Many of the problems surrounding funding of meaningful efforts to treat aging, eliminate age-related disease, and extend healthy life come about because the people with the biggest megaphones are also doing the least useful work.
This is true outside the scientific community, in the "anti-aging" marketplace that tries to convince people they should take supplements rather than support research.
This is true inside the scientific community, where the Sinclair labs and their work on sirtuins - which is about as useless as supplements based on the last ten years of work - get far more attention than anything that is actually likely to produce meaningful results.
This article is an example of high-road hype and nonsense. More than a decade of work on sirtuins have failed to reliably produce even a tiny fraction of the gains to health and life provided by calorie restriction or exercise. This is just one tiny slice of the broader mainstream scientific approach of attempting to alter the operation of metabolism in order to provide benefits. This is vastly complex, and will take a very, very long time to get anywhere. When scientists speak of not seeing any real progress towards human longevity in the near future, this is the approach they are talking about: take this thing, the interaction space of metabolism with aging, which is vast, and about which nowhere near enough is understood, and then try to make a better version of it.
Sure, it's possible in the long term. But we'll all be old before anyone even makes a good first pass through this enormous complexity.
Yet there is a much better path forward towards treatment of aging. This is to identify the differences between old and young tissues, something that has already been done and agreed upon by the scientific community, more or less settled for the past 20 years, and then fix them all. You don't need to delve into the interaction space to understand why or how or process or progress. You just fix it. It is the difference between repainting a wall versus understanding the deep molecular interactions of wall, paint, and weather so that you can build a better lasting paint. One of those choices is evidently much more efficient than the other.
When it's a wall, who cares? Let the paint scientists get on with it. But in the case of aging, tens of millions of lives are lost every year that passes while the mainstream screws around with metabolism to slow aging rather than building the means to repair the identified causes of aging.
Even better, while the metabolic engineers have no clear plan to produce a good end state, just a bunch of plans that have not yet panned out as expected despite great expense, the "just fix it" approach to aging has clear paths to the development of repair therapies for each identified difference between young and old tissues. So they are only limited in progress by funding.
Why does this situation exist? I blame regulation. If your work doesn't result in something that looks like a drug, sounds like a drug, and walks like a drug it isn't going to be approved. Further, treating aging is not a result recognized by the FDA - so whatever you do has to be sidelined to treat some disease of aging. In other words only applied after it's too late to prevent things from going awry. So we see marginal unambitious work on marginal unambitious treatments, the continuing random walk through the natural world's pharmacology in search of chemicals that can be crudely administered to do slightly more good than harm, because that's the only way to have even a slight chance of getting to market. Highly regulated systems perpetuate their current state at all expense, and treat change as a threat.
The treatments for aging that might actually do some good in the future are radically different from today's pharmacology. These are the repair strategies: mitochondrial gene therapy, adapted bacterial enzymes let loose in the body, targeted destruction of stem cells and immune cells run wild, that sort of thing. You can find them described if you look up SENS, the strategies for engineered negligible senescence, but there are other similar lists put forward by different research groups. The repair approach is the disruptive newcomer to the field, barely ten years old, but gathering support. We should hope that it soon wins over the mainstream, and relegates the era of paying billions for sirtuin research and other dead-ends to the dustbin of history.