Scientists haven’t figured out a really good way to measure the rate of aging yet. But there’s progress, as I wrote in the New York Times this week. The growing evidence that “epigenetic” changes are correlated with chronological aging, and possibly can be used to get a handle on the rate of biological aging, is one of the most promising recent developments on this front. It’s especially important stuff, in my view, because we need good biomarkers of aging in order to assess the human anti-aging effects, if any, of drugs like rapamycin, which appear to slow aging in mice.
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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.
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. Read More
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.
Several people emailed me recently for my reaction to media stories on a University of Pittsburgh study in which the short lifespans of mice with a severe form of progeria (accelerated aging) were extended by injections of stem-cell-like muscle cells from young mice. So I took a look at the study and some related research, and here are some things that jumped out at me.
First, it has never been clear how much progerias can tell us about normal aging. Further, it’s not even clear which life-shortening syndromes to anoint as forms progeria, which implies that they have something to do with aging—there are a myriad degenerative diseases that shorten life and cause forms of bodily decay reminiscent of aging’s toll, and it’s a judgment call, sometimes rashly made, to label one of them a form of accelerated aging. Besides, no one knows whether 10% or 90% of the zillion forms of deterioration caused by aging, or something in between, must be present in a purported form of progeria in order for it to tell us truly interesting things about aging. As a general rule, I tend to think that progerias that kill very early in life, as does the one investigated in the Pittsburgh study (it’s called XFE progeroid syndrome, by the way, and it kills mice with a few weeks of birth), are usually less like normal aging than ones that work slower. Thus, I didn’t find the Pittsburgh study all that interesting at first glance—it seemed to be about a possible treatment for a rare congenital disease, not a study on aging.
When I recently speculated that taking vitamin pills may contribute to unhealthy choices because many people assume the pills shield them from the choices’ ill effects, I figured there was no way to support my hunch. But I was mistaken: A recent Taiwanese study demonstrated that taking multivitamins does indeed make people feel protected against health hazards and thus more likely to indulge in unhealthy choices.
Led by Wen-Bin Chiou at National Sun Yat-Sen University, the researchers gave daily placebos for a week to 82 adults (45 women, 37 men, average age 31). They told half of the group that they were taking multivitamins, and at the end of the week administered surveys on the subjects’ health-related inclinations. The results: Those who thought they were taking vitamins reported a 44% higher tendency to partake in risky activities (examples included casual sex, sunbathing, and binge drinking), and a 61% higher preference for all-you-can-eat buffets over healthy meals, compared with those who knew they were taking placebos. The “multivitamin” group also reported exercising 14% less. The researchers concluded that multivitamin takers may experience an “illusory invulnerability” contributing to all kinds of risky behaviors.
If you follow aging science—and my guess is that you’re one of those mortal, aging types who do—you might want to take a look at the latest issue of Scientific American (the January 2012 issue), which has a cover story I wrote for the magazine about research on target of rapamycin (TOR) and its implications for aging and finding ways to slow it down. Accompanying the article is a blog I wrote about how politics and faulty perceptions are preventing the huge practical promise of aging research from being realized, and why we should change that ASAP. There’s also a slide show about the very different rates of aging (and longevity) across mammals, and a piece on the extraordinary longevity of naked mole-rats, an adaptation of part of my book’s chapter on aging across species.
If you’ve tuned into the resveratrol story over the past five years, you’ve probably heard that you’d need to take giant doses of the red-wine ingredient to do any good. That idea was based on mouse studies in 2006 that showed massive doses of the compound blocked bad effects of eating too much fat. A front-page New York Times story on the studies, memorably headlined “Yes, Red Wine Holds Answer. Check Dosage,” conveyed the conventional wisdom at the time that “a 150-lb person would need to drink 750 to 1,500 bottles of red wine a day to get such a dose.”
Recent placebo-controlled clinical trials with resveratrol, however, suggest that much smaller doses—maybe a tenth as much as suggested by the Times‘ story—can have significant cardiac benefits. These smaller doses are still too large to get from drinking wine—you’d need to take resveratrol pills to equal them. But evidence is plainly growing that a rethink is in order.