Alzheimer’s and Copper Toxicity: Related?

Copper and Alzheimer's

 

Recently an article was published online (2/6/19) linking Alzheimer’s disease (AD) to copper toxicity. The article author is George J. Brewer, Professor Emeritus of Human Genetic and Internal Medicine, at the University of Michigan (USA).

Professor Brewer has published related papers/studies on copper and AD in the past.  The author’s claims are ambitious and proposed solutions are startlingly simplistic.  So, we thought it necessary to review the study and its claims.

Before diving in, a brief description of copper, and its forms, is necessary for understanding Professor Brewer’s assertions.

 

The Science Behind Copper

 

Humans constantly ingest copper.  It’s essential for living.  Copper helps maintain your healthy bones, immune function, and helps the body to form new red blood cells, which carry hemoglobin.

Copper is available in two forms.

Monovalent copper (copper-1) is the copper in most food.  Divalent copper (copper-2), on the other hand, is often present in drinking water/water piping and supplement pills (esp. multivitamins).  Copper-2 is what Professor Brewer focuses on in his article and cited studies.

 

Alzheimer’s Study Overview

 

Professor Brewer’s hypothesis is this.  Copper-2 ingestion (form of copper found in drinking water and supplement pills) is the cause of the Alzheimer’s epidemic (1).

As evidence for copper toxicity’s role in AD, Professor Brewer draws on several phenomena.

Developed vs. Developing Countries

First, the author compares developed countries (high rates of AD + copper plumbing) to undeveloped countries (low rates of AD, no copper plumbing) to highlight his hypothesis.

One of the more interesting parts of the article was the case study on Japanese immigrants and their rates of AD.  As Professor Brewer explains:

“Japan is a developed nation but has a low prevalence of AD, and the Japanese have shunned copper plumbing for fear of toxicity. But when Japanese migrate to Hawaii, where copper plumbing is used, their prevalence of AD increases to match that of other developed countries” (3).

While compelling, the role of copper plumbing isn’t clear.  It could easily be correlational.  Perhaps it’s other Western lifestyle factors that cause their AD rates to match that of developed countries.  A study on residents of a European or Asian country with copper plumbing, who migrate to the US, would make the role of copper most clear.

Copper and Drinking Water + Nutrition

To address confounding factors, Brewer draws on two studies linking divalent copper ingestion to amyloid plaque buildup (the cornerstone of the “amyloid hypothesis”)

First, Professor Brewer cited a study published in the Journal for Nutrition Health and Aging linking copper in drinking water to AD.

Specifically, the researchers found adding “0.12 parts per million (ppm) of copper to the distilled drinking water significantly enhanced the amyloid plaques of AD in the brain, and caused memory loss in the animals” (2).

Copper in drinking water is copper-2.

Lastly, Professor Brewer used a nutritional study of a Chicago population subset. According to the study, “Among persons whose diets were high in saturated and trans fats, higher copper intake was associated with a faster rate of cognitive decline” (4).

 

Alzheimer’s and Saturated Fats?

 

Hold on, you might say.  Don’t you recommend eating plenty of saturated fats, as part of the Health & Life Diet?

Yes, and we still support that recommendation.

(bear with us for a brief tangent to the article’s main topic)..

The important information is, as always, in the details.

As the researchers say, “consistent with our hypothesis, among the 604 persons (16.2%) who consumed a diet high in saturated and trans fat, a faster decline was seen with higher copper consumption” (5).

Importantly, the researchers grouped trans fat and saturated fats.  Plenty of research has come out highlighting the damaging effects of trans fats and vegetable oils.  We believe the negative outcomes of the study are from trans fat consumption, not saturated fat consumption.

Furthermore, if you look at the researchers explanations, it’s clear they are linking saturated fat to cognitive decline (AD) contingent on copper ingestion.

Let us be more clear.  They compared high fat (saturated and trans) groups to low fat groups with high copper intake to see the cognitive outcomes.  But the negative relationship described is entirely conditional on copper intake.  

As the researchers later acknowledge, “The interaction with a high-fat diet was specific to copper intake and was not apparent with intakes of zinc or iron” (6).

While the high fat groups were negatively affected more than the low fat groups, the high-fat detail is in no way causational, and is less relevant, in this context, than the copper-2 ingestion.

 

Alzheimer’s Study Limitations

 

The first limitation to Brewer’s assertions, and the mentioned studies, is the assumption that a toxic dose of divalent copper in rats translates to a toxic dose in human beings.  This assumption, that humans are toxic at equivalent doses to rats, isn’t universally applicable.

Broadly speaking, the author’s argument is limited in its focus on the relationship between copper toxicity and amyloid plaque buildup.

The issue is that the “amyloid hypothesis” has been in fashion for over 15 years now.  Yet, no medication targeting amyloid plaque removal has been successful in reducing associated symptoms (memory loss, confusion, etc).

Did you know just one Alzheimer’s Alzheimer’s drug (memantine) was approved from 2000-2010?  It was in 2003 (7).

What about the number of experimental drugs tested by the FDA during that same time period? 244 (8).

The vast majority of experimental drugs were targeting the amyloid hypothesis- and the experiment compounds did just what the scientists hoped- to remove the amyloid plaques. Yet, patients symptoms didn’t improve or got worse.

 

Conclusion

 

There is certainly validity and evidence to back up the author’s claims.

Big pharma may even be working to suppress awareness of this sort of AD research, for fear of its impact on demand for their AD medication (ambitious claim).  We just don’t know.

Our main point is this- while Professor Brewer may effectively link copper-2 ingestion with amyloid plaque buildup, it isn’t clear that amyloid plaque buildup (and its removal) is what characterizes AD.

If it was, the hundreds of drugs that have successfully removed amyloid plaques in the brain would have improved symptoms in AD patients.  But they haven’t.

So, perhaps Professor Brewer’s claims are most flawed in his single-dimensional approach to AD treatment.  Alzheimer’s disease is a complicated disease with many contributing factors.  The right treatment, then, can’t just be a magic pill or solution (reducing copper-2 exposure).  Rather, the optimal AD treatment will target all of the disease’s contributing factors, recognizing the brain for the complicated organ that is it.

 

References:

 

(1) //journals.sagepub.com/doi/abs/10.1177/1535370219827907

(2) //www.ncbi.nlm.nih.gov/pubmed/16886094

(3) //journals.sagepub.com/doi/abs/10.1177/1535370219827907

(4) //jamanetwork.com/journals/jamaneurology/fullarticle/792043

(5) Ibid.

(6) Ibid.

(7)  Bredesen, The End of Alzheimer’s. 

(8)  Ibid.

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