Fight Aging!

Here's a little slice of recent scientific history for today via GRG mailing list. The capabilities of biotechnology continue to improve, and scientists are mapping and understanding ever more of the complex web of human biochemistry and genetics. As this process continues, I think we'll see many more proposals along the lines of the conclusion to this PDF-format scientific paper from 2004 on angiotensin I-converting enzyme (ACE). The authors connected this particular small component of human biochemistry to a range of age-related conditions and concluded:

Genomic epidemiologic data, increasingly supported by clinical outcomes results, strongly suggest that overactivity of angiotensin I-converting enzyme (ACE) may underlie most age-related diseases. Angiotensin II, the main product of ACE, is a pleiotropic hormone, capable of serving as a neurotransmitter, growth factor, angiogenesis factor, vasoconstrictor, pro-thrombotic agent, and cytokine. So it is perhaps not surprising that the ACE DID genotype is associated with several major psychiatric diseases, most cancers except prostate cancer (where the DID genotype is actually protective), most cardiovascular diseases, most autoimmune diseases, and even infectious diseases like tuberculosis and HIV.

...

For example, calorie restriction prolongs life-span in a number of species. With less fuel consumption, mitochondrial electron transport and production of ROS are decreased. sACE overactivity as a cause of aging is entirely consistent with this model, since angiotensin II stimulates mitochondrial electron transport, oxygen consumption, and production of ROS. Chronic angiotensin II signaling leads to mitochondrial hypertrophy and proliferation. Eventually, angiotensin II leads to mitochondrial dysfunction, with increased uncoupling of electron transport from A TP synthesis, and increased production of ROS. Inhibition of ACE in old animals restores mitochondrial function.

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In summary, population morbidity and mortality should be significantly reduced, and longevity enhanced, by widespread use of an ACE inhibitor or ARB. The only caveat is that white men taking an ACE inhibitor or ARB will need to check their PSA at least once a year.

The authors may have been overreaching, although the mitochondrial connection is especially interesting in light of what we presently know, but I think we'll be seeing more of this sort of review and proposal in the future. Understanding a system implies understanding how to fix and improve that system - and an increased understanding is certainly one of the things we need in the fight to cure aging.

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