A groundbreaking study reveals that oxytocin, a hormone traditionally linked to childbirth, lactation, and mother-infant bonding, may play an unexpected role in delaying pregnancy in times of maternal stress. The findings, published in Science Advances, highlight how oxytocin can temporarily halt the development of an embryo after conception, offering potential new understandings of infertility and pregnancy-related complications.
Led by researchers at NYU Langone Health, the study investigates a phenomenon called “diapause,” in which embryos pause their growth early in development before implanting in the mother’s uterus. This delay in development allows the mother to conserve resources, such as milk, to ensure successful offspring care later. Diapause is observed in various animal species, including armadillos, pandas, and seals, and has now been linked to stress factors like lactation in rodents.
The researchers found that when lactating mice were also pregnant, the typical gestation period of 20 days was extended by about a week. The delay was triggered by an increase in oxytocin levels, known to rise during nursing. The team demonstrated that even small doses of oxytocin were enough to delay embryo implantation by several days, confirming the hormone’s role in regulating diapause.
However, the study also showed that when oxytocin levels surged to mimic those observed during lactation, it caused pregnancy loss in nearly all the mice. These findings suggest that while oxytocin can temporarily delay pregnancy, high levels can have a detrimental effect on embryo survival.
Dr. Moses V. Chao, co-author of the study, explained, “Our findings shed light on oxytocin’s role in diapause, suggesting that abnormalities in its production could contribute to infertility, premature or delayed birth, and miscarriage.”
Further investigation revealed that oxytocin affects embryos by binding to receptors on the trophectoderm, a cell layer surrounding the early embryo that eventually becomes the placenta. Embryos genetically modified to lack oxytocin receptors were less likely to implant into the uterus, indicating that the ability to respond to oxytocin is crucial for embryo survival and development.
The study’s senior author, Dr. Robert Froemke, emphasized the significance of these findings in understanding infertility and pregnancy complications, which often remain poorly understood despite their widespread impact. “A deeper understanding of these factors may lead to better solutions for couples facing reproductive challenges,” said Froemke.
Looking forward, the research team plans to explore how cells resume normal growth after diapause, as well as how the process may affect offspring health post-birth. However, Froemke cautioned that the reproductive processes of mice and humans differ significantly, and future studies must also account for the roles of other pregnancy-related hormones, such as estrogen and progesterone.
These discoveries not only enhance our understanding of mammalian reproduction but may also open doors to new approaches in reproductive medicine and contraception.
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