Having Polycystic Ovary Syndrome (PCOS) can make it difficult to conceive. In fact, PCOS is one of the main causes of infertility today. Approximately one third of couples who seek help for infertility find that it is due to anovulation and 80% of these cases are directly associated with PCOS. The good news however, is that the symptoms of PCOS are manageable and can quite often be fully reversed by implementing diet and lifestyle changes.
The main pregnancy complications reported to affect women with PCOS are hypertension, preeclampsia and gestational diabetes. A direct correlation between PCOS and increased risk of miscarriage has not been identified, however, women with a high Body Mass Index (BMI) are at greater risk of miscarrying and obesity is a common comorbidity of PCOS. Women with a high BMI are strongly recommended to lose weight prior to attempting to conceive.
Not all women with PCOS experience pregnancy complications
PCOS is not a simple condition; it is a syndrome, with a range of symptoms. It is widely recognised that of the three predominant clinical symptoms (hyperandrogenism, anovulation and polycystic ovaries), two of the three must be present for an accurate diagnosis to be made.
The different phenotypes have differing risk rates for adverse pregnancy outcomes. Women who experience anovulatory cycles will struggle to conceive naturally because without ovulation pregnancy cannot occur. For these women, identifying the reason why they are not ovulating and implementing lifestyle changes to rectify this may be sufficient to restore fertility. For those women who are morbidly obese (BMI >40), pharmacological ovulation induction will not usually be considered until attempts are made to reduce BMI through diet and lifestyle changes.
Women who experience irregular cycles because they have PCOS, have a 5-fold increased risk of adverse pregnancy outcomes, including gestational diabetes and preterm birth. Low progesterone levels, a sign of anovulation, are also a risk factor for miscarriage. Hyperandrogenic women, whose condition is confirmed biochemically by the presence of increased circulating androgens (male hormones), have a 4-fold increased risk of pregnancy complications. High androgen levels not only adversely affect the early stages of embryo implantation and placental formation, but also increase the risk of preeclampsia and reduced birth weight, possibly due to reduced nutrient transfer through the placenta.
No single cause, means no single treatment
One of the major problems with the management of PCOS is that it is a multi-factorial condition, with genes, hormones, the environment and inflammation all thought to play a role in its pathogenesis. Unfortunately, the infertility that accompanies the condition is also highly variable, often involving several coinciding factors. For example, as described above, women with PCOS often struggle with their weight, they are also often insulin resistant, both of which increase the risk of pregnancy complications. They may have chronic low-grade inflammation and/or placental abnormalities affecting nutrient transfer. Finally, a significant proportion will undergo additional infertility treatment, which in itself is a risk factor, not only for gestational diabetes, hypertension and preeclampsia, but also for multiple births.
Will there be long-term consequences for my child?
Further work is required to assess the long-term health implications for children born to mothers with PCOS. The risks regarding premature birth and low/high birth weight are already understood, but any impact on their future metabolic or reproductive health is inconclusive. There is increasing evidence to support a genetic component to PCOS, so females may inherit a predisposition to the condition from their mothers. Further research and awareness is needed to support implementation of such testing in OBGYN clinics.
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- Thessaloniki ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. “Consensus on Infertility Treatment Related to Polycystic Ovary Syndrome.” Human Reproduction, vol. 23, no. 3, Mar. 2008, pp. 462–477., doi:10.1093/humrep/dem426.