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In this commentary over at the Fight Aging! website, Reason addresses the question of whether CR postpones or simply slows the aging process. What's the difference you ask? Apparently it's pretty important. Here is how Reason puts it: It is worth bearing in mind that when we seek to build therapies to treat aging as a medical condition, to bring it under control, the ideal goal is to postpone it, not slow it. A therapy that can postpone aging is a therapy that can be reused later to postpone aging some more. A therapy that only slows aging has no such option: it has a flat maximum benefit to life span. Postponing aging, provided it works well enough and doesn't let any aspect of aging leak though to accumulate, has an unlimited upside in terms of the years of healthy life it can add. This is one of the reasons why I'm very focused on repair of damage after the SENS model as the path ahead for the treatment of aging. Repair of the forms of cell and tissue damage that cause aging can in principle produce rejuvenation and indefinite postponement of aging, provided it can be made comprehensive enough. In comparison, work aimed at modestly slowing aging by developing drugs to beneficially alter metabolic state, meaning slowing the pace at which damage accumulates rather than repairing existing damage, has no such upside and will be of very limited utility to people who are already old and damaged. Reason is not too optimistic about the benefits of CR in humans seeing it most likely providing only at best a 5% increase in human longevity. Reason says: There is no rigorous estimate for longevity added in humans practicing calorie restriction, and such an estimate is unlikely to emerge any time soon, but the much less rigorous process of theorizing and modeling suggests 5% as a reasonable ballpark. Anything much larger than that would appear as a strong statistical signal in many historical data sets that are known to show no such signs. Reason goes on to post excerpts from this paper , which looked at the detailed effects of CR and growth hormone knockout mutations in mice, to try to tease apart whether CR postpones aging or simply slows it. The analysis is rather complicated, by the authors summarize their findings rather simply: According to the classical method [Gompertz modelling - DP], caloric restriction and disruption of growth hormone signaling did not affect the aging rates, but would be interpreted to postpone aging [A good thing - DP]. The alternative method studied here, by contrast, yields age-dependent aging rates that allow for a more variegated assessment beyond the question of a mere postponement or slowing of aging. This method interprets these interventions to affect the aging rates in an age-dependent manner: aging was slowed at lower ages, postponed until higher ages, but quickened at higher ages. Such a pattern resembles a compression of aging, whereby aging is postponed as well as intensified, reflected by a risk of death that increases sharply at a high age . A compression of aging also becomes apparent from the life expectancies of the mice (Table 1): these interventions [CR and growth hormone genetic knockout mutations - DP] bring about an increase in median life expectancy that is two to four times larger than the increase in maximal life expectancy, indicating a sharper increase in the risk of death at a higher age. So what does this analysis of CR's impact on aging mean for us? I'm not entirely sure, and it would be interesting if someone (Michael) chimed in who has more expertise. But it would appear from the authors' analysis that CR postpones aging, at least to a certain degree, between young adulthood and one's elderly years. A possible interpretation of what this might mean for an individual is that damage accumulation is arrested during that mid-life period, rather than simply slowed down. So for example, a healthy CR diet which keeps our oxidized cholesterol very low may halt for a time (rather than just slow down) the accumulation of athrosclerotic plaques that normally build up in people's arteries as they age. If these authors are correct, we may play "catchup" down the line, with an increased rate of aging at an extreme age, so that the max lifespan of a group of CR folks wouldn't be extended by nearly as much as the median lifespan. But who knows, perhaps by then the SENS research agenda might have succeeded and be able to postpone aging through other means... --Dean ------------------  AGING, March 2016, Vol 8 No 3 Received: 01/12/16; Accepted: 02/03/16; Published: 03/07/16 Measuring aging rates of mice subjected to caloric restriction and genetic disruption of growth hormone signaling Jacob J.E. Koopman1,2, Diana van Heemst1,2, David van Bodegom1,2, Michael S. Bonkowski3,4, Liou Y. Sun3,5, and Andrzej Bartke3 Correspondence: Jacob J.E. Koopman, MD/PhD; E-mail: email@example.com Free full text: http://www.impactaging.com/papers/v8/n3/pdf/100919.pdf Abstract Caloric restriction and genetic disruption of growth hormone signaling have been shown to counteract aging in mice. The effects of these interventions on aging are examined through age-dependent survival or through the increase in age-dependent mortality rates on a logarithmic scale fitted to the Gompertz model. However, these methods have limitations that impede a fully comprehensive disclosure of these effects. Here we examine the effects of these interventions on murine aging through the increase in age-dependent mortality rates on a linear scale without fitting them to a model like the Gompertz model. Whereas these interventions negligibly and non-consistently affected the aging rates when examined through the age-dependent mortality rates on a logarithmic scale, they caused the aging rates to increase at higher ages and to higher levels when examined through the age-dependent mortality rates on a linear scale. These results add to the debate whether these interventions postpone or slow aging and to the understanding of the mechanisms by which they affect aging. Since different methods yield different results, it is worthwhile to compare their results in future research to obtain further insights into the effects of dietary, genetic, and other interventions on the aging of mice and other species. Key words: aging, aging rate, mice, caloric restriction, growth hormone, Gompertz model