The fascinating thing about the transition of aging research from mere investigation to the possibility of intervention is that many researchers don't even want

The fascinating thing about the transition of aging research from mere investigation to the possibility of intervention is that many researchers don't even want to talk about extending life, but only a small expansion of healthspan. This lack of ambition, and refusal to engage with the large body of evidence that suggests we can do far better, is why we need organizations like the SENS Research Foundation and Methuselah Foundation, working to make the better option happen. It is possible and plausible to extend healthy life and overall lifespan indefinitely by implementing the approach of repairing the cell and tissue damage that causes aging. Yet all too much of the rhetoric and effort in the scientific community still goes towards tinkering with the operation of metabolism to slightly slow the pace at which damage accumulates - a clearly far inferior approach, that can at best produce only marginal outcomes. All of the technologies and approaches mentioned in this article are marginal, ways to only modestly slow the damage of aging from accumulation. They are very limited in what they can achieve - adding five to ten years to life would be an enormous, unlikely success for any one of these. Calorie restriction we know doesn't add more than that to human life spans, since we have plenty of examples to look at. Metformin data is all over the map in animal studies, just as contradictory and half-refuted as sirtuins. The transfer of young plasma to old individuals doesn't extend life in animal studies; it is pretty unlikely to have the desired effect in humans - that isn't the same thing as parabiosis. Human Longevity Inc is a personalized medicine company in fancy clothing, doing nothing that will greatly extend life, but rather looking for incremental gains in ordinary medicine. And so on. Sadly journalists typically don't distinguish between the potential value and outcome of different approaches to aging - it is all the same to them, just a flat list. So they pull five or ten items from the larger list to populate their articles, and mark them all equivalent. That's something of a problem when the differences are in fact enormously important and the expected outcomes are night and day when comparing approaches that repair damage versus approaches that do not repair damage. If there is to be significant progress towards healthy life extension in our lifetimes, the better strategies, those involving damage repair, must gain far greater support. This means the SENS list: senescent cell clearance, mitochondrial DNA damage, clearing metabolic waste like amyloid, lipofuscin, and cross-links, and so on.