Clinically, the androgen excess in PCOS manifests as excessive body hair and acne, and anovulation manifests as irregular cycles and reduced fertility.
PCOS is also associated with insulin resistance/diabetes, and obesity worsens all symptoms. The mechanisms underlying the development of PCOS are poorly understood, but maternal obesity and androgen excess can impact fetal development and programming.
Women with PCOS have an increased risk for pregnancy complications as well as delivery complications, and frequently deliver babies born large or small for gestational age. Birth weight is a sensitive marker of the overall impact of the intrauterine environment on fetal development and predicts the risk to develop obesity, diabetes, cardiovascular disease in adult life.
The hypothesis that PCOS originates during fetal life is supported by the finding that daughters of women with PCOS are more likely to develop the condition. Women with PCOS display high androgens and low levels of the insulin-sensitizing hormone adiponectin during pregnancy. Low adiponectin levels increase the risk of develop gestational diabetes, suggesting low adiponectin levels leads to an impaired capacity to handle metabolic changes during pregnancy.
Adiponectin acts on the placenta during pregnancy and this fact allows for the interesting possibility that adiponectin can exert endocrine effects on the developing fetus and protect against the effects of obesity and androgen exposure on the offspring.
We work according to the hypothesis that elevated levels of adiponectin improves maternal metabolism and placenta function, and thereby protects against fetal overgrowth by preventing excess nutrient and androgen transport to the fetus, which in turn will prevent the development of PCOS and mood disorders in the offspring.