Does the gut microbiota play a role in male infertility?
Obesity and metabolic disorders caused by a high-fat diet may alter sperm count and the quality of sperm. Why? A study published in Gut blames an imbalance of the gut microbiota caused by the consumption of junk food.
Infertility affects between 10% and 15% of couples, with gender equality called for in this domain, since men are the origin of the problem in half of cases. Among the environmental factors to blame is obesity, which leads to a reduction in sperm quality. However, the excessively rich diet which causes obesity is also associated with a change in the composition of the gut microbiota (dysbiosis). Might the ecosystem in our gut be a key factor in male infertility linked to junk food?
Fewer and less mobile sperm
This is the hypothesis put forward by Chinese researchers. To assess its validity, they put together four groups of mice: one group received a balanced diet and another a high-fat diet. Both served as donors in a fecal microbiota transplant to two other groups of mice subsequently fed normally. Unsurprisingly, the junk food diet resulted in weight gain, but it was also accompanied by dysbiosis and by endotoxemia, a bacterial infection which causes a chronic local inflammation known to impair spermatogenesis. Analyses on the mice’s semen showed a significant decrease in sperm count and sperm motility. Comparable results were observed for mice fed normally but receiving a fecal transplant from fattened members of the same species, though without any weight gain or metabolic changes. Dysbiosis and endotoxemia are thought to cause inflammation of the intestines and scrotum, resulting in impaired sperm production and maturation. The link between dysbiosis, endotoxemia and lower sperm quality has also been confirmed in infertile men.
Treat dysbiosis to restore fertility?
Ding N., Zhang X., Zhang XD. et al. Impairment of spermatogenesis and sperm motility by the high-fat diet-induced dysbiosis of gut microbes. Gut. 2020 ; https://doi:10.1136/gutjnl-2019-319127