Although most research has focused on maternal obesity, there is growing data to indicate that obesity in the father can affect reproduction. Supporting data come from both mouse and human studies. Murine studies found that obese male mice exhibited decreased motility and reduced hyperactivated progression versus lean mice. Obese mice also exhibited sperm with increased levels of intracellular and mitochondrial levels of reactive oxygen species, increased sperm damage, and lower levels of capacitation, which has been shown to be associated with poor fertilization rates following in vitro fertilization, defective preimplantation embryonic development, and high rates of miscarriage and morbidity in the offspring. Furthermore, diet-induced paternal obesity was found to initiate intergenerational transmission of obesity and insulin resistance in two generations of murine offspring. Meta-analysis from human studies found obese males were more likely to demonstrate sperm DNA fragmentation, infertility, decreased live birth per cycle of assisted reproduction technology, and increased absolute risk of pregnancy nonviability, with no consistent effect on conventional semen parameters. There is a need for future studies to expound on the mechanisms of sperm DNA damage and the impact of weight loss in reversing this damage.