As a companion to yesterday's post on insulin metabolism and human longevity, here is an open access paper that looks at stem cells, insulin signaling processes, and aging. In short, the activity of stem cells is vital to your long-term health, but this activity declines with age - and this decline is linked to other age-related changes, such as in insulin metabolism:
Tissue and organ rejuvenation and senescence/aging are closely related to the function of stem cells. Recently, we demonstrated that a population of [pluripotent] very small embryonic-like stem cells (VSELs) resides in the adult murine bone marrow (BM) and other murine tissues. We hypothesize that these pluripotent stem cells play an important role in tissue/organ rejuvenation, and have demonstrated that their proliferation and potentially premature depletion is negatively controlled by epigenetic changes of some imprinted genes that regulate insulin factor signaling.
Since the attenuation of insulin/insulin growth factor (Ins/Igf) signaling positively correlates with longevity, we propose, based on our experimental data, that gradual decrease in the number of VSELs deposited in adult tissues, which occurs throughout life in an Ins/Igf signaling-dependent manner, is an important mechanism of aging. In contrast, a decrease in Ins/Igf stimulation of VSELs that extends the half life of these cells in adult organs would have a beneficial effect on life span. Our preliminary data in long-living Igf-1-signaling-deficient mice show that these animals possess a 3-4 times higher number of VSELs deposited in adult BM, lending support to this novel hypothesis.
The big picture here is that mammals have evolved a balance of mechanisms to (a) repair themselves, and (b) suppress cancer. Crudely, we might think of cancer as being caused by damaged repair mechanisms run amok. The loss of repair capacity with age - which involves stem cell populations being reduced in number or becoming inactive due to changes in signaling processes - is a way to reduce the risk of cancer. This loss of stem cell capacity is coordinated by changes in the controlling systems of our biology: responses to accumulated damage and dysfunction, for example.
Thus, we should not be surprised to find that longer-lived animals of a given species have a greater regenerative capacity: more stem cells, or more active stem cells, or both. Nor should we be surprised to find out that known biochemical changes associated with longevity are a part of the controlling systems for stem cell behavior.
It is clearly the case that the evolved present state of many species is not optimized for longevity, but individuals have the capacity for longer lives if their metabolism ran slightly differently. Life spans are more plastic than was thought even a few decades ago: members of a smaller mammalian species like mice can live 30% longer if calorie restricted, and a change to their insulin metabolism can achieve the same end. There are survival advantages for a species that can more easily evolve into different lengths of life, better allowing it to prosper even if the environment changes dramatically.