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Research shows Alzheimer’s disease relationship with obesity and testosterone

A diagram of the brain of a person with Alzheimer’s disease. The disease and other forms of dementia kill as many as one in three senior citizens in the United States. PUBLIC DOMAIN

Christian Pike, a professor of gerontology — the study of aging and the elderly — at the University of Southern California, spoke about Alzheimer’s disease and its relationship with obesity and testosterone on Thursday, Oct. 4 in the Life Sciences Building.

Alzheimer’s disease, a progressive disease that destroys memory and other important mental functions, and other dementias kill as many as one-third of seniors. At present, Alzheimer’s disease is the sixth leading cause of death in the United States, affecting an estimated 5.7 million Americans.

Though old age is the biggest risk factor for Alzheimer’s, Pike’s talk suggested that biological factors such as obesity and low testosterone levels in men can further increase risk of getting the disease.

“Male testosterone production peaks at age 25,” Pike said. “Then beginning around 30, you have a slow decline of about 1 percent per year, but then free testosterone decreases even more and you have a slow slide.” .

Longitudinal studies in men have allowed researchers to determine testosterone’s role in Alzheimer’s progression. For example, examining patients with and without Alzheimer’s over 10 years, researchers reliably predicted the likelihood of developing Alzheimer’s by monitoring testosterone levels over time. Those with lower testosterone levels consistently demonstrated higher Alzheimer’s risk at an earlier age. This suggests that having higher testosterone levels mitigates Alzheimer’s disease risk in men.

However, while testosterone offers protection against Alzheimer’s disease, testosterone injections can significantly increase prostate cancer risk. Pike thus tried to test a potentially less harmful approach by using selective androgen receptor modulators (SARMs) which imitate testosterone’s function in muscles but lack substantial androgen activity in the prostate. Pike’s research in mice indicates that SARMs provide a similar neuroprotective effect to testosterone.

Pike then transitioned to discussing obesity. More than two-thirds of U.S. adults are overweight or obese, and risk of dementia is increased approximately threefold with obesity, according to Pike. This is supported as the age of Alzheimer’s onset is typically lower in obese people.

“Obesity increases systemic inflammation and neural inflammation,” Pike said, which causes poor outcomes.

After Pike established the roles of obesity and testosterone in Alzheimer’s disease, he connected the two factors.

“[Obesity] and testosterone have a bidirectional relationship — that is, high levels of fat lower testosterone, low testosterone increases fat, vice versa with metabolic syndrome, which drives things like type 2 diabetes. It goes both ways,” Pike explained.

Combined with the primary Alzheimer’s risk factor, aging, obesity and low testosterone can dramatically increase Alzheimer’s susceptibility.

As such, it seems like avoiding obesity and low testosterone (for males) is prudent in postponing Alzheimer’s onset.

“Everything [Pike] presented is extremely important,” Maria Galatioto, an MS student in physiology and biophysics, said. “As we have a human population with a growing life expectancy, we are going to have more individuals with dementia and Alzheimer’s. It is essential that we are all taking necessary preventive measures to the best of our ability, so that we can hopefully live healthy and happily later on in our lives.”

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