Abstract
Healthy life span is rapidly increasing and human aging seems to be postponed. As recently exclaimed in Nature, these findings are so perplexing that they can be dubbed the 'longevity riddle'. To explain current increase in longevity, I discuss that certain genetic variants such as hyper-active mTOR (mTarget of Rapamycin) may increase survival early in life at the expense of accelerated aging. In other words, robustness and fast aging may be associated and slow-aging individuals died prematurely in the past. Therefore, until recently, mostly fast-aging individuals managed to survive into old age. The progress of civilization (especially 60 years ago) allowed slow-aging individuals to survive until old age, emerging as healthy centenarians now. I discuss why slow aging is manifested as postponed (healthy) aging, why the rate of deterioration is independent from aging and also entertain hypothetical use of rapamycin in different eras as well as the future of human longevity.
Highlights
Healthy life span is rapidly increasing and human aging seems to be postponed
Life expectancy was less than 16 years and 75% of people born in London in 1662 died before they reached the age of 26 (Graunt’s life table)
“Taken together, these findings are so perplexing that they can be dubbed the ‘longevity riddle’: why do the evolutionary forces that shaped human aging provide a license to alter the level of health but not the rate of debilitation?” [3]
Summary
Death from aging is technically death from age-related diseases, which are manifestations of advanced aging [1]. The progress of civilization eliminated many causes of death that killed young people in the past The mTOR intracellular signaling pathway is activated by numerous signals including glucose, amino acids, fat acids and other nutrients, insulin and some other hormones, growth factors and cytokines [9,10,11] It increases cellular functions and cellular mass growth [12]. Cellular aging can be defined as over-activation of signaling pathways (such as mTOR) with secondary signal resistance [14] In turn this slowly leads to diseases of aging (hypertension, atherosclerosis, macular degeneration, insulin resistance, obesity, neurodegeneration, cancer, osteoporosis, organ hypertrophy). TORdependent activation of osteoclasts causes bone resorption (osteoporosis) [15] These aging processes are relatively silent (subclinical, no obvious deterioration) until aging culminates in “catastrophes” – organ damage. Deterioration can be quick, leading to death in a mater of hours or years or decades, depending on the level of medical care
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
