One of the largest, longest studies of aging in men found one more reason to stay trim and active: it could greatly raise your odds of living to at least age 85.
The number one factor in longevity is genes. Studies have already shown that those who exercise and watch their diet can expect to live on average only six months longer than those who don't.
I remember the great runner James Fix and his wonderful fitness program. He said in his book on running that it was goal of men to exceed 52. Because that was the age that seemed to catch those prone to heart disease. And Fix confirmed his speculation. Trim, healthy and vigorous, he died at - 52.
Hey Colpy, sorry about your brother, man, that's way too young to die. It's gotta be mostly just the luck of the draw with genetics. I'm 57 and (as far as I know) perfectly healthy, despite some decades in which I drank and smoked far too much. At my age my father was diabetic, hypertensive, had high cholesterol, had been operated upon for gallstones and a bleeding ulcer, and was a few years away from a major episode of congestive heart failure that resulted in open heart surgery, a valve replacement, and a quadruple bypass. And at my age my dad's brother was dead of cardiovascular disease. Somehow it seems significant that they were both about 50 kg overweight for most of their lives, and I've never been overweight. But I also seem to have the genes from my mother's side. Her father smoked like a steam engine from the time he was 11 years old until well into his 70s, he got no exercise anybody ever heard of, and ate mostly brown and white food, no vegetables. And he almost made it to 100. But he was lean all his life.
Look around: fat men don't get old.
A major cause of aging is thought to result from the cumulative effects of cell loss over time. In yeast, caloric restriction (CR) delays aging by activating the Sir2 deacetylase. Here we show that expression of mammalian Sir2 (SIRT1) is induced in CR rats as well as in human cells that are treated with serum from these animals. Insulin and insulin-like growth factor 1 (IGF-1) attenuated this response. SIRT1 deacetylates the DNA repair factor Ku70, causing it to sequester the proapoptotic factor Bax away from mitochondria, thereby inhibiting stress-induced apoptotic cell death. Thus, CR could extend life-span by inducing SIRT1 expression and promoting the long-term survival of irreplaceable cells.
The team also asked if SIRT1 was activated by resveratrol in mice, as Sir2 is in lower organisms. To determine this, they looked at the amount of a specific chemical modification (acetylation) on the molecule PGC-1alpha. Removal of the "acetyl" chemical groups on PGC-1alpha activates this protein so that it can turn on certain genes that generate mitochondria and turn muscle into the type suited for endurance. The only enzyme known to remove the acetyl chemical groups on PGC-1alpha is SIRT1, and therefore the activity of PGC-1alpha is one of the most reliable and specific markers of SIRT1 activity in mammals. The research team found that levels of PGC-1alpha were three-fold lower in the HCR fed mice than in the HC mice, consistent with what would be expected when SIRT1 was being activated by resveratrol.
WASHINGTON — Obese mice on a high-fat diet got the benefits of being thin — living healthier, longer lives — without the pain of dieting when they consumed huge doses of red wine extract, according to a landmark new study.