The idea was that such agents, if identified and removed from the environment, were the causes of disease and death that prevented us from reaching our 'lifespan potential' as it was called. Then, in the last 50 years of luxury, when famine and plague were not big problems in the industrialized world, aging itself became the target of substantial research. Why not? We can manipulate everything else about the world as we choose, so why not create the ultimate manipulation: immortality!
Since we in science need not just to identify causes and study their nature, but to proclaim ourselves geniuses with fundamental new theories (and the research funding we thus deserve), there have been many grand one-cause 'theories' of aging. Somatic mutation, apoptosis (programmed cell death), the loss of telomeres (chromosome ends), the idea that cells can only divide so many times before becoming permanently senescent (called the 'Hayflick' limit), and others: antioxidants prevent cancer and other diseases, and so on.
There are many reasons why no one cause can be responsible for aging, reasons both evolutionary and due to how genomes construct and maintain organisms.
Now, a new study published in Nature and described here, reports the latest miracle claim. This refers to the Hayflick limit in a sense: it is that seenescent cells that are past their dividing prime, send off signals targeting them for self-destruction, which leads to inflammation, which causes aging-symptoms. From the abstract to the paper:
Cellular senescence, which halts the proliferation of damaged or dysfunctional cells, is an important mechanism to constrain the malignant progression of tumour cells. Senescent cells accumulate in various tissues and organs with ageing and have been hypothesized to disrupt tissue structure and function because of the components they secrete. However, whether senescent cells are causally implicated in age-related dysfunction and whether their removal is beneficial has remained unknown. To address these fundamental questions, we made use of a biomarker for senescence, p16Ink4a, to design a novel transgene, INK-ATTAC, for inducible elimination of p16Ink4a-positive senescent cells upon administration of a drug. Here we show that in the BubR1 progeroid mouse background, INK-ATTAC removes p16Ink4a-positive senescent cells upon drug treatment. In tissues—such as adipose tissue, skeletal muscle and eye—in which p16Ink4acontributes to the acquisition of age-related pathologies, life-long removal of p16Ink4a-expressing cells delayed onset of these phenotypes. Furthermore, late-life clearance attenuated progression of already established age-related disorders. These data indicate that cellular senescence is causally implicated in generating age-related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend health span.It is interesting that many genomewide disease mapping studies (GWAS) for diverse chronic and late-onset diseases, have found genes related to inflammatory responses to be involved. Yet the diseases ranged from cancers, to diabetes, to digestive disorders, to loss of mental function. So the current study may be helping to explain that.
However, several caveats must be added. First, these are manipulated laboratory mice, not 'real' animals, and not humans. Secondly, as the authors themselves note, the aspects of aging that they studied were only one set of things that goes sour over time, so this is not 'the' theory of aging, even if it is supported by further work. Thirdly, if we avoid the diseases that are currently the targets of so much research, we will be left with a drawn-out process of physical and mental degradation that may likely be even worse than what we experience already.
The Be Careful What You Wish for Department:
In the past, pneumonia was often called the old person's friend, because when you were only a shell of your former self, and dependent on others just for day to day survival, pneumonia killed you quickly and in that sense with minimal suffering. Anyone visiting a nursing home might feel nostalgic about those good old days. And fourthly, if people lived much longer, the problem of world overpopulation and of too many depending on too few younger people to care for them, will be much exacerbated--and that will lead to other kinds of negative payoff: deeper poverty, wars for resources that involve massive suffering, and so on. So even a single aging theory would not be an unmixed blessing of more person-years of misery per person, or even worse.
There are many other interesting facts that need accounting for as well. Mice are orders of magnitude smaller than we are, with fewer cells to become senescent or acquire mutations. They acquire similar diseases to those we suffer, on a similarly accelerating pattern with age. But this occurs over only two years, while for us it takes 60 or more. This relates to the general relationship between body size and longevity among mammals. So other more basic issues of mammalian biology must be involved--an issue we've been aware of and that one of us (Ken) even did research on decades ago, in regard to cancer.
Aging has been programmed by evolution only to the extent that longevity for evolving species was long enough for it to evolve. Anything genetic that trimmed individuals away 'too soon' for their local circumstances, was trimmed away as well. The aggregate of what worked, in combination, well enough is what is here today. It need not be simple, nor is there any reason to think it would be--and a wealth of evidence to suggest that these things really are complex (GWAS results, for example).
As we went to great lenghts to try to explain in our book MT, this almost has to be the case (rather than single-causation) because of the complex nature of gene-gene interactions and so on.
So there are interesting biological and evolutionary problems to address, as well as the personal ones related to how long each of us is going to last.