No, no, no.<p>This is just an argument for putting more effort into a failed strategy. The reason why we haven't made much progress towards extending healthy human life isn't because the disease state is complex, it is because the primary strategy adopted by the research community is to reverse engineer the disease state, and then work backwards towards its cause.<p>Typical project: pick away at a small chunk of the altered metabolism of [age-related disease of choice]. Find a proximate cause of pathology that has some small contribution to the whole - an altered gene expression level, say, something really, really far removed from root causes. Find a small molecule that adjusts expression. Publish. Patent. Tech transfer finds someone willing to tinker with that family of small molecules to have a short at achieving a small alteration in the disease state. Goes into trials, fails at phase II or phase III.<p>This happens constantly. It is the bulk of all medical research for age-related disease. It is pointless. May as well not happen. Applying computational prowess to this process won't make it any better. You'll just have a lot more low yield approaches that still do nothing more than tinker with proximate causes in late stage disease, and will do next to nothing for patients. (With the occasional success like statins, which produce the amazing-for-this-strategy result of a 22% reduction in mortality. You still die, just slightly less often).<p>The only practical way forward for age-related disease is to entirely reject this approach to medicine in favor of a much, much better one.<p>1) Infer the root causes of aging and best points of intervention (already done, several times over).<p>2) Fix one of those causes, in isolation.<p>3) Observe the results.<p>Steps 1-3 have been achieved for removal of senescent cells. The results in animal studies are absolutely amazing, robust, night and day better than anything else anyone has done for the treatment of aging and age-related disease. Reversal of scores of diseases and measures of aging, every lab can do it, replicated many, many times via numerous different approaches.<p>Everyone is now backfilling their models of age-related disease, their understanding of disease etiology, to add senescent cells. Because they are clearly an important cause.<p>Once Unity Biotechnology has stopped being silly about their subpar approach to senescent cell clearance, and the rest of the dozen or so companies have started their trials, we should expect those human trials to follow the same sort of pattern.<p>This is the way to make progress. Infer root causes, target root causes, figure out which work by trying them. Backfill your understanding of age-related disease based on new data.