Oxytocin, the hormone widely known for its role in childbirth, lactation, and maternal bonding, may play a crucial role in fertility and pregnancy outcomes, according to a groundbreaking study. The research, led by scientists at NYU Langone Health and published in Science Advances, reveals that oxytocin may trigger a phenomenon known as “diapause,” where an embryo’s development is delayed after conception. This discovery, based on rodent studies, could provide new insights into human fertility challenges, including infertility, miscarriage, and premature or delayed birth.
Diapause is a process observed in several mammalian species, such as armadillos, pandas, and seals, where the embryo temporarily halts its development after fertilization. This pause allows the mother to conserve resources, like breast milk, until conditions are more favorable for successful reproduction. While similar evidence of diapause has been suggested in humans, the mechanisms behind it remained elusive until now.
The study, which focused on mice, found that maternal stress—particularly lactation—can induce diapause. The process of nursing demands significant energy and nutrients from the mother, leading to delays in the embryonic development of new offspring. The research demonstrated that in pregnant rodents already nursing a litter, the usual 20-day gestation period was extended by about a week. The delay was linked to an increase in oxytocin levels, which rise during lactation.
In laboratory tests, embryos exposed to small doses of oxytocin showed implantation delays of up to three days. When the hormone’s levels were elevated to mimic the surge observed during nursing, the pregnancy was often lost altogether.
“This finding reveals a previously unexplored role for oxytocin in controlling embryonic development,” said Moses Chao, Ph.D., a co-author of the study. “Abnormalities in oxytocin production could contribute to a variety of reproductive issues, including infertility, miscarriage, and birth timing problems.”
The research also uncovered the mechanism by which oxytocin impacts the embryo: the hormone binds to receptors on the trophectoderm, the outer layer of cells that forms the placenta. Mice with genetic alterations that disabled these receptors had much lower success rates of implanting into the uterus, highlighting the importance of oxytocin signaling in embryo survival.
Dr. Robert Froemke, senior author of the study, emphasized the significance of understanding these hormonal interactions, especially given the profound impact infertility and pregnancy complications can have on families. “A better grasp of the factors contributing to these issues will help us address them more effectively in the future,” Froemke noted.
Future research will investigate how cell growth resumes after diapause and how it might affect the long-term health of offspring. The team also plans to explore whether the findings can inform treatments in reproductive medicine. However, Froemke cautioned that while these results are promising, there are important differences between human and rodent reproductive processes that need to be carefully considered in future studies.
Despite the challenges, this research marks an exciting step toward uncovering the underlying causes of infertility and pregnancy-related complications, potentially paving the way for new therapeutic strategies.
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