This is the first experimental evidence that in lactating women, a family history of alcoholism in first-degree relatives is a determinant of hormonal and behavioral responses to breast stimulation and alcohol consumption. FHN and FHP women did not differ in their baseline prolactin values, and both exhibited an increase in prolactin in response to breast stimulation, although later and for a shorter period of time in FHP women compared with FHN women. Whereas moderate alcohol consumption increased the rapidity and duration of the prolactin response to breast stimulation in all women, only FHN women exhibited an increase in peak prolactin response to breast stimulation after alcohol consumption. These differences were not attributable to differences in alcohol pharmacokinetics.
As expected, differences in the effects of alcohol consumption on prolactin responses between FHP and FHN lactating women were qualitatively consistent with but more robust than those reported between FHP and FHN men and nonlactating women.19,20
FHP lactating women also exhibited increased stimulant-like effects of alcohol than did FHN women, despite similar BACs and drinking histories, as reported previously in FHP and FHN men and nonlactating women.35
A higher subjective response to alcohol is associated with higher dopamine (D2) receptor availability in the nucleus accumbens.36
Although never studied in lactating women, it has been suggested that dopaminergic dysregulation, characterized by lower D2 receptor availability in the striatum37
and larger prolactin responses, when challenged with dopamine antagonists32
is associated with certain behavioral phobias. Maternal neophobia, which is known to increase during lactation, promotes focus on and protection of the infant.33,38
Our study, which demonstrates a positive correlation between neophobia and prolactin response to breast stimulation, supports a neuroendocrine basis for maternal neophobia. Perhaps higher-than-normal levels of dopamine receptors in the caudate and striatum (in contrast to individuals with social phobia)32
might explain the reduced neophobia and smaller prolactin responses when challenged with alcohol in FHP lactating women (whose levels of neophobia were similar to those of nulliparous women31,39
). Taken together, these observations support the hypothesis that unaffected adult progeny from alcoholic pedigrees exhibit a fundamental dopaminergic dysregulation that affects personality-related differences in susceptibility of different brain areas.40
Familial history of alcoholism in nonalcoholic lactating women disrupts the lactational hormone milieu, resulting directly or indirectly in altered breastfeeding patterns during established lactation. This phenotype, a blunted prolactin response, is now considered an important risk factor for failure to initiate and sustain lactation among obese women,3,41
perhaps as a result of the obesity-related alterations in dopaminergic neurotransmission.42
Despite more persistent attempts to breastfeed in the first week postpartum, 3
obese women exhibit delayed secretory activation and, ultimately, premature cessation of breastfeeding than normal-weight women. As a consequence of this discovery, prolactin-promoting interventions, such as putting infants to the breast soon after birth and promoting frequent suckling, have substantially improved breastfeeding outcomes in obese women.3
Whether such prolactin-promoting strategies contributed to the breastfeeding success of the FHP women in this study, all of whom were of normal weight, is an important area for future research. Their more frequent breastfeeding during the afternoon and evening hours, the time of day when prolactin levels are naturally lowest because of circadian periodicity,4,43
may suggest another prolactin-promoting intervention for women with blunted prolactin responses (perhaps more infant-led feeding patterning). In other words, a blunted prolactin response to suckling does not mean that a woman cannot
successfully breastfeed. Regardless of the prolactin response, alcohol consumption did not result in greater milk production during the 16-minute pumping period, a finding that adds to the growing body of scientific literature that refutes the folklore that alcohol is a galactagogue.14,15,17
National estimates of the prevalence of family history of alcoholism in the United States are at least as high as those for adult obesity.44,45
Whether the hormonal and behavioral differences noted in FHP women contribute to early weaning and whether FHP women warrant similar support during the early stages of lactation as do obese women are still unknown. Addressing the limitations that such familial factors may impose on breastfeeding performance and the development of evidence-based strategies that lead to lactation success will be useful to help new mothers overcome breastfeeding barriers and to health officials who attempt to devise targeted breastfeeding interventions as well as to provide sound guidelines for ethanol consumption during lactation.46
WHAT’S KNOWN ON THIS SUBJECT
Studies indicate that men and nonlactating women with a family history of alcoholism but no alcoholism themselves display blunted prolactin responses to an alcohol challenge when compared with individuals without a family history; however, there are no such studies of lactating women.
WHAT THIS STUDY ADDS
Family history of alcoholism is associated with blunted magnitude, rapidity, and duration of prolactin responses to breast stimulation and an alcohol challenge in lactating women. More frequent breastfeeding by FHP women suggests behavioral compensation for perceived and/or actual poor lactation.