The aging research community might be divided into two camps. The much larger camp sees aging as a process of damage accumulation and reactions to that damage. There is a lot of argument over which forms of damage are more important and how they lead to the observed age-related changes in biochemistry, but the primary forms of damage are well described and that list has existed in its present form for more than thirty years. The smaller camp in the research community sees aging as an evolved genetic program of changes that cause damage. So we have a cart and a horse and debate over which is which. For my part I see the balance of evidence as leaning strongly towards aging as damage.
It can be the case that researchers well understand the fundamental damage of aging but yet argue over whether it is a cause or a consequence because metabolism - the day to day operation of our biochemistry, and the way in which it reacts to circumstances - is fantastically complex. Even in this age of advanced biotechnology and large-scale computation we stand a long, long way from a full model of its operation. So it seems likely that settling the debate over aging as damage versus aging is program will occur when the first damage repair treatments are rolled out and trialed in mice. They should be very effective if aging is in fact the results of damage. If aging is a program, well, they will be much less effective and the results transient. The cost of performing this grand experiment is very low in comparison to the cost of trying to build a complete understanding of metabolism. At this point in time it requires hundreds of millions of dollars and a decade of work to chase down answers in the roles of just a few genes and proteins out of the thousands of noteworthy types of molecule involved in metabolism: just look at sirtuin research as an example. In the world of SENS rejuvenation research, hundreds of millions of dollars would buy most of a rejuvenation toolkit for laboratory mice and the proof as to whether it works or not.
We live in a world that isn't all that rational, however, as illustrated by the fact that damage repair approaches like SENS are not well funded. Despite the fact that a majority in the research community work from the hypothesis that aging is caused by cellular and molecular damage in tissues, they work on treatments that make much more sense for the programmed aging school of thought. Generally research focuses on the end stages of age-related conditions, working backwards to identify proximate causes of pathology. Scientists identify the next to last changes before the end, which of course are very rarely the same thing as the primary forms of damage that are thought to cause aging. Only in some diseases, such as macular degeneration, is there a very short chain of steps from fundamental damage (build up of metabolic waste products called lipofuscin) to disease process (death of retinal cells), and that chain is well understood.
So instead of root causes, researchers are far more often studying the details of metabolic disarray in late stage disease. Simple causes spiral out into highly complex dysfunction in a system, our metabolism, that is researchers are still figuring out piece by piece as they go. Since genetic and epigenetic studies are becoming popular - they are newly cheap and funding is easily raised - the proximate causes latched onto are often epigenetic changes. These are consequences, reactions to damage, if you think that aging is damage, and primary causes of damage if you think that aging is programmed. So we have researchers who are firmly in the aging as damage camp nonetheless working hard to create treatments that should, by their own hypotheses, have only marginal benefits. Treatments that won't in any way deal with the underlying problem, but rather are attempts to force a dysfunctional metabolism to work better under a high load of damage. This is patching the problem, and will be expensive and provide little in comparison to the results that damage repair could achieve.
But anyway, there are plenty of examples to point out. Most research into treating aging is as I've described above, and the "repair the damage" approach of SENS is still the disruptive minor newcomer. It's strange, given that the majority of the field considers aging to be a process of damage. Here is one example in which researchers pick out an epigenetic change that occurs in aging, resulting in altered levels of one particular protein, and discuss the prospects for altering it in order to adjust the operation of metabolism. Read the open access paper, and bear in mind that this is what the ultimately futile path looks like, the way forward that will not greatly help us when we are old:
During human aging there is an increase in the activity of inflammatory, cancer promoting, and tissue destructive genes plus a decrease in the activity of regenerative and reparative genes. The human blood tripeptide GHK possesses many positive effects but declines with age. It improves wound healing and tissue regeneration (skin, hair follicles, stomach and intestinal linings, and boney tissue), increases collagen and glycosaminoglycans, stimulates synthesis of decorin, increases angiogenesis, and nerve outgrowth, possesses antioxidant and anti-inflammatory effects, and increases cellular stemness and the secretion of trophic factors by mesenchymal stem cells.
GHK was discovered during studies comparing the effect of human plasma from young persons (age 20-25) to plasma from older persons (age 50-70) on the functioning of incubated slices of human hepatic tissue. The younger plasma more effectively induced a profile associated with youth by suppressing fibrinogen synthesis. The active factor was found to be GHK. Since then numerous studies over the course of four decades demonstrated that this simple molecule improves wound healing and tissue regeneration.
Even though numerous and diverse beneficial effects of GHK have been known for decades, it was not clear how one simple molecule could accomplish so much. The use of gene expression data greatly extends our understanding of GHK's effects and its potential treatments of some of the diseases and biochemical changes associated with aging. As a potential therapeutic agent GHK has a clear advantage over many other active chemicals that may also show promising results in gene profiling experiments, its gene modulating effects correspond to findings from in vivo experiments. When GHK is administered internally to an animal, it induces actions throughout the body.
There is still not enough information to translate gene profiling data into biological effects. However, based on the documented activity of GHK in vivo, we can predict [various] beneficial actions from our gene profiling data. Most current theories and therapies to treat disease tend to target only one biochemical reaction or pathway. But for human aging, our data suggests that we must think of simultaneously resetting hundreds to thousands of genes to protect at-risk tissues and organs. GHK may be a step towards this gene resetting goal.