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Is it possible that excess NMN supplementation could result in hair loss due to upregulation of SASPs

I have a question, while attempting to connect some dots (I am way over my head) Is it possible that excess NMN supplementation could result in hair loss due to upregulation of SASPs My question arose after reading https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6448588/ Here is a short version https://www.tandfonline.com/doi/full/10.1080/23723556.2019.1605819 I am asking this question after bumping into this article https://www.nature.com/articles/s43587-021-00103-w … on the understanding that Stem Cell exhaustion can occur in response to SASP exposure. Pushing the envelope – would sudden (an otherwise unexplained) hair loss possibly serve as a metric for overdoing MNM/NR supplementation? Thank you again for your patience and for your indulgence.

Yamanaka Factors and Making Old Cells Young - Off-label use of doxycycline or other rejuvenants?

The latest podcast on Everything Testosterone was fantastic! Bravo! ... to the team... I offer for your considerations an intriguing (to me) paper quick outtake "Perhaps the most effective strategies so far have been those that focus on the removal of senescent cells with ‘senolytic’ drugs [2,3]. In some ways, however, we feel this is too focused on the symptoms of aging whereas perhaps the most promising strategy for the future would be to focus on the causes of aging and its corollary, the rejuvenative capacity of stem cells." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8070588/ Amen! ... explaining my applause for Peter's interviews with David Sinclair. This paper cites another which I find VERY exciting! https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7093390/ Quick Outtake of second embedded paper "The process of nuclear reprogramming to induced pluripotent stem cells (iPSCs) is characterized, upon completion, by a profound resetting of the epigenetic landscape of cells of origin, resulting in reversion of both cellular identity and age to an embryonic-like state1–4. Notably, if the expression of the reprogramming factors is only transiently applied and then stopped (before the so-called Point of No Return, PNR)5, the cells return to the initiating somatic cell state. These observations suggest that, if applied for a short enough time, the expression of reprogramming factors fails to erase the epigenetic signature defining cell identity; however, it remains unknown whether any substantial and measurable reprogramming of cellular age can be achieved before the PNR" Peter has discussed, on several occasions, and in detail the topic of off-label use of Rapamycin as a senolytic (most recently with Mat Kaemberlein) I was wondering if Peter would care to broach the subject of off-label use of Doxyclycin and/or other presumed "rejuvenants"

Insulin resistance and Parkinson’s

Hello. I am a Practicing physician with Parkinson’s. I understand you’re getting a lot of questions about GLP1 agonists and insulin resistance. You may be interested to know that ( as far as I know) the only phase 3 trial for a disease modifying PD medication is for Exenatide in the UK and a ( phase 2) study for lixisenatide here in the US. Can this topic be integrated into an AMA or a stand alone podcast. Dr Michael Tagliati at Cedar Sinai is a great interview and is heading the US study. Thank you so much.

Prolong fast - Testosterone

How does prolong fast (3-5 days) influences the testosterone levels in male, the same question for time restricting eating

Rapamycin starting age

In your prior episodes, you mentioned that you would not advise starting rapamycin before age 25 or so. If you could go back to your 20s, armed with your current rapamycin-related knowledgebase, at what age would you start pulsing rapamycin? Also, given that mTOR inhibition blunts/decelerates attempts to grow muscle/heal from injuries, is there anything you do to offset this effect?