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Puerperal breast feeding does not stimulate circulating opioids in humans
Journal of Endocrinological Investigation
|November 1, 1982
Summary
Breastfeeding rapidly normalizes hormone levels like ACTH and cortisol post-delivery. Suckling stimulates prolactin (PRL) release via distinct serotoninergic pathways, indicating it
Area of Science:
- Reproductive Endocrinology
- Neuroendocrinology
- Lactational Physiology
Background:
- Postpartum hormone dynamics are crucial for maternal adaptation.
- Proopiocortin (POMC)-related peptides and prolactin (PRL) play key roles in lactation and stress response.
- Serotoninergic pathways are implicated in both PRL release and POMC peptide regulation.
Purpose of the Study:
- To investigate the changes in ACTH, beta-lipotropin (beta-LPH), beta-endorphin (beta-EP), PRL, and cortisol during early puerperium.
- To assess the hormonal response to suckling in healthy lactating women.
- To explore the neuroendocrine mechanisms underlying PRL release and POMC peptide secretion during breastfeeding.
Main Methods:
- Hormone levels (ACTH, beta-LPH, beta-EP, PRL, Cortisol) were measured in 7 healthy lactating women.
- Measurements were taken on days 1-5 postpartum, at 9:00 AM, before and 30 minutes after suckling.
- Analysis focused on hormonal changes from delivery levels and responses to suckling stimulation.
Main Results:
- ACTH, beta-LPH, beta-EP, and cortisol levels decreased significantly from delivery, stabilizing by day 2 postpartum.
- Plasma PRL levels declined but remained elevated, with suckling stimulating a further increase.
- Suckling did not alter ACTH, beta-LPH, beta-EP, or cortisol levels, suggesting a lack of stress response.
Conclusions:
- Early postpartum hormone profiles show a rapid normalization of POMC-related peptides and cortisol.
- Breastfeeding is not a stressful event, as evidenced by the absence of a typical POMC peptide stress response.
- PRL release during suckling is mediated by serotoninergic neurons distinct from those controlling POMC peptide secretion.