The fixation of people outside the scientific community on things like this is irrational. If it works out stupendously well? You get to live a couple of years longer, and suffer a tiny bit less age-related disease. The cost of that is billions in research.<p>For the same amount of money, actual, serious rejuvenation of the double the remaining healthy life span following treatments type could be built in mice by following the SENS vision of repairing the cell and tissue damage that causes aging [1]. People should be chasing that dream.<p>Inside the scientific community, it is completely rational from a short term career still have a job a few years from now perspective to be investigating metabolism and the end state of a disease/old metabolism and proposing drug candidates that might slightly alter the situation for the better. That is the proven path to getting grants awarded, to moving with the grain of the system that wants drug candidates based on metabolic alteration that do a little bit of good, and no-one really cares that you're tinkering with proximate causes, not root causes, trying to get a little bit more mileage out of a damaged engine rather than fixing the damage.<p>It's a mess of perverse incentives. The only way to break out of the hole of misallocated funded (or at least misallocated if your goal is to effectively treat aging as a medical condition rather than, say, gain more data on the fine details of metabolism, or further your career within the system) is to bootstrap SENS therapies to the point of showing that you get far better results for far less funding, and with far less work.<p>Fortunately this is starting to happen. See, for example:<p>1) amyloid clearance: <a href="http://www.uclb.com/news-and-events/news-post/potential-new-approach-to-the-treatment-of-systemic-amyloidosis" rel="nofollow">http://www.uclb.com/news-and-events/news-post/potential-new-...</a><p>2) senescent cell clearance: <a href="http://www.scripps.edu/news/press/2015/20150309agingcell.html" rel="nofollow">http://www.scripps.edu/news/press/2015/20150309agingcell.htm...</a><p>3) mitochondrial DNA damage bypass: <a href="http://www.gensight-biologics.com/index.php?page=mts" rel="nofollow">http://www.gensight-biologics.com/index.php?page=mts</a><p>There are others moving into startups for development; more senescent cell clearance at Oisin Biotech, clearance of metabolic waste products that contribute to atherosclerosis at Human Rejuvenation Technologies. And so on.<p>Billions have been spent on the investigation of sirtuins and other excessively hyped alleged paths to ways to slightly, slightly slow down the aging process. They have gone nowhere, produced nothing beyond more knowledge of metabolism. It is well past time to accept that that game is broken, it's a path to nowhere other that the comprehensive mapping of cellular metabolism: very useful for the next generation of science, but not a road to extending healthy life and eliminating age-related frailty and disease. The only way to achieve that end is to repair the root causes of aging. For so long as the majority of the research community insists on metabolic tinkering that can in principle only achieve marginal results, progress to meaningful therapies will be slow.<p>[1]: <a href="http://sens.org/research/introduction-to-sens-research" rel="nofollow">http://sens.org/research/introduction-to-sens-research</a>