Oxytocin—the “feel-good” hormone our bodies naturally produce—is central to a lot of important physiological functions:
feelings of social connectedness and attachment, orgasm, breastfeeding, and labor among them.
But when its synthetic form (usually Pitocin) is given, especially before and during childbirth to stimulate contractions and prevent postpartum hemorrhage, subtle changes in how the hormone is expressed in the brain and circulated in the blood may put women and their babies at greater risk for depression.
“There are many things across pregnancy that we know can impact postpartum depression and the oxytocin receptor in our genes, but this is one factor that we can do something about.”Maria McDonald, FNP, PhD candidate, and NIH grantee
It was observing transgenerational depression as a family nurse practitioner and wondering what biological factors triggered its passage from parent to child that first stirred questions in Maria McDonald’s (PhD `24) mind. In the pediatric ICU, she often felt helpless to improve the clinical outcomes of depressed children. In an adult psychiatric clinic, she cared for suffering mothers who battled it, too. Those experiences deepened McDonald’s interest in depression’s biological underpinnings, and the role that epigenetics—a concept in which behaviors and environment change how your genes do their work—might play.
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It’s not entirely clear whether and how severely doses of synthetic oxytocin increase mothers’ chances for developing postpartum depression (PPD), but what is clear is the devastating toll PPD exacts. In mothers, PPD is linked to anxiety, fatigue, difficulties bonding, and, in the most acute cases, debilitating psychosis. Infants and small children exposed to it can face delayed cognition, impaired social functioning, behavioral problems, and mood disorders. With stakes that high, understanding what might influence its likelihood, said McDonald, is critical.
“There are many things across pregnancy that we know can impact postpartum depression and the oxytocin receptor in our genes,” she said, “but this is one factor that we can do something about.”
A year ago, McDonald—who earned a $77,000 NIH Diversity Supplement grant in 2021—began work with UVA Psychology Professor Jessica Connelly whose lab investigates DNA methylation of the oxytocin receptor and consequent behavior changes. The partnership means bench science for McDonald, who skillfully pipettes tiny brain and blood samples on a pyro-sequencer to measure the saturation of genetic material present. Though currently focused on tissue from prairie voles, she’ll soon move to saliva and blood samples from humans to better understand how administering extra oxytocin during certain critical periods might pave the way for depression to pass more readily from one generation to the next.
And while McDonald’s and her colleagues’ work may ultimately provide a potentially divisive, cautionary tale about Pitocin’s unintended consequences in both nursing and neuroscience, the cross-the-aisle collaboration she has with her colleagues is powerful. Each profession, she says, brings perspective to the other.
“I hear women talk about their symptoms while my colleagues try to understand the animal model and biological aspects of things,” McDonald said. “But what’s important is that we all have the opportunity to sit in a room together . . . and step into each other’s worlds for a little bit to understand what all of this means for us as humans.”