A fascinating article in this month’s health policy journal Health Affairs concludes that by focusing on diseases one at a time—trying to prevent heart disease or cancer or dementia—we are shooting ourselves in the foot. Instead, we should devote greater effort to delaying the aging process altogether. If we could slow aging, we could in principle delay the onset and progression of all fatal and disabling diseases at once. Instead of surviving your heart attack and then going on to suffer from dementia or cancer, you would remain healthy longer, perhaps dying suddenly, as centenarians have been reported to do. But will delaying aging improve the quality of life? And how likely are we to actually postpone aging any time soon?
Using a complicated model known as the Future Elderly Model (FEM), the authors predict what will happen to health care spending, functional status, and life expectancy under various scenarios. What they find is that decreasing the incidence of heart disease by 25% between 2010 and 2030 wouldn’t do very much for disability rates or overall mortality. Ditto for decreasing the incidence of cancer the same amount during the same period. In fact, mortality and disability would be much the same as what we can expect if the incidence of cancer and heart disease stayed the same and all that changed is that the number of older people increased, as we can expect when the baby boomers reach old age. Delaying aging, by contrast, would have a dramatic effect on both length and quality of life. These benefits would come at a considerable cost—by 2060, costs would be $295 billion greater in the delayed aging scenario than in the status quo scenario because all those people who live longer would typically qualify for Medicare and Social Security. The good financial news, however, is that changing the age of eligibility for Medicare from 65 to 68 and raising the age of eligibility for Social Security from 67 to 68 would offset the increased costs.
All very compelling. But just what are these potential advances that will allow us to delay aging? The Health Affairs authors cite two scientific papers, one in the Journal of Clinical Investigation and one in a journal called Experimental Gerontology, both published this year. The papers are very intriguing.
The two papers focus on the fact that aging cells secrete a variety of nasty substances that cause chronic inflammation, at least in mice. These chemicals are collectively referred to as SASP (senescence-associated secretory phenotype). SASP or the cells that make them are potential targets for drugs to delay the aging process. So far so good. But as one of the authors points out, it’s not known if SASP causes chronic age-related disease in people. Moreover, it’s entirely possible that disrupting the processes that cause aging and death will turn on the processes that promote cancer. Finally, as another of the authors argued, actually carrying out clinical research in humans, testing whether a drug (if we had one) has a beneficial effect, will take an estimated 17 years. This would bring us to 2030, the exact date in the Health Affairs article by which all the good effects of delaying aging are assumed to have already happened, according to their model. If we aren’t likely to have any aging-delaying drug available for clinical use before 2030, we can’t plausibly expect any beneficial effect until well after that time.
So by all means, let’s go ahead and invest in the basic science of aging. Let’s encourage more clinically trained geriatricians to go into this kind of research (reportedly of 7000 board certified geriatricians, only 12 have research grants from the biological division of the National Institute on Aging). But in the mean time, let’s figure out how best to care for the many frail elders who will be with us for years to come.