7:47 p.m. EDT, May 1, 2012
Resveratrol, the plant compound found in red wine and
reputed to have anti-aging effects, including protection against cancer and diabetes, has just had a "told-you-so"
moment.
Resveratrol's discoverer, the embattled Harvard professor who hopes it will point the way to new anti-aging drugs, long argued that the phytonutrient worked its magic by "turning on" the SIRT1 gene. The SIRT1 gene, one of a family of genes, the Sirtuins, is believed to control the good function and longevity of cells and, in turn, of their host.
But Harvard professor David Sinclair's critics argued, in effect, that the SIRT1 gene was not the lock for which Resveratrol was the key. Rather, they said, Resveratrol had its effect by a somewhat less magical route: it turned up the activity of an important metabolic sensor called the AMP-activated protein kinase. Some even argued that outside the test tube, Resveratrol loses its anti-aging power of cells completely.
By breeding a mouse that can live without the SIRT1 gene, Sinclair showed otherwise. His study is published in the journal Cell Metabolism. Mice who lacked the SIRT1 gene got no benefit from Resveratrol. But those that had the gene responded to Resveratrol with improved vascular and metabolic function, reduced inflammation and overall, cells that use fuel and clean up waste more efficiently. Even chubby mice responded to Resveratrol with improved function.
The discovery of how Resveratrol works should "allow the development of more potent and specific molecules"--drugs that could prevent diseases of aging more powerfully and with less risk of side effects than Resveratrol.
Speaking of side effects, the study also found that like any powerful agent, Resveratrol could have toxic effects at too-high doses. At high doses, researchers found, Resveratrol induced changes in cells and their activity that made them vulnerable to early death and inefficient fuel use. For the growing numbers of people considering Resveratrol, that should serve as a warning that more is not always better.
Resveratrol's discoverer, the embattled Harvard professor who hopes it will point the way to new anti-aging drugs, long argued that the phytonutrient worked its magic by "turning on" the SIRT1 gene. The SIRT1 gene, one of a family of genes, the Sirtuins, is believed to control the good function and longevity of cells and, in turn, of their host.
But Harvard professor David Sinclair's critics argued, in effect, that the SIRT1 gene was not the lock for which Resveratrol was the key. Rather, they said, Resveratrol had its effect by a somewhat less magical route: it turned up the activity of an important metabolic sensor called the AMP-activated protein kinase. Some even argued that outside the test tube, Resveratrol loses its anti-aging power of cells completely.
By breeding a mouse that can live without the SIRT1 gene, Sinclair showed otherwise. His study is published in the journal Cell Metabolism. Mice who lacked the SIRT1 gene got no benefit from Resveratrol. But those that had the gene responded to Resveratrol with improved vascular and metabolic function, reduced inflammation and overall, cells that use fuel and clean up waste more efficiently. Even chubby mice responded to Resveratrol with improved function.
The discovery of how Resveratrol works should "allow the development of more potent and specific molecules"--drugs that could prevent diseases of aging more powerfully and with less risk of side effects than Resveratrol.
Speaking of side effects, the study also found that like any powerful agent, Resveratrol could have toxic effects at too-high doses. At high doses, researchers found, Resveratrol induced changes in cells and their activity that made them vulnerable to early death and inefficient fuel use. For the growing numbers of people considering Resveratrol, that should serve as a warning that more is not always better.
