Antidepressant Medication Use in Pregnancy

Barbara Hackley, CNM, MSN

Disclosures

J Midwifery Womens Health. 2010;55(2):90-100. 

In This Article

Physiologic Changes in Pregnancy

Changes in brain chemistry have been theorized to be the underlying trigger for the development or worsening of depression during pregnancy and postpartum. Changes in thyroid function are of concern because mood disorders are associated with abnormal thyroid function. Overt thyroid dysfunction appears to be more common during the first year postpartum than in pregnancy; prevalence rates have been reported to be 6% to 9% in the first year after birth compared to less than 1% during pregnancy.[17] Other hormones, such as estrogen, progesterone, and prolactin, also increase significantly over the course of the pregnancy and then decline precipitously postpartum. Estrogen has been theorized to sensitize the brain to neurotransmitters and to cause significant fluctuations in their release.[14] It also appears to affect degradation of monamine oxidase, which catabolizes serotonin, increases the number of serotonergic receptors, and affects the transport and uptake of serotonin. Estrogen is thought to be a serotonin agonist.[18]

Elevated levels of cortisol and cortisol-releasing factor, which are thought to lead to dysregulation of the HPA axis in depression, also occur in pregnancy. Despite profound changes in the hormonal milieu during pregnancy and the early postpartum period, several comprehensive literature reviews concluded that studies have not consistently demonstrated a correlation between changes in gonadal hormones, thyroid levels, or cortisol and postpartum mood disorders.[17,19] A more recent study concurred; women with major depression at birth did not differ from healthy controls in the magnitude of the decline in estrogen and progesterone from postpartum day 1 to day 3 and in fact had significantly higher levels of estrogen on day 3 (P < .05).[20]

Indeed, the trigger for depression in pregnancy appears to be same as that for nonpregnant women (i.e., undue stress in vulnerable women). Recent studies have found that individuals with certain variations in the serotonin transporter gene (5-HTTLPR) who are subjected to stressful life events are at higher risk of depression than those without these variations.[21] Scheid et al.[22] reported similar findings in pregnant women.

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