Candidate mechanisms for physiological aging include free radical production and resulting oxidative damage, progressive erosion of telomeres and cellular senescence, age-dependent trade-offs in hormone signaling pathways, and immunosenescence, leading to an increased risk of infection, autoimmune disease, and cancer. These mechanisms are inter-related, not mutually exclusive, and probably all contribute to the aging phenotype. To date, most studies on mechanisms of aging are based on cell culture or lab animals, but interest in comparative studies is growing rapidly. Compared to mammals, birds have long life spans for their body sizes. Birds also appear to have lower rates of free radical production and oxidative damage than mammals, despite higher levels of oxidative metabolism. High levels of the antioxidant, uric acid, in birds may help protect against oxidative damage. Cultured bird cells are more resistant to oxidative damage than mammal cells, and membrane phospholipids of birds are less susceptible to peroxidation than those of mammals of the same size, but show a similar susceptibility as those of mammals with the same life span. In birds, telomeres shorten with age, and the rate of shortening is proportional to life span. Telomerase has a higher activity in long-lived than in short-lived species. Within a species, short telomeres correlate with reduced survival. Birds have higher plasma glucose than mammals, but lower levels of protein glycation, which contributes to aging damage. Immunosenescence is linked to both oxidative damage and telomere shortening. Patterns of cellular and humoral immunosenescence differ among species in birds. The rate of decline in cell-mediated immune function is inversely correlated with life span. Comparative studies on mechanisms underlying senescence in birds will continue to provide us with valuable information on how aging mechanisms have evolved.