The "Slow Aging with Drugs" Viewpoint
Most of that portion of the aging research community interested in intervening in the aging process to extend healthy life focus on near term drug discovery and reuse. They recognize that the gains here will be small and the process, like all drug development, will be enormously expensive. They are trying to alter the operation of metabolism in order to slow down the pace at which it damages itself, but the ongoing interactions of metabolism and aging form an enormously complex and still poorly understood system. Researchers still don't have a full understanding of the easily replicated and widely studied life extension produced by calorie restriction in most species, for example. Even if drugs can be produced to recapture some of this alteration without meaningful side-effects, that will result in only a small gain in human life span, and it will do little to help the old. What use is a drug to slightly slow down the damage of aging when you are already so damaged as to be near death?
In short, the traditional approach of drug development to alter the operation of our biochemistry is a terrible way forward to extend healthy life. It is an expensive path to a mediocre result, and the research community is doing the worst thing that it could do: aiming very low and digging through drugs that already exist rather than building new technologies. But this is the mainstream today, and that is something that must change. The need for change is why I support disruptive next-generation research programs such as those of the SENS Research Foundation, where the focus is on evading the complexities of metabolism to focus on repair of clearly understood damage. Clean up the damage in the machinery, rather than try to change the whole machine to slow down the pace of damage. It's a much better path forward, and the only one likely to produce actual rejuvenation in the old.
Millions of people are taking anti-ageing drugs every day - they just don't know it. Drugs to slow ageing sound futuristic but they already exist in the form of relatively cheap medicines that have been used for other purposes for decades. Now that their promise is emerging, some scientists have started using them off-label in the hope of extending lifespan - and healthspan. "We are already treating ageing. We have been doing ageing research all along but we didn't know it. We can develop effective combinations for life extension right now using available drugs."One of the most promising groups of drugs is based on a compound called rapamycin. It was first used to suppress the immune system in organ transplant recipients, then later found to extend lifespan in yeast and worms. In 2009, mice were added to the list. This led to an explosion of research into whether other structurally similar compounds - called rapalogs - might be more potent. Now the first evidence has emerged of one such drug having an apparent anti-ageing effect in humans. A drug called everolimus, used to treat certain cancers, partially reversed the immune deterioration that normally occurs with age in a pilot trial in people over 65 years old.
Other familiar drugs might also fit the bill. Low-dose aspirin and statins are widely taken by healthy people to reduce their risk of heart disease. Both extend lifespan in animals and seem to have anti-inflammatory effects. Inflammation is one of the proposed mechanisms behind ageing, so aspirin and statins could be effective heart drugs in part because they slow ageing.
The fact that common mechanisms seem to be behind the major diseases of ageing, like heart disease, stroke and dementia, is good news, as it suggests we should be able to extend our lifespan while also extending healthspan. Indeed, it would be difficult to imagine an effective longevity agent that worked without alleviating or delaying such conditions. Rapamycin, for instance, has been found to reduce the cognitive decline that accompanies ageing in animals.
I like this analogy that you give, and agree with this in principle....."Clean up the damage in the machinery, rather than try to change the whole machine to slow down the pace of damage". But it should be noted that not all drug interventions are focused on slowing down the machine, some are focused on enhancing the body's self repair systems.
@JohnD: Yabbut those self-repair systems are, themselves, also damaged by aging. And there are not only genetic constraints on how far you can push that machinery, but inevitably Janus-faced effects: the DNA repair machinery is itself responsible for a significant amount of mutations; upregulating autophagy too much can be very destructive (as it is in heart failure); stem cell proliferation is at the heart of (most? All?) cancer; the immune system is needed to clear out harmful antigens and microbial invaders, but its chronic or over-activation leads to inflammation, can be destructive to tissues, and, in the end, likely weakens itself; etc.
I can't wait until this slowing aging nonsense is dead and buried. Don't smoke, drink or eat badly and give money to charitable organisations that work on damage repair.
@Michael:
It is said that throughout evolutionary time protein sequences tend to be conserved while it is primarily regulatory sequences that are changed. AFAIK, long lived negligible senescence organisms do not show substantial accumulation over time of at least most types of molecular damage, even the oldest of them, though maybe they do and I've not heard.
What this suggests to me is that it is likely that with existing machinery damage accumulation can not only be slowed but accumulation stopped, probably by exporting undegradable stuff(as seems to happen in the brain through the glymphatic system, iirc). In the case of things like atherosclerosis, there are even claims of not only stopping accumulation but reversal of already accumulated damage.
Regards damage to these systems by aging, even some of the most rapidly dividing cells accumulate only a few hundred mutations even in adverse aging environment even after a century of living, a few fold more mutations than a newborn's.
Again I say similarity at the genetic level between most primates is likely around 90+%, yet some live about a decade while others like us live over a century. Again what would be the sens proponent response to increasing the lifespan of the shortest lived primates if we didn't know about longer lived primates? The SENS solutions, but nature merely mostly tweaked gene expression/regulation and virtually multiplied lifespan by ten. Nothing suggests that the next jump is exponentially harder. Basically doubling maximum lifespan from the relatively long lived chimp to humans involves less than 2% change in genetic data(as many if not most changes are unrelated to lifespan).