Abstract
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.
Keywords
obesity - infertility - reproduction - DNA fragmentation - sperm damage - systematic
review - meta-analysis - andrology
