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  1. Dr. Alan Green just opened a medical practice focused on rapamycin. His site is probably the first on its own. https://www.rapamycintherapy.com/
  2. This all started when I found an article about a method that increased the viability of sperm stem cells by culture them in a low oxygen, high glucose medium. This promoted the stem cells to use glycolysis as their energy source instead of mitochondrial oxidative phosphorylation (OXPHOS) for their energy needs. The article went on to explain that glycolysis produces a lot less ROS than OXYPHO and it prevents a lot of DNA damage. So i went on to look if this was just a specific case but it appears that Haematopoietic SCs, Embryonic SCs, pluripotent SCs, and most adult stem-cells, use glycolysis as their main way to create energy. I couldn't figure out if its because of a predominant hypoxic environment or if this is a trait of stem-cells. When stem-cells go on to differentiate, they go through a metabolic reprogramming and start using the mitonchondrion (OXPHOS). [2] CR is known to cause a shift away from Glycolysis to OXPHOS, so its not clear how this would be beneficial. Could be part of a hormesis response. Its likely that stem-cells do not go through this metabolic shift, only differentiated cells. I tried look for rapamycin and mTOR inihibition and how it effects stem-cells, and it appears some mTOR activation is beneficial in ESCs: But lower mTOR activation is better on the long-run as it prevents stem-cell exhaustion. I was thinking of doing a 1-month intake of rapamycin while on CR to further suppress mTOR activity. I don't know now if this is a good idea. We know that whatever happens here and the shift in metabolism to OXPHOS in cells during starvation will lead to a healthier life, but i can't reconcile this stuff as it appears glycolysis is a lot better to avoid DNA damage as you can see from the sperm cells that reached 40% viability from 5% when using OXPHOS. [1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3575699/ [2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4095859/
  3. All, At the recent CR conference, Dr Richard Miller from the University of Michigan gave a great talk on the Interventions Testing Program, a NIA-sponsored, rigorous, multi-center effort to investigate the potential of various drugs, supplements and nutriceuticals to extend lifespan in mice. Dr. Miller shared with us some results which have now been published. Here is a good summary of the latest results. It looks like the most promising interventions were metformin+rapamycin, acarbose, and 17-α-estradiol (in males only). I'm not planning on running out to take any of these, but I find acarbose interesting. It works by blocking the breakdown of carbohydrates, and suppressing hunger - in many ways like eating extra dietary fiber (a controversial topic itself) as discussed here on the Dietary Fiber - Health Promoter or Anti-CR Hunger-Suppressor? thread. --Dean
  4. All: Rapamycin is by far the best-supported drug (or "drug-type" supplement) potential anti-aging therapy, as most or all of you should know; it is thought to work by inhibiting mTOR, thereby inhibiting protein synthesis and boosting autophagy. Its interactions with the mechanisms of CR in mammals are complex but seemingly not very overlapping, as discussed eg here , here, and most cogently in this context here, suggesting the tantalizing possibility that rapamycin might not be a "CR mimetic" as once thought, but engage a different anti-aging pathway that might be additive to or synergistic with CR mimetics or CR itself. The biggest heretofore-identified potential roadblocks to the use of rapamycin or some modified mTOR inhibitor as anti-aging interventions in humans are diabetic-like side-effects and immune suppression seen in patients given rapamycin for existing indications (mostly, exactly to suppress the immune system, as especially after transplantation). Now, a new study reports that rapamycin can actually enhance the immunological response to vaccination in aging humans: The most immediate caveat: simply showing the mounting of a better antibody response after short-term use of the drug is not the same thing as actually showing more effective defense against and clearance of the target pathogen after long-term use of the drug to slow the aging process. In (2), The latter study has been discussed in this thread on the CR Society Listserv; I should have, but haven't yet, responded to some of Tom's objections to the latter. References 1. Joan B. Mannick, Giuseppe Del Giudice, Maria Lattanzi, Nicholas M. Valiante, Jens Praestgaard, Baisong Huang, Michael A. Lonetto, Holden T. Maecker, John Kovarik, Simon Carson, David J. Glass, and Lloyd B. Klickstein mTOR inhibition improves immune function in the elderly Sci Transl Med 24 December 2014: Vol. 6, Issue 268, p. 268ra179 Sci. Transl. Med. DOI: 10.1126/scitranslmed.3009892 [No PMID yet] 2. Lifespan-extending caloric restriction or mTOR inhibition impair adaptive immunity of old mice by distinct mechanisms. Goldberg EL, Romero-Aleshire MJ, Renkema KR, Ventevogel MS, Chew WM, Uhrlaub JL, Smithey MJ, Limesand KH, Sempowski GD, Brooks HL, Nikolich-Žugich J. Aging Cell. 2014 Nov 26. doi: 10.1111/acel.12280. [Epub ahead of print] PMID:25424641[PubMed - as supplied by publisher] Free Article