Selenium is a trace mineral that has powerful antioxidant properties. It is a co-factor enzyme and its main job as an antioxidant is to protect against oxidative damage, so it can help with chronic conditions that include inflammation. A new mouse study demonstrated that adding selenium to diets can protect against obesity as well as provide metabolic benefits.
The findings were published in the journal eLife in a paper titled, “Selenium supplementation inhibits IGF-1 signaling and confers methionine restriction-like healthspan benefits to mice,” and was led by researchers at the Orentreich Foundation for the Advancement of Science (OFAS) in Cold Spring, NY.
Methionine restriction (MR) has been shown to extend the healthspan of several organisms. The researchers sought to determine whether selenium supplementation offered the same protection against obesity as methionine restriction.
“…Methionine-restricted rodents have less age-related pathology and increased longevity as compared with controls, and recent studies suggest that humans might benefit similarly,” wrote the researchers. “Mechanistically, it is likely that the decreased IGF-1 signaling that results from MR underlies the benefits of this regimen. Thus, we hypothesized that interventions that decrease IGF-1 signaling would also produce MR-like healthspan benefits.”
The researchers fed young male and older female mice one of three high-fat diets: a control diet containing typical amounts of methionine, a methionine-restricted diet, and a diet containing typical amounts of methionine as well as a source of selenium. The researchers observed that selenium supplementation completely protected against the dramatic weight gain and fat accumulation seen in mice fed the control diet, and to the same extent as restricting methionine.
They then explored the effects of the three diets on physiological changes normally associated with methionine restriction. They noted reduced levels of IGF-1 in both male and female mice. They also saw reductions in the levels of the hormone leptin, which controls food intake and energy expenditure.
Their results demonstrated that selenium supplementation produces most of the hallmarks of methionine restriction, which suggests that this intervention may have a similar positive effect on healthspan.
To further gain insight into the benefits of selenium supplementation, the researchers used yeast and found that yeast grown under selenium-supplemented conditions had a 62% longer chronological lifespan (from 13 days to 21 days) and a replicative lifespan extended by nine generations as compared with controls.
“One of the major goals of aging research is to identify simple interventions that promote human healthspan,” noted senior author Jay Johnson, senior scientist at OFAS. “Here we present evidence that short-term administration of either organic or inorganic sources of selenium provides multiple health benefits to mice, the most notable of which being the prevention of diet-induced obesity. In the long term, we expect that supplementation with these compounds will also prevent age-related disease and extend the overall survival of mice. It is our hope that many of the benefits observed for mice will also hold true for humans.”
“In the current study, we present a novel mechanism by which selenium supplementation contributes to mammalian healthspan. We propose that this intervention downregulates IGF-1 signaling, thereby activating pathways that are both beneficial to healthspan and shared with MR. In the short term, this results in total protection against diet-induced obesity. However, we expect that, in the long term, this intervention will also produce an MR-like extension of overall survival, as well as an amelioration of age-related pathologies,” concluded the researchers.
