Fight Aging!

Laboratory mice are little cancer factories in comparison to humans, and so any mechanism that reduces cancer risk is going to extend life expectancy in a study group. That's one of many reasons why it is a good idea to pay more attention to research that shows a gain in maximum life extension rather than just mean life span extension. There is some debate over whether reducing cancer risk counts as an anti-aging therapy: the argument in favor suggests that since cancer is an age-related condition, risk rising to a plateau with advancing age, and since aging can be defined as increasing risk of mortality, of course reducing incidence of cancer counts as an anti-aging treatment. On the other side of the fence, there is the tendency of the research community to carve away named diseases from aging as new knowledge arises, and talk about treating those diseases rather than treating aging. See, for example, sarcopenia as the comparatively new designation for age-related loss of muscle mass and strength.

This seems to come down to how well researchers understand a given method of extending life in laboratory animals. No idea how it works, and the older individuals in the study are looking healthier? Then suggest that it is a slowing of aging. If, on the other hand, the precise mechanisms of action can be identified and have to do with cancer, then there is a reluctance to talk about the pace of aging. In this we might see some of the consequences of the remaining divisions and uncertainties over what exactly aging is, how it is caused, and how it progresses at the level of cells, cellular machinery, and biological systems.

An example of this sort of debate showed up recently in connection to rapamycin. Reputable researchers have run sizable studies on mouse life span under treatment with rapamycin: some conclude that rapamycin definitely slows aging, while others conclude that the effect on life span is due to reduced cancer risk, and yet more argue that there is no real difference in this case between life extension and reduced cancer risk as it all stems from the same underlying collection of mechanisms.

I can't say as I have a strong opinion on this topic insofar as it touches on rapamycin: research into drugs to modestly slow aging isn't the future of human longevity. Rather it is a sidebar to learning more about the operation of mammalian biology and how it adapts to various circumstances, such as calorie restriction and aging. But on this subject, I noticed a recent paper on a less well studied longevity-enhancing genetic alteration in which the authors also postulate that the mechanism is reduced cancer risk:

Reduced Malignancy as a Mechanism for Longevity in Mice with Adenylyl Cyclase Type 5 (AC5) Disruption

Disruption of adenylyl cyclase type 5 (AC5) knockout (KO) is a novel model for longevity. Since malignancy is a major cause of death and reduced lifespan in mice, the goal of this investigation was to examine the role of AC5KO in protecting against cancer. There have been numerous discoveries in genetically engineered mice over the past several decades, but few have been translated to the bedside. One major reason is that it is difficult to alter a gene in patients, but rather a pharmacological approach is more appropriate.

The current investigation employs a parallel construction to examine the extent to which inhibiting adenylyl cyclase type 5 (AC5), either in a genetic knockout (KO) or by a specific pharmacological inhibitor protects against cancer. This study is unique, not only because a combined genetic and pharmacological approach is rare, but also there are no prior studies on the extent to which AC5 affects cancer.

We found that AC5KO delayed age-related tumor incidence significantly, as well as protecting against mammary tumor development, [which] can explain why AC5KO is a model of longevity. In addition, an FDA approved anti-viral agent, adenine 9-β-D-arabinofuranoside (Vidarabine or AraAde), which specifically inhibits AC5, reduces [lung and melanoma] tumor growth. Thus, inhibition of AC5 is a previously unreported mechanism for prevention of cancers associated with aging, and which can be targeted by an available pharmacologic inhibitor, with potential consequent extension of life span.