A 21-Year Longitudinal Analysis of the Effects of Prenatal Alcohol Exposure on Young Adult Drinking

Baer, John; Sampson, Paul D.; Barr, Helen M.; Connor, Paul; Streissguth, Ann P.

doi:10.1097/01.ogx.0000088884.79233.a8

Cited by 61 publications

(80 citation statements)

References 33 publications

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“…Overall, prenatal exposure to alcohol, cigarettes, and street drugs has been reported to be associated with long-term changes in growth and development, neuropsychological deficits, and behavioral sequelae such as increased use of substances in young adulthood (Baer et al, 2003). However, it has not been a common feature of these studies to include other potentially salient causes of these abnormalities such as having a familial diathesis for psychiatric disorders.…”

Section: Discussionmentioning

confidence: 99%

Offspring from families at high risk for alcohol dependence: Increased body mass index in association with prenatal exposure to cigarettes but not alcohol

Hill¹,

Shen²,

Wellman³

et al. 2005

Psychiatry Research

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The prevalence of overweight and obese children is increasing, a tendency that can be expected to increase the risk of adverse outcomes in adulthood. The aim of this study was to determine if prenatal exposure to alcohol, cigarettes, and street drugs would be associated with differences in body mass index (BMI) in childhood and adolescence in offspring from families at high and low genetic risk for developing alcohol dependence. Annual follow-up of offspring (N =288) provided 1200 height and weight assessments for analysis. Maternal substance use data were available for 235 offspring from families stratified for familial/genetic risk for alcohol dependence (high or low risk), providing the opportunity to assess prenatal exposure and familial/genetic risk in relation to BMI in the offspring. When data were grouped by the presence or absence of any prenatal cigarette exposure, a significant difference in offspring BMI was seen for 8-to 11-year-olds. Significant group differences were also seen at ages 12-15 and 16-18 years. A dose-response relationship between cigarette use by the mother and offspring BMI was also seen. With the strong tendency for individuals who are overweight in childhood and adolescence to become overweight adults, prenatal exposure to nicotine may be a harbinger of increased risk for numerous adultonset, weight-related health problems.

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Section: Discussionmentioning

confidence: 99%

Offspring from families at high risk for alcohol dependence: Increased body mass index in association with prenatal exposure to cigarettes but not alcohol

Hill¹,

Shen²,

Wellman³

et al. 2005

Psychiatry Research

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show abstract

“…An emerging question is whether early developmental drug exposure can increase the liability for addictive behaviors later in life. While prenatal exposure to alcohol Baer et al, 2003) and to tobacco Cornelius et al, 2000;Kandel et al, 1994) have been shown in clinical studies to be associated with an increased risk of alcohol and nicotine abuse, respectively, in adolescents and young adults, similar studies on the rate of adolescent or adult drug abuse in cocaine-exposed children have not yet been published.…”

Section: Introductionmentioning

confidence: 99%

Prenatal exposure to cocaine alters the development of conditioned place-preference to cocaine in adult mice

Malanga

Pejchal

Kosofsky

2007

Pharmacology Biochemistry and Behavior

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As addiction is increasingly formulated as a developmental disorder, identifying how early developmental exposures influence later responses to drugs of abuse is important to our understanding of substance abuse neurobiology. We have previously identified behavioral changes in adult mice following gestational exposure to cocaine that differ when assessed with methods employing contingent and non-contingent drug administration. We sought to clarify this distinction using a Pavlovian behavioral measure, conditioned place-preference. Adult mice exposed to cocaine in utero (40 or 20 mg/kg/day), vehicle and pair-fed controls were place-conditioned to either cocaine (5 mg/kg or 20 mg/kg, i.p.) or saline injections. The development of conditioned place-preference to cocaine was impaired in mice exposed to cocaine in utero, and was abolished by fetal malnutrition. A context-specific place-aversion to vehicle but not cocaine injection was observed in prenatally cocaine-exposed mice. Locomotor behavior did not differ among prenatal treatment groups. We conclude that early developmental exposure to cocaine may diminish the subsequent rewarding effects of cocaine in adulthood measured with classical conditioning techniques, and that this is not due to changes in locomotor behavior. Sensitivity to acute stress is also altered by prenatal cocaine exposure, consistent with earlier findings in this model.

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“…Individuals with histories of PAE are at increased risk for substance and alcohol abuse problems later in life [Baer et al, 2003;Alati et al, 2008]. Both prevention and intervention programs are needed for this population to provide alcohol-related education to individuals with FASDs and their parents and caregivers (including the risks of drinking during pregnancy), to teach them strategies for avoiding situa-tions and behaviors that may encourage high-risk drinking, and to address ongoing substance and alcohol use/ abuse problems.…”

Section: Substance and Alcohol Abuse Problemsmentioning

confidence: 99%

Intervention for individuals with fetal alcohol spectrum disorders: Treatment approaches and case management

Paley¹,

O’Connor²

2009

Dev Disabil Res Revs

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Exposure to alcohol in utero is considered to be the leading cause of developmental disabilities of known etiology. The most severe consequence of such exposure, fetal alcohol syndrome (FAS), is characterized by a distinct constellation of characteristic facial anomalies, growth retardation, and central nervous system (CNS) dysfunction. Some individuals with prenatal alcohol exposure (PAE) do not meet the full criteria for FAS, but instead are diagnosed with partial FAS, alcohol related neurodevelopmental disorder (ARND), or alcohol related birth defects (ARBD). The entire continuum of effects from PAE is increasingly being referred to under the umbrella term of fetal alcohol spectrum disorders (FASDs). An extensive body of research has documented major cognitive, behavioral, adaptive, social, and emotional impairments among individuals with FASDs. Although FAS was identified in the U.S. over 35 years ago, the development, evaluation, and dissemination of evidencebased interventions for individuals with FASDs have lagged behind significantly. Encouragingly, however, in recent years there has been a marked increase in efforts to design and test interventions to remediate the impairments associated with prenatal alcohol exposure. This article will review treatment needs and considerations for individuals with FASDs and their families, current empirically tested treatment approaches, case management issues, and suggestions for future directions in research on the treatment of FASDs. ' 2009 Wiley-Liss, Inc. Dev Disabil Res Rev 200915:258-267.

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A 21-Year Longitudinal Analysis of the Effects of Prenatal Alcohol Exposure on Young Adult Drinking

Abstract: Background: Prenatal alcohol exposure may be a risk factor for the development of alcohol problems in humans.

Cited by 61 publications

References 33 publications

Offspring from families at high risk for alcohol dependence: Increased body mass index in association with prenatal exposure to cigarettes but not alcohol

Offspring from families at high risk for alcohol dependence: Increased body mass index in association with prenatal exposure to cigarettes but not alcohol

Prenatal exposure to cocaine alters the development of conditioned place-preference to cocaine in adult mice

Intervention for individuals with fetal alcohol spectrum disorders: Treatment approaches and case management

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