Yes: different phenotypes. I am convinced of this, that we are all on a spectrum from anabolic to catabolic. Just as there are body types: mesomorph, endomorph, ectomorph, there are genetic profiles that are high growth or low growth. Synthesizing everything I have read, a drug like rapamycin that reduces mTOR, thus reducing protein synthesis and growth, is a good fit for someone with an anabolic phenotype, who could benefit from a push toward slower growth. I myself am the catabolic type --slow growth, small stature, early menopause.
And, to your point about insulin: I am convinced that my low insulin levels are a result of a mutation in the genes that control production of glucokinase. I am quite insulin sensitive: I just don’t produce very much insulin. This is not classic diabetes, but some sort of rare variant, caused solely by genetics (and can be confirmed through genetic testing for glucokinase mody, though docs and insurance won’t do the testing because there is no treatment required. GKM manfests simply as a pre-diabetic glucose level that does not progress.
That is why I lit up when I read about intranasal insulin as a possible therapy for preventing or forestalling AD. It makes perfect sense: too little endogenous insulin available to the brain, but the IN insulin goes right into the brain via the olfactory and trigeminal nerves, and does not get into the body at all. I wrote to a leading practitioner/clinician expert on insulin and type 1 DM, laid this out, and asked for his thoughts on IN insulin. He responded – keep using it. He did caution that I should have an effective delivery instrument, and I suspect that the little Snoot bottles are far from efficient but that’s all I can find . . .
Also, my conviction that I am this catabolic type made me decide not to take rapa – I do not need a push toward reducing mTOR, reducing growth.
I feel like a spoiler in this community of avid rapa users. I do believe it is a fantastic intervention, and I gave my stash to my son who seems to be a more anabolic type, very much like his father. But I believe that we need a model for prescribing / taking drugs that takes this anabolic/catabolic paradigm into consideration. One size does not fit all.
I wonder what is the opposite of rapamycin that I should be taking. My tiny mother, before she developed dementia, continually craved red meat, and she consumed massive quantities, dripping blood. (no fruits or vegetables unfortunately). I don’t want to eat red meat but have started taking leucine.
So yes, there are these types – high growth, higher cancer, etc, and low growth – long life, lower cancer, higher Alzheimers. I believe that some day all therapies will be prescribed based not merely on the symptoms a patient presents, but on an assessment of phenotype.
I am so grateful to this forum and all the information out there that enabled me to figure this out.
