Longstanding questions about how the red-wine ingredient resveratrol works at the molecular level have been answered by Harvard’s David Sinclair and colleagues in a paper that just appeared in Science. The new research supports the idea that the compound directly activates an enzyme called SIRT1 to induce effects in cells that are similar to those caused by calorie restriction, which is known to slow aging in various species. You can read about my take on the new findings in this Scientific American blog.
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If you set out to learn a foreign language along with your kid, get ready for a provocative lesson about brain aging: At some point, you’re likely to find yourself falling ever farther behind, laboriously struggling to implant new words in your plainly decayed memory while your youngster absorbs them like animal crackers.
But the standard picture of one-way cognitive decline after about age 25 is way too simple, according to psychologists who study brain aging. In fact, their work suggests that cognitive development actually continues through middle age, and even beyond. The gist of this later development was nicely captured by the great Polish-American pianist Arthur Rubenstein, who continued to perform until he was pushing 90 (he died at 95): When asked at 80 how he managed to continue giving such good concerts, he explained that he relied on three strategems–he played fewer pieces, he practiced the pieces more often, and he used dramatically contrasting tempi to make it appear that he could play the piano faster than he actually could.
Since 1935, scientists have known that putting rodents on very low calorie diets extends their lifespans. Scores of studies since then have shown that such calorie restriction (CR) can extend lifespan across species in a way suggesting it delays the onset of diseases of aging, extending healthspans (the proportion of life spent in good health) as well as lifespans. But, as detailed in my book, CR hasn’t extended lifespan in all species, nor has it worked in certain strains of rodents. In the latest study on the topic, it failed to extend lifespan in a long-term study in rhesus monkeys at the National Institute on Aging (NIA). The finding conflicts with results of another long-term CR study in rhesus monkeys at the Wisconsin National Primate Research Center in Madison, which showed that CR significantly improved late-life health in the primates; the Wisconsin study also offered evidence, though it wasn’t conclusive, that CR can extend lifespan in monkeys.
What all this means is that CR is probably more like medicine than magic. That is, almost all medicines work well for some individuals while doing little or nothing for others. Fewer than half of people put on antidepressants respond to them. And I can testify from personal experience that my genotype is virtually immune to Tylenol’s pain-killing effect.
The first strong evidence that a drug could slow aging in mammals came out in 2009 when scientists reported that chronically feeding doses of rapamycin to mice significantly extended their average and maximum lifespans. Yet rapamycin, a drug used to help prevent rejection of transplanted organs, causes multiple side effects in people, including elevated triglycerides and cholesterol, increasing the risk of heart disease; moderate immune suppression, perhaps increasing infection risks; and low blood platelet levels, which raises the specter of dangerous bleeding. In recent years another especially surprising and troubling side effect has come to the fore: Chronically taking large doses of rapamycin induces “insulin insensitivity” in both rodents and humans, leading to rising blood sugar and potentially to type 2 diabetes.
How do we reconcile such adverse effects with the drug’s unprecedented ability to boost healthy aging and longevity, at least in mice?
Some telling insights on this burning issue were recently published in two reports on rapamycin’s effect on insulin and blood sugar: a mouse study that revealed a probable mechanism behind the effect and a theory paper suggesting that the purported diabetes risk has been overblown. Continue Reading
It’s not every day that scientists base a study on an idea behind the story of Peter Pan. But as the research showed, the notion that slow development goes with longer life—which in the immortal Peter’s case meant completely arrested development along with no aging—has implications that reach far beyond Neverland: Led by Rong Yuan at the Jackson Laboratory in Bar Harbor, Maine, the study has demonstrated a nifty new way to find genes that enhance longevity and healthy aging.
The hunt for such “gerontogenes” took off around 1990 when scientists discovered that mutations in certain roundworm genes could double their lifespans. A few years later, similar genes were found in mice, thanks partly to pioneering research at Jackson Laboratory led by two coauthors of the new study, Kevin Flurkey and David Harrison. The findings helped turn aging science into a hot field and raised hopes that drugs could be found that would mimic the effects of the mutations and thus slow human aging.