Attention Problems among Children with a Positive Family History of Alcohol Abuse or Dependence and Controls

Barnow, Sven; Schuckit, Marc A.; Smith, Tom L.; Spitzer, Carsten; Freyberger, H. J.

doi:10.1159/000095808

Cited by 9 publications

(7 citation statements)

References 85 publications

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“…That said, better measurements of the relationship of cognitive impairment to later alcoholism are made by family history and longitudinal studies. One study that tested family history positive teens found no impairment on attentional measures (Barnow et al., 2007), but when multigenerational or higher familial alcoholism density are used as factors, attentional impairment can be detected (Corral et al., 1999, 2003). An 8‐year longitudinal study with high‐risk youths found that attentional impairment/executive functioning predicted later substance use, even when controlling for intake substance involvement, gender, education, conduct disorder, family history, and learning disabilities (Tapert et al., 2002).…”

Section: Discussionmentioning

confidence: 99%

Pharmacologic Dissociation Between Impulsivity and Alcohol Drinking in High Alcohol Preferring Mice

Oberlin

Bristow

Heighton

et al. 2010

Alcoholism Clin & Exp Res

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Background Impulsivity is genetically correlated with, and precedes addictive behaviors and alcoholism. If impulsivity or attention is causally related to addiction, certain pharmacological manipulations of impulsivity and/or attention may affect alcohol drinking, and vice versa. The current studies were designed to explore the relationship among impulsivity, drinking, and vigilance in selectively bred High Alcohol Preferring (HAP) mice, a line that has previously demonstrated both high impulsivity and high alcohol consumption. Amphetamine, naltrexone and memantine were tested in a delay discounting (DD) task for their effects on impulsivity and vigilance. The same drugs and doses were also assessed for effects on alcohol drinking in a two-bottle choice test. Methods HAP mice were subjected to a modified version of adjusting amount DD using 0.5 sec and 10 sec delays to detect decreases and increases, respectively, in impulsive responding. In 2 experiments, mice were given amphetamine (0.4, 0.8 or 1.2 mg/kg), naltrexone (3 and 10 mg/kg), and memantine (1 and 5 mg/kg) before DD testing. Another pair of studies used scheduled access, two-bottle choice drinking to assess effects of amphetamine (0.4, 1.2, or 3.0 mg/kg), naltrexone (3 and 10 mg/kg), and memantine (1 and 5 mg/kg) on alcohol consumption. Results Amphetamine dose-dependently reduced impulsivity and vigilance decrement in DD, but similar doses left alcohol drinking unaffected. Naltrexone and memantine decreased alcohol intake at doses that did not affect water drinking, but had no effects on impulsivity or vigilance decrement in the DD task. Conclusions Contrary to our hypothesis, none of the drugs tested here, while effective either on alcohol drinking or impulsivity, decreased both behaviors. These findings suggest that the genetic association between drinking and impulsivity observed in this population is mediated by mechanisms other than those targeted by the drugs tested in these studies.

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Section: Discussionmentioning

confidence: 99%

Pharmacologic Dissociation Between Impulsivity and Alcohol Drinking in High Alcohol Preferring Mice

Oberlin

Bristow

Heighton

et al. 2010

Alcoholism Clin & Exp Res

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“…Less is known about the manner in which attributes such as BU contribute to alcohol-related problems in groups with higher education, higher income and who were not selected for pre-existing problems [29,44,45]. Because the lifetime risk for more extreme disorders such as CD and ASPD in males is estimated to be less than 5%, and only 20% of male alcoholics entering treatment fulfill criteria for ASPD [46,47], it is important to establish whether a characteristic such as BU still contributes to the AUD risk in less deviant groups who may be more representative of non-treated populations.…”

Section: Introductionmentioning

confidence: 99%

“…While there is little doubt regarding the importance of externalising characteristics such as BU to the pattern of heavier drinking and associated problems, most studies of these relationships have been carried out in adolescents and populations chosen at least in part for deviant behaviours [42,43]. Less is known about the manner in which attributes such as BU contribute to alcohol-related problems in groups with higher education, higher income and who were not selected for pre-existing problems [29,44,45]. Because the lifetime risk for more extreme disorders such as CD and ASPD in males is estimated to be less than 5%, and only 20% of male alcoholics entering treatment fulfill criteria for ASPD [46,47], it is important to establish whether a characteristic such as BU still contributes to the AUD risk in less deviant groups who may be more representative of non-treated populations.…”

Section: Introductionmentioning

confidence: 99%

The relationship of behavioural undercontrol to alcoholism in higher-functioning adults

Schuckit

Smith

2006

Drug and Alcohol Review

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Externalising behaviours, including the personality characteristics of behavioural undercontrol (BU), represent one of several genetically influenced domains that impact on the alcoholism risk. Because genes explain only about 60% of the vulnerability toward alcohol use disorders (AUDs), an optimal understanding of how such behaviours affect the risk requires evaluation of their impact in the context of additional influences. Few studies have addressed this question regarding BU among relatively well-functioning adults. This paper presents results from testing a BU-based mediational model of risk in men from the San Diego Prospective Study. Structured research instruments were used with 430 adult Caucasian males to evaluate the performance of BU in predicting AUDs at the 15-year follow-up using Pearson product - moment correlations among domains and an AMOS-based structural equation model (SEM). While both the family history of AUDs (FHalc) and BU predicted alcohol-related outcome, BU by itself did not mediate the relationship of the FH to alcohol disorders. The impact of BU on alcohol problems was mediated by alcohol expectancies, peer drinking and by coping. The SEM explained 42% of the variance for AUDs. The current results indicate that BU contributed to the risk for alcohol-related problems, even among more highly functional subjects and after excluding the impact of the antisocial personality disorder, but by itself did not mediate the relationship of FH to outcome in these subjects.

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“…Concerning ADHD, earlier work defines it as narrow DSM-IV ADHD (Knopik et al, 2006), ‘any ADHD,’ symptom count, and ADHD with or without clinical impairment (Knopik et al, 2005). Considering the larger literature, other definitions such as dimensions of ADHD (Barnow et al, 2007), laboratory tasks (Corral et al, 1999), behavioral undercontrol (Sher, 1991), and attention and memory deficits (Tarter et al, 1989) have been used. Further, even when parental alcoholism has been found to predict ADHD, non-genetic and genetic explanations have often been difficult to untangle from one another since most studies in this literature have not used genetically informative design (Knopik et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Paternal Alcoholism and Offspring ADHD Problems: A Children of Twins Design

Knopik¹,

Jacob

Haber

et al. 2009

Twin Res Hum Genet

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Objective A recent Children-of-Female-Twin design suggests that the association between maternal alcohol use disorder and offspring ADHD is due to a combination of genetic and environmental factors, such as prenatal nicotine exposure. We present here a complementary analysis using a Children-of-Male-Twin design examining the association between paternal alcoholism and offspring attention deficit hyperactivity problems (ADHP). Methods Children-of-twins design: offspring were classified into 4 groups of varying genetic and environmental risk based on father and co-twin’s alcohol dependence status. Results Univariate results are suggestive of a genetic association between paternal alcohol dependence and broadly defined offspring ADHP. Specifically, offspring of male twins with a history of DSM-III-R alcohol dependence, as well as offspring of non-alcohol dependent monozygotic twins whose cotwin was alcohol dependent, were significantly more likely to exhibit ADHP than control offspring. However, multivariate models show maternal variables independently predicting increased risk for offspring ADHP and significantly decreased support for a genetic mechanism of parent-to-child transmission. Conclusions In support of earlier work, maternal variables (i.e., maternal ADHD and prenatal exposure) were strongly associated with child ADHP; however, the role of paternal alcohol dependence influences was not definitive. While genetic transmission may be important, the association between paternal alcohol dependence and child ADHP is more likely to be indirect and a result of several pathways.

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Attention Problems among Children with a Positive Family History of Alcohol Abuse or Dependence and Controls

Cited by 9 publications

References 85 publications

Pharmacologic Dissociation Between Impulsivity and Alcohol Drinking in High Alcohol Preferring Mice

Pharmacologic Dissociation Between Impulsivity and Alcohol Drinking in High Alcohol Preferring Mice

The relationship of behavioural undercontrol to alcoholism in higher-functioning adults

Paternal Alcoholism and Offspring ADHD Problems: A Children of Twins Design

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