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Physiological mechanisms underlying lactational amenorrhea
A S McNeilly1, C C Tay, A Glasier
1MRC Reproductive Biology Unit, University of Edinburgh, United Kingdom.
Annals of the New York Academy of Sciences
|February 18, 1994
Summary
Breastfeeding delays ovarian cycles by disrupting gonadotropin-releasing hormone (GnRH) pulsatile release. Reduced luteinizing hormone (LH) prevents ovulation until suckling stimulus decreases sufficiently.
Area of Science:
- Reproductive endocrinology
- Neuroendocrinology
- Lactational physiology
Background:
- Breastfeeding is known to delay the return of ovarian cyclicity.
- The hormonal mechanisms underlying this delay are complex and not fully understood.
Purpose of the Study:
- To elucidate the neuroendocrine mechanisms by which suckling disrupts the hypothalamic-pituitary-ovarian axis.
- To understand how these disruptions affect follicle development and ovulation during lactation.
Main Methods:
- The study reviews existing literature on hormonal regulation during lactation.
- It analyzes the interplay between suckling, hypothalamic GnRH release, and pituitary gonadotropin secretion (FSH and LH).
Main Results:
- Suckling disrupts pulsatile GnRH release, leading to inadequate LH pulses.
- This results in reduced estradiol production, impaired follicle development, and anovulation or cystic follicles.
- Ovulation only resumes when suckling stimulus allows for a normal preovulatory LH surge.
Conclusions:
- Suckling delays ovarian cyclicity by disrupting GnRH release patterns, not by complete inhibition.
- The precise mechanism of suckling-induced GnRH disruption remains unclear, with potential roles for prolactin, dopamine, or opiates.
- Optimizing lactation for contraceptive potential may require focusing on stress-free oxytocin release for milk letdown.