Likely Cause of Postpartum Blues and Depression Identified
News Aug 14, 2008
Unique biochemical crosstalk that enables a fetus to get nutrition and oxygen from its mother's blood just may cause common postpartum blues, researchers say.
That crosstalk allows the mother's blood to flow out of the uterine artery and get just a single cell layer away from the fetus' blood, says Dr. Puttur D. Prasad, biochemist in the Medical College of Georgia School of Medicine.
That controlled exchange between the blood of mother and fetus is courtesy of the placenta regulating levels of serotonin, a neurotransmitter commonly associated with depression. But platelets that enable blood clotting also secrete serotonin which prompts platelets to aggregate and the placenta to want to get rid of it.
"If there were no proper control here, blood leaving the mother's blood vessel would trigger release of serotonin, platelets would aggregate, vessels constrict and the fetus wouldn't get what it needs," says Dr. Prasad. An MCG research team led by Dr. Vadivel Ganapathy first reported evidence of serotonin transporter gene expression in the placenta back in 1989 in the Journal of Biological Chemistry. Now they know the gene plays an important role in the crosstalk that forestalls clotting until after birth.
When the fetus and placenta are gone, blood continues flowing from the mother's uterine artery until platelets move in to stop it, Dr. Prasad explains. Serotonin levels begin to rise and interact with receptors on the smooth muscle of the uterus. This stimulates production of interleukin-1 beta which the MCG researchers found regulates expression of serotonin-hoarding transporters. Interleukin-1 beta gets in the mother's bloodstream, crosses the blood brain barrier and creates more serotonin transporters on the neurons when they are not needed.
Until interleukin-1 beta levels normalize, there's too little communication between serotonergic neurons and moms get the blues, says Dr. Prassad.
"We believe that 80 percent of women experience postpartum blues because of this effect of interleukin-1 beta. If our hypothesis holds true, lowering interleukin-1 beta levels may be a better treatment option." He notes that while serotonin reuptake inhibitors, commonly used for depression, work well in these women, transferring the drug to the baby during nursing can be problematic.
But there's more. In more serious postpartum depression, polymorphisms or variations of the serotonin transporter gene - which already have been linked to non-pregnancy related depression - appear to make bad matters worse because they are even better at taking up serotonin, he says.
Dr. Prasad, in collaboration with Dr. Sandra Pittman, director of MCGHealth's Healthy Start program, already put the laboratory findings into practice in a small study of 50 women enrolled in the federally funded program for women with high-risk pregnancies in the rural Georgia counties of Burke and McDuffie. The program was a perfect fit for the research. Healthy Start identifies women as early in pregnancy as possible who are at risk because of medical, psychosocial and/or environmental problems, Dr. Pittman says.
Many studies have looked at these genetic variations in non-pregnancy-related depression but not in postpartum depression, Dr. Prasad says.
They expect their studies will advance the understanding of the biochemical basis of postpartum blues and depression and point toward ways to better identify and treat it.
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