Effect of Breast-Feeding on Pituitary-Ovarian Function After Childbirth

Bonnar, J.; Franklin, M.; Pn, Nott; As, Miller

doi:10.1097/00006254-197605000-00003

Cited by 4 publications

(4 citation statements)

References 1 publication

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“…During the first week after delivery the concentration of PRL in both groups was grossly elevated above the value found in nonpregnant women, confirming previous reports (21)(22)(23). The progressive rise in the concentration of PRL during pregnancy is probably due to the elevated level of estrogen, which is known to stimulate the secretion of PRL (24).…”

Section: Estrogen Provocation Testsupporting

confidence: 89%

Failure of Estrogen-Induced Discharge of Luteinizing Hormone in Lactating Women

Baird

McNeilly

Sawers

et al. 1979

The Journal of Clinical Endocrinology & Metabolism

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Pituitary-ovarian relationships were studied in seven lactating women by measuring the basal plasma concentrations of pituitary and ovarian hormones and their responses to an estrogen provocation test at 7, 30, and 100 days after delivery. The results were compared to a similar group of seven women who did not breast feed. The first ovulation occurred in five of the nonlactating women beteen 43-87 days after delivery, as judged by the urinary excretion of total estrogen and pregnanediol. In all lactating women, ovarian cyclicity was suppressed for at least 150 days after delivery or until weaning. The basal concentration of PRL in lactating women was significantly higher than in the nonlactating women at all three times measured. At 30 and 100 days, the concentration of estradiol was significantly lower in the lactating women, although the basal concentrations of FSH were similar in the two groups. After an injection of 1 mg estradiol benzoate, the concentrations of FSH and LH in plasma were suppressed to a greater extent in lactating than in nonlactating women. In addition, fewer of the lactating group (one of seven and none of seven at 30 and 100 days, respectively) than the nonlactating group (two of seven and five of seven) subsequently showed a rise in the concentration of LH 58--96 h after the estrogen injection (positive feedback). These results suggest that during lactation the hypothalamic-pituitary system is more sensitive to the negative feedback and relatively insensitive to the positive feedback of estrogen.

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Section: Estrogen Provocation Testsupporting

confidence: 89%

Failure of Estrogen-Induced Discharge of Luteinizing Hormone in Lactating Women

Baird

McNeilly

Sawers

et al. 1979

The Journal of Clinical Endocrinology & Metabolism

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“…Circulating concentrations of PRL are at least highly correlated with the duration of post-partum infecundity (Bonnar et al, 1975;Delvoye et al, 1978;. Strong, if circumstantial, evidence for a direct causal effect of PRL comes from studies of pathological hyperprolactinaemia associated, for example, with pituitary adenomas.…”

Section: Introductionmentioning

confidence: 99%

Lactation and birth spacing in highland New Guinea

et al. 1985

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The effects of infant suckling patterns on the post-partum resumption of ovulation and on birth-spacing are investigated among the Gainj of highland New Guinea. Based on hormonal evidence, the median duration of lactational anovulation is 20-4 months, accounting for about 75% of the median interval between live birth and next successful conception (i.e. resulting in live birth). Throughout lactation, suckling episodes are short and frequent, the interval changing slowly over time, from 24 minutes in newborns to 80 minutes in 3-year olds. Maternal serum prolactin concentrations decline in parallel with the changes in suckling patterns, approaching the level observed in non-nursing women by about 24 months post-partum. A path analysis indicates that the interval between suckling episodes is the principal determinant of maternal prolactin concentration, with time since parturition affecting prolactin secretion only in so far as it affects suckling frequency. The extremely prolonged contraceptive effect of breast-feeding in this population thus appears to be due to (i) a slow decline in suckling frequency with time since parturition and (ii) absence of a decline over time in hypothalamic-pituitary responsiveness to the suckling stimulus.

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“…However serum oestradiol concentra¬ tions were below normal levels and significantly lower in lactating compared to non-lactating mo¬ thers, supporting the view that the ovaries do not respond to FSH stimulation in the presence of increased prolactin levels (Bonnar et al 1975).…”

Section: Discussionmentioning

confidence: 63%

Influence of lactation on oral glucose tolerance in the puerperium

Lenz¹,

Kühl²,

Hornnes³

et al. 1981

Acta Endocrinologica

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The influence of endogenous hyperprolactinaemia on oral glucose tolerance in normal women post-partum was studied. An oral glucose tolerance test (OGTT) was performed 8 weeks after delivery in 23 women, 13 of whom were breastfeeding. The lactating women had significantly higher plasma prolactin values before and during the OGTT than the non-lactating women (P < 0.005). Fasting values of serum FSH, LH, progesterone and plasma glucagon were similar in the two groups. The non-lactating women had higher fasting concentrations of serum oestradiol (P < 0.0005), plasma glucose (P < 0.05) and insulin (P < 0.05) than the lactating women. After oral glucose no differences were found between lactating and non-lactating women in changes in plasma glucose, insulin and glucagon concentrations. It is concluded that lactating women 8 weeks post-partum do not have an impaired OGTT compared to non-lactating women despite elevated plasma prolactin levels.

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Effect of Breast-Feeding on Pituitary-Ovarian Function After Childbirth

Cited by 4 publications

References 1 publication

Failure of Estrogen-Induced Discharge of Luteinizing Hormone in Lactating Women

Failure of Estrogen-Induced Discharge of Luteinizing Hormone in Lactating Women

Lactation and birth spacing in highland New Guinea

Influence of lactation on oral glucose tolerance in the puerperium

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