At present the research community cannot robustly connect underlying causative processes of aging, such as those described in the SENS view of damage and rejuvenation, or some of the hallmarks of aging, to higher level manifestations of aging, such as declining function or changing biomarkers associated with age-related disease. This gives great freedom to theorize on how exactly the present voluminous but disconnected body of data on aging, cellular biochemistry, and age-related disease all fits together. There is no shortage of theories of aging, and no sign that the research community will cease to create new ones at any point in the near future. Some are quite interesting, as in the case here, regardless of what might think of the likelihood of such mechanisms playing an important role in degenerative aging.
We recently published selective destruction theory (SDT), which suggests a mechanism of ageing which is both independent of accumulating damage and consistent with epigenetic rejuvenation. We argue that in multicellular organisms, neighbouring cells are in constant competition. When mutations arise that increase a cell's growth rate, they bestow a selective advantage (an extreme example would be cancer, but most will not be). If these cells are uncontrolled, their growth advantage will allow them to spread, and their overactive metabolism could result in a host of detrimental or even lethal overactivity disorders. For example, in β-cells where growth is tied to insulin production, fast mutants spreading could produce a lethal drop in blood glucose. Another less tissue-specific example is the increased propensity of fast growing/metabolising fibroblasts to reach the critical threshold required for fibrosis.
Fast mutants are also likely to be more tumorigenic, while slow mutants will be less active, less fibrotic, and less tumorigenic even compared to wildtype cells. We therefore proposed that a maintenance mechanism which selectively destroyed fast cells might undergo positive selection even if it caused the spread of slow mutants as it would reduce the risks of overactivity disorders. The mechanism of selective destruction is currently theoretical. In our most developed model, we demonstrated that if slow cells induced epigenetic changes in faster cells causing their metabolism to slow (rather than killing them) it not only reduced unnecessary cell death, but also further reduced the likelihood of overactivity disorders by preventing the spread of fast cells. The resulting epigenetic growth suppression could therefore reflect a kind of ageing program designed to prevent overactivity disorders, and may explain why the methylation of specific CpG islands provides such accurate ageing clocks. It would also explain epigenetic rejuvenation by Yamanaka factors and parabiosis, so we predict that methylation of CpG islands will affect cell growth.