As predicted by hyperfunction theory, rapamycin treatment during development extends lifespan

to reverse damage. It might prevent diabetes and obesity but not diabetic gangrene and stroke. It might prevent macular degeneration but will unlikely cure blindness. Rapamycin will not rapamycin most as anti-aging drug to slow down senescence and to prevent diseases” to to human studies in demonstrated that rapamycin extends in Hyperfunction theory predicts that rapamycin can slow down aging by two complementary mechanisms:

To maximally extend health and lifespan in humans, it was suggested that the treatment with rapamycin should be started at a young age: "As an anti-aging drug, rapamycin will prevent diseases rather than cure complications of diseases. Rapamycin will prevent [organ] damage but not to reverse damage. It might prevent diabetes and obesity but not diabetic gangrene and stroke. It might prevent macular degeneration but will unlikely cure blindness. Rapamycin will not repair broken bones but might prevent osteoporosis… rapamycin will be most useful as [an] anti-aging drug to slow down senescence and to prevent diseases" [1]. The hyperfunction theory explains why a large-body correlates with longevity between species (for example, elephants live longer than mice, which live longer than flies), but in contrast, within each species, it is a small body size that is associated with longevity [40]. Lifelong small body size after a brief treatment is consistent with reprogramming of the growth program.
Notably, life extension by rapamycin was mostly observed in male mice [2]. This is consistent with the finding that mTOR is overactivated in young male mice compared with young female mice, thus explaining robustness of males at young age and their shorter lifespan [41].
Supporting the notion of rapamycin-induced reprogramming, previous studies found that (a) even transient treatment with rapamycin can extend lifespan [27,36,39] (b) a single rapamycin injection can lower body weight set point in the long run [42] and (c) rapamycin can affect the mTOR pathway activity long term by preventing obesity [43,44].

Further suggestions
To further study rapamycin-induced reprogramming of aging, pregnant mice should be treated with a single subcutaneous injection of rapamycin and the lifespan of their offspring should be measured. Prenatal (before birth) rapamycin treatment on early postnatal development has been studied [45][46][47]. For example, prenatally rapamycin-treated neonates are small, and body weight and left ventricular mass remain reduced in adulthood [47]. However, lifespan was not measured. (Note: rapamycin pre-treatment increased mortality immediately after the birth [47] because mTOR is essential early in life. Early-life death is not agingdriven and should be excluded from the age-related mortality curve).
At what age may rapamycin treatment be started in order to maximally extend human lifespan? Based on murine data, treatment with rapamycin can be started at a very old age. Still, in theory, the maximal effect potentially may be achieved before age-related diseases and pre-diseases become apparent in humans [1]. However, it should not be started too early because mTOR is essential for growth and early life fitness. In my opinion, rapamycin treatment (for anti-aging purposes) may only be started when a young adult can make informed decisions and should not be allowed before the age of 21. Doctors should consider that rapamycin may negatively affect reproduction, albeit reversibly. I believe that the initial dose should be very low and gradually increase with older age, when full individual doses are achieved. An anti-aging dose/ schedule is a maximum dose that do not yet cause side effects in a particular person [48]. Self-treatment is unacceptable and doses are highly individual [48,49].

Disclaimer
This commentary is for information purposes, not medical advice.

CONFLICTS OF INTEREST
The author declares no conflicts of interest.