Women who carry elevated body weight often have infrequent periods and/or fertility concerns.  This is most often diagnosed as polycystic ovary syndrome (PCOS).  Conversely, men with obesity can have low testosterone and fertility concerns due to a different reason, called central hypogonadism.  In this condition, the excess body fat turns down the signals coming from the brain (specifically, two hormones called LH and FSH) to direct the testicles to make testosterone and sperm.    So if men can have the signal from the master gland of the brain dampened by obesity, could this also happen in women?

A review article, published in Endocrine Reviews, poses this exact question. They challenge the notion that all obesity-related infrequent periods and infertility in women is PCOS, and question whether some women may in fact have central hypogonadism, similar to what we see commonly in men with obesity. They have called this FOSH (female obesity-related secondary hypogonadism).

The article then gets into a pretty heavy scientific discussion about the hormones involved, and I encourage interested readers to dig into the details in the review article itself. Some of the key points:

  • Women with obesity can have reduced LH levels, similar to men with obesity.
  • Increased leptin levels and chronic low grade inflammation are key features of obesity (in any gender), and are potential reasons for having lower LH levels.
  • Women with elevated weight can have increased androgen (testosterone) production even without PCOS.

The concept of FOSH makes a lot of sense to me. While unproven and hypothetical at this point, it may explain why some women’s blood work doesn’t look quite classic for PCOS.  Would women with FOSH respond differently to treatments to restore periods or fertility differently than women with PCOS? These and other important questions need to be explored to deepen our our understanding of reproductive function in women with obesity. I think the idea of FOSH is well worth investigating further. 


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