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24-11-2008 | Mental health | Article

Serotonin transporter variant risks post-partum depression

Abstract

Free abstract

MedWire News: Women with variant forms of the serotonin transporter gene may be particularly vulnerable to depressive symptoms after childbirth, research shows.

The effect may be more pronounced under certain environmental conditions such as depletion of the amino acid tryptophan, which often accompanies pregnancy and delivery, study co-author Julio Sanjuán (Universidad de Valencia, Spain) and colleagues note.

They comment in the British Journal of Psychiatry: “Post-partum depression has a great impact on the family and economy, and is considered a major public health problem.

“Pregnancy and delivery are accompanied by hormonal changes as well as lower plasma tryptophan levels, both of which are thought to be etiologically relevant to the mood changes that follow childbirth.”

Noting that tryptophan is precursor to the neurotransmitter serotonin, the researchers investigated whether known variants in the serotonin transporter gene influence post-partum depression.

They recruited 1804 depression-free Spanish women who were assessed using the Edinburgh Postnatal Depression Scale (EPDS) at 2–3 days, 8 weeks, and 32 weeks post-partum.

The team genotyped women for two polymorphisms in the serotonin transporter gene, both of which affect expression level: 5-HTTLPR, a 44-base pair insertion/ deletion in the promoter region, and STin2, a multi-allelic 17-base pair variable number of tandem repeats (VNTR) within intron 2.

In all, 173 (12.7%) women experienced major depression during the 32-week post-partum period.

Notably, serotonin transporter genotype was not significantly associated with major depression.

However, depressive symptoms increased in a dose–response fashion with increasing copies of high-expression serotonin transporter gene variants at 8 weeks post-partum, but not at 32 weeks.

The researchers speculate that such high expression of the serotonin transporter gene may actually deplete serotonin by removing it from the synaptic cleft. This would exacerbate any existing depletion of serotonin through, for example, a decrease in plasma tryptophan levels after delivery.

“This study supports a new hypothesis for understanding the biological mechanisms underlying depressive symptoms after delivery and encourages further study of gene–tryptophan interactions in mood disorders,” Sanjuán and colleagues conclude.

By Andrew Czyzewski