Eat right. Get regular exercise. Don't smoke, don't use drugs and avoid stress. These pieces of advice are the mantras of most health professionals. If the goal is to live a long life, following these recommendations will definitely improve the odds.
Indeed, many of the trappings of "modern" life such as better nutrition, more accurate information on disease and better access to medical care are the reason some of us are living longer. Is it always the environment, however? A recent study at Northwestern University suggests that a rare genetic mutation found in a single family living in the Old Order Amish community near Berne, Indiana could be the cornerstone of developing an anti-aging drug that would increase longevity.
The study revealed that some of the Indiana Amish kindred (immediate family members and relatives) who have the mutation live longer, by about 10%, than those without it. Along with the mutation, this group of Amish also have longer telomeres. Telomeres are structures, which resemble an end cap on strands of DNA. They can be compared to the bits of plastic at the end of shoelaces (Trivia tip, those are called aglets) and when cells divide, which happens as we age, they get shorter and shorter. The genetic mutation that causes longer telomeres has a protective effect against aging because, with more material, cells stay healthier longer.
One of the benefits the study found was that Amish participants who have the mutation, also have a lower incidence of diabetes and lower levels of fasting insulin. These patients also have better vascular health, with increased flexibility in blood vessels and less arterial stiffening, which results in less heart disease.
Dr. Douglas Vaughan, the lead author of the study, explained another bonus the Amish with the mutation have, which is a lower level of a protein called PAI-1 (plasminogen activator inhibitor,) which is known to be involved in the aging process. Dr. Vaughn explained, "The findings astonished us because of the consistency of the anti-aging benefits across multiple body systems. For the first time we are seeing a molecular marker of aging (telomere length), a metabolic marker of aging (fasting insulin levels) and a cardiovascular marker of aging (blood pressure and blood vessel stiffness) all tracking in the same direction in that these individuals were generally protected from age-related changes. That played out in them having a longer lifespan. Not only do they live longer, they live healthier. It's a desirable form of longevity. It's their ‘health span.'"
The mutation is that only one copy of the relevant gene exists in some of the Amish. Those who have two copies do not have the same protective effect against diabetes. So what can be done with this information? Vaughn's team at Northwestern has partnered with scientists at Tohoku University in Japan and is testing an oral medication, TM5614, which tamps down the action of PAI-1. The drug has been tested in Japan on humans already, with Phase 1 trials complete and Phase 2 beginning soon. Northwestern will be starting trials of it, with study participants who have Type 2 diabetes and obesity, shortly. Check out the video below to see how this work could advance the science of aging.
Sources: Northwestern University, Journal article, Science Advances, New York Times
