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Postpartum depression descended on Kristina Leos like a heavy fog that separated her from everyone she loved. She could see her newborn baby girl, her two older kids, and her husband, but she felt like a ghost passing through their world. “I was going through the motions, but it was like I was looking down on my family,” she recalls.

Leos, 40, a nurse who lives in Midlothian, Tex., tried several different antidepressants and doses. None helped. She messaged a friend, anxious that she was unfit to be a mother. She even asked if they would take her new baby, Victoria. Although Leos never considered hurting her kids, there were times when she was driving home from work and wondered what it would be like to drive off a bridge. “I just had no fear of dying,” she says. “I didn’t care what happened.”

In December 2023, nine months after Leos gave birth to Victoria, her doctor told her they were running out of options. She was down to serious choices, including infusions of ketamine (a drug that alters the anatomy and activity of brain cells), electroconvulsive therapy, or admission to a psychiatric hospital.

Then Leos remembered seeing something on social media about a new drug specifically for postpartum depression. Unlike older antidepressants such as Prozac, this medication worked on brain chemicals that are particularly affected by pregnancy. She asked her doctor about it, and they decided to give it a try. Leos began the medication on New Year’s Day 2024. Three days later, her world shifted. “I was driving on the highway, and I could literally feel this huge cloud lifting over me,” she says. “And every day I got better and better.” The drug, called zuranolone and approved by the U.S. Food and Drug Administration in 2023, has since relieved depression in thousands of women.

This kind of help is needed desperately. For new mothers, the overall leading cause of death during the first year after childbirth is not bleeding or infection, according to one study encompassing 36 states. What kills more are mental health problems, which account for approximately 23 percent of maternal deaths in the country. These disorders include a lot of cases of postpartum depression. Yet fewer than half of the women who show signs of such illness are diagnosed, and even fewer receive any form of treatment.

Emerging research on the biology of postpartum depression shows that it is not like other severe mood disorders neurologically or biochemically. Rather, it is a result of dramatic changes in hormone levels that come with pregnancy and childbirth. Studies have shown that levels of progesterone and a related hormone, allopregnanolone, rise significantly during pregnancy. Then the levels drop sharply after delivery. Some women are particularly sensitive to this drop, which can disrupt the brain circuitry that regulates mood, leaving them unable to effectively deal with the stresses of motherhood. Zuranolone is designed to offset that drop-off.

Growing knowledge of the neurobiology of postpartum depression is also pointing toward methods for earlier and more reliable detection. Many experts hope that identifying biomarkers that predict which women will develop the condition, as well as the introduction of the new medication, will take the stigma away from the illness and stop both health-care workers and patients from viewing it as a sign of personal weakness or poor parenting. “It is a serious mental illness,” says Kristina Deligiannidis, a reproductive psychiatrist at the Feinstein Institutes for Medical Research at Northwell Health in New York State. “We just want to empower women to seek treatment.”

Challenges do remain. The price tag for the two-week course of zuranolone is nearly $16,000, raising concerns about how insurance coverage and looming Medicaid-eligibility cuts could restrict access, especially because Medicaid covers about 40 percent of births in the U.S., and researchers are still trying to figure out why the pill doesn’t work for everyone. “Not every single person that takes it is going to have a fabulous remission of their symptoms,” says Samantha Meltzer-Brody, a psychiatrist and founder of the perinatal psychiatry program at the University of North Carolina School of Medicine in Chapel Hill. Still, she views the medication as a major milestone. “It can work remarkably well for more than half of people, and it’s rapid-acting,” she says. “That’s a game changer.”

For centuries, medicine has struggled to fully grasp the causes and consequences of postpartum depression. Descriptions go as far back as ancient Greece: physicians wrote about women who showed signs of a depressed mood, and even psychosis, after childbirth. During the Middle Ages, new mothers with depressive symptoms were often believed to be possessed by demons or suffering from an imbalance of bile or other body fluids. Postpartum mood disturbances have also been grouped into vague or broad diagnoses such as melancholia, mania, or neurosis, which did little to help patients.

Even in modern times, such distress is often dismissed as “baby blues”—the mood swings that affect most new moms but typically resolve within a couple of weeks. But postpartum depression is more intense and long-lasting. It can cause profound sadness and despair, disrupting the crucial bond between mother and child, and its consequences can affect multiple generations. Every yea,r approximately 500,000 women in the U.S. experience the condition. Approximately 30 percent of women with postpartum depression continue to experience symptoms one year after giving birth. For some, these problems can persist for as long as 11 years.

Yet postpartum depression is not officially recognized as a standalone illness. It did not appear in the Diagnostic and Statistical Manual of Mental Disorders (DSM), the so-called bible of psychiatry, until 1994. Even then it was listed as a subtype of major depression. In the most recent major edition, DSM-5, released in 2013, it is still subsumed under the “major depression” label, with the added phrase “with peripartum onset.” These additional three words reflect evidence that almost half of women develop symptoms during pregnancy, not just after.

Because postpartum depression has been lumped in with major depression, the two have often been treated the same way. Therapy has relied on traditional antidepressants such as selective serotonin reuptake inhibitors (SSRIs) or serotonin and norepinephrine reuptake inhibitors. This approach is rooted in the idea that depression stems from low levels of chemical messengers such as serotonin and norepinephrine that help to govern mood. These antidepressants aim to boost levels of these messengers in the brain.

Not everyone who takes zuranolone is going to have a fabulous remission. Still, it works well for more than half the people. That’s a game-changer.

But in recent decades, the research community has recognized that focusing only on these chemical imbalances leaves out other factors that may underlie postpartum depression—including genetics, inflammation, hormonal changes, and neuroplasticity, the brain’s ability to adapt and form new connections.

Some scientists suspected that fluctuations in hormones such as estrogen and progesterone—called neurosteroids because they act in the brain—played an important role. Yet when research groups started examining the levels of various hormones and neurosteroids, they did not see consistent differences that explained why some new mothers developed depression, and others did not.

Then, about 17 years ago, Jamie Maguire, a neuroscientist now at Tufts University, stumbled on some unusual behavior in mice that had just given birth, and her observation helped to connect the dots. At the time, Maguire was a postdoctoral fellow at the University of California, Los Angeles, studying an ailment called catamenial epilepsy, in which brain seizures become more frequent or more severe during certain phases of the menstrual cycle. She was interested in how neurosteroids might protect against these seizures. Some neurosteroids have been shown to dampen brain activity by strengthening certain effects of a neurotransmitter called gamma-aminobutyric acid, or GABA. This chemical can inhibit neurons, making them less likely to fire. Maguire genetically engineered mice to have altered receptors for GABA on their neurons, making it hard for them to react to the chemical. Without this “brake” on neural activity, the mice’s brains became hyperexcitable. That extreme state can contribute to seizures.

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