Epigenetic variation can predict the risk of post-natal depression symptoms in women without a history of depression, researchers from the UK and US have found.
As this epigenetic regulation can be measured in blood, the finding could lead to a blood test for post-natal depression susceptibility.
'Our data need to be replicated, but it is our hope that the oxytocin receptor marker we have identified will be useful to clinicians in identifying women at risk for postpartum depression,' said first author Dr Aleeca Bell of the University of Illinois, Chicago.
The researchers used blood samples and psychological data on 500 women to determine the association between an OXTR variant, the level of OXTR methylation, and post-natal depression. Depressive symptoms were evaluated at 32 weeks gestation and eight weeks postpartum.
They found that in women without depression during pregnancy, the presence of a specific OXTR genotype, coupled with high methylation levels in OXTR, were nearly three times more likely to develop post-natal depression than other women.
In these women, the risk of post-natal depression more than doubled with each 10 percent increase in DNA methylation in the gene. This finding also remained significant when the researchers excluded women who had a previous history of depression outside of pregnancy.
There was no association between the genotype or methylation levels and postpartum depression for women with depression during pregnancy.
'We know that women who have experienced depression before pregnancy are at higher risk of developing depression in the postpartum period,' said Dr Jessica Connelly, assistant professor of psychology at University of Virginia, and senior author of the study. 'However, women who have never experienced depression also develop postpartum depression. These markers we identified may help to identify them in advance.'
Previous research has linked oxytocin levels as well as several OXTR SNPs, single nucleotide polymorphisms, to postpartum depression.
Writing in Frontiers in Genetics, the researchers explain that oxytocin promotes wellbeing and is involved in maternal bonding. They hypothesise that mothers with low oxytocin or receptor levels may become insensitive to its effects and thus do not benefit from its protective effects during the stressful post-natal period.
'The role of the oxytocin system in maternal behaviour is well known in rodents,' said study co-author Professor Sue Carter, director of the Kinsey Institute at Indiana University. 'Our work emphasises its importance in the human maternal condition and places the epigenetic regulation of the oxytocin receptor at the forefront.'