The Oxford study is big and I am sure well done, but it boils down to what I hope we all knew—human health and healthspan are both mainly about non-genetic fact

The Oxford study is big and I am sure well done, but it boils down to what I hope we all knew—human health and healthspan are both mainly about non-genetic factors. Avoid pestilence, famines, wars, and crazy leaders; eat right, exercise, do not smoke. Have a good social network at all ages. Stay active. The estimate of the magnitude of genetics effects in this study is “silly low”, roughly by an order of magnitude. (Notice the hedging in the PR piece.) The heritability of a trait is a function of environmental stability and quality. In a stable environment—Sweden or Iceland from 1900 to 2000—-heritability of lifespan is still low; about 15 to 25%. But that is way different than 2%. Claiming 2% is more of a socio-political statement: to focus on what we can influence ourselves. Re telomere length. I wish it were that simple. Telomere length is not the main cause of aging in mammals. Read the title if the paper that you cite: “correlates with”! My presbyopia correlates beautifully with my age but did not cause me to age. I would not even rank telomere length among the top ten (the putative “Hallmarks of Aging”). But it is a great story which makes good headline fodder. I think the comment about dogs is really just highlighting the wide range of differences in maximum lifespan among species. This indicates that DNA variants indirectly or directly modulate the baseline tempo of aging between a short lived mammal (less than a year) to species like us that live 100 years. There is really no doubt about this. And of course DNA variants do the same thing but over a much more modest range within a sexually reproducing species. Some mice make it to 500 days, some make it to 1000 days in exactly the same environment. Reduce environmental variance sufficiently and heritability begins to get up to 40%. Out in the wild here almost no mouse dies of natural cause heritability should approach zero. Aging is highly polygenic. There will be 100s of DNA variants and de novo mutations contributing to aging per se and to disease risks. And many processes.