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  1. As I've indicated many times in the past, one should ignore studies on interventions in aging in nematode worms (C. elegans), fruitflies (Drosophila), and all other non-mammalian species: they age and anti-age too differently to be given any credence until at least translated into mice. One of the most remarkable broad categories of such findings is the remarkable number of "hormetic" interventions reported to increase maximum LS in C. elegans, despite the fact that no such interventions with the pseudo-exception of CR have done so in mice. A remarkable new study turned up in a professional-oriented science news outlet by Al Pater finally gets to the bottom of this: it's not just (as I had assumed) an interspecies difference, but a freakin' experimental artifact! Apparently, researchers performing LS studies in C. elegans routinely dose the animals with low levels of 5-fluorodeoxyuridine (FUdR), a drug usually used in chemotherapy as an alternative to 5-fluorouracil, "a thymidylate synthase (TS) inhibitor. Interrupting the action of this enzyme blocks synthesis of the pyrimidine thymidine, which is a nucleoside required for DNA replication." By interfering with cells' ability to replicate their DNA, these drugs drugs work to shut down cancer by preventing them from replicating — and ferocious, unregulated cell replication is the very definition of cancer. Of course, many kinds of normal cells have occasional need to replicate too, which is why you get the awful side-effects of these drugs. Well, apparently (and I assume that my eyeballs must at least have passed over this info on a few occasions, but it never registered — I probably figured "those worm guys know what they're doing"), FUdR is also routinely used at low dose to sterilize the worms and prevent them from laying eggs, both because the new "born" C. elegans mess up their worm counts when they later conduct survival studies, and because reproduction itself reduces the lifespan of C. elegans. This has been thought harmless because FUdR That may be the biggest understatement to appear in a scientific abstract since Watson and Crick's "It has not escaped our notice that the specific pairing we have postulated immediately suggests a possible copying mechanism for the genetic material" in their landmark paper proposing the double helical structure of DNA as the structural basis of genetic inheritance (Nature 171: 737-738 (1953)). Even studies in mice don't always translate directly to humans -- look at all the failed cancer drugs that cure the disease in mice -- but they're a much better start. Now we know one more massive reason why. Reference 1: Anderson EN, Corkins ME, Li JC, Singh K, Parsons S, Tucey TM, Sorkaç A, Huang H, Dimitriadi M, Sinclair DA, Hart AC. C. elegans lifespan extension by osmotic stress requires FUdR, base excision repair, FOXO, and sirtuins. Mech Ageing Dev. 2016 Mar;154:30-42. doi: 10.1016/j.mad.2016.01.004. Epub 2016 Feb 22. PubMed PMID: 26854551.
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