Reducing calorie intake has extended lifespan in animals including mice, rhesus monkeys, and fruit flies. In some studies, the animals also remained healthier for longer. But severe calorie restriction can come with serious costs.
Mice placed on a diet with 40% fewer calories, for instance, become more vulnerable to infections, reproduce less successfully, and show impaired growth. That has left scientists with a difficult question: Could humans gain some of the longevity benefits of calorie restriction without experiencing those harmful effects? A new study, published in Nature Aging, points to a possible answer involving an immune protein called complement component 3 (C3).
Yale researchers have previously shown that people who followed moderate calorie restriction, cutting calorie intake by 14% for two years, developed stronger immune defenses without experiencing problems related to growth or reproduction. "This concept demonstrates that aging is actually malleable and a process that can be targeted," says senior author Vishwa Deep Dixit, PhD, Waldemar Von Zedtwitz Professor of Pathology, professor of immunobiology and of comparative medicine, and director of the Yale Center for Research on Aging (Y-Age) at Yale School of Medicine. Calorie Restriction Lowers an Inflammation-Linked Protein For the new study, Dixit and his colleagues at YSM examined plasma samples from 42 people who participated in a National Institutes of Health-funded two-year study called the Comprehensive Assessment of Long-Term Effects of Reducing Intake of Energy or CALERIE.
"It's the only trial of its kind that has been done with such rigor and control and demonstrates relevance to human physiology," Dixit says. During the trial, participants reduced their calorie intake by 11 to 14% without feeling deprived. The researchers measured more than 7,000 proteins across plasma samples collected over time.
One stood out: complement component 3 (C3), an immune protein whose levels fell significantly after calorie restriction. C3 drew particular attention because earlier research has suggested that activation of the complement system, a network of proteins that helps defend the body against pathogens, may contribute to chronic inflammation. That persistent inflammation is considered a major feature of aging and many age-associated diseases.
"But the causal effects of C3 in aging and chronic inflammation have not been identified. So, we were very excited to find that in our study," says Hee-Hoon Kim, PhD, a postdoctoral associate in the Dixit lab and a co-first author of the paper. Fat Tissue Emerges as a Key Source of C3 By comparing protein levels before and after two years of calorie restriction, the team found that white adipose tissue, the main form of fat tissue in mammals, appeared to be the primary tissue affected by the dietary change.
Extract — continue reading at the source.
