The popular science article I'll point out here is written from a programmed aging point of view, in which - to simplify greatly - epigenetic change is considered to be the root cause of aging, changing the operation of cellular metabolism so as to generate damage, dysfunction, and death. One of the authors maintains a blog, and you'll find much more on his take on programmed aging there. I consider the opposite view to be more plausible, that the root cause of aging is accumulated damage, produced as a side-effect of the normal operation of metabolism, and that where we observe epigenetic changes in aging, they are a response to rising levels of damage. Placing this crucial difference to one side for one moment, the article below does makes an entirely valid point, which is that the enormous evolved variation in life histories in the natural world - in the pace and character of aging and species longevity - indicates that it is in principle possible to engineer a radically different human metabolism in order to create individuals who undergo slower aging, and down the line that sort of approach could be used to produce negligibly senescent or even ageless branches of humanity.
Humans age gradually, but some animals do all their aging in a rush at the end of life, while others don't age at all, and a few can even age backward. The variety of aging patterns in nature should be a caution sign to anyone inclined to generalize - particularly the generalization that aging is inevitable. Life spans range from Methuselans great and small to genetic kamikazes that die of a spring afternoon. Submerged dragonflies live four months, adult mayflies half an hour. We live some 70-odd years; but the meristem of the ginkgo may be millions of years old. This range becomes all the more impressive when we realize that the genetic basis for aging is widely shared across different species, from yeast cells on up to whales. Somehow, the same genetic machinery, inherited from our common ancestors at the dawn of life on Earth, has been molded to generate life spans ranging from hours (yeast cells) to thousands of years (sequoia trees and quaking aspen).
And it is not only the length of life but the pattern of deterioration within that time that varies widely. Aging can occur at a steady pace through the course of an entire lifetime (most lizards and birds), or there can be no aging at all for decades at a time, followed by sudden death (cicadas and century plants). Our own "inner assassin" works with stealth, like an evil empress gradually poisoning her husband; but other species have inner killers that do their deed far more quickly, and still others appear to have no genetic death programs at all. Such variety is a sure signal for a feature molded by active natural selection, not an immutable law of entropy. The great variety of aging styles among plants and animals suggests it can be controlled.
Suppose we were to remove length of life completely from consideration and compare different species based on the shape rather than the duration of their life histories. However long or short the life span, we display it in the same size box for comparison. Rather than asking how long they live, ask instead whether their populations tend to die out gradually, or if many die in infancy and fewer later on, or if all the deaths bunch up at the end of the life cycle. The strange bedfellows that appear as neighbors on the chart are utterly unexpected. For example, at the top of the chart, with low mortality that rises suddenly at the end of life, humans are joined by lab worms and tropical fish (guppies)! In fact, in terms of aging profiles, we humans look more like the lab worm than the chimpanzee.
Styles of aging in nature are just about as diverse as they can be, which suggests that nature is able to turn aging on and off at will. With this in mind, we may be forgiven for regarding theories that explain why aging must exist with extreme skepticism. Whatever our theory of aging turns out to be, it had better make room for plasticity, diversity, and exceptions.
I do not believe that building a variant of human biochemistry to produce negligibly senescent individuals is a near term project in any way, shape, or form. It is certainly possible, and may well be accomplished, but in the same sense as building out human habitats in high Jupiter orbit is possible, and may well be accomplished. Both are projects that could be eclipsed and rendered retro-futures by any number of advances over the decades ahead: why invest in building a negligibly senescent human biochemistry in a world in which we can discard our biology to merge with the machinery of a mature molecular nanotechnology industry, becoming ageless, durable, and repairable, for example? Or why do it if by the time it is plausible the medical community can already comprehensively repair the biological damage that causes aging?
At the present time we stand at least decades from even a comprehensive map of healthy, normal metabolism. Applications of that knowledge will require longer to arrive, and based on existing experience that work will be painfully challenging. Over the past fifteen years, it has required scores of researchers and a few billion dollars to somewhat improve the state of knowledge for one small set of genes and processes involved in calorie restriction, a very well-studied altered state of metabolism that modestly increases health and longevity. The research community is nowhere near a full accounting of how calorie restriction works, or any way to turn it on safely all the time, or even good ways to recreate some of its effects using the standard panoply of drugs and gene therapies. All of that effort could be repeated ten times over between now and 2030 and researchers would still be only a little further along in the process of figuring out how it all works in detail. The molecular biology of life is fantastically complex.
I point this out, as usual, to illustrate why the SENS approach of repairing damage is really the only viable way forward to radical life extension in our lifetimes. The cell and tissue damage that causes aging - that is the signature difference between old and young tissues - is well cataloged, agreed upon in many diverse fields of medical research, and there are plausible ways to repair it either under development or that are planned out in some detail. Given the vast costs and length of time needed to get to the point of being able to defeat aging by creating a new human metabolism, it is vitally important that we have an alternative approach to rejuvenation and agelessness that requires little to none of that effort in order to progress. It really is as simple as periodically fixing the damage and observing the results, a process that is taking place for senescent cell clearance in mice right now, today. This and other similar efforts in the years ahead will help map cause and effect and relative contributions to specific age-related diseases, but much more importantly will also produce the basis for rejuvenation therapies - and produce them soon enough to matter to people alive today.