A Malfunction of Homeostatic Control Theory of Aging
There are many theories of aging, and we should expect more of them arise in the years ahead. On the one hand there is a growing interest in the science of aging as a place where careers can be made and on the other hand there is a great gulf of missing knowledge when it comes to a full and detailed catalog of exactly how aging actually progresses at the very detailed level of cells and cellular mechanisms. That is very much the type of environment that will lead to more theorizing. The research community has a very defensible list of fundamental differences between old and young tissues, changes that result directly from the ordinary operation of metabolism. There is, however, endless debate over which of these forms of damage are important, how they interact, and how they cause other changes and dysfunction. There is even a higher level debate over whether accumulated damage is in fact the cause of aging, or whether damages instead results from the operation of an epigenetic program that is itself the root cause of aging.
Mountains of data are being gathered on an ongoing basis to feed into this mill. As a process that is actually fairly typical for modern fields wherein the researchers study very complex systems but are collectively nowhere near attaining a full understanding of those systems. We live in an age in which obtaining and managing data in massive volumes is now feasible, and the all too human researchers are often playing catch up in the analysis. So there is a lot of back and forth, many conflicting study results, and everyone of note has their own pet hypotheses when it comes to poorly understood areas of the field. Aging research is far from the only area of scientific study that looks this way at present, and this is how science is done at the cutting edge.
As an aside, the primary and most important conceptual innovation contained in the Strategies for Engineered Negligible Senescence (SENS) is to note that since there exists a defensible list of fundamental differences between old and young tissues, we can skip the full understanding that will likely require decades further to arrive and use that list to work directly on repair biotechnologies now. The majority of the as yet unknown details of how and why simply don't matter all that much from a practical engineering perspective of producing rejuvenation treatments. In this, SENS is firmly in the aging as damage accumulation camp.
Over at the Russian end of the research community there tends to be more support for programmed aging theories. In their most common manifestation these theories suggest that aging is driven by epigenetic changes, and evolutionary processes select for aging to exist in this form. This might be because specific mechanisms are beneficial in youth and are thus selected for despite the fact that they run awry after reproductive life span is ended, a concept known as antagonist pleiotropy. It may be because aging allows for more successful adaptation of the species in the face of environmental change. There are many other evolutionary theories of aging, and there is some overlap between those used to explain programmed aging versus those used to explain aging as an accumulation of damage. The evolutionary explanations for aging are "why" and the mechanisms by which we age are "how", and those two questions can be considered separately from one another.
Just as there is a lot of debate among researchers who see aging as damage accumulation, there is similarly a lot of debate among researchers who theorize on programmed aging. This is an interesting if fairly dense paper from Russian researchers. If I'm reading it correctly, they are suggesting that aging is caused by a drift of set points in the biological mechanisms collectively responsible for maintaining homeostasis, keeping everything roughly the same and in place throughout an organism. That seems to me a layer of explanation on top of the more general idea that epigenetic changes happen in aging and they are the fundamental cause of damage rather than being responses to damage, though the researchers here declare their theory a third way, neither programmed nor damage-based:
There are two well-known but opposing concepts of the reason for aging. The first supposes that senescence is programmed similarly to the genetic program of development from a zygote up to a mature organism. Genetically determined senile wasting is thought to be associated with the necessity to renovate the population to ensure its adaptation and survival. According to the concept of the stochastic aging (due to accumulation of occasional error and damage), there is no built-in program of aging. There is only a program of development up to the state of maturity, and then the organism should be able to maintain itself limitlessly. However, although the efficiency of repair systems is assumed to be rather high, it is less than 100%. Just this has to result in aging because of accumulation of various errors.We have continued and developed another approach that considers both programmed and stochastic concepts to be incorrect. Aging is a simple deprivation syndrome driven by preventable and even reversible drifts of control systems set points because of an inappropriate "organism-environment" interaction.
Reading the whole thing, which isn't long enough to fully outline the thinking here, it seems pretty easy to pick holes in this. But the core idea of a set point drift is an interesting one in the context of present debates over the details of aging. That said it is probably not very relevant to the type of research strategy that I support. Fix the damage first, move as rapidly as possible towards saving lives, and then figure out how young turns to old in as much detail as you like - you'll have the time for it.