Another recent study that has implications for what kind of diet might lead to a longer life was done at the Buck Institute for Age Research and is published in the current edition of Cell. Flies fed an "anti-Atkins" low protein diet lived longer because their mitochondria functioned better. The research shows that the molecular mechanisms responsible for the lifespan extension in the flies have important implications for human aging and diseases such as obesity, diabetes and cancer. Mitochondria act as the powerhouse of the cells, and mitochondrial function worsens with age in many species and in humans with Type 2 diabetes and obesity. "Our study shows that dietary restriction can enhance mitochondrial function, offsetting the age-related decline in its performance," said Buck faculty member Pankaj Kapahi, PhD, lead author of the study. The research provides the first genome-wide study of how proteins are translated under dietary restriction in any organism. The researchers report the unexpected finding that while there is a reduction in protein synthesis globally with the low protein diet, the activity of specific genes involved in generating energy in the mitochondria are increased, Kapahi said. That activity, which takes place at the level of conversion of RNA to protein, is important for the protective effects of dietary restriction, Kapahi said. "There have been correlative studies that show mitochondria change with dietary restriction—this research provides a causal relationship between diet and mitochondrial function," he said. The research calls into question the health benefits of high-protein diets, often used to lose weight. The long-term impacts of such diets have not been examined in humans; they are likely to be harmful, he said. "In flies, we see that the long-lived diet is a low protein diet and what we have found here is a mechanism for how that may be working."