Research has lagged far behind other areas of medicine and psychiatry. There is a dearth of knowledge and of theories. There is a much evidence of heritability, both from family studies and molecular genetics. Early onset cases occur more frequently in first time mothers, but this is not true of late postpartum or pregnancy onset. There are not many other predictors. Sleep deprivation has been suggested. Inhibition of steroid sulphatase caused behavioural abnormalities in mice. A recent hypothesis, supported by collateral studies, invokes the re-awakening of auto-immunity after its suppression during pregnancy, on the model of multiple sclerosis or autoimmune thyroiditis; a related hypothesis has proposed that abnormal immune system processes (regulatory T cell biology) and consequent changes in myelinogenesis may increase postpartum psychosis risk. Aberrant steroid hormone–dependent regulation of neuronal calcium influx via extracellular matrix proteins and membrane receptors involved in responding to the cells microenvironment might be important in conferring biological risk. Another promising lead is based on the similarity of bipolar-cycloid puerperal and menstrual psychosis; many women have had both. Late-onset puerperal psychoses, and relapses may be linked to menstruation. Since almost all reproductive onsets occur when the menstrual cycle is released from a long period of inhibition, this may be a common factor, but it can hardly explain episodes starting in the 2nd and 3rd trimesters of pregnancy. History
Between the 16th and 18th centuries about 50 brief reports were published; among them is the observation that these psychoses could recur, and that they occur both in breast-feeding and non-lactating women.
Harwood D (2017) Birth of a New Brain - Healing from Postpartum Bipolar Disorder. Brentwood, Post Hill Press. References


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