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What diet helps Alzheimer’s? Why are Alzheimer’s NZ selling biscuits to raise money?


A year or so ago I spent a fair few hours doing an assignment looking at the relationship of diet to Alzheimer’s disease (AD). One fact is very clear, biscuits are probably the worst food you can eat if you have this disease or want to stay free of it. Saturated fat (I know this is contentious – but there is a link), omega 6 fats (high in most margarines and therefore commercial baking), refined grains which are nutrient free and have a very high glycemic index, sugar – again nutrient free, and intake is linked to obesity, inflammation and type 2 diabetes – all risk factors for AD.

I saw this in the supermarket today – it just makes me feel sad. Why aren’t Alzheimer’s NZ selling a product that reduces the risk of Alzheimer’s?

So how does diet impact Alzheimer’s? Unfortunately the diet you ate consistently over the last 15 to 25 years has already affected your brain. But you can still help your brain now. I’ll just post this concept-map I’ve done so you can see what causes problems for your brain, and what helps your brain – it is self explanatory. The reference list is also posted below.

Nutrition and Alzheimer’s Disease Concept map

Question for concept map: What is the relationship between nutrition and Alzheimers disease?

Design of Concept Map

When I started to research this topic – I found there were multiple dietary factors contributing to the aetiology of Alzheimer’s disease. Diet contributed to many different factors causing brain degeneration, for example oxidative stress, inflammation, and high homosysteine levels – these factors are inter-related.

I started by looking at dietary patterns that were proven to be protective. {4,15, 22, 26} I then listed all the nutrients found in these beneficial diets, {1,7,8,9,12,13,16,17,18,19,20,21,24,25,27} and looked at the mechanisms and effect of these nutrients; how and why they were protective. Where there were confusing or conflicting studies – I looked deeper – for example Vitamin E. Supplements appear to have mixed effects, and when I researched why this might be, I found evidence that the 8 natural forms might work together to be protective. I also found tocotrienols have shown neuro-protective properties, yet are not included in vitamin E supplement  intervention studies. {1,24}

I then looked at dietary factors that increased the risk of Alzheimer’s or sped up cognitive decline, and again researched the mechanisms and specific effects. {2,3,4,5,6,8,10,12,20,23,26}

This concept map links diet to nutrients and then to their effects on Alzheimer’s pathology, both those that are protective and those that increase risk of neurological damage.

For a PDF of this concept map click here: Alzheimers and diet concept map

Click on picture below for a larger copy:

Alzheimers and diet concept map (3)



**Outstandingly important


***Text provided in course notes

  1. **Mangialasche, F., et al., Serum levels of vitamin E forms and risk of cognitive impairment in a Finnish cohort of older adults. Experimental Gerontology, 2013. 48(12): p. 1428-1435.

This study analysed the baseline levels of serum tocopherols and tocotrienols and Vitamin E and oxidative damage, and compared them to cognitive impairment 8 years later. Those with the highest levels of all vitamin E forms had lower levels of cognitive impairment, the association was particularly significant for g-tocotrienol, a form not used in supplement studies.

  1. Hao, Q. and W. Maret, Imbalance between pro-oxidant and pro-antioxidant functions of zinc in disease. Journal of Alzheimers Disease, 2005. 8(2): p. 161-170.

This paper discusses how both an overload and deficiency of zinc can cause oxidative stress and lead to death of nerve cells.

  1. *Martins, I.J., et al., The acceleration of aging and Alzheimer’s disease through the biological mechanisms behind obesity and type II diabetes. Health, 2013. 5(5): p. 913-920.

Mechanisms that link calorie overload, obesity and type 2 diabetes to alterations in Sirt1 (the nutrient sensitive gene), shortened telomeres, and AD are discussed.

  1. Luchsinger, J.A., et al., Caloric intake and the risk of alzheimer disease. Archives of Neurology, 2002. 59(8): p. 1258-1263.

This longitudinal study followed 980 elderly, free of dementia, and looked at the association between developing AD and intake of calories and fat. Those with the Apolipoprotein E e4 allele showed an increased risk of developing AD on a high fat and high calorie diet.

  1. Bitanihirwe, B.K.Y. and M.G. Cunningham, Zinc: The Brain’s Dark Horse. Synapse, 2009. 63(11): p. 1029-1049.

Zinc overload and deficiency is associated with central nervous system pathologies, including oxidative stress, apoptosis, and amyloid plaque formation. This paper contains a section explaining the mechanism of zinc imbalance in the pathology of AD.

  1. Lakhan, S.E. and A. Kirchgessner, The emerging role of dietary fructose in obesity and cognitive decline. Nutrition Journal, 2013. 12.

This paper discusses the links between obesity and metabolic syndrome and cognitive decline. Dietary fructose from sugar and high fructose corn syrup has increased in the Western diet in the last 3 decades, and its link to metabolic syndrome and cognition is discussed.

  1. Dickens, A.P., et al., Vitamin D, Cognitive Dysfunction and Dementia in Older Adults. Cns Drugs, 2011. 25(8): p. 629-639.
  1. Cardoso, B.R., C. Cominetti, and S.M.F. Cozzolino, Importance and management of micronutrient deficiencies in patients with Alzheimer’s disease. Clinical Interventions in Aging, 2013. 8: p. 531-542.
  1. Li, F.-J., L. Shen, and H.-F. Ji, Dietary Intakes of Vitamin E, Vitamin C, and beta-Carotene and Risk of Alzheimer’s Disease: A Meta-Analysis. Journal of Alzheimers Disease, 2012. 31(2): p. 253-258.
  1. Rao, J.S., S.I. Rapoport, and H.W. Kim, Altered neuroinflammatory, arachidonic acid cascade and synaptic markers in postmortem Alzheimer’s disease brain. Translational Psychiatry, 2011. 1.
  1. ***Kamphuis, P.J. and R.J. Wurtman, Nutrition and Alzheimer’s disease: pre-clinical concepts. European Journal of Neurology, 2009. 16(s1): p. 12-18.
  1. Hu, N., et al., Nutrition and the Risk of Alzheimer’s Disease. Biomed Research International, 2013.
  1. ***von Arnim, C.A.F., U. Gola, and H.K. Biesalski, More than the sum of its parts? Nutrition in Alzheimer’s disease. Nutrition, 2010. 26(7-8): p. 694-700.
  1. Hussain, G., et al., Fatting the brain: a brief of recent research. Frontiers in Cellular Neuroscience, 2013. 7.
  1. Scarmeas, N., et al., Mediterranean Diet and Mild Cognitive Impairment. Archives of Neurology, 2009. 66(2): p. 216-225.
  1. **Butterfield, D.A., et al., Nutritional approaches to combat oxidative stress in Alzheimer’s disease. Journal of Nutritional Biochemistry, 2002. 13(8): p. 444-461.

This paper discusses nutrients needed for production of endogenous antioxidants, and dietary nutrients required to reduce oxidative stress in Alzheimers disease. Studies supporting the role of antioxidants and mechanisms of action are discussed.

  1. Rafnsson, S.B., V. Dilis, and A. Trichopoulou, Antioxidant nutrients and age-related cognitive decline: a systematic review of population-based cohort studies. European Journal of Nutrition, 2013. 52(6): p. 1553-1567.
  1. ***Ramesh, B.N., et al., Neuronutrition and Alzheimer’s Disease. Journal of Alzheimers Disease, 2010. 19(4): p. 1123-1139.
  1. *Loef, M. and H. Walach, The Omega-6/Omega-3 Ratio and Dementia or Cognitive Decline: A Systematic Review on Human Studies and Biological Evidence. Journal of Nutrition in Gerontology and Geriatrics, 2013. 32(1): p. 1-23.

This review looks specifically at the ratio of omega 6 to omega 3 and its association to the risk of AD. Most other studies and reviews look at omega-3 intake alone, so this review provides additional information on the importance of omega 6 intake as it affects omega 3 by competing for rate limiting enzymes.

  1. Amtul, Z., et al., Structural Insight into the Differential Effects of Omega-3 and Omega-6 Fatty Acids on the Production of A beta Peptides and Amyloid Plaques. Journal of Biological Chemistry, 2011. 286(8): p. 6100-6107.
  1. Cho, E., et al., Dietary choline and betaine assessed by food-frequency questionnaire in relation to plasma total homocysteine concentration in the Framingham Offspring Study. American Journal of Clinical Nutrition, 2006. 83(4): p. 905-911.
  1. **Singh, B., et al., Association of Mediterranean Diet with Mild Cognitive Impairment and Alzheimer’s Disease: A Systematic Review and Meta-Analysis. Journal of Alzheimers Disease, 2014. 39(2): p. 271-282.

This is a systematic review of all quality longitudinal studies looking at the association between a Mediterranean diet the risk of developing MCI and AD. Five studies fitted a strict criteria.

  1. Tolppanen, A.-M., et al., Midlife and Late-Life Body Mass Index and Late-Life Dementia: Results from a Prospective Population-Based Cohort. Journal of Alzheimers Disease, 2014. 38(1): p. 201-209.
  1. *Sen, C.K., S. Khanna, and S. Roy, Tocotrienols in health and disease: The other half of the natural vitamin E family. Molecular Aspects of Medicine, 2007. 28(5-6): p. 692-728.

Intervention studies with vitamin E usually only use one form a-tocopherol, and these have shown mixed results in studies on AD patients. This review paper looks at the properties and mechanisms of tocotrienols. It is hypo-cholesterolemic and neuro-protective, but needs further research in AD models.

  1. Poly, C., et al., The relation of dietary choline to cognitive performance and white-matter hyperintensity in the Framingham Offspring Cohort. American Journal of Clinical Nutrition, 2011. 94(6): p. 1584-1591.
  1. *Grant, W.B., Trends in Diet and Alzheimer’s Disease During the Nutrition Transition in Japan and Developing Countries. Journal of Alzheimers Disease, 2014. 38(3): p. 611-620.

The prevalence of AD rose from 1 to 7% in Japan between 1985 and 2008. Dietary changes that preceded this increase are discussed, they have a lag of 15 to 25 years.

  1. **Otaegui-Arrazola, A., et al., Diet, cognition, and Alzheimer’s disease: food for thought. European Journal of Nutrition, 2014. 53(1): p. 1-23.

Recent review providing summaries of studies on the role of nutrition in AD, including Omega-3, antioxidants, B vitamins, neutraceutical formulations, and dietary patterns. Clinical trials and mechanisms are discussed.

  1. *de Waal, H., et al., The Effect of Souvenaid on Functional Brain Network Organisation in Patients with Mild Alzheimer’s Disease: A Randomised Controlled Study. PLoS ONE, 2014. 9(1).

This 24 week RCT using a nutraceutical supplement (highly promoted by company making it) containing a combination of nutrients shown in theory to be effective in preserving brain network connectivity, is shown to be effective for mild AD. However with respect to secondary measures of cognition; the Rey Auditory Verbal Learning Test, the cognitive subscale of the Alzheimer’s Disease Assessment Scale, the Letter Digit Substitution Test, and the Wechsler Memory Scale, results did not differ from placebo.

Addition November 2016

Activated B vitamins and N-A-C slows down Alzheimers



  1. The thing about your ref. 20 is, of course, that saturated fats can be produced endogenously as well as sourced from the diet – in this regard they differ from omega-3 and 6, with the total amount of serum SFA being controlled by dietary carbohydrate.

    Another paradigm I will throw in here is brain insulin resistance. When serum insulin is sustained at excessive levels the brain transport of insulin closes down; the BBB downregulates insulin uptake, the brain becomes insulin-deficient. At the same time, foods that stimulate insulin also stimulate amylin release, and pancreatic amylin does cross the BBB and is a source for amyloid.

  2. Love the concept map and agree that biscuits are a very poor choice for a fundraiser.

    I think a potential problem here is that so much of medical/physiology research is geared to ultimately develop new drugs. This is based on the premise that people generally don’t adopt sufficient healthy lifestyle behaviours despite knowing more or less what they should be doing*. I’m sure Alzheimers NZ know of a link between junk food and Alzheimers, but they also know selling biscuits will raise more money than selling fish (for example) and perhaps they are trying to create a future where people can eat what whatever they want and no one develops Alzheimers due to a miracle drug, a model which is currently working out really badly

    * This line of thinking is probably more relevant for obesity and T2D and perhaps less so for Alzheimers where the discussion ends with non-modifiable risk factors (age, family history, etc) and ‘healthy diet’. But never the less, it sets up a bit of a self-fulfilling prophecy. If there isn’t much research on the effects of various healthy lifestyle behaviours (and in combination), and which gets trickled down to the public and reinforced, then why should we expect the average person to be particularly empowered, and so they think Alzheimers is just what happens if you’re old and unlucky

    • Great points Steven. Our current medical model is so influenced by the pharmaceutical industry. I wonder what the message would be if the same number of dollars was thrown at marketing a healthful diet?

  3. Thanks for sharing the fruits of your hard work, Julianne. I’ll save the graphic as desktop wallpaper on my work PC and that way it gets blown up and frequently studied.

  4. Apologies, I didn’t have time to complete that comment.
    It appears that amylin is not problematic and even beneficial at normal insulin concentrations, and insulin is beneficial if it can be delivered directly to the brain.


    So we have a divergent effect:
    In individuals with hyperinsulinaemia, meals that increase insulin and amylin (carbohydrate meals) result in an imbalance (high amylin, low insulin) which favours formation of amyloid; and of course there is also the presence of excessive glucose which mucks up the intercommunication of neurons.
    In individuals who are still insulin sensitive, the flux of insulin, amylin and glucose is just right to keep the brain working.

    Shortbread, by definition a mixture of sugar, starch and fats (unlikely to be much omega 3, but some mix of SFA, MUFA, trans fats, and maybe omega 6) with little in the way of micronutrition let alone antioxidants, would be the sort of food you would design if you were trying to a) increase serum saturated fats in the short term, or b) produce insulin resistance in the long term, as well as c) cause a substantial release of insulin and amylin.

    Did anyone see the movie Iris? In it, Irish Murdoch (Dame Judy Dench) dies of Alzheimer’s. There are a few scenes set in the supermarket and kitchen which basically show Dame Judy and Jim Broadbent shopping for high carbohydrate processed food and eating it with minimal preparation.
    These are the most tragic scenes in the movie.
    I’m sure they would have bought the AD fundraising biscuits had they been on sale.

    • Thanks George! I didn’t see that movie. But speaking of Dame Judi Dench – I believe she has macular degeneration. I also did a bit of study on that, diet of course can protect. Another blog post in the pipeline from way back.

  5. Macular degeneration is one of the few diseases where the evidence against 18:2 omega 6 is consistent; the other is skin cancer. Both involve the cells most directly exposed to UV light.
    About amylin – type 1 diabetics have no pancreatic amylin. Though type 1 has many features that should be taxing on the brain, they don’t have a high rate of AD at all. Compared to type 2 diabetics, who have lots of amylin, and a very high rate of AD, they seem to do fine.
    I thought up a formula to explain the relation between amylin insulin and energy
    our two natural (adaptive) settings protect the brain – these are
    1) + insulin, + amylin, and + glucose
    2) – insulin, – amylin, and + ketones

    The harmful combo is (from the point of view of the brain)
    3) – insulin, ++ amylin, ++ glucose

    If your brain is at 3 you will find it hard to get back to 1, but you can go back to 2 quite easily. Hence the coconut oil and low carb etc. protocols.

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