Antidepressants During Pregnancy: The Drug Companies Tip the Scale

Baum Hedlund Law
February, 2007

Persistent pulmonary hypertension of the newborn is a life-threatening disorder in which the newborn's arteries to the lungs remain constricted after delivery, limiting the amount of blood flow to the lungs and therefore the amount of oxygen into the bloodstream. Newborns who have PPHN are typically full-term or near-term infants who are born without associated congenital abnormalities, yet present after birth with severe respiratory failure. Babies born with this condition often require intubation and mechanical ventilation. Despite this treatment, 10 to 20 percent of affected infants do not survive.

The connection between PPHN and selective serotonin reuptake inhibitors -- a class of antidepressants used in the treatment of depression, anxiety disorders, personality disorders and several other conditions -- was first reported in the scientific literature in 1996. That year, Dr. Christina Chambers and several of her colleagues performed a case-controlled study of women on Prozac and discovered that infants born to women who took Prozac late in their pregnancy had a host of breathing difficulties, including PPHN. See Christina D. Chambers et al., "Birth Outcomes in Pregnant Women Taking Fluoxetine," N. Engl. J. Med. 1996; 335; 14: 1010-1015.

In a follow-up study, Chambers and her colleagues concluded that mothers who took SSRIs in the second half of their pregnancies were six times more likely to give birth to a baby with PPHN. Christina D. Chambers et. al., "Selective Serotonin-Reuptake Inhibitors and Risk of Persistent Pulmonary Hypertension of the Newborn," N. Engl. J. Med. 2006; 354; 6: 579-587. Despite this research, it was not until July 19, 2006, that a public health advisory from the U.S. Food and Drug Administration alerted physicians and patients about the Chambers studies and the risk of PPHN. 

Although researchers admit their studies cannot conclusively establish causality, they have offered an explanation as to why SSRI exposure causes PPHN. It has been discovered and discussed among researching physicians that the lung acts as a reservoir for antidepressant drugs and, in fact, a 1998 study in The Lancet reported substantial accumulation of SSRIs within the lungs. Moreover, serotonin has vasoconstrictive properties that increase pulmonary vascular resistance, and at the same time has mitogenic and comitogenic effects on pulmonary smooth-muscle cells. Therefore, higher levels of serotonin circulating within the growing fetus and the accumulation of serotonin within the fetus's lungs may result in the proliferation of smooth-muscle cells that is characteristic of PPHN.  In addition, SSRIs have an inhibitory effect on the synthesis of nitric oxide, a vasodilator that may have a role in the regulation of vascular tone and reactivity both in utero and during postnatal life.

Less severe complications occur in 20 to 30 percent of all newborns with prenatal exposure to SSRIs late in the pregnancy. These complications include mild respiratory distress, transient tachypnea of the newborn (a condition that results when there is extra fluid in the lungs or the fluid in the lungs is absorbed too slowly, making it more difficult for the baby to take in oxygen properly and requiring the baby to breathe faster and harder to compensate), failure to cry, and cyanosis (the bluish coloration of the skin due to the presence of de-oxygenated hemoglobin in blood vessels near the skin surface suggesting a circulatory or ventilatory problem). According to Chambers' research, it is possible that these respiratory problems represent the less severe end of the spectrum in a range of outcomes consistent with PPHN. When considered along with the new information that women who take certain doses of some antidepressants during their pregnancy are three times more likely to have a baby with a congenital heart malformation, why would anyone take an SSRI while pregnant?

Confusing the Issue
Even in the face of this new information of potentially devastating results from SSRI use during pregnancy, a group of physicians has been speaking out about the "harm" that may result to mothers who stops taking the medications during pregnancy -- complicating and confusing the issue at hand.

Prominent physicians are publishing articles warning mothers that they may experience a recurrence of depression or other underlying conditions if they stop taking whatever antidepressant they are presently prescribed. See, e.g., Lee S. Cohen et al., "Relapse of Major Depression During Pregnancy in Women who Maintain or Discontinue Antidepressant Treatment," J. Am. Med. Ass'n, 2006; 295: 499-507.

They caution that there is a high risk of relapse of depression following discontinuation of antidepressant therapy, and suggest women need to consider the risks of depressive relapse during pregnancy and the effects of untreated depression on fetal and maternal well-being. However, the doctors are extremely vague as to what are the "risks of untreated depression on fetal and maternal well-being."  It should also be noted that some of these physicians are spokespersons for, and therefore, paid by the drug companies.

In the absence of solid evidence regarding the risks of untreated depression and mounting evidence of harm, it is believed that most mothers would not risk the death of a newborn child from PPHN or other life-threatening birth defects for the sake of their own sense of "well-being." According to the information reviewed, almost without exception, mothers who have been treated with an antidepressant during pregnancy and given birth to children with PPHN or other birth defects say they never would have taken the risk, had they known it existed.

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