On 2016 Oct 14, Attila Csordas commented:

Authors finish the article with the following suggestion: "To further extend human lifespan beyond the limits set by these longevity-assurance systems would require interventions beyond improving health span, some of which are currently under investigation (15). Although there is no scientific reason why such efforts could not be successful, the possibility is essentially constrained by the myriad of genetic variants that collectively determine species-specific lifespan(16).”

Authors seem to be suggesting that all the current experimental efforts won’t be enough to increase maximum life span over a biological limit that has been reached already and overcome or counterbalance the collective effect of those “myriad of genetic variants”.

In fact, there is at least one experimental result that leaves this question definitely open, and this is the scenario of clearing-out senescent cells from the aging organism, see mouse studies summarised in http://www.nature.com/nature/journal/v530/n7589/full/nature16932.html where concerning maximum lifespan the results are mixed: “Maximum lifespan was significantly increased for mixed AP-treated males and females combined (P = 0.0295), but not for females and males individually. Maximum lifespan was not extended for C57BL/6 AP-treated animals, either combined or separately”. Indeed this is the approach taken by biotech companies like http://unitybiotechnology.com/ amongst others.

I wonder how a study, also appearing in Nature, earlier this year, February, 2016, have slipped through the attention of the authors?

The assumption of my argument is that mouse studies can be relevant for human trials. After all mice have those “myriad of genetic variants” too.

On 2016 Oct 14, Attila Csordas commented:

Authors finish the article with the following suggestion: "To further extend human lifespan beyond the limits set by these longevity-assurance systems would require interventions beyond improving health span, some of which are currently under investigation (15). Although there is no scientific reason why such efforts could not be successful, the possibility is essentially constrained by the myriad of genetic variants that collectively determine species-specific lifespan(16).”

Authors seem to be suggesting that all the current experimental efforts won’t be enough to increase maximum life span over a biological limit that has been reached already and overcome or counterbalance the collective effect of those “myriad of genetic variants”.

In fact, there is at least one experimental result that leaves this question definitely open, and this is the scenario of clearing-out senescent cells from the aging organism, see mouse studies summarised in http://www.nature.com/nature/journal/v530/n7589/full/nature16932.html where concerning maximum lifespan the results are mixed: “Maximum lifespan was significantly increased for mixed AP-treated males and females combined (P = 0.0295), but not for females and males individually. Maximum lifespan was not extended for C57BL/6 AP-treated animals, either combined or separately”. Indeed this is the approach taken by biotech companies like http://unitybiotechnology.com/ amongst others.

I wonder how a study, also appearing in Nature, earlier this year, February, 2016, have slipped through the attention of the authors?

The assumption of my argument is that mouse studies can be relevant for human trials. After all mice have those “myriad of genetic variants” too.