By lowering the expression of a single gene, researchers at the National Institutes of Health have extended the average lifespan of a group of mice by about 20 percent — the equivalent of raising the average human lifespan by 16 years, from 79 to 95. This study appears in the August 29th edition of Cell Reports .
If there is one thing that the sugar free, low carb, low fat, and gluten free dieting trends of the past few decades have taught us, it’s this: a calorie is a calorie is a calorie. Right? Wrong! Whereas the source of the calories you consume might not have much bearing on the amount of weight you gain, when you consume them very well might. Research in both mice and humans demonstrates that eating whenever one pleases (mice) or later in the day (humans) causes significantly more weight gain than consuming the same diet in a time restricted manner, in keeping with the cyclical nature of the body’s energy metabolism.
Mitochondria are specialized subunits inside a cell that produce the cell’s energy and regulate its metabolism. Research suggests that mitochondria may play a central role in neuronal cell survival because they regulate both energy metabolism and cell death pathways. Using genetic mouse models of Alzheimer’s disease, researchers from Mayo Clinic have found that mitochondria in the brain are dysfunctional early in the disease. The findings were recently published in the open access journal PLoS ONE.
Earlier this year, researchers at the Max Plank Institute for Evolutionary Anthropology, the Shanghai branch of the Chinese Academy of Sciences and Cambridge University published a study in the journal Genome Biology providing further evidence that the evolution of human cognitive abilities was accompanied by adaptive changes in brain metabolism, potentially pushing the human brain to the limit of its metabolic capabilities . The results support the theory that schizophrenia is a consequence of human brain evolution.