Seifer, D. B., & Collins, R. L. (1990). Current concepts of beta-endorphin physiology in female reproductive dysfunction. Fertility and Sterility, 54(5), 757-771. https://doi.org/10.1016/s0015-0282(16)53928-4
Seifer DB, Collins RL. Current concepts of beta-endorphin physiology in female reproductive dysfunction. Fertil Steril. 1990;54(5):757-771. doi:10.1016/s0015-0282(16)53928-4
Seifer, D. B., and R. L. Collins. "Current concepts of beta-endorphin physiology in female reproductive dysfunction." Fertility and Sterility, vol. 54, no. 5, 1990, pp. 757-771.
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Beta-endorphin is linked to several menstrual cycle disorders
A 1990 review by two physicians reports that beta-endorphin, a brain hormone, has a role in the menstrual cycle and is associated with several disorders. Levels were higher in the studies of athletic and stress-related amenorrhea and polycystic ovarian syndrome. Levels were lower in the studies of premenstrual syndrome and menopause.
Key Findings
Beta-endorphin concentrations are highest in the luteal phase, slightly lower in the late follicular phase, and lowest during menstruation and the early follicular phase.
Women with exercise-associated amenorrhea had higher resting beta-endorphin and cortisol than nonathletic women with regular menses. In one study, athletes with amenorrhea had higher basal beta-endorphin than athletes with regular cycles.
Women with premenstrual syndrome had lower plasma beta-endorphin than controls in the luteal phase. Placebo-controlled trials of clonidine (24 women with low beta-endorphin) and naltrexone (20 women) reported better symptoms.
Naltrexone given daily for 28 days produced ovulatory cycles in three women with hypothalamic amenorrhea. Each became amenorrheic again after it stopped.
Several studies found raised plasma beta-endorphin in women with polycystic ovarian disease compared with controls.
Interpretation
The paper is a narrative review of animal experiments, hormone measurements and small clinical trials. Most human data come from blood samples. The authors suggest beta-endorphin may change the pulsed release of GnRH, the brain signal that drives ovulation. The authors ask whether altered levels are merely associated with a disorder or a cause of it.
RRM Context
Restorative reproductive medicine reads the menstrual cycle as a vital sign. The review points to the GnRH signal as a possible meeting place for stress, heavy training and sex steroids. Hypothalamic amenorrhea and polycystic ovarian syndrome (PCOS), also called PMOS (Polyendocrine Metabolic Ovarian Syndrome), both raise the question of what stops ovulation. The review links both to altered GnRH release.
Our editorial summary of this paper, not the article's abstract.
Abstract
beta-Endorphin has a role in the regulation of the normal menstrual cycle and possibly in the onset of puberty. We have reviewed the evidence pointing to an alteration in this neuropeptide that may contribute to the pathogenesis of various reproductive dysfunctions. Elevated or high levels of beta-endorphin have been associated with exercise-associated amenorrhea, stress-associated amenorrhea, and polycystic ovarian syndrome. Depressed or low levels of beta-endorphin have been associated with PMS and menopause. Alterations in the levels of beta-endorphin may change the pulsatile release of GnRH via noradrenergic and/or dopaminergic pathways. We have primarily focused on beta-endorphin as representative of the endogenous opioid peptides, but other opioid peptides may also contribute to the pathogenesis of various types of reproductive dysfunction. Perhaps it will become possible to characterize and hone our understanding of the function of beta-endorphin and the other substances composing the endogenous opioid peptides. A better understanding of their role in physiological as well as pathophysiological processes may allow for the development of rational approaches to the treatment of specific disorders pertaining to reproduction. Many questions remain unanswered. Among the most relevant are: what is the precise mechanism of action by which beta-endorphin exerts its influence on pulsatile GnRH release? Is there a functional relationship between CNS and peripheral (serum) levels of beta-endorphin? Are the detected changes in beta-endorphin levels merely associated, or are they a cause of a particular disorder? Since it took almost 40 years between the time prostaglandins were first discovered and eventual realization of their clinical application, it may take some time before the beta-endorphin story is complete.
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