Life expectancy has doubled in the last 150 years and with it has come the proverbial “silver tsunami” – a cost to society for increasing lifespan with a concomitant rise in chronic disease incidence. Geroscience is essentially an interdisciplinary field at the crossroads of aging and age-related diseases.
Given this dramatic increase and that age is the greatest risk factor for a majority of chronic diseases driving both morbidity and mortality, the National Institutes of Health’s Geroscience Interest Group (GSIG) – an interdisciplinary band of researchers – is calling for more collaboration, both within the NIH and with its funded external researchers.
They say it is critical to expand geroscience research directed at extending human healthspan, pointing out that 46 percent of Medicare spending is for people with six or more chronic conditions, including diabetes and heart disease.
Clearly, living longer doesn’t always mean living better. “Healthspan,” the length of a lifetime that is spent in optimal health, is the lynchpin for better aging. Age itself is the predominant risk factor for most diseases and conditions that limit healthspan. This knowledge launched the idea of geroscience, which strives to understand how aging enables chronic disease and seeks to develop novel multi-disease preventative and therapeutic approaches.
Researchers studying epigenetics say that the lack of validated biomarkers of human aging has impeded progress in solving the mysteries of the molecular underpinnings of aging. They argue that epigenetic changes present promising biomarkers, and, if validated, could be used to examine deterioration associated with abnormal aging, and ultimately, to test interventions to bolster normal aging.
But, it remains unclear whether these markers forecast chronologic or biologic age, which are likely distinct. That is, there may be changes to the epigenetic modification that always occur with the aging clock, whether or not abnormal deterioration to cells occur. If the status of the chemical modifications to the epigenome does indeed indicate biologic age – normal healthy aging compared to abnormal – then a major hurdle to initiating human studies will be overcome because status of the epigenetic modification will indicate the age-related deterioration state.
Also, if similar modifications are identified in mice, they could then be validated by determining whether chronic stressors, such as alcohol, accelerate the abnormal epigenetic changes, and importantly, whether interventions such as epigenetic pharmacological drugs could delay the negative changes.
“The epigenetic landscape could reveal and explain the relationship between aging and the increase in chronic diseases that manifest throughout the body, such as inflammatory problems, because epigenetic mechanisms occur throughout all cells in the body,” says Berger. “This, we hope, may one day lead to finding epigenetic therapeutics to hold back the aging epigenome and delay the onset of multiple, co-occurring chronic diseases.”