Finding a way to slow the biological processes of aging will do more to extend the period of healthy life in humans than attacking individual diseases alone, according to some of the nation's top gerontologists writing in the latest issue of Public Policy & Aging Report (PP&AR), titled "The Longevity Dividend: Geroscience Meets Geropolitics." The authors showcase work in the emerging interdisciplinary field of geroscience, which is based on the knowledge that aging itself is the major risk factor for most chronic diseases prevalent in the older population.
The new PP&AR, published by The Gerontological Society of America (GSA), will be released during a November 22 press briefing at GSA's 66th Annual Scientific Meeting in New Orleans. Both the issue and the briefing were developed in partnership with the American Federation for Aging Research.
"In recent years, researchers studying the biological underpinnings of the aging process have made impressive progress in understanding the genetics, biology, and physiology of aging," said GSA Executive Director and CEO James Appleby, RPh, MPH. "With adequate research support, we could be in reach of a breakthrough similar to those in public health in the 19th century and medicine in the 20th."
The PP&AR contains seven articles that discuss the contemporary pursuit of scientific means to extend the period of healthy life by slowing aging in people - known as the Longevity Dividend Initiative - and some of the obstacles that stand in the way of what many consider to be one of the most exciting breakthroughs in the history of science and public health.
"In this new issue, we are proud to spotlight the pioneering work of high-profile researchers who add visibility to the value of geroscience in the eyes of both the scientific community and the general public," said AFAR Executive Director Stephanie Lederman, EdM.
As author Gordon J. Lithgow, PhD, points out, many childhood diseases were brought under control by antibiotics and vaccines once scientists understood they essentially had a single cause: microbes. If the diseases of late life also have a single cause (aging itself), then researchers should be able to develop classes of therapeutics by targeting aging mechanisms in a way similar to targeting microbial infection.
Yet PP&AR Editor Robert B. Hudson, PhD, explains that scientists may face difficulty in convincing skeptics - among the biomedical community, public and private funders of research, and the general public - that attacking aging is a viable and more efficient approach to reducing the risk of all fatal and disabling diseases and improving well-being across the life cycle.
Author S. Jay Olshansky, PhD, additionally emphasizes that the Longevity Dividend Initiative is not focused on delaying aging at the expense of an extended period of infirmity at the end of life. He writes that "although people who benefit from advances in aging science will probably live longer, the extension of healthy life is the primary goal. In addition, reductions in the infirmities of old age and increased economic value to individuals and societies would accrue from the extension of healthy life."