Most women experience some form of premenstrual syndrome (PMS) at some point in their menstrual cycle. However, a small percentage suffer with a more extreme version of this called premenstrual dysphoric disorder (PMDD). The symptoms of this are so severe that it can interfere with the ability to lead a normal life. Yet a new study has illuminated the molecular and genetic mechanisms behind this very real and debilitating condition.
The symptoms of PMDD are largely psychiatric, including depression, anxiety, sleep disturbance and extreme irritability, but also include physical manifestations such as nausea and muscle aches. Some have criticised the labelling of this issue as a medical condition as it de-emphasises the potential social causes of premenstrual distress in women. Others welcome studies like this as they provide further evidence of the difficulties experienced by these women and make it harder to dismiss it as something to simply ‘get over’.
This study, published in Molecular Psychiatry, involved deregulating ovarian hormones, progesterone and oestrogen, in both women diagnosed with and without PMDD. The PMDD symptoms were significantly reduced during this period, compared to when the hormones were ‘turned on’. The control women did not experience any change. This suggested that it was not the amount of hormones that caused the difference, but rather the contrasting reaction to them.
The indication was that the brain cells’ reaction to the hormones was causing the difference. As white blood cells (WBC) express most of the same genes as brain cells, the researchers continued the experiment using WBCs from the subjects. They found a difference between the WBCs that had been exposed to the hormones and those that had not. The difference was in a specific gene complex that controls the expression of genes in response to various hormones.
It was found that certain genes in the cells of PMDD women were being overexpressed, whereas no such mutation was found in those without PMDD. The results suggest that something about the molecular pathway in women with PMDD is causing extreme sensitivity to ovarian hormones. Peter Schmidt, a co-author of the study, described the results as “cellular evidence of abnormal signalling in cells derived from women with PMDD”.
Although this study was very small and is in need of replication, it offers some first steps in providing a plausible biological cause for this condition. No longer can women experiencing this be deemed ‘over-emotional’ and in need of better self-control. The struggle is very real and this study could even lead to improved treatments for this condition and similar diagnoses.
Sarah Barfield Marks is studying for an MSc in Science Communication
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