Vitamin D: low vitamin D levels in childhood are related to behaviour problems in adolescence (25) and are significantly linked to a higher risk of dementia and cognitive decline. (26, 27, 28) 

Chromium, copper, zinc, and magnesium: children with ADHD tend to have lower levels of zinc, chromium, and magnesium, with some having low levels of copper (29). One study found a higher copper to zinc ratio in neurodivergent children compared to neurotypical children, predicting the degree of ADHD (30). Zinc supplementation has been shown to improve memory and attention spans in ADHD (31). Additionally, magnesium deficiency is common in ADHD, and supplementation has been linked to reduced hyperactivity (32). Deficiencies in these minerals can contribute to symptoms of ADHD and other neurodevelopmental disorders.

So are we Neurodivergent or Neurodeficient?

In the chart below I’ve listed the most common characteristics in those with autistic spectrum disorder by the US Center for Disease Control and Prevention 

I’ve added a column for the nutrients, when deficient, that have been shown to induce these symptoms.

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Ending your sweet tooth…

It’s not just about specific nutrients, the amount of sugar you consume has a big impact on your brain health.

Too many carbs and ultra-processed foods are bad for anyone at any age, as is too much sugar. They are linked to children’s mental health issues relating to symptoms of ADHD (33) and autism and adult anxiety and depression, (34) and strongly linked to increased risk of age-related cognitive decline, dementia and Alzheimer’s. 

Going back to childhood, even the glycemic load of a mother’s diet predicts a massive four-fold risk of anxiety in toddlers, with five times more impulsivity in boys, and four times as many sleeping problems, while girls have 15 times the likelihood of anxiety in those in the top third for glycemic load. (35)

So while you probably already know it, reducing sugar is imperative to your brain health. 

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Gut health & food intolerances

Dr Alessio Fasano, who is 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. (36)

Professor Fasano’s research finds that neurodivergent guts show high levels of zonulin, which can lead to leaky gut. (37) The gluten in wheat makes the zonulin levels go up. 

Opioid-like wheat and milk proteins have been found in the urine samples of those with ASD, 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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The four drivers of ADHD 

Optimum nutrition has a big role to play in helping ameliorate negative symptoms of neurodivergence.

Multi-nutrient trials have shown improvements in irritability, hyperactivity and self-harm in children with ADHD.(39) Raised homocysteine and low B12 or folate are associated with greater risk of developing ASD and worse symptoms, (40) creating methylation abnormalities that could explain many of the symptoms. (41) Supplementing homocysteine- lowering B vitamins makes symptoms better. (42)

So to summarise 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 (read more about how food intolerance can impact the brain here)

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What you can do 

For adults managing ADHD, a holistic approach that incorporates dietary changes and supplementation can be highly effective. Here are some strategies:

Feed your brain! The food you eat provides the ‘raw material’ for your brain and body. Focus on a diet rich in whole foods, including 3-5 portions of oily fish a week, nuts, seeds, leafy greens, and vegetables, to ensure adequate intake of essential nutrients.
Add in key nutrients. Consider supplementing with B-vitamins, zinc, magnesium, copper, chromium, and other essential nutrients to address deficiencies and support optimal brain function. Find out more about recommended supplements and dose requirements here
Test don’t guess. Test your vitamin D, omega-3, and sugar levels, along with your homocysteine to get accurate data on what you need to focus on or supplement with. Find out more about the accurate, at-home tests here
Mindful Eating. Pay attention to food intolerances and adopt a low-glycemic load (low sugar) diet to stabilise blood sugar levels and improve cognitive function.
Complete the Cognitive Function test below to get personalised information on your area of risk and what you can do to mitigate them and upgrade your brain over the next 6 months..
Reclaim your brain so that your neurodivergence can serve and support you, and no longer create additional struggle in your life.

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 Barkley RA. Attention-Deficit Hyperactivity Disorder: A Handbook for Diagnosis and Treatment. New York: Guilford Press; 2010.

2 Kooij JJS, Bejerot S, Blackwell A, et al. European consensus statement on diagnosis and treatment of adult ADHD: The European Network Adult ADHD. BMC Psychiatry. 2010;10(1):67.

3 Asherson P, et al. Attention deficit hyperactivity disorder in adults: A review of the literature. Nat Rev Neurol. 2012;8(2):93-104.

4 Brown TE. Attention Deficit Disorder: The Unfocused Mind in Children and Adults. New Haven: Yale University Press; 2005.

5 Faraone SV, Biederman J, Mick E. The age-dependent decline of ADHD: A meta-analysis of follow-up studies. Psychol Med. 2006;36(2):159-165.

6 Willcutt EG, et al. Validity of DSM-IV attention deficit/hyperactivity disorder symptom dimensions and subtypes. J Abnorm Psychol. 2012;121(4):991.

7 Shaw P, et al. Emotion dysregulation in attention deficit hyperactivity disorder. Am J Psychiatry. 2014;171(3):276-293.

8 Surman CB, et al. Emotional dysregulation in adult ADHD and response to atomoxetine. J Atten Disord. 2011;15(5):354-368.

9 Quinn PO, Madhoo M. A review of attention-deficit/hyperactivity disorder in women and girls: Uncovering this hidden diagnosis. Prim Care Companion CNS Disord. 2014;16(3):PCC.13r01596.

10. Williamson D, Johnston C. Gender differences in adults with attention-deficit/hyperactivity disorder: A narrative review. Clin Psychol Rev. 2015;40:15-27.

11.Loo SK, et al. Cognition in girls with attention-deficit/hyperactivity disorder: Executive functions, emotion regulation, and comorbidity. J Am Acad Child Adolesc Psychiatry. 2008;47(3):262-274.

12 Babinski DE, et al. A meta-analysis of neuropsychological functioning in posttraumatic stress disorder. Arch Clin Neuropsychol. 2015;30(8):724-743.

13 Skogli EW, et al. Emotional lability in children and adolescents with attention deficit/hyperactivity disorder (ADHD): Clinical correlates and familial prevalence. J Affect Disord. 2013;145(2):241-249.

14 Grevet EH, et al. Gender differences in prevalence of symptoms of attention deficit and hyperactivity disorder in adults. Rev Bras Psiquiatr. 2005;27(1):21-24.

15 Solanto MV, et al. The prevalence of sluggish cognitive tempo in psychiatric outpatients with ADHD, anxiety, and mood disorders. J Atten Disord. 2017;21(8):666-674.

16 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.

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

18 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. 

19. 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.

20 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.

21 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.

22 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.

23 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.

24 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

25 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.

26 Jayedi A, Rashidy-Pour A, Shab-Bidar S. Vitamin D status and risk of dementia and Alzheimer’s disease: A dose-response meta-analysis. Nutr Neurosci. 2019 Nov;22(11):750-9. doi: 10.1080/1028415X.2018.1436639.

27 Chai B, Gao F, Wu R, Dong T, Gu C, Lin Q, et al. Vitamin D deficiency as a risk factor for dementia and Alzheimer’s disease: an updated meta-analysis. BMC Neurol. 2019 Nov 13;19(1):284. doi: 10.1186/s12883-019-1500-6.

28 Melo van Lent D, Egert S, Wolfsgruber S, Kleineidam L, Weinhold L, Wagner-Thelen H, et al. Low Serum Vitamin D Status Is Associated with Incident Alzheimer’s Dementia in the Oldest Old. Nutrients. 2023;15(1):61. https://doi.org/10.3390/nu15010061

29 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. PMID: 31869738.

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

31 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.

32 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

33 Farsad-Naeimi A, Asjodi F, Omidian M, Askari M, Nouri M, Pizarro AB, Daneshzad E. Sugar consumption, sugar sweetened beverages and Attention Deficit Hyperactivity Disorder: A systematic review and meta-analysis. Complement Ther Med. 2020 Sep;53:102512. doi: 10.1016/j.ctim.2020.102512. Epub 2020 Aug 16. PMID: 33066852.

34 Haghighatdoost F, Azadbakht L, Keshteli AH, Feinle-Bisset C, Daghaghzadeh H, Afshar H, Feizi A, Esmaillzadeh A, Adibi P. Glycemic index, glycemic load, and common psychological disorders. Am J Clin Nutr. 2016 Jan;103(1):201-9. doi: 10.3945/ajcn.114.105445. Epub 2015 Nov 25. PMID: 26607943.

35 Alick CL, Maguire RL, Murphy SK, Fuemmeler BF, Hoyo C, House JS. Periconceptional Maternal Diet Characterized by High Glycemic Loading Is Associated with Offspring Behavior in NEST. Nutrients. 2021 Sep 13;13(9):3180. doi: 10.3390/nu13093180. PMID: 34579057; PMCID: PMC8469715.

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 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.

38 http://www.espa-research.org.uk/linked/sunderlandprotocol.pdf.

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

40 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.

41 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.

42 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.

By Professor Michael Crawford

The brain of H. sapiens evolved from a chimpanzee cranial capacity of 340cc to the peak of 1,500 to 1,700cc about 28,000 – 32,000 years ago. That encephalization was powered by the epigenetic force of wild foods, in which marine foods would have been essential to provide omega 3 DHA, and trace elements including iodine, essential for brain growth, function and maintenance. (Encephalization is an evolutionary increase in the complexity or relative size of the brain, involving a shift of function from non-cortical parts of the brain to the cortex.) The brain evolved in the sea some 500 million years ago using such nutrients and science shows they are still required today.

In recent times, the brain has been shrinking, likely due to the increasing reliance on intensively produced land foods and the decline in fish and seafoods.  

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Since 1950 there has been a 40% per capita decrease in fish landings in the UK and a decline in the fishing communities and ports.  At the same time, there has been a decline in average IQs and an escalation of mental ill-health. Just recently the Children’s Society declared that there had been a 3-fold increase in hospital referrals for mental ill-health in children in the last 3 years. In March 2023, the Federation of European Neuroscientists declared that brain health was now a global emergency. 

The continued shrinking of the brain and escalation of mental ill health can only end in disaster. 

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How do you know if you are eating enough seafood? Check your omega-3 levels! Buy youR 4 in 1 DRIft at home test kit here OR buy the single omega-3 test kit here.

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The solution lies in the restoration of destroyed sea beds with marine pastures, planting of kelp forests, farming of shellfish and the planting of artificial reefs to provide surfaces for marine flora to flourish and as with the seagrass, enhance the natural productivity. 

At the same time this solution of marine enhancement fixes CO2. This has been done in Japan, starting in 1991. It is also being started in many other places including Scotland, Korea, Oman, Saudi, Australia, and in the US.  It now needs to be escalated with energy which could create a new industrial revolution and a sea change in nutrition and brain health. It is all in our book, The Shrinking Brain by Crawford and Marsh, just published.

‘Totally essential for everyone to see’

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Want to find out more? Watch ‘Why the Brain is Shrinking’ with Patrick here for a small ‘pay what you can’ donation.

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Other resources:

Listen to his podcast with Patrick Holford here
Read his book The Shrinking Brain, by Professor Michael Crawford and David March
How do you know if you are eating enough seafood? Check your omega-3 levels! Buy your 4 in 1 DRIft at home test kit here OR buy the single omega-3 test kit Here.
Want to dive even deeper? Then you can get instant access to the Upgrade Your Brain Conference, with world-class speakers like Dr David Perlmutter, Dr Robert Lustig and many more!

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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.

The Upgrade Your Brain Conference was a legendary event!

A few weeks ago we co-hosted a truly epic event – the Upgrade Your Brain Conference.

We aimed to bring world experts and healthcare professionals together to address the mental health crisis we are facing…and we did just that.

Hundreds of people from across the world joined together to learn, discuss and share research on what we CAN do to prevent and shift the (depressing) trajectory of decline. When we come together things can change, not just for adults but for children and future generations to come.

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‘Thank you so much for organising this amazing day! So, SO interesting…’
Audrey – practitioner

This conference is great, really enjoying it! Anon.

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The variety and depth of information was excellent, and to see so many people coming together and the variety of tools available to help create this change in mental health was inspiring and hopeful.

If you have ever felt confused by all the ‘pieces’ that play a role in brain health this event will bring more clarity and help you know what to focus on in your own life or with your clients.

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This has been super interesting and everyone should listen to it!

Wonderful Conference – thank you.

Get access to the Upgrade Your Brain Conference Replays HERE >>>

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Takeaways and what you can expect to learn:

Why amyloid is a consequence NOT a cause.
The role of a ketogenic diet in depression, bipolar and cognitive decline with Dr Georgia Ede and why the Mediterranean diet is not the ‘perfect’ diet.
Debate on how healthy legumes are, should we promote fish more than meat and intermittent fasting
Victoria Sampson discusses the oral microbiome and how gum disease can increase risk of Alzheimer’s by up to 70%…plus some debate around fluoride and what toothpaste we need to be using!
The link between fluoride mouthwashes and Alzheimer’s with Dr David Perlmutter
Tommy Wood brilliantly explained how so many of these things fit together in terms of structure, supply, utilisation.
Robert Lustig on fructose and its impact on the brain.
Why is it not just about omega 3 or B Vitamins – but rather how they all work together. (Omega 3 being the metaphorical plank of wood, the ‘nail’ being phospholipids and the hammer is the B-vitamins that do methylation.)
Polyphenols and fibre with Dr Christina Singer and the impact on brain health and learning.
Why we are underestimating the power of prevention and the power we have through the food we eat.
An indepth look at the four horsemen of the mental health apocalypse with Patrick Holford.
Why we should all be eating more caviar and oysters.
Dr Bill Harris on why cholesterol levels that are too low can be problematic for the brain, along with the importance of DHA fatty acids.
Plus SO much more

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Change is happening and as healthcare professionals and active members of the public, we must be equipped with the tools and research we need to make an impact. Every brain matters!

We want as many practitioners and interested members of the public to see this conference as possible so we have made the replays available for purchase at a special discounted rate for the next month.

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What an amazing day it has been! Louise – practitioner.

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Click here to register and get instant access the Conference for £65 
8 hours CPD/CE points available
Instant access to all replays
This is aimed at practitioners but ALL people are welcome to watch and learn from this conference.

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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

If you look up the Oxford Dictionary definition of the word neurodivergent it is this: ‘divergence in mental or neurological function from what is considered typical or normal (frequently used with reference to autistic spectrum disorders).’ 

Other types of neurodivergence include Tourette’s, dyspraxia, synaesthesia, dyscalculia, Down syndrome, epilepsy, and chronic mental health illnesses such as bipolar disorder, obsessive-compulsive disorder, borderline personality disorder, anxiety, depression and ADHD.  More recently the overlapping of symptoms within diagnoses of ADHD and ASD has led to the term AuDHD.  

So the word refers to the idea that a person’s brain is processing things differently.

Before getting into the nutrition and potential driving forces that lead to some neurodivergent traits, it is important to understand the difference between ‘neurodiversity’ and ‘neurodivergence’.  Neurodiversity includes us all and works on the assumption that every human is unique. I’ve long argued how biologically and biochemically unique we are. “Neurodiversity as a biological fact applies to everyone” says Psychology Today.

However, differences do not have to be seen as a disorder, but as natural variations of the human brain. Although some neurodivergent people really struggle to fit in, as they think, process information and communicate in ways that are different from the norm, some of the brightest and most creative people have been diagnosed as neurodiverse.

Dr Rona Tutt, former president of the National Association of Head teachers and a scientific advisor and Trustee of the charity says “sometimes people are divided into a majority who are described as ‘neurotypical’ – although it’s debatable whether there’s such a thing as ‘typical’ – and a minority who are described as ‘neurodivergent’ or ‘neurodiverse’. (These 2 adjectives are used interchangeably, which sometimes causes confusion).” Rona was one of the first to highlight ‘overlapping dis-orders’.  She says “At one time, it was thought that if you had one diagnosis, you couldn’t have another. Then it became obvious that neurodevelopmental disorders in particular, such as autism, ADHD, Developmental Language Disorder (DLD) – formerly known as Specific Language Impairment (SLI) and the Specific Leaning Difficulties of dyslexia, dysgraphia, dyscalculia and dyspraxia, have a tendency to co-occur with each other – hence AuDHD – and with other disorders such as OCD, Tourette’s etc.”

Click here to watch the New Frontiers in Autism Masterclass >>>

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“It is the case that these neurodevelopmental disorders run in families – there’s plenty of evidence of this in some special school populations, including where I’ve worked.” She goes on to say, “But this is only part of the story and most agree that the environment is another part of the equation. At least part of the rise in these conditions might be attributed, as you’ve said, to the unnatural environment in which we live, with the polluted air we breathe, the chemically-laden food we eat, and perhaps the way technology dominates our lives, having an adverse effect both before and after we are born.”

I’d also like to point out a common error when issues or traits run in families these are often described in as inherited, implying that it is genetic, when it may be the shared environment – be it nutritional, environmental or psycho-social that drives the heritability, not ‘genes.’ The fact that so many of these conditions have escalated beyond what could reasonably be fobbed off as ‘more awareness hence more diagnoses’ suggests a large part of the problem is not ‘genetic’. 

An example of this is that the number of children diagnosed with ADHD and autism and other developmental problems classifying them as ‘neurodivergent’ has rocketed in both the UK and US. “Now, one in six children in the US are classified as neurodivergent and one in 36 as autistic – a fourfold increase in 20 years.” says professor of paediatrics, Alessio Fasano from Harvard Medical School. (1) 

A practical measure of neurodivergence is whether a child is classified as SEN – in need of Special Education. One in six children now are. While it is possible to argue that some of this might be to do with ‘better diagnosis’, classifying a child as in need of special education is one that both parents and schools are keen to avoid unless absolutely necessary. 

Some children cannot cope with the noise, the number of children and the intensity of interactions hence prefer not to be in mainstream school. My first teacher, Dr Carl Pfeiffer, taught me back in the 1970’s that zinc deficiency and pyroluria are biological imbalances that lead to difficulties with such sensory overload.  

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Is autism, ADHD and other such conditions preventable?

In a wider sense, the question ‘is neurodivergence preventable?’ also means, are autism, ADHD, Tourette’s, dyspraxia, synesthesia, dyscalculia, Down syndrome, epilepsy, and chronic mental health illnesses such as bipolar disorder, obsessive-compulsive disorder, borderline personality disorder, anxiety, and depression all preventable? 

Preventable in this context doesn’t have to mean ‘completely preventable’ but rather ‘can prevent to an extent’. Thus, anything that lessens the chance of someone becoming neurodivergent or alleviates any of the unpleasant or undesirable symptoms of neurodivergence is helping achieve a degree of prevention.

Since it is not reasonable to argue that the increase in neurodivergence over the past two decades is simply down to better diagnosis, it must follow that part of what is driving the increase is not ‘in the genes’ but in the environment. This could be the nutritional environment, the psychosocial environment and exposure to potential neurotoxins; possibly from industrial, building, agricultural, cosmetic or food chemicals and medicines. Vaccines and ingredients of vaccines would potentially fit in this category.

As a psychologist and nutritionist, my primary interest is in relieving suffering. Many, but certainly not all those either classified as ‘neurodivergent’ or autistic are ‘suffering’. The definition of suffering in this instance could include for example, emotional problems from anxiety and aggression to depression or cognitive problems including a hyperactive and inattentive mind, sleeping problems and feeling stressed, to name a few. Psychologically, Oscar Ichazo proposes that some of us use panic, anxiety, fears, phobias, obsessions, compulsions, hypochondria and even psychosis as a ‘door of compensation’ – a way to let off psychological steam when unable to cope with reality. Building resilience, both physically, biochemically and psychologically, is a key part of my integral medicine model.

Since there has been an escalation in the number of children classified as neurodivergent, autistic, or with attention-deficit-hyperactive disorder (ADHD), with special educational needs to the point where one in six children are so classified, we do need to ask why? Also, can a child so classified, be helped to feel, think or behave better in a way that helps them fulfil their potential enough to be happy and able to socialise with peers?

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Neurodivergent or Neurodeficient?

In the chart below I’ve listed the most common characteristics in those with autistic spectrum disorder by the US Center for Disease Control and Prevention 

I’ve added a column for the nutrients, when deficient, that have been shown to induce these symptoms.

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The hard truth…

Most importantly, the hard truth is that many of the brain cells, neurons in the brain are formed by birth; literally 70% of all neurons are already there. What happens at every stage of pregnancy, and especially early on, has a major impact on the child’s development. Consequently, some neurodevelopmental issues that result in these symptoms are largely irreversible. Foetal alcohol syndrome is such an example. Knowing this makes it imperative to encourage as much as we can, women who are likely to become pregnant to first optimise their diet and nutrients intake and avoid anti-nutrients – alcohol and smoking are two such anti-nutrients.

As well as avoiding alcohol and smoking during pregnancy we know from a study of 11,875 pregnant women, there is 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.(2) 

Also, a lack of vitamin A during pregnancy, which is another nutrient rich in seafood, can affect brain development and lead to long-term or even permanent impairment in the learning process, memory formation, and cognitive function. (3) 

You can do the DRIfT test on children over 2 years old.

We also know that a mother’s folate intake predicts the child’s performance in cognitive tests at the age of nine to ten (4) and the higher a baby’s B-vitamin status, the higher their cognitive function at the age of 25. (5) Supplementing mothers-to-be with folic acid (400mcg/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) 

Folate is required for healthy methylation and nothing can be built properly in the brain without healthy methylation, which is reflected by 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. (7) 

We hope that some of the deficit in brain function can be recovered. The starting point is to provide all brain-dependent nutrients at an optimal level and see what happens. In the UK, fewer than 5 per cent of children achieve the basic dietary recommendations for omega-3 and fish. (8) Lower DHA concentrations are associated with poorer reading ability, poorer memory, oppositional behaviour and emotional instability. (9) Several studies have shown increased aggression in those with low omega-3 DHA and EPA, and giving more omega-3 reduces aggression. (10)

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 level. (11) 

A study in Northern Ireland found that half of schoolchildren were deficient in vitamin D, with a level below 50nmol/l (I recommend above 75 nmol/l). Another found that low vitamin D levels in childhood were related to behaviour problems in adolescence. (12) 

There is, for many children, plenty of room for improvement and relief from suffering. Additionally, for parents-to-be, it is of vital importance to optimise nutrition throughout pregnancy.  It is critical that we don’t ‘normalise’ the consequences of sub-optimum nutrition either during pregnancy or childhood development.

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Summary

In summary, to build healthy young brains and minimize the risk of developing undesirable symptoms associated with neurodivergence, including ADHD and autism, it is important for mothers-to-be, pregnant women and breastfeeding mothers and their children to: 

Avoid alcohol and smoking, especially during pregnancy but also while breast-feeding.
Limit or avoid foods with added sugar and follow a low-GL diet 
Avoid chemical colouring and flavour additives such as MSG 
Optimise omega-3 intake, as phospholipids, from seafood and eggs, and supplement omega-3 DHA and EPA 
Optimise 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. 
Also note you can do the DRIfT test on any child over 2 years old. Find out more about the DRIfT test here

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Click here to watch the New Frontiers in Autism Masterclass >>>

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.cdc.gov/ncbddd/autism/data.html

2. 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.

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

4. 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.

5. 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: PMC56117

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. 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.

8. 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

9. 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.

10. 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.

11. 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-w12. 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.

TODAY is the first, global Alzheimer’s Prevention Day!

An initiative created by a group of world-leading experts on Alzheimer’s prevention have designed a free, online 3-minute Alzheimer’s Prevention Check that helps you see, at a glance, what simple diet and lifestyle changes most help to dementia-proof your diet and lifestyle. 

Over 7000 people have already taken part in this never-been-done global initiative – it’s time for you to join them and help us spread the word!

What to do:

Share the Alzheimer’s Prevention Check with EVERYONE. Put the link in your WhatsApp group, text or email it to a friend, post it on social media, and send it around your office. (Plus if you have not yet done the Cognitive Function Test then this is a great place to start) https://ffb-upgradedcft.org/apc
Share this post. Download the image here and share it on any platform you use and link to https://www.alzheimersprevention.info/
Do the challenge! Record your short video on your smartphone and tell us what you do every day to help prevent Alzheimer’s. Find out how to do that here & see other people’s videos here

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What the experts want YOU to do to prevent Alzheimer’s

Your Daily Lifestyle Choices Matter | Dr David Perlmuter

The Ketogenic Diet for Alzheimer’s Disease | Georgia Ede MD

Address the Energy Gap with MCT oil or Intermittent Fasting | Profesor Stephen Cunnane

Build Your Muscles to Build Your Brain | Dr Tommy Wood

Alcohol Use & Dementia Risk | Chris Palmer MD

Fish Really IS Brain Food! | Professor William Harris

Resistance Training and Alzheimer’s | Louisa Nicola

You can also download and share this graphic to spread the word!

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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.

Yesterday’s announcement by the Alzheimer’s Society that dementia will cost the UK almost £91bn a year by 2040 highlights why prevention has to be the way forward. (See the Guardian Article here) 

“Dementia’s devastating impact is colossal – on the lives of those it affects, on the healthcare system and on the economy”, said Kate Lee, the Alzheimer’s Society’s chief executive who is calling for the ‘urgent need to prioritise early diagnosis.’ We know here at Food for the Brain, that these costs, could easily be halved by focussing on prevention. A recent study from the UK Biobank data and conducted by two of the charity’s scientific advisors, China’s leading dementia prevention Professor Jin-Tai Yu from Fudan University, and by former deputy head of Oxford University’s school of medical science, Professor David Smith, concluded that “up to 73% of dementia can be prevented” right now by focussing on prevention. (1) The Biobank research, however, didn’t measure homocysteine and thus excluded one of the most easily actioned prevention steps – lowering homocysteine with B vitamins – which the US National Institutes of Health says accounts for 22% of the risk for Alzheimer’s. (2)

Patrick Holford our CEO says “the reality is that over 80 percent of dementia could be prevented right now if we took prevention seriously. The quickest wins are testing people, for free, for cognitive function then identifying those at risk and why they are at risk. Dementia is diagnosed with a cognitive function test and changes occur at least thirty years before a diagnosis. This is doable right now with no cost at all.” We have tested 425,000 people to date with 200 taking the free, validated test every day. This is followed by a ‘cognition’ questionnaire that shows the person exactly what is driving their future risk. 

The quick wins are increasing omega-3 fats from seafood and supplements, and lowering high homocysteine with B vitamins. The higher a person’s omega-3 level the better their cognition and the more brain density they have, according to research from Loma Linda University in California. (3) “Half of those over 65 have raised blood homocysteine which is easily lowered with a 10p a day B vitamin supplement.” says Holford “The health economist at Oxford University costed the saving just from this one prevention step as £65 million a year. (4) B vitamins with omega-3 have already been shown to reduce the annual rate of brain shrinkage by 73% in those at risk.” (5) The other big driver, he says, is sugar and ultra-processed foods. “Diabetes doubles dementia risk and accelerates brain shrinkage (6) but we can pick up those with the beginnings of blood sugar problems in mid-life with high but ‘normal’ levels of blood sugar which has been shown to increase Alzheimer’s risk by 14.5%. (7)” he says.

We also offer a ‘home-test kit that those at risk can use to measure homocysteine, omega-3, vitamin D and sugar balance (HbA1c – the test used by GPs to diagnose diabetes) then tells the individual what actions to take to protect their brain and improve their cognition. Research shows that having a low vitamin D level increases triples risk for Alzheimer’s (8) and those who supplement vitamin D cut Alzheimer’s risk by a third. (9)

“None of the major charities are taking prevention and the role of nutrition in brain health seriously.” says Holford, author of a new book Upgrade Your Brain which explains how to dementia-proof your diet and lifestyle. “Kate Lee of the Alzheimer’s Society told me they spend nothing on prevention. Alzheimer’s Research UK told us they spend 4.3% of all research money on non-drug prevention. When 80 percent is preventable surely at least half of research funds should be spent on non-drug prevention? We do not need to wait for more research. Dementia is diagnosed using a cognitive function test done in memory clinics. But by the time a GP refers a patient, it is often too late. We offer exactly this cognitive function test for free, online at foodforthebrain.org. There is no need to wait for a mythical blood test to ‘diagnose early’. 

This is like having a blood test to diagnose how unfit you are.” says Holford. “Even if this existed, the critical question for those at risk is how to reduce it. All that is needed is to take prevention seriously. It is not difficult. The government have pledged £166 million for dementia a year but no-one can tell us if any of this is actually to be spent on prevention research or putting prevention into action.”

We are supporting World Alzheimer’s Prevention Day – see alzheimersprevention.info – on Wednesday (May 15^th), with the support of thirty of the world’s leading dementia prevention experts.

Where to start in reducing your risk:

Take the FREE Cognitive Function Test here
Order your at-home blood tests here
Support our research and become a FRIEND here
Participate in Alzheimer’s Prevention Day

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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 Zhang, Y., Chen, SD., Deng, YT. et al. Identifying modifiable factors and their joint effect on dementia risk in the UK Biobank. Nat Hum Behav 7, 1185–1195 (2023).
2 Beydoun MA, Beydoun HA, Gamaldo AA, Teel A, Zonderman AB, Wang Y. Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis. BMC Public Health. 2014 Jun 24;14:643. doi: 10.1186/1471-2458-14-643. PMID: 24962204; PMCID: PMC4099157.
3 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.
4 https://doi.org/10.1016/j.trci.2016.07.0
5 Jernerén F, Elshorbagy AK, Oulhaj A, Smith SM, Refsum H, Smith AD (2015). 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
6 Arvanitakis Z, Wilson RS, Bienias JL, Evans DA, Bennett DA. Diabetes mellitus and risk of Alzheimer disease and decline in cognitive function. Arch Neurol. 2004 May;61(5):661-6. doi: 10.1001/archneur.61.5.661. PMID: 15148141; see alsoYaffe K, Blackwell T, Kanaya AM, Davidowitz N, Barrett-Connor E, Krueger K. Diabetes, impaired fasting glucose, and development of cognitive impairment in older women. Neurology [Internet]. 2004 Aug 24 [cited 2022 Mar 16];63(4):658–63. Available from: https://n.neurology.org/content/63/4/658; see also Tiehuis AM, van der Graaf Y, Visseren FL, Vincken KL, Biessels GJ, Appelman APA, et al. Diabetes Increases Atrophy and Vascular Lesions on Brain MRI in Patients With Symptomatic Arterial Disease. Stroke. 2008 May;39(5):1600–3; see also Samaras K, Lutgers HL, Kochan NA, Crawford JD, Campbell LV, Wen W, et al. The impact of glucose disorders on cognition and brain volumes in the elderly: the Sydney Memory and Ageing Study. AGE [Internet]. 2014 Jan 9 [cited 2022 Aug 5];36(2):977–93. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4039246/
7 Zhang X, Tong T, Chang A, Ang TFA, Tao Q, Auerbach S, Devine S, Qiu WQ, Mez J, Massaro J, Lunetta KL, Au R, Farrer LA. Midlife lipid and glucose levels are associated with Alzheimer’s disease. Alzheimers Dement. 2023 Jan;19(1):181-193. doi: 10.1002/alz.12641. Epub 2022 Mar 23. PMID: 35319157; PMCID: PMC10078665.
8 Vitamin D deficiency increases the risk of Alzheimer’s.112 In a study in France involving 912 elderly patients followed for 12 years, a total of 177 dementia cases occurred. Those with low vitamin D levels had a nearly three-fold increased risk of Alzheimer’s.113
9 Ghahremani M, Smith EE, Chen HY, Creese B, Goodarzi Z, Ismail Z. Vitamin D supplementation and incident dementia: Effects of sex, APOE, and baseline cognitive status. Alzheimers Dement (Amst). 2023 Mar 1;15(1):e12404. doi: 10.1002/dad2.12404. PMID: 36874594; PMCID: PMC9976297.

The food you eat feeds your brain but how can you consistently eat healthy even on the go, or when life is busy?

We know here at Food for the Brain that a low Glycemic Load diet is one of the 8 ways you can reduce your risk of dementia and Alzheimer’s (and improve your Cognitive Function score – take the free validated online test here) – which is why we are creating our Recipe App so that you have access to lots of brain loving recipes.

But what can you eat when travelling, on the go or for an easy snack?

That is why we want to introduce you to FATT bars. As one of our supporting organisations, FATT provides a variety of good quality, sugar free, convenient and tasty snacks.

So if you are preparing for summer holidays, work trips or have a busy schedule then these might be the perfect way to nourish your brain!

Introducing FATT – Real Keto Snacks!

Feeding the brain is a no-brainer but picking the right foods can be hard.

At FATT we really love the brain and because we love the brain, we also love the gut.

Everything we pick must be right for both brain and gut which is why we really do love nuts and in particular almonds and macadamias. Nuts are smart as they are rich in protein, B vitamins and vitamin E but are also a good source of potassium, selenium, magnesium, zinc and copper.

Macadamias are also rich in omega 3 to help balance any omega 6 in your diet.

We then add in the inulin and chicory fibre for a prebiotic kick to feed your healthy gut bio.

Whether you are eating a cookie or a brownie, a bar or a bite, you can be sure that you are getting food for the brain and gut without compromise. At FATT we do not use any sweeteners (artificial or otherwise) that might interfere with your gut and your brain or even fool your body into thinking it is digesting sugar.

We allow the natural sweetness of nuts or butter or chicory to give you a gentle sweet taste knowing that your body will not have any blood sugar spike or any insulin release.

Try our unique range of healthy low carb but indulgent snacks at a special discount and we will also make a further charitable contribution to Food for the Brain and its amazing work.

You can pick from Almond + Vanilla Keto Cookie, Double Chocolate Keto Brownie, Caramel + Sea Salt Keto Bar, Chocolate + Mint Bites and MORE!

Go and order your first box or single bars at www.livefatt.com and use the unique code FFTB10 to get a special Food for the Brain charity discount.

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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.

Author of the article is Patrick Holford and the Alzheimer’s Prevention Expert Group.

The single greatest genetic predictor of Alzheimer’s disease is the presence of the ApoE4 variant of the ApoE gene, carried by about one in five people. Having this contributes 4% to 6% of the absolute risk for Alzheimer’s disease. (1)


This is often exaggerated as a risk factor because, if a person is an Apoe4 carrier, and changes nothing, they have about a 20% greater chance of developing Alzheimer’s later in life than someone who doesn’t. This is called ‘relative risk’. It doesn’t mean, however, that someone with the ApoE4 gene has a 20% chance of developing Alzheimer’s. This is because, as an example, a person without the ApoE4 gene at a certain age might have a 4% chance of developing Alzheimer’s, while someone with the ApoE4 gene might have a 5% chance, so their risk has gone up by, in this example, 20%. In absolute terms, the risk would be only 1% higher.

This new study 2 shows two things: the first is that most ApoE4 carriers show some of the biomarkers for developing Alzheimer’s later on, namely higher levels of toxic amyloid and – p-tau proteins. This is not surprising. However, and this is key, quoting the paper “In the dementia stage, there were no differences in amyloid or tau despite earlier clinical and biomarker changes.” In other words, even these indicators of risk had vanished, or were no longer more prevalent in those with vs without this gene variant. This means that, even if you could lower levels of amyloid earlier in the disease process, this is highly unlikely to have any effect.

This so-called ‘Alzheimer’s gene’ can only exert effects via non-genetic mechanisms, and these mechanisms are often susceptible to modification with a person’s nutrition having the most direct influence. In other words, genes only tell us about susceptibilities, tendencies – they are not (at least in this case) determinative of whether one does or does not develop Alzheimer’s in their lifetime because other factors can modify the effects of carrying the ApoE4 gene variant. In other words, a gene variant such as ApoE4 it is more like a dimmer switch and can be ‘over-expressed’ or ‘down-regulated’, turned up or dimmed down by a variety of lifestyle factors.

The ApoE4 gene is downregulated by eating a low-glycemic load (GL) or low sugar diet or more ketogenic diet with specific Mediterranean-style food choices including fatty fish, cruciferous vegetables, olive oil, low alcohol consumption. Four supplemental nutrients have reasonably good evidence of blunting the effects of the ApoE4 variant. These are omega-3 DHA, B vitamins (B2, B6, B12 and folate) and vitamin D. (3)

But what happens to risk if a person is well-nourished with these dietary factors already? A good example of this is a recent study in China, involving 29,072 people of which 20% had the ApoE4 gene. 4 Each participant had their diet and lifestyle assessed over the 10 year period of the study to see who would or wouldn’t develop cognitive decline or dementia.

What the study showed was that whether or not a person had the ApoE4 ‘Alzheimer’s gene’ made no difference to the positive reduction in risk achievable by simple diet and lifestyle changes. “These results provide an optimistic outlook, as they suggest that although genetic risk is not modifiable, a combination of more healthy lifestyle factors is associated with a slower rate of memory decline, regardless of the genetic risk,” wrote the study authors. Eating a healthy diet was also the most important prevention step, followed by an active lifestyle, with one’s intellectual life, then physical activity, then social interactions being the next most important steps. Eating a healthy diet was about twice as important as exercise in
predicting cognitive decline. Those with a healthy diet were about seven times less likely to have age-related cognitive decline or dementia than those with an ‘average’ diet and about nine times less likely to develop dementia than those with an unfavourable diet.

All major studies on people at risk of, or already with, dementia or Alzheimer’s have measured whether the study participants do or don’t have the ApoE4 variant. We’ve looked at the major studies that have measured the impact of a change in diet or nutrition or lifestyle and they almost all show no difference in outcome if you do or don’t have the gene.

A good analogy is that having the ApoE4 gene variant is like a weak beam of light which, in the darkness, increases one’s risk a bit, but once you shine the strong light of actually doing something such as changing your diet or supplementing omega-3 fish oils, B vitamins or vitamin D, the effect of being an ApoE4 carrier seems to be invisible in that there is no significant difference in outcome between those who had or didn’t have this gene variant.

Please note: the pharmaceutical industry is keen to promote a drug that lowers amyloid or p-tau. 14 trials have shown that anti-amyloid drugs do lower amyloid but none has had clinically significant effect on actual dementia or cognitive decline. 5 In other words the amyloid theory is bust. Amyloid is not a cause of Alzheimer’s – it’s a result. Raised toxic P-tau is a direct consequence of raised homocysteine, driven by a lack of B vitamins. See the p-tau delusion article here. Lowering homocysteine with B vitamins, which is an established cause, lowers p-tau.

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Take the FREE Cognitive Function Test 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.

References

1 Heininger, K. (2000), A unifying hypothesis of Alzheimer’s disease. III. Risk factors. Hum.
Psychopharmacol. Clin. Exp., 15: 1-70. https://doi.org/10.1002/(SICI)1099-
1077(200001)15:1<1::AID-HUP153>3.0.CO;2-1; see also Ridge PG, Mukherjee S, Crane PK,Kauwe JSK, (2013) Alzheimer’s Disease: Analyzing the Missing Heritability. PLoS ONE 8(11): e79771. doi: 10.1371/journal.pone.0079771

2 https://www.nature.com/articles/s41591-024-02931-w.pdf

3 Norwitz,N.G.;Saif,N.; Ariza, I.E.; Isaacson, R.S. Precision Nutrition for Alzheimer’s
Prevention in ApoE4 Carriers. Nutrients 2021, 13, 1362. https://doi.org/10.3390/
nu13041362

4 Jia J, Zhao T, Liu Z et al., Association between healthy lifestyle and memory decline in olderadults: 10 year, population based, prospective cohort study BMJ 2023;380:e072691
http://dx.doi.org/10.1136/ bmj-2022-072691

5 https://www.bmj.com/content/372/bmj.n156/rr

Written by Jerome Burne, see the original article at the Daily Mail here. Find out about Jerome here.

It is over 20 years since I discovered in my fifties that I have a copy of the gene, ApoE4, that’s been linked to a raised risk of Alzheimer’s.

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It is over 20 years since I discovered in my fifties that I have a copy of the gene, ApoE4,that’s been linked to a raised risk of Alzheimer’s.

It’s the same gene that the actor Chris Hemsworth carries, although he has two copies, one from each of his parents – he learned this in 2022 after having tests for a documentary series he was making about longevity.

Now comes news of a major study that’s found that almost everyone who has two copies of this gene goes on to develop early signs of Alzheimer’s – researchers at the Sant Pau Research Institute in Barcelona looked at data from 10,000 people and 3,000 brain donors and found that the majority of those with two copies showed signs of Alzheimer’s by the time they reached the age of 55. The researchers estimate that around 2 percent of people have this gene profile.

My ApoE4 gene was identified when I was writing about the gene tests then just becoming publicly available, and as a health journalist I took one. It was an alarming discovery, since not only do I have no family history of Alzheimer’s, but back then there was nothing to be done about it, and for a while,  common moments such as forgetting why I was peering into the fridge or a cupboard felt like a sinister warning. 

But I quickly persuaded myself that any brain malfunction wouldn’t begin for years.

Anyway, a cure might come along any time and as a health journalist I could keep up with the latest research. 

Yet for years there was little to be hopeful about – the few drugs that were available didn’t make a difference to the disease progression.

Small bits of cutting-edge research I came across here and there convinced me to try various lifestyle approaches (more on the specifics later), but the expectation has long been that once you’re heading into the medical territory that is Alzheimer’s, you need heavyweight
pharmaceuticals.

But the cheering, and very surprising news, is that nutritional and lifestyle advice, with some additions and tweaks, is the very latest thing in Alzheimer’s prevention, with several UK charities and academic centres – including Imperial College, London, Exeter University, and Alzheimer’s Research UK – now actively investigating lifestyle.

What’s driving this dramatic U-turn is the failure of the drug industry to come up with effective and safe products. Even the newer ‘wonder’ drugs such as donanemab and lecanemab, which can delay the worsening of the disease by around a third in patients, can have serious side-effects – around a quarter of those who take them suffer bleeding or swelling in the brain, and some patients have experienced brain shrinkage. 

These drugs work by clearing the brain of amyloid plaques – the sticky protein deposits thought to cause symptoms by disrupting communication between brain cells.

The problems with the latest drugs are detailed in a new book by leading neurologist Professor Karl Herrup, of Philadelphia University. In ‘How not to study a disease: The story of Alzheimer’s’ he writes: ‘In our rush to find a cure we have gone down a blind alley. For decades we have focused more on salesmanship than scholarship. The amyloid cascade hypothesis has become a steamroller, intent on crushing any alternative models.’

One problem is that having the plaque doesn’t necessarily mean you will have Alzheimer’s and not having it doesn’t mean you won’t.

As Professor Herrup points out, ‘we need to rebalance this amyloid hypothesis about the cause of Alzheimer’s to include other worthy ideas about its nature, such as those indicated by the links with diabetes and blood vessel damage and the insights gained from approaches involving diet, nutrition, and lifestyle’.

What’s so radical about the nutritional and lifestyle approach is that it doesn’t target a single
cause but aims to improve the health of many of the body’s systems – such as metabolism (how energy is used), the immune system and the vast colony of bacteria and other microbes (the microbiome) in your guts, that have a two-way connection with the brain.  Keeping them all healthy can do the same for the brain.  

And it means we can all take steps to protect themselves, which is what I’ve tried to do. 

I spoke to Tommy Woods, an Assistant Professor of neuroscience and paediatrics at the University of Washington, who is a principal investigator for the research charity, the Food for the Brain Foundation, which is looking at dementia amongst other brain disorders. The charity offers a free online test to both measure your cognitive function but also a questionnaire that works out your dementia risk. I did the test and it showed me exactly what, in my diet and lifestyle, was driving my risk.

He told me: ‘I first came across the idea of multiple approaches to health and fitness when I worked with athletes as a performance consultant. Many of the systems that affected their cognitive and physical abilities were the same as the ones we concentrate on at the charity with much older people.’

Robert Lustig, who is professor emeritus and an international expert on metabolism, based at the University of California San Francisco, explains why both blood sugar levels and insulin need to be kept at a low level to protect the brain.

Insulin’s job is to help the body use blood sugar (glucose) as fuel to clear it away into storage as fat. Professor Lustig, who is also advising the Food for Brain Foundation, says high levels of glucose – from a high carb diet – lead to higher levels of insulin. ‘Fairly soon, however, your system stops responding to insulin – known as insulin resistance – which is bad news because insulin delivers the glucose needed for energy in the brain and muscles.’

This is the kind of information that convinced me over the years to make changes to my diet.

The standard advice to have plenty of carbs and pick the low-fat option was reversed, and I started following a ketogenic diet that involves eating much more fat, mostly saturated and is very low in carbs.

The fat gets turned into small packets of energy, known as ketones, that can power brain cells.

I also started stepping up gym visits from a couple of times a week, to three or four. Exercise improves blood circulation which is needed to clear waste products from the brain.

I started paying attention to my microbiome – the colony of microbes that lives in the gut. This involved eating more fibrous vegetables, as well as making and drinking kefir – a fermented drink that delivers probiotics to the guts, every day.

And I started taking B vitamins.

A decade after my gene was spotted, a randomised trial at Oxford University, run by Professor Emeritus David Smith, showed that B vitamins were essential for clearing a toxic compound called homocysteine from blood.

Homocysteine comes from the breakdown of proteins, and can damage cells. High levels often found in the brains of Alzheimer’s patients.

In the Oxford study, which involved over 200 people with mild cognitive impairment (MCI) – where memory and clear thinking are impaired – half were given a daily high dose of a B vitamin, the rest a placebo. A proportion of each group had a brain scan at the beginning end of the two-year trial.

The results, published in the journal PLOS One in September 2010, were impressive: those in the vitamin group not only had reduced homocysteine levels but brain shrinkage – the sign brain cell death – was half that of those in the placebo group.

Rather than being welcomed, however, the trial set off a long running academic battle. Alzheimer’s charities, including one that contributed funding, ignored it. 

Another study which found no benefit from B vitamins was published four years later, but it didn’t convince me. While the participants in the Oxford trial had mild cognitive impairment, those in the later trials did not. So I kept taking the tablets.

One senior academic who has picked up on this research is Professor Peter Garrard, a specialist in neurodegenerative diseases such as Alzheimer’s, at St George’s Hospital in London. 

When his mother Sheila started losing words and describing things in roundabout ways at the age of 78, he put her on a daily dose of high strength B vitamins. 

‘It was very encouraging that despite having had a brain scan that showed significant cell damage, she didn’t get any worse and then gradually started doing a lot better,’ says Professor Garrard. Sheila died at the age of 89. ‘We’ll never know how long she would have lived without the vitamins, but it must have made a difference that she stayed very fit and active.’

Professor Garrard told me that he’d been impressed by the B vitamin research done at Oxford and regarded claims that the vitamins had no benefit inaccurate. ‘I check all my patient’s homocysteine levels and give them B vitamins if they are over the healthy level,’ he says.

Evidence for the benefit of B vitamins continued to mount, including in 2020, a review published by Professor Jin-Tai Yu from Fudan University in Shanghai, China’s leading Alzheimer’s prevention expert. Published in Journal of Neurology, Neurosurgery and Psychiatry, this analysed the results of 153 randomised trials and concluded that:  ‘Homocysteine-lowering treatment seems the most promising intervention for Alzheimer’s disease prevention. ’ (The homocysteine-lowering treatment reviewed involved using folic acid (B9), vitamin B12 and vitamin B6).
 
As for me, I’m sanguine about the latest research about the ApoE4 gene: I’m currently feeling fit and well, thanks to a programme that seems a sensible way to stave off physical decline in general, and neurological decline in particular.

For more information and to reduce your risk you can:

Take the FREE Cognitive Function Test here
Order your at-home blood tests here
Support our research and become a FRIEND here
Participate in Alzheimer’s Prevention Day

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.

Everybody wants a cure for Alzheimer’s. 

The medical industry has spent around $100 billion searching for one and so far, come up relatively empty-handed with over thirty failed drug trials. The focus has been on drugs that lower two of the chemical compounds associated with Alzheimer’s and dementia in general – amyloid and p-tau, a pair of messed up proteins that can lead to plaques in the brain and tangled nerves. There is a third compound – an amino acid called homocysteine – that becomes toxic if you have too much, that the drug industry and the Alzheimer charities don’t talk about, for reasons that will become clear.

The actual clinical measures that are used to diagnose Alzheimer’s are a decline in cognitive function and shrinkage of the central area of the brain called the medial temporal lobe. Both changes in cognitive function and brain shrinkage can be picked up thirty years before a diagnosis of Alzheimer’s is made.  

So now a £10 million study is underway to see if a blood test for p-tau, or amyloid, will ‘predict’ if you are more likely to develop the disease and there are plans for a major programme to identify those at risk so they can be treated as early as possible.  This sounds sensible but there are serious drawbacks. To begin with not everyone with raised p-tau or amyloid go on to develop Alzheimer’s. 

This means, as a recent article in the New York Times entitled, ‘Apparently healthy but diagnosed with Alzheimer’s,’ pointed out, people without a diagnosis or no brain scan showing shrinkage, could well be offered new drug treatments that are so far, only marginally better than placebos but can have awful adverse effects. 

These include brain bleeding or swelling which has occurred in more than one in four in the last two drug trials and resulted in seven deaths. Medical agencies in the US, EU and UK are reluctant to licence their use but are under a lot of pressure to do so. 

So thousands of desperate people with early stage Alzheimer’s or cognitive decline, hoping for a cure, are queuing up to join these drug trials because they perceive these drugs, that so far come with little or no benefit plus highly unpalatable side effects, are a better alternative than doing nothing.

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There are alternatives – you just haven’t been told about them!

But are there really no alternatives? Well, none that patients are routinely told about. They involve changes in diet and lifestyle that are very likely to improve your overall health, including that of your brain, and very unlikely to cause damaging side effects. 

Almost all money for research, pledged by governments and raised by Alzheimer’s charities, is going in the direction of drug treatments. Alzheimer’s Research UK’s (ARUK) website says “we exist for a cure”. Most of the money is going toward amyloid and p-tau related research, neither of which have been established as causal. In other words, high levels may just be a consequence of the disease process.

The same is not true for raised blood levels of homocysteine. If levels rise in the brain, it shrinks faster and cognitive abilities decline. If it goes down, they improve, and brain shrinkage slows. This means that it is causing the damage and so would logically be a target for treatment. The only way to do it, however, is with high dose B vitamins (B6, B12 and folate). Several gold standard, placebo-controlled trials have found this to be very safe and effective. But this approach is not patentable and so yields nothing like a drug profit.

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This is a much better biomarker than p-tau

But the benefits of treating homocysteine don’t stop there. It is a much better biomarker of risk for Alzheimer’s than plaque and p-tau both because it is more easily measured and more safely lowered. And when it is lowered, unlike those two, it actually improves cognitive function and slows brain shrinkage by as much as two thirds. It also helps to stop p-tau formation.

Routinely checking homocysteine levels could prevent thousands of cases. Just doing this “could save costs to the UK economy of approximately £60 million per year,” says Dr Apostolos Tsiachristas, Associate Professor in Health Economics at the University of Oxford. His research also estimated it would promote healthy longevity, adding 14 years to life expectancy. 

About half of people over 65 have a homocysteine level above 11 mcmol/l, which is where it starts to become damaging. In one study a third of those treated ended the study with no clinical dementia rating, meaning they could no longer be diagnosed with cognitive impairment. Those with sufficient omega-3 DHA, which is the most important structural fat in the brain, had 73% less brain shrinkage compared to placebo when given the B vitamin treatment. In contrast, in the last anti-amyloid treatment trial, brain shrinkage accelerated by about a fifth in those getting the drug, compared to placebo and not one person achieved a clinical dementia rating of zero.

It should be clear by now, after decades of scientific research that amyloid plaque is not a cause of Alzheimer’s, but a consequence. The same is likely to be true for p-tau tangles.

As an analogy, consider your teeth. Is plaque the cause of tooth decay?  Sure, flossing your teeth and getting the plaque scraped off by the dental hygienist helps, but what causes the plaque? The answer is a bad diet – in this case, one high in sugar and low in fibre. Despite fifty years of research, there is no ‘cure’ for tooth decay, but it can be prevented. The same concept applies to Alzheimer’s, which is as preventable as tooth decay with the right diet and nutrition and lifestyle – which also happens to include less sugar and more fibre.

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Alzheimer’s Prevention

How preventable is Alzheimer’s? It accounts for two thirds of dementia cases. The most conservative figure is 40% . More optimistic estimates say around 80%. Since only one in a hundred cases is caused by genes Alzheimer’s may be entirely preventable in those 99% who do not have the rare causative genes and act early enough to optimise all diet and lifestyle factors. It is not an inevitable consequence of the ageing process as evidenced by the fact that the majority of people don’t get it.

Why the difference in figures? It’s all to do with what is or isn’t included in prevention studies. The most widely used review for dementia prevention in the UK is the 2020 report of the Lancet Commission, authored by Professor Gill Livingston. Both this and the first edition in 2017 failed to even mention homocysteine, despite being repeatedly sent all the evidence of the undeniable beneficial effects of homocysteine-lowering B vitamins by the Oxford Project to Investigate Memory and Ageing (OPTIMA) at the University, headed by former Deputy Head of Medical Science, Professor David Smith.

This is a major and damaging error and has led to the widespread belief that B vitamin supplements are not part of the usual list of preventive actions. But it should be corrected, especially considering that a US National Institutes of Health study attributes 22% of the risk of Alzheimer’s to raised homocysteine. Also, the best study of all, looking at 396 studies in total, published in 2020, concluded: ‘Homocysteine-lowering treatment seems the most promising intervention for Alzheimer’s disease prevention.’

Other prevention studies you may have read are possibly based on data from the UK Biobank. This major research data bank also ignores homocysteine, not for any malevolent reason but simply because it wasn’t measured when it was enrolling people. So, one of the single biggest risk factors and arguably the simplest to change, is repeatedly ignored.

Given that a conservative half of Alzheimer’s cases could be prevented, shouldn’t half the available research money be spent on prevention? 

This certainly doesn’t happen at the moment. Of the three leading charities, two spend nothing on prevention. ARUK claims to spend 5% but none of this goes towards B vitamins or other brain-friendly nutrients such as omega-3 or vitamin D. They, too, ignore homocysteine, and the beneficial effects of lowering it with B vitamins, as first shown in a 2010 Oxford University study they actually helped fund!

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1+1=3

Prevention studies are almost always going to underestimate (never overestimate) the power of prevention due to excluding risk factors, but also because they largely ignore the ‘1+1=3’ compounding impact of interactive risk factors. B vitamins, for example, don’t work without sufficient omega-3 and omega-3 fish oils don’t work in people with raised homocysteine, because of a lack of B vitamins. This has been shown in four trials – in the UK, Holland, Sweden and China. The combination of B vitamins given to people sufficient in omega-3 DHA improved the reduction in brain shrinkage from 53% to 73%. 

Pollution exposure is a risk factor but, in those with lower homocysteine, this effect is much reduced. Poor sleep is a risk factor, but less so in those who exercise. 

For the past five years leading UK researchers, led by neurologist Professor Peter Garrard, who is the Director of the dementia research group in the St George’s, University of London Neuroscience Research Section, have tried to get funding to test the most promising combination – B vitamins and omega-3 – to no avail. Such a trial is badly needed and would cost a fraction of that being spent on amyloid or p-tau.

So. What if a person does everything right – enough B vitamins to keep homocysteine low, sufficient omega-3, low sugar, high fibre diet, enough vitamin D (Alzheimer’s is four times less likely in those with sufficient vitamin D), and an active physical, intellectual and social lifestyle, plus good sleep and not too much stress? 

The only ongoing study and database that assesses all these risk factors as well as including blood tests of four critical biomarkers, homocysteine, omega-3 index, vitamin D and HbA1c, which measures glucose control, is our COGNITION Biobank. We describe it as ‘citizen science’ because anyone can get involved doing a free online Cognitive Function Test, filling in a questionnaire about their diet, lifestyle and medical history, and sending in a blood sample from our home test kit available for purchase. 

So far, over 400,000 people have done our test. But, unlike the £10 million trial, funded by the People’s Lottery, the Gates Foundation, ARUK and the Alzheimer’s Society, it gets no funding. It is literally funded by our citizen scientists who chip in £50 a year and pay for their own tests. Their message is simple: prevention is better than cure – don’t jump.

Action:

Take the FREE Cognitive Function Test here
Order your at-home blood tests here
Support our research and become a FRIEND here
Participate in Alzheimer’s Prevention Day

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A world-class group of Alzheimer’s prevention experts are launching Alzheimer’s Prevention Day on May 15^th. See alzheimersprevention.info.

(The 3-minute Alzheimer’s Prevention Check goes live on May 1^st).

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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 & Info

These are key papers regarding stated facts in this article.

New York Times article: https://www.nytimes.com/2024/03/04/health/alzheimers-amyloid-diagnosis.html

Homocysteine and p-tau: https://foodforthebrain.org/the-p-tau-delusion/

Donanemab review in the British medical Journal: BMJ 2023;382:p1852 

http://dx.doi.org/10.1136/bmj.p1852; 

Telegraph reports 7 deaths and brain shrinkage: https://www.telegraph.co.uk/news/2024/02/19/alzheimers-drugs-shrink-brain-scientists-warn/

Health economics of B vitamins: Tsiachristas A, Smith AD. B-vitamins are potentially a cost-effective population health strategy to tackle dementia: Too good to be true? Alzheimers Dement (N Y). 2016 Aug 11;2(3):156-161. doi: 10.1016/j.trci.2016.07.002. PMID: 29067302; PMCID: PMC5651357.

Omega-3 and B vitamin interactions and studies: Smith AD, Jernerén F, Refsum H. ω-3 fatty acids and their interactions. Am J Clin Nutr. 2021 Apr 6;113(4):775-778. doi: 10.1093/ajcn/nqab013. PMID: 33711096.

Less brain shrinkage and cognitive decline with B vitamins and sufficient omega-3: 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; see also  Oulhaj A, Jernerén F, Refsum H, Smith AD, de Jager CA. Omega-3 Fatty Acid Status Enhances the Prevention of Cognitive Decline by B Vitamins in Mild Cognitive Impairment. J Alzheimers Dis. 2016;50(2):547-57. doi: 10.3233/JAD-150777. PMID: 26757190; PMCID: PMC4927899.

NIH Alzheimer’s prevention review: Beydoun MA, Beydoun HA, Gamaldo AA, Teel A, Zonderman AB, Wang Y. Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis. BMC Public Health. 2014 Jun 24;14:643. doi: 10.1186/1471-2458-14-643. PMID: 24962204; PMCID: PMC4099157.

Meta-analysis of 396 studies favouring homocysteine-lowering B vitamin treatment: Prof Yu study Yu JT, Xu W, Tan CC, Andrieu S, Suckling J, Evangelou E, Pan A, Zhang C, Jia J, Feng L, Kua EH, Wang YJ, Wang HF, Tan MS, Li JQ, Hou XH, Wan Y, Tan L, Mok V, Tan L, Dong Q, Touchon J, Gauthier S, Aisen PS, Vellas B. Evidence-based prevention of Alzheimer’s disease: systematic review and meta-analysis of 243 observational prospective studies and 153 randomised controlled trials. J Neurol Neurosurg Psychiatry. 2020 Nov;91(11):1201-1209. doi: 10.1136/jnnp-2019-321913. Epub 2020 Jul 20. PMID: 32690803; PMCID: PMC7569385.