For those who might not be aware, Polycystic Ovary Syndrome is a very common condition. And sadly, it has caused various reproductive issues (including infertility) among women worldwide.

Polycystic Ovary Syndrome also known as PCOS, affects between 8 and 20 percent of reproductive-aged women across the globe. While the exact number of women in the United States with this is not known, it is estimated at around 5 million. Personally, I know several people with it.

PCOS can affect anyone and can even affect girls who are as young as 11 and have not even begun their menstruation cycles yet. However, most women are not diagnosed until their 20s or 30s. This is basically something that revolved around a set of symptoms that are related to hormone imbalances that have no universal definition.

That being said, we are learning more and more about it in current times. A recent study has found evidence that it might start in the brain, which really makes researching it a lot more in depth. This study was led by researchers from the University of Lille in France. It seems PCOS is developed when a hormone produced by the ovaries interacts with a set of neurons in the mother’s brain.

This interaction can initiate what seems to be a cascade effect. It disrupts enzymes in the placenta causing PCOS for the child to be. This also kind of helps to explain how PCOS can usually run in families. The results of this study most likely will change a lot about what we think in regards to PCOS.

The abstract of this study goes as follows:

Polycystic ovary syndrome (PCOS) is the main cause of female infertility worldwide and corresponds with a high degree of comorbidities and economic burden. How PCOS is passed on from one generation to the next is not clear, but it may be a developmental condition. Most women with PCOS exhibit higher levels of circulating luteinizing hormone, suggestive of heightened gonadotropin-releasing hormone (GnRH) release, and anti-Müllerian hormone (AMH) as compared to healthy women. Excess AMH in utero may affect the development of the female fetus. However, as AMH levels drop during pregnancy in women with normal fertility, it was unclear whether their levels were also elevated in pregnant women with PCOS. Here we measured AMH in a cohort of pregnant women with PCOS and control pregnant women and found that AMH is significantly more elevated in the former group versus the latter. To determine whether the elevation of AMH during pregnancy in women with PCOS is a bystander effect or a driver of the condition in the offspring, we modeled our clinical findings by treating pregnant mice with AMH and followed the neuroendocrine phenotype of their female progeny postnatally. This treatment resulted in maternal neuroendocrine-driven testosterone excess and diminished placental metabolism of testosterone to estradiol, resulting in a masculinization of the exposed female fetus and a PCOS-like reproductive and neuroendocrine phenotype in adulthood. We found that the affected females had persistently hyperactivated GnRH neurons and that GnRH antagonist treatment in the adult female offspring restored their neuroendocrine phenotype to a normal state. These findings highlight a critical role for excess prenatal AMH exposure and subsequent aberrant GnRH receptor signaling in the neuroendocrine dysfunctions of PCOS while offering a new potential therapeutic avenue to treat the condition during adulthood.

What do you think about this? I for one am quite impressed and a bit shocked. Their findings were nothing I would have expected.

 

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