Tuesday, January 7, 2020

Retrospective #325: Supplemental Ketones, a Prophylactic Strategy

In the introduction to this series in #322, I say, “I have become newly motivated…to introduce ketones to my body every day…as a prophylactic and perhaps therapeutic practice.” And that after I said I was motivated to continue “…to be very low carb/keto-adapted in my dietary practices.” For the new reader, I have been a Type 2 Diabetic for 34 years and an advocate of Very Low Carb eating for almost 18. With this WOE (Way of Eating), I have achieved and maintained 1) weight loss (150+ lbs.), without hunger, 2) infinitely better blood sugar control, and 3) blockbuster improvements in blood lipids, specifically much higher HDL-C and much lower serum triglycerides.
This motivation in 2016 came from having attended the Nutritional Ketosis and Metabolic Therapeutics Conference in Tampa, FL, in January of that year. The sold-out meeting was presented by and intended for academics and clinicians (PhDs and MDs mostly), and included many icons and luminaries in the field. As one of very few lay people attending, it was both eye opening and inspirational and a privilege to be present in this rarefied environment.
My biggest takeaway was the very strong association shown in several presentations between the metabolic diseases whose incipient cause is insulin resistance at the cellular level both in the body and in the brain, i.e. Type 2 Diabetes, and Alzheimer’s Disease (AD), the latter characterized by insulin resistance and glucose disregulation in specific regions of the brain. This similarity is explored in depth (for the serious reader) in a 2008 peer- reviewed article, now cited 190 times in PubMed, “Alzheimer’s Disease is Type 3 Diabetes – Evidence Reviewed,” by Suzanne M. de la Monte, M.D. I found this link on the website of Dr. Mary Newport, a conference presenter.
For an easier read, Mark Bittman, former food writer at The New York Times, in 2012 wrote an opinion piece, “Is Alzheimer’s Type 3 Diabetes?” He must have seen Suzanne de la Monte on The Oz Show, where she appeared and then wrote a “fantastic and detailed summary” (Bittman), “Alzheimer’s: Diabetes of the Brain?” The best précis of the de la Monte piece, however, was in Bittman’s NYT piece. Here are selected excerpts:
“Let’s connect the dots: We know that the American diet is a fast track not only to obesity but to Type 2 diabetes and other preventable, non-communicable diseases, which now account for more deaths than all other causes combined. We also know that people with diabetes are at least twice as likely to get Alzheimer’s, and that obesity alone increases the risk of impaired brain function. What’s new is the thought that while diabetes doesn’t ‘cause’ Alzheimer’s, they have the same root: an over consumption of those foods that mess with insulin’s many roles.”
Bittman, never one of my favorite food writers, especially after writing “VB6, Vegan before 6:00,” concluded,
“The link between diet and dementia negates our notion of Alzheimer’s as a condition that befalls us by chance. Adopting a sane diet, a diet contrary to the standard American diet [referred to as SAD], would appear to give you a far better shot at avoiding diabetes in all of its forms, along with its dreaded complications” [my emphasis].
So far these points only make an argument for what I am already doing personally and cajoling my readers to do. However, the evidence presented at this conference, and in follow-up reading, has persuaded me to introduce ketones to my body every day as a prophylactic and/or therapeutic practice. Why? To avoid damage to the brain that evidence suggests occurs long before mild cognitive impairment (MCI) begins or is detectable. Why ketones?
Ketone bodies are an alternative fuel for brain cells when glucose availability is insufficient,” Richard L. Veech says in an academic article in the Neurobiology of Aging: “A ketone ester diet exhibits anxiolytic and cognition-sparing properties, and lessens amyloid and tau pathologies in a mouse model of Alzheimer’s disease.” Dr. Veech concludes:  
“The present findings show that long-term feeding of ketone esters not only improved cognitive function but also decreased Aβ and pTau pathologic changes. The increase in blood ketone bodies, by either a ketogenic diet or by feeding a ketone ester, would be expected to alleviate the impaired brain glucose metabolism that precedes the onset of AD. Ketone bodies can bypass the block in glycolysis resulting from impairment of insulin function…”
Thus, absent strict, daily adherence to a ketogenic diet, which is an onerous task, my “insurance” to assure the prophylactic and/or therapeutic benefit of ketone bodies on my brain metabolism is to supplement with ketones.

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