On September 28th, I decided to stop rapamycin, ending almost 5 years of experimentation with this molecule for its longevity potential. I have tested various rapamycin protocols including weekly (5, 6, and 10 mg dose schedules), biweekly (13 mg) and alternating weekly (6/13mg) to optimize rejuvenation and limit side effects. Despite the immense potential from pre-clinical trials, my team and I came to the conclusion that the benefits of lifelong dosing of Rapamycin do not justify the hefty side-effects (intermittent skin/soft tissue infections, lipid abnormalities, glucose elevations, and increased resting heart rate). With no other underlying causes identified, we suspected Rapamycin, and since dosage adjustments had no effect, we decided to discontinue it entirely. Preclinical and clinical research has indicated that prolonged rapamycin use can disrupt lipid metabolism and profiles [1], as well as induce insulin and glucose intolerance [2] as well as pancreatic Beta-cells toxicity [3]. Despite anecdotal evidence of rapamycin slowing down tumor growth, its effect in inhibiting natural killer cells [4]  do raise concern for anti-cancer immune surveillance and cancer risk in the longer run. Additionally, on October 27th, a new pre-print [5] indicated that Rapamycin was one of a handful of supposed longevity interventions to cause an increase/acceleration of aging in humans across 16 epigenetic aging clocks. This type of evaluation is the first of its kind, as most longevity interventions up to date have been tested against one or two aging clocks, leading to invisible biases and potential intended “cherry picking” of favorable clocks for the tested interventions. Longevity research around these experimental compounds is constantly evolving, necessitating ongoing, close observation of the research and my biomarkers which my team and I do constantly. Sources: [1] pubmed.ncbi.nlm.nih.gov/1217… [2]pmc.ncbi.nlm.nih.gov/article…. [3]diabetesjournals.org/diabete… [4]pmc.ncbi.nlm.nih.gov/article….