Psychological medicine · 2023
Prenatal cocaine exposure and self-reported behavioral adjustments from ages 12 to 21: environmental pathways.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Min Meeyoung O, Albert Jeffrey M, Minnes Sonia, Kim June-Yung, Kim Sun-Kyung, Singer Lynn T
Аннотация
BACKGROUND: In a birth-cohort study, we followed offspring with prenatal cocaine exposure (PCE) to investigate longitudinal associations of PCE with self-reported behavioral adjustment from early adolescence to emerging adulthood (EA). Environmental pathways (family functioning, non-kinship care, maltreatment) were specified as potential mediators of PCE.
METHODS: Participants were 372 (190 PCE; 47% male), primarily Black, low socioeconomic status, enrolled at birth. Internalizing and externalizing behaviors were assessed using Youth Self-Report at ages 12 and 15 and Adult Self-Report at age 21. Extended random-intercept cross-lagged panel modeling was used to account for potential bidirectional relationships between internalizing and externalizing behaviors over time, examining potential mediators.
RESULTS: Adjusting for covariates, significant indirect effects were found for each mediator at different ages. For family functioning, these were both internalizing (β = 0.83, p = 0.04) and externalizing behaviors (β = 1.58, p = 0.02) at age 12 and externalizing behaviors at age 15 (β = 0.51, p = 0.03); for non-kinship care, externalizing behaviors at ages 12 (β = 0.63, p = 0.02) and 15 (β = 0.20, p = 0.03); and for maltreatment, both internalizing and externalizing behaviors at ages 15 (β = 0.64, p = 0.02 for internalizing; β = 0.50, p = 0.03 for externalizing) and 21 (β = 1.39, p = 0.01 for internalizing; β = 1.11, p = 0.01 for externalizing). Direct associations of PCE with internalizing and externalizing behaviors were not observed, nor cross-lagged relationships between internalizing and externalizing behaviors.
CONCLUSIONS: Negative associations of PCE with behavioral adjustment persist into EA via environmental pathways, specifying intervention points to disrupt adverse pathways toward healthy development.
METHODS: Participants were 372 (190 PCE; 47% male), primarily Black, low socioeconomic status, enrolled at birth. Internalizing and externalizing behaviors were assessed using Youth Self-Report at ages 12 and 15 and Adult Self-Report at age 21. Extended random-intercept cross-lagged panel modeling was used to account for potential bidirectional relationships between internalizing and externalizing behaviors over time, examining potential mediators.
RESULTS: Adjusting for covariates, significant indirect effects were found for each mediator at different ages. For family functioning, these were both internalizing (β = 0.83, p = 0.04) and externalizing behaviors (β = 1.58, p = 0.02) at age 12 and externalizing behaviors at age 15 (β = 0.51, p = 0.03); for non-kinship care, externalizing behaviors at ages 12 (β = 0.63, p = 0.02) and 15 (β = 0.20, p = 0.03); and for maltreatment, both internalizing and externalizing behaviors at ages 15 (β = 0.64, p = 0.02 for internalizing; β = 0.50, p = 0.03 for externalizing) and 21 (β = 1.39, p = 0.01 for internalizing; β = 1.11, p = 0.01 for externalizing). Direct associations of PCE with internalizing and externalizing behaviors were not observed, nor cross-lagged relationships between internalizing and externalizing behaviors.
CONCLUSIONS: Negative associations of PCE with behavioral adjustment persist into EA via environmental pathways, specifying intervention points to disrupt adverse pathways toward healthy development.