A research team recently demonstrated that a diet lower in advanced glycation endproducts (AGEs) extended life in mice: "Aging is accompanied by increased oxidative stress (OS) and accumulation of [AGEs]. AGE formation in food is temperature-regulated, and ingestion of nutrients prepared with excess heat promotes AGE formation, OS, and cardiovascular disease in mice. We hypothesized that sustained exposure to the high levels of pro-oxidant AGEs in normal diets (RegAGE) contributes to aging via an increased AGE load [and a same-calorie] AGE-restricted (by 50%) diet (LowAGE) would decrease these abnormalities. ... This was associated with a reduction in systemic AGE accumulation and amelioration of insulin resistance, albuminuria, and glomerulosclerosis. Moreover, lifespan was extended in LowAGE mice, compared with RegAGE mice. Thus, OS-dependent metabolic and end organ dysfunction of aging may result from life-long exposure to high levels of glycoxidants ... A reduced AGE diet preserved these innate defenses, resulting in decreased tissue damage and a longer lifespan in mice." More attention should be given to developing AGE breaker drugs. Diet is just one source - your body also creates AGEs itself as a byproduct of metabolic processes.