JulieGee wrote:Stavia, per these results, I agree with your stance on using the LEAST amount of dietary fat necessary to obtain ketosis. That philosophy has worked well for me in the past. I strongly believe there is much evidence to support ketosis for the neuroprotection element, but applying exercise and CR (which I've consistently done) reduces the need for dietary fat and may be the safest path for us.
In conclusion, despite the relatively small size of this study, genetic influences on cognitive scores in response to induced ketosis were noted. The main modulator of induced ketosis appears to be the carriage status of APOE4. It may not be a coincidence that APOE4 is also the major genetic risk factor for late onset AD. The failure of APOE4 carriers to respond to ketosis may indicate a more insidious metabolic problem. APOE4 carriers may be overly reliant on glucose and hence, over a lifetime, cerebral neurons are deprived of the metabolic advantages conferred by ketone body metabolism and this may be crucial to etiology of AD . Importantly, this type of pharmacogenomic profiling not only offers insights into the disease process, it also allows targeting of patients who are most likely to respond to therapy. In this way, better and more effective therapeutics can be developed.
GenePoole0304 wrote:All the mono fats he suggests can shift ones omega3 index unfavorably to more inflammatory status
Welcomeaboard wrote:I may have said this as I know I have thought about it. That is that Gundry's idea of eating 1 meal a day in winter seems to be his idea of trying to live like ancient man before he knew how not to try and starve himself to death. Sometime ideas of living like ancient man is absurd as I am sure if you asked ancient man if he enjoyed and welcomed the days of stress that starvation brought on he would probably just kill you and throw you on the grill and say nope thank god that meal came so easily. It may sound bad but they had Pacific Islanders practicing canabalism into the 1900's and they pretty much lived that ancient man life style as well.
As well as one of the pharaoh's of Egypt about 4500 years ago give or take a few hundred lived to 92 and you can bet your damn ass he was not on the ancient man starvation diet plan to reach 92. Or eating one meal a day because it was good for him.
There have been people documented living to their 70's to 100 years of age for 400 hundred years or more and I have not read where any of them said they chose to starve themselves so they could live long and prosper.
Now, in his defense the diet plan for certain people with bad genetics leading to cvd issues probably need some type of restricted diet to help them live past 50, including heart operations as required.
In summary, H1R and H2R signaling may play important roles in glucose and lipid metabolism, which seems to be mediated through both central and peripheral pathways. H1R signaling would be involved in central nervous system and pancreatic tissue to regulate glucose metabolism, while H2R signaling would be mainly related to peripheral action in the liver and skeletal muscle via adiponectin system to regulation both lipid and glucose metabolisms.
These results indicate that histamine could have a certain effect on lipid metabolism in liver cells... Furthermore, HDC expression in the pancreatic islet cells (73) also suggests a close relationship between histamine and energy metabolism, along with insulin and glucagon. The system effects of histamine on energy or lipid metabolism, which would modify atherogenesis, are still controversial.
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