Association Between Length of Maternity Leave and Breastfeeding Duration in the United States: A Systematic Review.

OBJECTIVE: To perform a systematic review to assess the association between the length of maternity leave and breastfeeding duration in the United States. DATA SOURCES AND METHODS OF STUDY SELECTION: This review was conducted with a five-stage model for reviews. We included publications from 2000 to 2023, U.S.-based studies written in English, and primary research and peer-reviewed articles. In February 2023, a medical librarian conducted a search across seven databases, yielding 1,540 results. ClinicalTrials.gov was later searched, yielding no results. After duplicates were removed, 835 abstracts were screened. A full-text article review was then conducted of the remaining 34 articles. TABULATION, INTEGRATION, AND RESULTS: Twenty-three articles met inclusion criteria, two of which were reviews. Of the nonreview articles, all found a positive relationship between increased maternity leave and duration of breastfeeding. Data showed that earlier return to work for the birth parent decreased the odds of breastfeeding dyads meeting breastfeeding recommendations. Many studies adjusted for confounders (eg, race, socioeconomic status); however, Black or Latinx mothers still experience shorter breastfeeding durations or lower breastfeeding exclusivity when given equal leave compared with White mothers. CONCLUSION: Results show a positive relationship between length of maternity leave and breastfeeding duration. Advocacy for longer, paid parental leave and more robust research rooted in rigorous methods are needed.

Disruption of DNA methylation-mediated cranial neural crest proliferation and differentiation causes orofacial clefts in mice.

Orofacial clefts of the lip and palate are widely recognized to result from complex gene-environment interactions, but inadequate understanding of environmental risk factors has stymied development of prevention strategies. We interrogated the role of DNA methylation, an environmentally malleable epigenetic mechanism, in orofacial development. Expression of the key DNA methyltransferase enzyme DNMT1 was detected throughout palate morphogenesis in the epithelium and underlying cranial neural crest cell (cNCC) mesenchyme, a highly proliferative multipotent stem cell population that forms orofacial connective tissue. Genetic and pharmacologic manipulations of DNMT activity were then applied to define the tissue- and timing-dependent requirement of DNA methylation in orofacial development. cNCC-specific Dnmt1 inactivation targeting initial palate outgrowth resulted in OFCs, while later targeting during palatal shelf elevation and elongation did not. Conditional Dnmt1 deletion reduced cNCC proliferation and subsequent differentiation trajectory, resulting in attenuated outgrowth of the palatal shelves and altered development of cNCC-derived skeletal elements. Finally, we found that the cellular mechanisms of cleft pathogenesis observed in vivo can be recapitulated by pharmacologically reducing DNA methylation in multipotent cNCCs cultured in vitro. These findings demonstrate that DNA methylation is a crucial epigenetic regulator of cNCC biology, define a critical period of development in which its disruption directly causes OFCs, and provide opportunities to identify environmental influences that contribute to OFC risk.