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The relation of parent alcohol disorder to young adult drinking outcomes mediated by parenting: Effects of developmentally limited versus persistent parent alcohol disorder.

ABSTRACT: BACKGROUND:Parent alcohol use disorder (AUD) is a well-established risk factor for the development of offspring AUD and is associated with poor parenting. However, few studies have examined heterogeneity in trajectories of parental AUD and its influence on adolescent offspring drinking, and no studies to date have considered the differential risk to offspring conferred by parental AUDs that are limited to early adulthood. Specifically, AUDs limited to the period of emerging adulthood may confer less risk to a child's environment as recovery following emerging adulthood coincides with the typical ages of entry into the parenting role. The present study tested whether parental AUDs developmentally limited to emerging adulthood (DLAUD) transmit less risk for alcohol problems and alcohol consumption in offspring compared to offspring of parents with AUDs spanning across multiple developmental periods (persistent AUD), as mediated by positive parenting strategies. METHOD:Pathways were examined using longitudinal mediation models (N?=?361) comparing offspring with parental DLAUD, persistent AUD, and no AUD. RESULTS:Parents with DLAUD do not transmit the same risk for alcohol problems to offspring as parents with persistent AUD (B?=?0.173, SE?=?0.067, p?

SUBMITTER: Sternberg A

PROVIDER: S-EPMC6029693 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature

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The relation of parent alcohol disorder to young adult drinking outcomes mediated by parenting: Effects of developmentally limited versus persistent parent alcohol disorder.

Sternberg Ariel A Pandika Danielle D Elam Kit K KK Chassin Laurie L

Drug and alcohol dependence 20180425

<h4>Background</h4>Parent alcohol use disorder (AUD) is a well-established risk factor for the development of offspring AUD and is associated with poor parenting. However, few studies have examined heterogeneity in trajectories of parental AUD and its influence on adolescent offspring drinking, and no studies to date have considered the differential risk to offspring conferred by parental AUDs that are limited to early adulthood. Specifically, AUDs limited to the period of emerging adulthood may ...[more]

PMID: 29783094

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Project description:BACKGROUND:Liver damage is a serious and sometimes fatal consequence of long-term alcohol intake, which progresses from early-stage fatty liver (steatosis) to later-stage steatohepatitis with inflammation and fibrosis/necrosis. However, very little is known about earlier stages of liver disruption that may occur in problem drinkers, those who drink excessively but are not dependent on alcohol. METHODS:We examined how repeated binge-like alcohol drinking in C57BL/6 mice altered liver function, as compared with a single binge-intake session and with repeated moderate alcohol consumption. We measured a number of markers associated with early- and later-stage liver disruption, including liver steatosis, measures of liver cytochrome P4502E1 (CYP2E1) and alcohol dehydrogenase (ADH), alcohol metabolism, expression of cytokine mRNA, accumulation of 4-hydroxynonenal (4-HNE) as an indicator of oxidative stress, and alanine transaminase/aspartate transaminase as a measure of hepatocyte injury. RESULTS:Importantly, repeated binge-like alcohol drinking increased triglyceride levels in the liver and plasma, and increased lipid droplets in the liver, indicators of steatosis. In contrast, a single binge-intake session or repeated moderate alcohol consumption did not alter triglyceride levels. In addition, alcohol exposure can increase rates of alcohol metabolism through CYP2E1 and ADH, which can potentially increase oxidative stress and liver dysfunction. Intermittent, excessive alcohol intake increased liver CYP2E1 mRNA, protein, and activity, as well as ADH mRNA and activity. Furthermore, repeated, binge-like drinking, but not a single binge or moderate drinking, increased alcohol metabolism. Finally, repeated, excessive intake transiently elevated mRNA for the proinflammatory cytokine IL-1B and 4-HNE levels, but did not alter markers of later-stage liver hepatocyte injury. CONCLUSIONS:Together, we provide data suggesting that even relatively limited binge-like alcohol drinking can lead to disruptions in liver function, which might facilitate the transition to more severe forms of liver damage.

Dataset Information

The relation of parent alcohol disorder to young adult drinking outcomes mediated by parenting: Effects of developmentally limited versus persistent parent alcohol disorder.

Publications

The relation of parent alcohol disorder to young adult drinking outcomes mediated by parenting: Effects of developmentally limited versus persistent parent alcohol disorder.

Similar Datasets

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