Is breastfeeding linked to how strongly a mother's body releases growth hormone after stimulation?

Details

Human prolactin (PRL), growth hormone (GH), and their respective receptors have closely related origins. Around childbirth, physiologically elevated prolactin is associated with markedly reduced GH secretion, a pattern that remains incompletely characterized. PRL-secreting “pregnancy cells” may influence the secretory function of GH-producing cells, called somatotropes, through local, paracrine signaling; somatotropes are known to express PRL receptors.

In a randomized, placebo-controlled design, researchers examined GH responsiveness in 10 nonpregnant women and 58 mothers. The mothers were studied either early postpartum—a median of 48 hours after delivery, with a range of 42–54 hours, all lactating—or late postpartum—a median of 10 weeks, with a range of 3–25 weeks, including lactating and nonlactating subgroups. To stimulate GH release, the researchers used GH-releasing peptide-1 (GHRP-1), given as a 100-microgram intravenous bolus.

Baseline serum PRL concentrations were similarly low in nonpregnant controls and nonlactating women in the late postpartum period, with a median of 5 micrograms/L. Concentrations were elevated in lactating women, particularly early postpartum: the median was 102 micrograms/L early postpartum, compared with 27 micrograms/L late postpartum.

GHRP-1 stimulated a GH response in every study group, but lactation was associated with smaller and slower responses. At 20 minutes after GHRP-1 treatment, the median serum GH concentration in controls was 78 micrograms/L. The control concentration was 7-fold higher than in early-postpartum lactating women and 5-fold higher than in late-postpartum lactating women. Baseline PRL concentrations were inversely correlated with GH responsiveness: the higher the baseline PRL concentration, the smaller and slower the GH response to GHRP-1.

The findings further characterize reduced GH responsiveness after childbirth by showing that it includes the GHRP pathway. The inverse relationship between baseline PRL and GH responsiveness is consistent with the idea that pregnancy cells may directly or indirectly inhibit the secretory capacity of somatotropes; the abstract presents this as a possible explanation, not an established mechanism.