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Here, using biological rhythms to assess the effects of exogenous S -adenosylmethionine, we reveal that excess S -adenosylmethionine disrupts rhythms and, rather than promoting methylation, is catabolized to adenine and methylthioadenosine, toxic methylation inhibitors

While the high upfront cost of these drugs is a significant barrier, they could represent a significant source of savings in the later years from lower rates of obesity, cardiovascular, and kidney disease

This phenomenon is central to its study in models of tissue aging and repair

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