UCSF Biochemistry and Biophysics Professor Cynthia Kenyon, PhD, presented her research on roundworms last week, revealing insights into the cellular mechanisms of aging. Since humans share many of the same genes as roundworms, Kenyon believes her findings offer clues to increasing human youthfulness and longevity, and can lead to treatments for heart disease, Huntington's disease, cancer and other diseases associated with aging.
The presentation, followed by a reception, was held at the Mission Bay Branch Library to an audience of 70 people, primarily from the Mission Bay neighborhood. This community event was sponsored by UCSF, the San Francisco Public Library and Friends of the San Francisco Public Library.
"We used to think that when we aged, we just wore out like an old car. But I questioned this because different animals have different life spans, so there must be genes that influence aging," said Kenyon, who is also the director of the Hillblom Center for the Biology of Aging at UCSF's Mission Bay campus.
Kenyon's lab analyzes the 20,000 genes of the microscopic roundworm C. elegans. The first breakthrough occurred 10 years ago, when Kenyon identified a long-lived worm, and she began to search for the mutated gene that caused its increased longevity. Seven years later, Kenyon identified the gene daf-2 that codes for hormone receptors that bring insulin and IGF-1, an insulin-like growth factor, into cells.
"When insulin and IGF-1 enter cells, they promote food storage and growth," said Kenyon. "Lower levels of these hormones promote cell maintenance and stress resistance. If there is no receptor for the insulin to enter the cell, cells remain in this maintenance phase and age at a slower rate."
By treating worms with a chemical mutagen that damages daf-2, Kenyon found that the worm's life span increased up to six times its normal existence. These worms, which typically live for two weeks, remained active and apparently healthy for 12 weeks and, in a few cases, more than 20 weeks. Not only did the worms live longer, but they aged more slowly, and mutant worms were more active and disease-resistant than worms half their age.
Other scientists duplicated Kenyon's technique in fruit flies and mice and found similar results, implying that several biological mechanisms are conserved throughout the animal kingdom. Although humans have 10,000 more genes than C. elegans, Kenyon believes that much of the basic biochemistry is the same and that increases of insulin and IGF-1 in human cells also speed up the aging process.
"Although insulin is essential for nutrient uptake, I personally reduce my intake of sugar and other high-glycemic carbohydrates, which increase insulin levels," said Kenyon.
Kenyon explained that humans have evolved these "grim reaper" genes that speed up aging to benefit the species as a whole. She said it is better for the survival of a species if individuals don't live too long because once they reproduce, they are competing with their progeny for food and resources.
"I'm not saying that people will be able to live for 500 years," said Kenyon. "But my prediction is that these two hormones also affect aging in humans and that therapies can be developed to ward off age-related diseases and provide five to 10 additional healthy years of life."