Cholesterol Leads to Alzheimer's? Nonsense!

Neurologist & New York Times Bestselling Author By David Perlmutter, M.D.
Neurologist & New York Times Bestselling Author
Dr. Perlmutter is a Board-Certified Neurologist, four-time New York Times bestselling author, and fellow at the American College of Nutrition.

Recently, JAMA Neurology published a study that looked at the connection between cholesterol levels and Alzheimer's disease, and it got a lot of attention in the press. Somehow it was widely reported that the study showed a direct relationship between cholesterol levels and Alzheimer’s risk.

Is that really what the research showed? Let’s take a look.

The study evaluated total cholesterol levels, levels of HDL and LDL in a group of 74 elderly adults. They also underwent a special type of brain scan to determine how much beta-amyloid their brain contained. Beta-amyloid, a chain of amino acids, was studied because some researchers believe there's a relationship between beta-amyloid levels and Alzheimer’s risk.

The study found a small increased risk of having higher beta-amyloid if the subjects had higher levels of LDL and lower levels of HDL.

Does this mean there's a definite connection between high LDL or low HDL and Alzheimer’s disease risk?

No. The problem with this hypothesis is the assumption that beta-amyloid is responsible for Alzheimer’s disease, when in reality it's a symptom of it.

This idea that β-amyloid is responsible for Alzheimer’s disease was popular for years among neuroscientists, especially those involved in drug development. Millions of dollars have been spent to develop a drug therapy to rid the brain of beta-amyloid in hopes of offering up a treatment for Alzheimer’s disease.

And each and every trial has failed, with the most recent report in the New England Journal of Medicine showing that a drug, Semagacestat, designed to lower beta-amyloid, actually made people more demented and increased the risk for other threatening issues.

So what's the role of beta-amyloid?

New research is directly challenging the hypothesis that β-amyloid causes Alzheimer’s disease. Rudy J. Castellani, Jr., MD, Director of Neuropathology at the University is among the critics of this view.

His research on this subject has been published in the Journal of Alzheimer’s Disease, and key points are found on the very insightful website The Tangled Neuron – A Layperson Reports on Memory Loss, Alzheimer’s & Dementia. They suggest that beta-amyloid may actually protect the brain, going so far as to suggest that β-amyloid may be a brain-protective antioxidant.

Other researchers believe that β-amyloid may actually represent the brain’s response to invading viruses. Dr. Ruth Itzhaki from the University of Manchester has published extensively demonstrating compelling evidence of the central role of the herpes simplex virus in being a risk factor for Alzheimer’s disease.

Consider that beta-amyloid is increased in Alzheimer’s not as a cause, but rather as an effect. This protein, the target of so many failed pharmaceutical campaigns, may well be our brain’s desperate response to an invading organism, herpes simplex, or who-knows-what-else.

So we should reconsider our thought process on what underlies this devastating disease, especially as it relates to the role of beta-amyloid. Remember, the enemy of my enemy is my friend.

It’s so important to provide the full story when media spins research like we saw with this recent publication. The mission is to light the single candle and, while not cursing the darkness, reveal how misguided are the ongoing efforts to castigate and medically remediate parameters that may actually be doing no harm.

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