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Rasmussen KM & Kjolhede CL (2004). Prepregnant overweight and obesity diminish the prolactin response to suckling in the first week postpartum. Pediatrics, 113(5), e465-e471. Article available online: http://pediatrics.aappublications.org/cgi/content/full/113/5/e465

Abstract:
<< Objective. The population subgroups with the highest proportion of overweight and obese women often are characterized by the lowest rates of initiation and shortest durations of breastfeeding. We previously documented that these 2 population-level trends may be related. In a population of white women who lived in a rural area, we observed that prepregnant overweight and obesity were associated with failure to initiate and also to sustain lactation. The means by which being overweight or obese negatively affect lactational performance is unknown and likely to be multifactorial in origin, including the simple mechanical difficulties of latching on and proper positioning of the infant. In addition, we have shown that prepregnant body mass index (BMI) is negatively associated with the timing of lactogenesis II, the onset of copious milk secretion. Although the effects of obesity on the prolactin response to infant suckling have never been studied, we postulated that maternal obesity could compromise this important response. We proposed that this might occur because obesity alters the 24-hour spontaneous release of prolactin and also because prolactin secretion is blunted in response to various stimuli among obese subjects. The fall in progesterone concentration that occurs immediately postpartum is the trigger for the onset of copious milk secretion, but maintenance of prolactin and cortisol concentrations is necessary for this trigger to be effective. Adipose tissue concentrates progesterone. We proposed that this additional source of progesterone would lead to consistently higher progesterone concentrations among obese compared with normal-weight women. This, in turn, would lead to a delay in reaching the appropriate concentration to trigger the onset of lactogenesis II. We tested the hypotheses that a reduced prolactin response to suckling and higher-than-normal progesterone concentration in the first week after delivery might be among the means by which maternal overweight could compromise early lactation.

Methods. We enrolled 40 mothers of term infants from the same population that we studied previously. We measured serum prolactin and progesterone concentrations by radioimmunoassay before and 30 minutes after the beginning of a suckling episode at 48 hours and 7 days after delivery. We used path analysis to develop a parsimonious multivariate prediction of the prolactin response to suckling at 48 hours and 7 days postpartum.

Results. As expected, prolactin values decreased from 48 hours to 7 days postpartum. Women who were overweight or obese (using the Institute of Medicine’s cutoff for women of a BMI >26 kg/m2) before conception had a lower prolactin response to suckling than normal-weight women at 48 hours but not at day 7. In multivariate analyses, overweight/obesity, primiparity, and birth weight were negatively associated with the prolactin response to suckling at 48 hours. After adjustment for confounding by time since delivery and the duration of the nursing episode, only overweight/obesity remained a significant negative predictor of prolactin response to suckling at day 7. Concentrations of progesterone decreased dramatically from 48 hours to 7 days postpartum but did not differ between normal-weight and overweight/obese women at either time. In addition, the decreases in progesterone concentrations from 48 hours to 7 days postpartum did not differ between the prepregnant BMI groups.

Conclusion. The unique and important finding from this study is that overweight/obese women had a lower prolactin response to suckling. This would be expected to compromise the ability of overweight/obese women to produce milk and, over time, could lead to premature cessation of lactation. These findings are important because, during our observation period (just before and after lactogenesis II, the time of onset of copious milk secretion), the prolactin response to suckling is more important for milk production than it is later in lactation. We have previously shown that a high proportion of the overweight and obese women in this population who give up on breastfeeding do so at this time. This finding thus provides evidence of a biological basis for this association, and additional study of it is likely to be informative. We postulated that there would be consistently higher progesterone concentrations in the early postpartum period among obese compared with normal-weight women because adipose tissue is an extraplacental source of this hormone. This hypothesis was not supported in this study because there were no significant differences between normal-weight and overweight/obese women in progesterone concentrations at either 48 hours or 7 days postpartum. The values that we observed at these times were similar to those reported by others in the early postpartum period. The findings from this study add plausibility to our observation that initiation, not just duration of breastfeeding, is negatively affected by maternal overweight/obesity. Although women should begin pregnancy at a healthy weight and gain reasonably during gestation, not all will. Pediatricians can help overweight/obese women to succeed at breastfeeding by targeting them for contact with a lactation consultant before discharge from the hospital to be sure that they have received optimal advice on breastfeeding techniques. In addition, early contact with the mother after discharge—by calling her at home to offer her support and counseling for breastfeeding, by scheduling the first pediatric visit earlier than for other patients, or by enlisting the assistance of public health nurses for a home visit if this is possible—would help overweight/obese women to continue to breastfeed. Being overweight or obese is negatively associated with the prolactin response to suckling in the first week postpartum and, thus, may contribute to early lactation failure.


Key Words: obesity • prolactin • breastfeeding • lactogenesis • estrogen • progesterone • leptin

Abbreviations: BMI, body mass index
Although we have made progress in meeting national goals for initiation of breastfeeding in recent years, we have made disturbingly little progress toward national goals for maintenance of breastfeeding in this same period1—despite overwhelming scientific evidence that documents the benefits of this method of feeding infants.2 Simultaneously, American women in general and some racial/ethnic subgroups in particular have gotten fatter.3 The population subgroups with the highest proportion of overweight and obese women often are characterized by the lowest rates of initiation and shortest durations of breastfeeding. We have previously documented that these 2 population-level trends may be related. In a population of white women who lived in a rural area, we observed that those who were overweight or obese before conception had a significantly increased risk of failing to initiate breastfeeding successfully.4 Those who did initiate breastfeeding successfully also stopped this practice significantly sooner than their normal-weight counterparts. These findings have been confirmed in larger, more diverse populations.5–7 Prepregnant body mass index (BMI) has been used as the measure of maternal fatness in nearly all of these studies because it is more readily available from medical records than BMI at delivery and is highly associated with maternal fatness at the time when breastfeeding begins.
The means by which being overweight or obese negatively affect lactational performance is unknown and likely to be multifactorial in origin, including the simple mechanical difficulties of latching on and proper positioning of the infant when the mother is obese. In another study in this same geographic area, we observed that prepregnant BMI was negatively associated with the timing of lactogenesis II, the onset of copious milk secretion.8 This association was not confounded by the tendency of heavier women to undergo cesarean sections, but it was reduced by primiparity, which was unexpectedly more common among the heavier women in this particular study population. Psychosocial factors, such as planned duration of breastfeeding, behavioral beliefs about breast- and bottle-feeding, and maternal knowledge of and confidence about or support for breastfeeding, were not associated with the timing of the onset of lactogenesis II.
The fall in progesterone concentration that occurs immediately postpartum is the trigger for the onset of copious milk secretion, but maintenance of prolactin and cortisol concentrations is necessary for this trigger to be effective.9 It is known that adipose tissue concentrates progesterone.10 We proposed that this additional source of progesterone, which remains after delivery of the placenta, would lead to consistently higher progesterone concentrations among obese compared with normal-weight women. This, in turn, would lead to a delay in reaching the appropriate concentration to trigger the onset of lactogenesis II. Although the effects of obesity on the prolactin response to infant suckling have never been studied, we postulated that maternal obesity could compromise this important response. This is because obesity alters the 24-hour spontaneous release of prolactin and also because prolactin secretion is blunted in response to various stimuli among obese subjects.11 Finally, we observed previously that insulin concentrations decrease less dramatically from the end of pregnancy to early lactation in obese than in nonobese rats.12 We postulated that this may also occur in obese women, which could result in less glucose being available for milk biosynthesis. The goal of the research reported here was to examine whether maternal fatness at the time of conception was associated with several biological factors that are known to be important for the successful initiation of lactation. >>

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