A mixed methods study of perinatal sleep and breastfeeding outcomes in women at risk for postpartum depression.

INTRODUCTION: Pregnant and postpartum women experience significant sleep disruption, but the role of perinatal sleep disturbances in breastfeeding is understudied. METHODS: In this observational cohort study, we used mixed methods to examine associations between perinatal sleep and breastfeeding. Forty-eight women (mean age 28.2 ± 4.9 years) who were euthymic at enrollment but had a history of major depression (n = 43) or bipolar disorder (n = 5) had sleep recorded with wrist actigraphy. We determined feeding status through daily diaries and used semi-structured interviews to identify themes regarding participants' experiences, breastfeeding decisions, and behaviors. To examine whether sleep disturbance during pregnancy predicted breastfeeding (BF) rates, we defined "lower sleep efficiency" (LSE) and "higher sleep efficiency" (HSE) groups based on the median split of actigraphic SE at 33 weeks' gestation (cutoff SE = 84.9%) and classified mothers as No-BF, Mixed-BF (BF + formula), and Exclusive-BF at 2 weeks postpartum. RESULTS: Percentages of women who did any breastfeeding were: Week 2 = 72.3%, Week 6 = 62.5%, Week 16 = 50%. LSE mothers were less likely than HSE mothers to initiate breastfeeding (percent No-BF: LSE = 45.8%, HSE = 16.7%, P < .05). Average actigraphic sleep onset, sleep offset, time in bed, sleep duration, and SE did not differ based on breastfeeding status at any time point. Qualitative themes included insufficient preparation for the demands of breastfeeding, interrupted and nonrestorative sleep, and unrelenting daytime tiredness. CONCLUSIONS: In our sample, preserved actigraphic SE during pregnancy was associated with initiation and continuation of breastfeeding. Future work should examine whether improving sleep in pregnancy improves mothers' feeding experiences.

ACTN3 allele frequency in humans covaries with global latitudinal gradient.

A premature stop codon in ACTN3 resulting in α-actinin-3 deficiency (the ACTN3 577XX genotype) is common in humans and reduces strength, muscle mass, and fast-twitch fiber diameter, but increases the metabolic efficiency of skeletal muscle. Linkage disequilibrium data suggest that the ACTN3 R577X allele has undergone positive selection during human evolution. The allele has been hypothesized to be adaptive in environments with scarce resources where efficient muscle metabolism would be selected. Here we test this hypothesis by using recently developed comparative methods that account for evolutionary relatedness and gene flow among populations. We find evidence that the ACTN3 577XX genotype evolved in association with the global latitudinal gradient. Our results suggest that environmental variables related to latitudinal variation, such as species richness and mean annual temperature, may have influenced the adaptive evolution of ACTN3 577XX during recent human history.