The self-experimentation rumor mill has it that presently available senolytic pharmaceuticals, repurposed chemotherapeutics that can selectively destroy some fraction of senescent cells, can show results for inflammatory conditions in elderly individuals. Equally, they don’t appear to produce evident benefits in basically healthy 40-somethings. While senescent cells are indeed a source of chronic inflammation, one should never act on whispers: wait until data from the present or near future clinical studies is published and ratified. We can certainly debate and hypothesize, however, where anecdotes overlap with existing animal data and supporting evidence from other lines of research.
My thinking runs much as follows: the immune system is responsible for destroying cancerous cells and those senescent cells that fail to self-destruct. Immune cells are very efficient when it comes to this task, and thus the risk posed by both of these classes of harmful cell remains low for much of life. This is the case until immune function has declined significantly with age; one can look at the models that correlate cancer risk with atrophy of the thymus, and therefore reduction in T cell generation, for example. It fits well. Peak cancer risk
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