Since late 2016 we have entered the age of disclosures! Fasten your mental safety belt and enjoy the ride! Heretic

Sunday, July 28, 2019

Keto diet overcomes unfavorable ApoE4 Alzheimer's genetics

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Wiki Rostas
Wiki Fish

... better way to put it - ketogenic diet renders some of the genetical conditions such as ApoE4+  irrelevant or not endangering an individual survival chances! It appears ApoE4+ does represent a handicap ONLY on a high carbohydrate diet! It is probably similar with many other genetic impairments. It seems one needs to have a more than "perfect" genetics to be able to remain healthy until a very old age on a high carbohydrate diet!

"Ketogenic diet rescues cognition in ApoE4+ patient with mild Alzheimer's disease: A case study.", by Morrill SJ, Gibas KJ, Diabetes Metab Syndr., March-April 2019


Quotes:


Abstract
It has been established that there is a correlation between Alzheimer's disease and apolipoprotein E, specifically the ApoE4 genetic variant. However, the correlation between Apoe4, insulin resistance and metabolic syndrome (MetS) pathologies still remains elusive. As apolipoprotein E has many important physiological functions, individuals with the ApoE4 allele variant, also known as the Alzheimer's disease gene, are primarily at a greater risk for physiological consequences, specifically cognitive impairment (Chan et al., 2016). In this case study, a 71-year old female, heterozygous for ApoE4 with a family history of Alzheimer's Disease (AD) and the dual diagnosis of mild AD/metabolic syndrome (MetS) was placed on a 10-week nutrition protocol purposed at raising plasma ketones through carbohyrdrate restricted, high fat ketogenic diet (KD), time- restricted eating and physical/cognitive exercise. Primary biomarkers for MetS were measured pre/mid-/post intervention. The MoCA (Montreal Cognitive Assessment) was administered pre/post intervention by a licensed clinical therapist. The results were statistically significant. The HOMA-IR decreased by 75% from 13.9 to 3.48. Triglycerides decreased by 50% from 170mg/dL to 85mg/dL. VLDL dropped by 50% from 34mg/dL to 17mg/dL, and HgA1c decreased from 5.7% to 4.9%. The baseline MoCA score was 21/30; post treatment score was 28/30. The significant results in both MetS biomarkers and the MoCA score suggest that a ketogenic diet may serve to rescue cognition in patients with mild AD. The results of this case study are particularly compelling for ApoE4 positive (ApoE4+) subjects as ketogenic protocols extend hope and promise for AD prevention.

UPDATE

Within a short time from posting the above, the following comments were posted on Twitter.
(BTW - Thanks Tucker Goodrich and Shaza!)


Indeed, it turns out that it is not the keto diet per-se but rather the improved DHA contents of such a diet that is the critical factor, not just the low carbohydrates aspect of it!    Tsimane (Bolivian natives) diet is high carbohydrate (vegetable & fruit) and low protein (16%), low fat but also most of the protein comes from fish.  The paper on "DHA brain uptake..." of ApoE4 versus non-ApoE4 carriers confirms that the critical factor is abundance of DHA in food for the ApoE4 carriers. In return they have a higher mass of grey matter in the brain than non-ApoE4, which appears to be confirmed by cognition tests [add study refs]. In return for having higher grey matter mass, the uptake of DHA is 20% higher for ApoE4 carriers, making them more vulnerable to DHA starvation.

It seems that this story has evolved in a direction that I did not expect. Perhaps the ApoE4 rather than being a mildly inconvenient adaptation requiring high fat/high fish diet, turns out to be a very beneficial genetic evolutionary trait helping in brain development and achieving higher IQ - which is clearly a survival advantage. Especially for navigation over the high seas or in the Arctic!






1 comment :

john said...

That's interesting.

Stan, have you read 'Neurons and the DHA Principle'? It's expensive for a book, but it's great for a compilation of DHA research, along with some hypotheses. My problem with a lot of the DHA papers is that they tend to be speculative, use mostly correlational evidence, and apply circular reasoning.

For example: What makes DHA beneficial? ..."It has a unique structure, and we selectively store it, so its structure is perfect for us and is be beneficial." Well, why does c elegans store EPA and not DHA? ..."EPA's structure and function is better for c elegans, which is clear because they selectively store it."

I'm never quite satisfied with the conclusions. Supplement results are mixed along with overexpression studies. Removing it entirely via knockout often comes with some negative consequences, but I'm not sure how much that tells us.