Can a Reasonable Argument be Made for Variations in Human Longevity to be Significantly Driven by DNA Repair?

As I’m sure you are all aware, we humans do not exhibit a uniform pace of aging. Setting aside mortality caused by anything other than aging, the vast majority of recorded life spans at the present time fall within a range of three decades, 65-95. A comparatively tiny number of exceptional outliers age to death at younger or older ages. Some of this variation can be attributed to secondary aging, which is to say the way in which circumstances and lifestyle choices interact with the biology of aging. Visceral fat tissue and smoking cause greater chronic inflammation, accelerating all of the common age-related conditions, for example. On the other hand, calorie restriction modestly slows most aspects of aging. The rest is due to differences in primary aging, meaning intrinsic differences in genetics that lead to differences in the operation of cellular mechanisms that occur more independently of lifestyle and environment. Some human mutants have lower blood cholesterol, and thus slower onset of atherosclerosis, for example.

secondary agingVisceral fat tissuesmokingchronic inflammationcalorie restrictionprimary agingatherosclerosis

Most accelerated aging conditions take the form of a mutational malfunction in DNA repair – cells become damaged and dysfunctional much more rapidly than is the case in normal individuals.

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