Nov 05 2007

Aluminum and Alzheimer’s

I have been hearing a lot of people talking about aluminum in deodorants (I think it’s aluminum sulfate that is the active ingredient? ), and that it results in a higher chance of developing Alzheimer’s disease. I doubt this claim, but don’t know of any scientific inquiry that either supports or disproves it. It just seems that with deodorant use being so widespread, a serious side-effect like this would have been detected, if by no other means, by the fact that we would have seen a huge surge in Alzheimer’s rates a little while after deodorants hit the market (whenever that was). Is there any truth to this rumor?Also, when I tell people my doubts on this, they often give the following response: “Whether or not it causes Alzheimer’s, it can’t be healthy to rub aluminum into your pores, so you are better off buying deodorants that do not include it (such as “natural” products)”. Isn’t this some kind of logical fallacy?Thanks so much for taking the time to read the email, and keep up the phenomenal work – I’ll be listening!
All the best,
Zach M.

The Aluminum hypothesis of Alzheimer’s disease has been around for 42 years, and the current bottom line is that at present there does not appear to be a causal relationship between aluminum and Alzheimer’s disease (AD) but aluminum may still be playing a role in the severity of the disease. But there is still no definitive scientific answer – the story of aluminum and AD reveals the complexity of such questions, and exposes the quality and integrity of news sources that report on it.

AD is a neurodegenerative disease resulting in the death of neurons (the brain cells that are responsible for the processing of information) that progresses over many years, resulting in chronic memory loss and impairment of all types of cognitive function (a clinical picture referred to as dementia). AD results in brain atrophy and specific pathological changes in neurons, most notably plaques and neurofibrillary tangles.

The exact causes of AD are not currently known, but what is known is that age is the strongest risk factor for AD. In addition genetic risk plays a role, most notably variants of the gene for apolipoprotein E (ApoE) predispose to AD. But age and genetics are not the only story, and there is likely also various environmental risk factors that play a role as well, in addition to other biological factors (the presence or absence of certain other diseases, for example). Like many neurodegenerative diseases, AD likely results from a combination of factors conspiring together, and these factors likely vary among patients. This makes it very difficult to pinpoint specific factors that cause or increase the risk of AD.

There are different kinds of evidence that we can bring to bear on questions such as the relationship between aluminum and AD. Only one type of evidence is not circumstantial, and that is the one type of evidence we do not have, and cannot have. Direct evidence, where all variables were controlled except for the one of interest, in this case aluminum, would involve comparing randomized groups of people, exposing them to various amounts of aluminum, following them over years or even decades, and tracking how many develop AD. There are significant practical reasons why such studies are difficult to perform, but this is irrelevant because such a study would be unethical. We cannot deliberately expose people to suspected toxins in order to measure their toxicity.

So we are left with the circumstantial, or inferential, evidence. This includes exposing brain cells to aluminum to see the effect, exposing animals to aluminum to see if they develop AD, correlating aluminum exposure to risk of AD, measuring aluminum levels in subjects with and without AD, looking to see if there is a role for aluminum in the pathological process of AD, and removing aluminum from subjects with AD to see if this results in an improved outcome.

These types of evidence are brought to bear on most questions of toxicity. It is rare for all the circumstantial evidence to point consistently in one direction. Even in well established cases, such as the link between smoking tobacco products and certain types of lung cancer, not all the evidence points toward a causal relationship. But the overwhelming majority of the evidence does point in this direction, so we accept as largely proven that smoking causes cancer.

As I have written about extensively before, the evidence for vaccines an autism points overwhelming in the direction of a lack of a causal relationship, and so the consensus of opinion (reflected by current policy) is that vaccines do not cause autism.

The evidence of aluminum and AD is mixed, without a clear direction. At present the best answer we have is that aluminum probably does not cause AD but appears to be playing some role, perhaps influencing severity. But even after 42 years, there remains a question mark next to these conclusions. We can rule out that aluminum is the single cause of AD, but whether or not it is an independent risk factor is a qualified “probably not.”

To summarize the specific types of evidence:

Aluminum is toxic to neurons in the petri dish, and causes some changes similar to AD, but not all.

Animal models show that aluminum does cause neurological damage, but in doses higher than likely human exposure, and without causing the tangles and plaques typical of AD – on the other hand rat and other animal brains may not form tangles and plaques like human brains do.

Epidemiological and exposure models are somewhat mixed, but mostly negative, without a consistent pattern of association. Of note, patients with kidney failure who have impaired clearing of aluminum do not have a higher risk of AD.

Aluminum has been detected inside AD plaques, and may play role in their formation. But a causal mechanism has not been identified.

While AD patients have aluminum in dying neurons, the total “burden” of aluminum in AD brains or bodies is not higher than controls. This leaves open the possibility that aluminum, while present, is incidental to the pathology of AD. This is always a source of complexity. When something goes biochemically or physiologically wrong in the body there are many downstream or secondary effects. Therefore, researchers can find many biological changes that correlate with the presence of a disease, but many of them are not the cause of the disease but rather the result of the disease.

And finally, studies that involve the removal or aluminum from AD patients did correlate with a mildly improved outcome, but these studies are complicated by the fact that the treatment also decreased iron stores, and this may have resulted in less oxidative stress on neurons. So the variable of aluminum was not isolated, complicating interpretation of the results.

You can see why this question has remained controversial for over four decades. The data is highly complex and mixed in terms of favoring or rejecting the aluminum-AD hypothesis. This will remain an area of active research for some time. I suspect the answer will be mixed – meaning that aluminum is not a significant cause of AD but is playing some role, resulting in the persistent if circumstantial signal in the research data.

The mainstream scientific and patient or disease-oriented groups accurately reflect the above interpretation of the research. But the complexity of the results make it very easy to exploit for the purpose of fear-mongering. The notorious crank website,, for example, cherry picks the evidence that suggests there is a correlation and piles it up to present a very distorted view of the issue. There will likely persist rumors, scare e-mails, and conspiracy websites promoting the idea that aluminum causes AD regardless of how the research progresses.

Regarding Zach’s last question, about the logic of the statement that “it can’t be healthy” to be exposed to aluminum, this argument is based upon an unstated major premise – namely that any exposure to a possible toxin, regardless of dose or mode of exposure, is a bad thing. This premise is false. We evolved in an environment that includes exposure to some extend to a wide range of elements and chemicals, so we have defense mechanisms to environmental toxins. Also, you cannot eliminate all exposure to any element or substance, you can only minimize it.

Therefore, the question is not whether or not it is a good thing to be exposed at all to something, but what are the safe levels of exposure. Toxicity is always about dose. The real question is whether or not current exposure levels pose any risk, and if the evidence suggests that this answer is no then it is likely a waste of effort and resources to minimize exposure further. You can also take a risk vs benefit analysis to such questions. What is the benefit of using certain substances and what is the risk. In this context I certainly do not blame anyone who chooses not to use a deodorant with aluminum – I would consider the benefit to be optional for most people, there are other options, and while the risk is probably low there is a small question mark next to risk. At the same time I think there is no reason for panic or extreme measures.

On a side note, questions about toxicity have a particular hold on the human imagination, beyond their purely practical implications. This is because we evolved the emotion of disgust, which motivates us to avoid potentially harmful substances, like spoiled food. This results in varying degrees of obsession with purity and cleanliness (varying both individually and by culture). The idea that some invisible toxin is assaulting our bodies has a strong emotional impact, and leads most people to conclude something along the lines of “why take a chance.” While it is rational to minimize exposure to known or possible toxins, rational calculations of probability and risk vs benefit often take a back seat to the raw emotion of disgust. Understanding this human tendency, however, helps us to take a step back and look at the data more dispassionately.

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