News | Could maternal stress cause embryos to ‘pause’? Oxytocin may be a key regulator
Oxytocin is well known for its important role in childbirth, breastfeeding, and mother-infant bonding. New research suggests that this “love hormone” may have another role in mammalian reproduction: delaying embryonic development and, under certain conditions, causing pregnancy loss.
An animal study led by NYU Langone Health found for the first time that when the mother is under certain physiological stress, such as lactation, elevated oxytocin may cause an embryo to enter diapause, stopping growth for days or weeks before implantation. This may be an evolutionary strategy that conserves maternal energy and protects offspring.
Exploring diapause: an embryo’s development placed on pause
Diapause is an active pause in early embryonic growth before implantation in the uterine lining. It occurs naturally in mammals ranging from armadillos to giant pandas and seals. Whether it occurs in humans or is linked to pregnancy complications remains unclear.
In mice, the study confirmed that elevated oxytocin during lactation can significantly delay implantation. A mouse pregnancy normally lasts 20 days, but concurrent pregnancy and nursing delayed delivery by about one week.
“Lactation consumes substantial maternal nutrients and places demands on both existing and developing offspring,” said co-author Dr. Moses Chao, professor of cell biology, neuroscience, and psychiatry at NYU. “Oxytocin may be one way the mother presses pause.”
Even small amounts of oxytocin delayed implantation
To test oxytocin’s role in diapause, researchers exposed early embryos to 1 or 10 micrograms of oxytocin. Even these small doses delayed implantation by up to three days.
When scientists simulated the oxytocin surges that occur during lactation, nearly all experimental mice experienced pregnancy loss. This suggests that oxytocin may not only pause pregnancy but may also end it.
Embryos can also detect oxytocin
The key appears to be the trophectoderm, the outer layer of the early embryo that later contributes to the placenta.
Oxytocin binds to specific receptors on trophectoderm cells. When researchers genetically removed these receptors, implantation rates fell sharply. Embryos can therefore detect oxytocin, and this ability appears important for survival.
Professor Chao said: “Diapause may be both a protective mechanism and an evolutionary strategy for adapting to environmental stress and optimizing reproductive timing.”
New clues to infertility and pregnancy loss
“Although infertility and abnormal early pregnancy development are extremely common, their mechanisms remain poorly understood,” said senior author Dr. Robert Froemke, Skirball Professor in NYU’s Department of Neuroscience. “This finding offers a glimpse of the underlying biology.”
The team plans to investigate:
When and how diapause ends
Whether diapause affects offspring health after birth
Whether this oxytocin effect could be used in assisted reproduction or contraception
Whether hormones such as estrogen and progesterone act with oxytocin in diapause
Froemke cautioned that although mice and humans are both mammals, their reproductive mechanisms differ substantially, so the findings should not yet be applied directly in clinical care. They nevertheless represent an important step toward more precise reproductive medicine.
Research team and funding
The study was funded by the U.S. National Institutes of Health under grants T32MH019524, NS107616, and HD088411. It was published March 5, 2025, in the Women’s Health special issue of Science Advances.
Authors included Jessica Minder, now a postdoctoral researcher at the University of California, Berkeley; Luisa Schuster; Habon Issa; Janaye Stephens; Michael Cammer; Latika Khatri; Maria Alvarado-Torres; Jie Tong; Orlando Aristizábal; Youssef Wadghiri; Sang Yong Kim; Catherine Pei-ju Lu; and Silvana Valtcheva.
News | Could maternal stress cause embryos to ‘pause’? Oxytocin may be a key regulator
News | Could maternal stress cause embryos to ‘pause’? Oxytocin may be a key regulator
Oxytocin is well known for its important role in childbirth, breastfeeding, and mother-infant bonding. New research suggests that this “love hormone” may have another role in mammalian reproduction: delaying embryonic development and, under certain conditions, causing pregnancy loss.
An animal study led by NYU Langone Health found for the first time that when the mother is under certain physiological stress, such as lactation, elevated oxytocin may cause an embryo to enter diapause, stopping growth for days or weeks before implantation. This may be an evolutionary strategy that conserves maternal energy and protects offspring.
Exploring diapause: an embryo’s development placed on pause
Diapause is an active pause in early embryonic growth before implantation in the uterine lining. It occurs naturally in mammals ranging from armadillos to giant pandas and seals. Whether it occurs in humans or is linked to pregnancy complications remains unclear.
In mice, the study confirmed that elevated oxytocin during lactation can significantly delay implantation. A mouse pregnancy normally lasts 20 days, but concurrent pregnancy and nursing delayed delivery by about one week.
“Lactation consumes substantial maternal nutrients and places demands on both existing and developing offspring,” said co-author Dr. Moses Chao, professor of cell biology, neuroscience, and psychiatry at NYU. “Oxytocin may be one way the mother presses pause.”
Even small amounts of oxytocin delayed implantation
To test oxytocin’s role in diapause, researchers exposed early embryos to 1 or 10 micrograms of oxytocin. Even these small doses delayed implantation by up to three days.
When scientists simulated the oxytocin surges that occur during lactation, nearly all experimental mice experienced pregnancy loss. This suggests that oxytocin may not only pause pregnancy but may also end it.
Embryos can also detect oxytocin
The key appears to be the trophectoderm, the outer layer of the early embryo that later contributes to the placenta.
Oxytocin binds to specific receptors on trophectoderm cells. When researchers genetically removed these receptors, implantation rates fell sharply. Embryos can therefore detect oxytocin, and this ability appears important for survival.
Professor Chao said: “Diapause may be both a protective mechanism and an evolutionary strategy for adapting to environmental stress and optimizing reproductive timing.”
New clues to infertility and pregnancy loss
“Although infertility and abnormal early pregnancy development are extremely common, their mechanisms remain poorly understood,” said senior author Dr. Robert Froemke, Skirball Professor in NYU’s Department of Neuroscience. “This finding offers a glimpse of the underlying biology.”
The team plans to investigate:
When and how diapause ends
Whether diapause affects offspring health after birth
Whether this oxytocin effect could be used in assisted reproduction or contraception
Whether hormones such as estrogen and progesterone act with oxytocin in diapause
Froemke cautioned that although mice and humans are both mammals, their reproductive mechanisms differ substantially, so the findings should not yet be applied directly in clinical care. They nevertheless represent an important step toward more precise reproductive medicine.
Research team and funding
The study was funded by the U.S. National Institutes of Health under grants T32MH019524, NS107616, and HD088411. It was published March 5, 2025, in the Women’s Health special issue of Science Advances.
Authors included Jessica Minder, now a postdoctoral researcher at the University of California, Berkeley; Luisa Schuster; Habon Issa; Janaye Stephens; Michael Cammer; Latika Khatri; Maria Alvarado-Torres; Jie Tong; Orlando Aristizábal; Youssef Wadghiri; Sang Yong Kim; Catherine Pei-ju Lu; and Silvana Valtcheva.
Source:
Collected online