Obesity may impair lactogenesis II.

Data from livestock species and experimental animal models suggest that excess body fatness may impair lactogenesis. For example, it has long been known that overfed dairy cows are at risk of fat cow syndrome, a condition characterized by lactation failure in the early postpartum period. Obese rats often lose their litters in the early postpartum period to primary lactation failure. A negative association between high body mass index (BMI) before conception and the duration of lactation has been documented in studies from diverse human populations. Findings from our laboratory establish that among women who ever attempted to breastfeed their infants, high BMI before conception was also associated with failure to initiate breastfeeding successfully. In a more recent study, we found that high prepregnant BMI was specifically associated with later onset of lactogenesis II. This was mediated by parity but not by breastfeeding behavior. Psychosocial factors related to a woman's intention to breastfeed and her planned duration of breastfeeding did not modify this association. Taken together, these findings in animals and women strongly suggest that maternal obesity in the perinatal period is a cause of delayed lactogenesis.

Maternal obesity and breast-feeding success in a rural population of white women.

Maternal obesity interferes with the initiation and maintenance of lactation in animal models but it has not been investigated widely in women. We reviewed medical records from a white population to examine the relation between prepregnant overweight [body mass index (BMI; in kg/m2) 26.1-29.0] and obesity (BMI > 29.0) on initiation and duration of breast-feeding. Logistic regression revealed that of those who ever put their infants to the breast (n = 810), women who were overweight [odds ratio (OR) = 2.54, P < 0.05] or obese (OR = 3.65, P < 0.0008) had less success initiating breast-feeding than did their normal-weight counterparts (BMI < 26.1). Proportional-hazards regression revealed higher rates of discontinuation of exclusive breast-feeding in overweight (RR = 1.42, P < 0.04) and obese (RR = 1.43, P < 0.02) women and higher discontinuation of breast-feeding to any extent in overweight (RR = 1.68, P < 0.006) and obese (RR = 1.73, P = 0.001) women. Controlling for parity, socioeconomic status, maternal education, and other factors that often covary with maternal obesity and breast-feeding did not change these results. These results suggest that excessive fatness in the reproductive period may inhibit lactational performance in women.

Analyses of response patterns clarify lead effects in olfactory reversal and extradimensional shift tasks: assessment of inhibitory control, associative ability, and memory.

Rats exposed to lead (Pb) chronically from conception were tested on (a) an olfactory serial reversal task and (b) an extradimensional shift (EDS) task. Pb exposure did not impair learning of the original olfactory discrimination but did impair learning of the 5 reversals and the EDS task. In the reversals, Pb exposure tended to shorten the initial period of persistent responding to the previously correct cue, but significantly prolonged the postperseverative learning phase (both the "chance" and "greater-than-chance" components). These effects are similar to those produced by lesions of the amygdala, a structure implicated in the process by which stimuli acquire incentive value. This similarity, coupled with the pattern of findings, suggests that Pb-induced impairment of reversal learning is due to a deficiency in learning the new contingencies of the task (an associative deficit), not inflexibility or deficient inhibitory control. These findings also illustrate the importance of analyzing the types of errors committed, rather than focusing solely on learning rate.