Hormonal pathways and neuroendocrine control Breastfeeding delays the resumption of normal ovarian cycles by disrupting the pattern of pulsatile release of gonadotropin-releasing hormone (GnRH) from the hypothalamus and hence luteinizing hormone (LH) from the pituitary. The plasma concentrations of follicle-stimulating hormone (FSH) during lactation are sufficient to induce follicle growth, but the inadequate pulsatile LH signal results in a reduced estradiol production by these follicles. When follicle growth and estradiol secretion does increase to normal, lactation prevents the generation of a normal preovulatory LH surge and follicles either fail to rupture, or become atretic or cystic. Only when lactation declines sufficiently to allow generation of a normal preovulatory LH surge to occur will ovulation take place with the formation of a corpus luteum of variable normality. Thus lactation delays the resumption of normal ovarian cyclicity by disrupting but not totally inhibiting, the normal pattern of release of GnRH by the hypothalamus. The mechanism of disruption of GnRH release remains unknown. In women, hyperprolactinemia is often associated with amenorrhea, a condition that resembles the physiological situation during lactation<unk> . Mechanical detection of suckling increases prolactin levels in the body to increase milk synthesis. Excess prolactin may inhibit the menstrual cycle directly, by a suppressive effect on the ovary, or indirectly, by decreasing the release of GnRH. Suckling stimulus Suckling intensity directly correlates with the duration of the amenorrheal period following birth. Suckling intensity has several dynamic components: frequency of suckling, duration of the suckling bout, and duration of suckling in a 24 hour period. It is not clear which of these plays the most critical role in maintaining amenorrhea. Suckling intensity is highly variable across populations. Studies of U.S. and Scottish women show that at least six bouts per day and 60 minutes of suckling in a 24 hour period will typically sustain amenorrhea. Concurrent studies of !Kung women in Botswana and Gainj women in Papua New Guinea have shown that very frequent, very short suckling bouts of about 3 minutes, 40 to 50 times per day correlate with typical amenorrhea of up to two years postpartum. When an infant suckles, sensory receptors in the nipple send a signal to the anterior pituitary gland in the brain, which secretes prolactin and oxytocin. Prolactin and oxytocin trigger the release (letdown) of milk and its ejection from the nipple in a positive feedback loop. It was previously thought that prolactin hormone, which is released by the anterior pituitary in response to the direct nerve stimulation of suckling, was responsible for creating the hormonal pathways necessary to sustain amenorrhea. Now, however, it seems that this relationship is one of correlation not causation as prolactin levels in the blood plasma are simply an indicator of suckling frequency. Suckling, and the subsequent release of prolactin, is not directly responsible for postpartum infecundity. Rather it is one mechanism that increases milk production, thereby increasing the metabolic cost of breastfeeding to mothers, which contributes to sustained infecundity. Suckling as proxy indicator of infecundity rather than a direct, hormonal causal factor is supported in studies contrasting the nursing intensity hypothesis, which says that more intense (prolonged, frequent) breastfeeding will result in a longer period of<unk> , and the metabolic load model, which posits that maternal energy availability will be the main factor determining postpartum amenorrhea and the timing of the return of ovarian function. Lactation and energy availability Postpartum ovarian function and the return of fecundity depend heavily on maternal energy availability. This is due to the relatively consistent metabolic costs of milk production across populations, which fluctuate slightly but represent a significant cost to the mother. The metabolic load hypothesis states that women with more available energy or caloric/metabolic resources will likely resume ovarian function sooner, because breastfeeding represents a proportionally lower burden on their overall metabolic function. Women with less available energy experience a proportionally higher burden due to breastfeeding and therefore have less surplus metabolic energy to invest in continued reproduction. The metabolic load model is therefore consistent with the nursing intensity hypothesis, in that more intense nursing increases the relative metabolic burden of breastfeeding on the mother. It also takes into account the overall energy supply of the mother in determining whether she has enough caloric/metabolic resources available to her to make reproduction possible. If net energy supply is high enough, a woman will resume ovarian cycling sooner despite still breastfeeding the current infant. Infecundity Amenorrhea itself is not necessarily an indicator of infecundity, as the return of ovarian cycling is a gradual process and full fecundity may occur before or after first postpartum menses. Additionally, spotting or the appearance of first postpartum menses can be a result of either lochia or estrogen withdrawal and not actual ovulation.<unk>  has evolved as a mechanisms for preserving the health of the mother. This period of infecundity allows the mother to focus her energy on breastfeeding as well as allow time for her body to heal between births. The frequency and durations of the feedings determine how long the mother will continue to be infecund during breastfeeding. However there is variation across different cultures. The Turkana, Gainj, and Quechua societies all breastfeed on demand until their child is around 2 years old. The timing of returned ovulation for these women is however varied. Because of this, interbirth intervals vary across these three societies.
Lactational amenorrhea
Exercise amenorrhoea
Polycystic ovary syndrome
Functional hypothalamic amenorrhea
Anovulation
Obstetric transition
Premenstrual syndrome
Postpartum physiological changes