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When compared to full-term infants, infants born prematurely often have lower effortful control throughout the lifespan, suggesting that time spent in the womb or factors associated with prematurity, such as obstetrical and birth complications, are responsible for such differences (Cassiano et al., 2020; Reyes et al., 2020). Thus, our first aim was to examine whether prematurity or neonatal medical risk explained differences in effortful control across childhood. Our second aim was to estimate the heritability of effortful control and examine changes in heritability when moderated by prematurity. Based on prior literature (Lemery-Chalfant et al., 2008), we expected that effortful control would be moderately-to-highly heritable, and vary by prematurity (Ganiban et al., 2021).
Our diverse sample included 1285 twin children (50.1% female; 58.5% non-Hispanic White, 27.3% Hispanic; 27.2% identical, 35.2% same-sex fraternal, 30% opposite-sex fraternal) and their parents from the ongoing longitudinal Arizona Twin Project (Lemery-Chalfant et al., 2019). 35.8% were full-term (>37 weeks gestation), 57.2% moderately premature, and 7% very premature (<32 weeks). Sample sizes varied across wave from 402 (age 5) to 744 (age 10). Gestational age was coded from medical records when available (19.44%) or taken from parent report. Neonatal medical risk was coded from medical records via the well-validated Obstetrical Complications and Neonatal Complications Scales (Littman & Paralee, 1974), and Neonatal Morbidity Scale (Minde et al., 1983). We obtained parent report of duration of orientating at 12 months and the three subscales of effortful control (inhibitory control, activation control, attentional focusing) 2.5, 5, 8, 9, and 10 years using the reliable and valid age-appropriate Rothbart measures of temperament (IBQ, Garstein & Rothbart, 2001; CBQ, Rothbart et al., 2001; TMCQ, Simonds, 2006; EATQ, Ellis & Rothbart, 2001; α = .59 - .91).
We compared effortful control scores from 12 months to 10 years at six timepoints in children born very prematurely and children who were born full-term by randomly selecting one twin and running t-tests. There were no differences in effortful control by prematurity. Next, we ran correlations between neonatal medical risk and effortful control, again randomly selecting one twin, and found no notable associations. Univariate twin models revealed that attentional focusing at age eight was explained by additive genetic (A), dominant genetic (D), and nonshared environmental influence (E) (-2LL=1984.09; A=.01, D=.80, E=.19) and inhibitory control was explained by additive genetic and nonshared environmental influence (-2LL=1168.38; A=.86, E=.14). We tested whether ADE influences on toddler attentional focusing were moderated by prematurity. The most parsimonious model did not include moderation (-2LL=1344; A=.41, D=.24, E=.35).
Components of effortful control across childhood were highly heritable and largely independent of prematurity and neonatal medical risk, considering both phenotypic associations and moderation of genetic and environmental variance. The lack of phenotypic association may differ from the literature because we used a larger, community sample of twins, compared to most existing studies with small samples (Ns<50) that likely included infants at higher medical risk. Genetically informed designs are useful for studying the influence of prematurity/neonatal medical risk on child development.