Alzheimers/dementia, Uncategorized

Diet can impact Alzheimer’s Disease?

The brain is often called the most sensitive part of the body to inflammation.  So, as we touched on earlier, high blood sugar can contribute to inflammation and that can manifest in the brain.  Alzheimer’s Disease and associated Cognitive Decline disorders are best considered a normal defense mechanism to protect the brain.  I have been following Dale Bredesen’s work for years (highly recommended), here is a clip from his book:

Alzheimer’s disease is what happens when the brain tries to protect itself from three metabolic and toxic threats: Inflammation (from infection, diet, or other causes) Decline and shortage of supportive nutrients, hormones, and other brain-supporting molecules Toxic substances such as metals or biotoxins (poisons produced by microbes such as molds)

Dale Bredesen, The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline, loc. 440

More specifically, constantly ringing the insulin bell with high blood sugar causes another pronounced problem.  Most people have heard of Beta-Amyloid plaques that are associated with Alzheimer’s Disease, and they are topics of much research by drug companies (unsuccessfully to this point, a recent headline from Forbes “Latest Alzheimer’s Flop Raises Doubts About ‘Amyloid Hypothesis'”). Beta Amyloid is actually a very useful substance that helps us clear infectious agents and toxins from the brain, so maybe we might not want to get rid of that function…I let you decide.  Ok, hold on for this one; again from Bredesen:

And insulin is intimately related to Alzheimer’s disease, by several mechanisms. For example, after insulin molecules do their job and lower the glucose, the body must degrade the insulin in order to prevent dropping the blood glucose too low. It does this via an enzyme called insulin-degrading enzyme (IDE). Guess what else IDE degrades? Amyloid, the protein fragment in the sticky, synapse-destroying plaques in Alzheimer’s disease. But the enzyme can’t do both at once. If IDE is breaking down insulin, it can’t break down amyloid, any more than a firefighter can battle a blaze at the north end of town if he/she is raining water down on a conflagration at the south end. By diverting IDE from destroying amyloid, chronically high levels of insulin increase the risk for Alzheimer’s disease.

Dale Bredesen, The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline, loc. 765

Read that again.  By keeping our insulin levels high, we prevent the clearance of Beta-Amyloid from the brain since IDE has to deal with insulin before it can deal with Beta-Amyloid.

The 400 words above here should produce a feeling of empowerment, I hope, that we have the ability to control the insulin levels we keep in our body.    Even though there are know genetic risks via the ApoE4 genetic variant, insulin resistance appears to be the biggest driver, which is great news since we don’t have full control over all of our genes.  David Perlmutter ( a must follow) recently summarized a new study, published in the March 27, 2018 issue of Neurology where they looked at insulin resistance and those with and without ApoE4, and when all lumped together without separating by the ApoE4 presence, insulin resistance was the best indicator by far:


Is this sufficient information to demonstrate for you that there are steps we can take to control our destiny with relation to Alzheimer’s Disease?

Part of this service is to offer personalized guidance on how to implement dietary strategies that can take advantage of this information, which may contribute to improving brain health.


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