SubscribeIt’s not often that 33 scientists jointly pen a public complaint that an article in Science got things wrong. But in this week’s issue of Science nearly three dozen researchers working on sirtuins, the enzymes thought by many scientists to help induce the health- and longevity-promoting effects of calorie restriction (CR), complain in a letter to the editor that the authors of a review of how CR works that appeared earlier in the journal committed a glaring sin of omission by failing to mention sirtuins.
By pointedly omitting mention of sirtuins, the April 16 article—by Luigi Fontana at Washington University in St. Louis, Linda Partridge at University College London, and Valter Longo at the University of Southern California—implicitly dismissed the idea that sirtuin-based drugs may mimic CR’s health- and longevity-promoting effects. In effect, that represented a broadside aimed at Sirtris Pharmaceuticals, which is developing such drugs, as well as at the work of MIT’s Lenny Guarente and Harvard’s David Sinclair, leading proponents of the idea that sirtuins play key roles in mediating CR’s effects. (Sinclair of course is famed for studies suggesting that resveratrol mimics CR’s health benefits by stimulating a mammalian sirtuin known as SIRT1.) Many other scientists who’ve conducted studies over the past decade linking sirtuins to CR and aging also were effectively in the broadside’s line of fire.
Ironically, the letter of complaint appears in an issue of Science that happens to include a study by prominent ant researchers at Arizona State University and other schools showing, among other things, that an ant version of SIRT1 is upregulated in extra-long-lived “functional queens” of Harpegnathos saltator, a species of predatory leaping ants whose genome was recently sequenced. While the study had nothing to do with CR, it added novel support to the idea that SIRT1 is part of a highly conserved pathway closely tied to aging, and that enhanced SIRT1 activity helps to extend lifespan. (Amazingly, queens of some ant species have been known to live for up to 30 years.) Read More
No subject has inspired more hype and wishful thinking through the ages than life extension. Not surprisingly, our inner skeptics tend to counsel extreme caution when the talk turns to anti-aging elixirs. For many of us after a certain age, the skepticism is reinforced each morning with that first grimacing glance in the bathroom mirror, showing once again that no matter how many vitamins we've popped, cups of ginkgo tea we've downed, or miles we've jogged, we are melting, melting—oh, what a world!
The Birth of Applied Gerontology
Gerontology, the study of aging, has long seemed a field of basic research that’s only tangentially related to the nitty-gritty world of geriatrics, the medical specialty devoted to ills of the elderly. But as gerontologists have delved deeper into the molecular roots of aging, they’ve increasingly found themselves shedding light on what gives rise to diseases of aging. That’s led to surprising insights that, in some cases, have life-or-death implications for the practice of geriatric medicine.
Example: Gerontologists studying “cellular senescence” have shown that the molecular damage that continually occurs in cells as they age often triggers a mechanism that stops them from dividing and induces a zombie-like state called the “senescent phenotype.” This static state presumably prevents the damaged cells from spiraling into the runaway proliferation of cancer. But as ever more of our cells become senescent—especially stem cells that regenerate our worn-out parts—our skin, immune cells, artery linings and other tissues lose their youthful powers of renewal. Worse, such senescent cells have been shown to secrete chemical messengers that promote local inflammation, a major contributor to aging diseases, including atherosclerosis, and ironically, even the malignant spread of cancer cells. Here’s one of the surprising and important medical implications of this developing picture: A study led by biogerontologist Judith Campisi at the Buck Institute for Age Research suggests that administering chemotherapy drugs to tumor patients can backfire by inducing such senescent secretions from early-stage cancer cells, fueling the development of deadly, secondary cancers.
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