Double Protection

Will Obesity Protect You from Alzheimer’s?

The answer is no. You better not count on obesity to protect you from Alzheimer’s disease, regardless of what you might read in the newspaper.

A study just published in Lancet Diabetes and Endocrinology led the Washington Post to proclaim that ”being fat in middle age reduces risk of developing dementia.” Of course, this is not what the study showed.

What they found is an association between higher weight and a lower incidence of Alzheimer’s disease. They did not show that higher weight reduced the risk. This distinction may seem small, but it makes a huge difference.

UAB Distinguished Professor David Allison pointed out that that these findings are neither entirely new nor accurately reported:

It is well documented that weight loss precedes the onset of frank cognitive symptoms of Alzheimer’s disease. This is an observational study which cannot show cause and effect. It is at least equally plausible that the underlying process of Alzheimer’s disease causes lower BMI long before the onset of notable cognitive decline.

Correlation proves nothing about causation. Finding a more fundamental truth of health research would be hard.

So why is it so easy for health reporters to forget it?

Click here to read the (flawed) coverage in the Washington Post and here to read the study. If you want to read more about spurious correlations, we highly recommend you click here.

Double Protection, photograph © Vida Dimovska / flickr

Subscribe by email to follow the accumulating evidence and observations that shape our view of health, obesity, and policy.


2 Responses to “Will Obesity Protect You from Alzheimer’s?”

  1. April 11, 2015 at 5:23 pm, George Henderson said:

    Rather than obesity being protective (type 2 diabetes is certainly not protective) there might be something about hormonal mechanisms that keep some people lean that promotes Alzheimer’s disease.
    For example
    “chronic infusion of amylin into the brain reduces body weight gain and adiposity”
    “In conclusion, our study shows, for the first time, that amylin derived from the pancreas accumulates in the brain precipitating as independent plaques or co-precipitating with Aβ to form complex amylin/Aβ plaques.”

    • April 11, 2015 at 7:36 pm, Ted said:

      Thanks for taking time to comment and provide these references, George!