Genetics, phenotype, Aging "Style," rapamycin

A thought experiment: there is a spectrum of aging styles, consistent with the concept of antagonistic pleiotrophy. On this spectrum, one end is: higher growth, may-be more mesomorphic muscular body type, high fecundity, later menopause (?), denser bones, very robust in early life, higher rates of cancer and other disease of inflammation or overgrowth in late life. On the other end: smaller body, lower BMI, smaller muscles, lower fecundity, tendency to earlier menopause, osteoporosis and frailty, possibly longer life length but with high tendency to neurodegeneration. This is the more “catabolic” style. Is this also consistent with the Indian dialectic between “hot” and “cold”?

Reading about Alzheimers and also listening to Nir Barzilai I have learned that I am highly aligned with the catabolic style and so likely to have longer life and develop Alzheimers. (like mother and grandmother).Early menopause, osteoporosis, high HDL, low TRIGS, low BMI, BP and pulse-- all line up perfectly with the high Alzheimers cohort and the long lived cohorts that I have read about.

So while I am trying to optimize bones, heart, anti cancer, it is clearly Alzheimers that is at the top of my ladder of worries and the area that I am most wanting to take action to prevent. Considering GHK-CU, tadalafil and already taking many supplements.

So, since Rapamycin seems to push toward the catabolic, acting as an mTOR switch and CR restriction mimetic, I wonder if that is the right strategy for me personally. I have the pills here but have not yet started taking.

Would appreciate insights on whether this “spectrum” from an anabolic to catabolic overall phenotype makes sense as a tool for guiding one’s personal overall longevity strategy and decisions on what interventions to puruse. With emphasis on Rapamycin, yea or nay, specifically.

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While I’m low risk for neuro issues like dementia, it is one of my concerns. With your profile I’d be doing what you are doing, added focus on this aging factor.

I do have some focus on dementia.

  1. Rapa every other week
  2. low dose selegline daily
  3. microbiome ongoing adventure
  4. various other interventions that may or may not be of benefit in this area but are (hopefully) beneficial for health span.

One person I chat with occasionally is Frank Bernier
https://www.alzforum.org/member-directory/frank-bernier-0
https://www.linkedin.com/in/francois-bernier-phd/

My main reason for focus on dementia is that I’ve been in over 300 medical facilites, over 200 of those were SNF’s (skilled nursing facilities) when I was in the wound care business. I’ve seen so many people stricken with dementia and housed like cattle that I have a pact with my wife that she won’t let me go there and will help me take advantage of the MAID program here in Canada.

My hope is that it never comes to that :slight_smile:

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Thank you so much for the links, and the info about what you are doing.

Like you have witnessed first hand (my mother). I have my exit pills sequestered away. But have some optimism that with what I have learned and new information coming as we boomers age, I can avoid this awful fate.

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One of the best things about this group is learning something new.

I use GHK-Cu topically in a skin care product I make for friends and family, and I’ve been aware of other uses both topically and subcutaneous injections (2 different versions of GHK-Cu are used) but never knew about the neuro protective potential.

It is an amazing peptide! one of over 7,000 that our body makes.

I’m going to have to get some of the injectable quality GHK-Cu as that would be the only version that you should use in a nasal spray. Not the cosmetic quality. Since the nose has a near direct path to the brain, one would want to use the purest form of GHK-Cu in a nasal spray.

I have made my own nasal sprays in the past using bromelain and NAC. That was like turning on a light. It’s tricky to make though and without care it will damage your nasal passages, don’t ask…

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This study is behind a pay wall, hoping someone here might have access and be able to get it :slight_smile:

What I’m interested in is the word optimization

The Optimization and Validation of Intranasal GHK-Cu Peptide Drug Delivery in Cognitive Impairment Pathology

https://digital.lib.washington.edu/researchworks/handle/1773/50223

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Many of us here are concerned about dementia. I think your thoughts (anabolic vs catabolic) are interesting and worth thinking about. I’m not sure rapamycin fits into one model or the other though. Many on this group take rapa primarily to prevent dementia, most commonly alzheimers. The proposed mechanism of alzheimers being inflammatory breakdown of the blood brain barrier and rapa proposed to subvert this process through various pathways. Some of this is nicely substantiated in animal models of Alzheimers though most animal models of this disease are poor approximations of the human condition. There are clinical trials underway to study the affect of rapamycin on alzheimers development in humans.

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