Do Multivitamins Really Increase The Risk Of Alzheimer’s Disease?

Claim

Multivitamins increase the risk of Alzheimer’s Disease.

Verdict

False

There is no definitive proof that multivitamins increase the risk of Alzheimer’s Disease.

Origin

Online interest in the relationship between multivitamins and Alzheimer’s Disease was sparked by a paper published in 2009 by Dr George Brewer from University of Chicago (1). Dr Brewer believes that copper (in unfiltered water and multivitamins) plays a key role in the development of Alzheimer’s Disease.

There are no randomised controlled trials or clinical studies to definitively establish a relationship between copper containing multivitamins and Alzheimer’s Disease. Dr Brewer has developed a hypothesis connecting Alzheimer’s Disease and copper and he has then supported the hypothesis with relevant studies where he can.

Dr Brewer believes that demographic data supports his hypothesis that Alzheimer’s is a disease of the twentieth century in the developed world (2). Not everyone agrees with Dr Brewer on this point and this issue has been debated over and back in the medical literature (3, 4). Disbelievers say that Alzheimer’s Disease is a disease of ageing and that life-expectancy increased in the twentieth century which explains the apparent increase in Alzheimer’s Disease. Dr Brewer disagrees.

Dr Brewer is convinced that a new environmental toxin/toxins must have emerged in the twentieth century to cause this increase in Alzheimer’s Disease. Dr Brewer has noticed a correlation between the timing of the introduction of copper plumbing and the increase in Alzheimer’s Disease (5). He also is convinced that the amount of copper that leaching from piping is enough to cause Alzheimer’s Disease (5).

Dr Brewer further develops his hypothesis quoting animal studies that showed that copper ingestion from drinking water in Alzheimer Disease animal models greatly enhanced the Alzheimer’s like disease in rabbits (6).  Additionally, humans studies showed that individuals with free copper levels higher than 1.6 μmol/L (the upper value of the normal reference range) were more frequent among people with Alzheimer’s Disease as compared to matched controls (p < 0.001) (7).

Dr Brewer advocates dietary modification, avoidance of copper containing multivitamins and filtering water to reduce intake of copper in order to avoid Alzheimer’s Disease (8).

Two small clinical studies looked at the effects of copper supplementation on cognitive function and cerebrospinal fluid in patients with Alzheimer’s Disease (9, 10). The authors of this study believed that dysregulation of copper metabolism rather than copper toxicity may relate to Alzheimer’s Disease. Copper supplementation had no impact on cognitive function but was associated with a significant decrease in Abeta42 which is a marker for Alzheimer’s Disease. This is completely at odds with the Brewer model.

In summary, there is no scientific evidence to support the claim that multivitamins cause Alzheimer’s Disease. Dr Brewer’s hypothesis is biologically plausible but unproven theoretical model.

 References

  1. The risks of copper toxicity contributing to cognitive decline in the aging population and to Alzheimer’s disease. Brewer GJ.J Am Coll Nutr. 2009 Jun;28(3):238-42. Review.
  2. Copper toxicity in Alzheimer’s disease: cognitive loss from ingestion of inorganic copper. Brewer GJ. J Trace Elem Med Biol. 2012 Jun;26(2-3):89-92. doi: 10.1016/j.jtemb.2012.04.019. Epub 2012       Jun 4. Review
  3. Age and Alzheimer’s Disease. Meunier B. Nutrients. 2016 Jun 16;8(6). pii: E372. doi: 10.3390/nu8060372
  4. Reply to B. Meunier’s Letter to the Editor Re: Brewer G. J.; Nutrients 2015, 7, 10053-10064. Brewer GJ. Nutrients. 2016 Aug 22;8(8). pii: E517. doi: 10.3390/nu8080517.
  5. Brewer, G.J. Copper-2 ingestion, plus increased meat eating leading to increased copper absorption, are major factors behind the current epidemic of Alzheimer’s disease. Nutrients 2015, 7, 10053–10064. [Google Scholar] [CrossRef] [PubMed]
  6. Trace amounts of copper in water induce beta-amyloid plaques and learning deficits in a rabbit model of Alzheimer’s disease. Sparks, D.L.; Schreurs, B.G. Proc. Natl. Acad. Sci. USA 2003, 100, 11065–11069.
  7. ATP7B variants as modulators of copper dyshomeostasis in Alzheimer’s disease. Squitti, R.; Polimanti, R.; Siotto, M.; Bucossi, S.; Ventriglia, M.; Mariani, S.; Vernieri, F.; Scrascia, F.; Trotta, L.; Rossini, P.M.   Neuromol. Med. 2013, 15, 515–522.
  8. Copper-2 Hypothesis for Causation of the Current Alzheimer’s Disease Epidemic Together with Dietary Changes That Enhance the Epidemic. Brewer GJ. Chem Res Toxicol. 2017 Mar 20;30(3):763-768. doi: 10.1021/acs.chemrestox.6b00373. Epub 2017 Mar 3.
  9. Effect of copper intake on CSF parameters in patients with mild Alzheimer’s disease: a pilot phase 2 clinical trial. Kessler H, Pajonk FG, Bach D, Schneider-Axmann T, Falkai P, Herrmann W, Multhaup G, Wiltfang J, Schäfer S, Wirths O, Bayer TA. J Neural Transm (Vienna). 2008 Dec;115(12):1651-9. doi: 10.1007/s00702-008-0136-2. Epub 2008 Oct 30.
  10. Intake of copper has no effect on cognition in patients with mild Alzheimer’s disease: a pilot phase 2 clinical trial. Kessler H, Bayer TA, Bach D, Schneider-Axmann T, Supprian T, Herrmann W, Haber M, Multhaup G, Falkai P, Pajonk FG. J Neural Transm (Vienna). 2008 Aug;115(8):1181-7. doi: 10.1007/s00702-008-0080-1. Epub 2008 Jun 28.
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