The effect of maternal employment on adolescents' transition to young adulthood

The purpose of this study was to examine relationships between multiple characteristics of maternal employment, parenting practices, and adolescents’ transition outcomes to young adulthood. The research addressed four main research questions. First, are the characteristics of maternal work (i.e., hours worked, multiple jobs held, work schedules, earnings, and occupation) related to adolescents’ enrollment in post-secondary education, employment, or involvement in neither of these types of activities as young adults? Second, are the work characteristics related to parental involvement and monitoring, and are the parenting practices related to adolescents’ transition outcomes? Third, do parental involvement and monitoring mediate any relationships between the characteristics of maternal employment and adolescents’ transition outcomes? Finally, do any associations between characteristics of maternal employment and parenting practices and adolescents’ transition outcomes vary by poverty status, race/ethnicity, or gender? To address these research questions, secondary data analysis was conducted, using data from the National Longitudinal Survey of Youth (NLSY) from 1998 through 2004. The study sample consisted of 849 youths who were 15 through 17 years of age in either 1998 or 2000, and were 19 through 21 years of age when their transition outcomes in young adulthood were measured four years later. Multinomial logistic and ordinary least squares regression models were estimated to answer the research questions. Study findings indicated that of the maternal work characteristics, mothers’ multiple jobs held, occupation, and work schedule were significantly related to the youths’ transition outcomes. When mothers held multiple jobs for 1 to 25 weeks per year, and when mothers held jobs involving lower levels of occupational complexity, their youths were more likely to experience employment rather than post-secondary education. Adolescents whose mothers worked a standard work schedule were less likely to experience other types of transitions than post-secondary education. With regard to the effects of maternal employment on parenting practices, none of the maternal work variables were related to parental involvement, and only one variable, mothers working less than 40 hours per week, was negatively related to parental monitoring. In addition, when parents were more involved with their youths’ education, the youths were less likely to transition into employment and other types of transitions rather than post-secondary education. The parenting practices did not mediate the relation between the significant work variables (holding multiple jobs, work schedule, and occupation) and youths’ transition outcomes. Finally, none of the interactions between maternal work characteristics and poverty status, race/ethnicity, and gender met the criteria for determining significance; but in a series of sub-group analyses, some differences according to poverty status and gender were found. Despite the lack of mediation and moderation, the findings of this study have important implications for social policy and social work intervention. Based on the findings, suggestions are made in these areas to improve working mothers’ lives and their adolescents’ development and successful transition to adulthood. Finally, directions for future research are discussed.

A decrease in dkk1, a Wnt inhibitor, contributes to placental and fetal lipid accumulation in an obesity-prone rat model

Placenta, as the sole transport mechanism between mother and fetus, links the maternal physical state and the immediate and life-long outcomes of the offspring. The present study examined the mechanisms behind the effect of maternal obesity on placental lipid accumulation and metabolism. Pregnant Obese Prone (OP) and Obese Resistant (OR) rat strains were fed a control diet throughout gestation. Placentas were collected on gestational d21 for analysis and frozen placental sections were analyzed for fat accumulation as well as β-Catenin and Dkk1 localization. Additionally, DKK1 was overexpressed in JEG3 trophoblast cells, followed by treatment with NEFA and Oil Red O stain quantification and mRNA analysis to determine the relationship between placental DKK1 and lipid accumulation. Maternal plasma and placental NEFA and TG were elevated in OP dams, and offspring of OP dams were smaller than OR. Placental Dkk1 mRNA content was 4-fold lower in OP placentas, and there was a significant increase in β-Catenin accumulation as well as mRNA content of fat transport and TG synthesis enzymes, including Ppar-delta, Fatp1, Fat/Cd36, Lipin1, and Lipin3. There was significant lipid accumulation within the decidual zones in OP but not OR placentas, and the thickness of the decidual and junctional zones was significantly smaller in OP than OR placentas. Overexpression of DKK1 in JEG3 cells decreased lipid accumulation and the mRNA content of PPAR-Delta, FATP1, FAT/CD36, LIPIN1, and LIPIN3. Our results indicate that Dkk1 may be regulating placental lipid metabolism through Wnt-mediated mechanisms. Additionally, recent studies have suggested that maternal obesity may also program early development of non-alcoholic fatty liver disease (NAFLD), rates of which have correlated with the increase in the obesity epidemic. In the current study, livers of OP offspring had significantly increased TG content (P<0.05) and lipid accumulation when compared to offspring of OR dams. Additionally, hepatic Dkk1 mRNA content was significantly decreased in OP livers when compared to OR (P<0.05), and treating H4IIECR rat hepatocyte cells with NEFA showed that Dkk1 mRNA was also decreased in NEFA-treated cells (P<0.05) that also had lipid accumulation. Chromatin Immunoprecipitation (ChIP) analysis of the Dkk1 promoter in fetal livers showed a pattern of histone modifications associated with decreased gene transcription in OP offspring, which agrees with our gene expression data. These results demonstrate that the hepatic Dkk1 gene is epigenetically regulated via histone modification in neonatal offspring in the current model of gestational obesity, and future studies will be needed to determine whether these changes contribute to excessive hepatic lipid accumulation in offspring of obese dams.