A Family Study of Alcohol Dependence

Nürnberger, John I.; Wiegand, Ryan E.; Bucholz, Kathleen K.; O’Connor, Sean; Meyer, Eric T.; Reich, Theodore; Rice, John P.; Schuckit, Marc A.; King, Lucy Jane; Petti, Theodore A.; Bierut, Laura J.; Hinrichs, Anthony L.; Kuperman, Samuel; Hesselbrock, Victor; Porjesz, Bernice

doi:10.1001/archpsyc.61.12.1246

Cited by 227 publications

(67 citation statements)

References 61 publications

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“…Probands were required to meet criteria for DSM-III-R alcohol dependence (42) and Feighner definite alcoholism (43), and to have at least 2 first-degree relatives available for study in the catchment area; all first-degree relatives were sought for baseline and follow-up interviews 5 years later (19, 44). The COGA protocol was approved by the institutional review board at each research site and all subjects provided written informed consent.…”

Section: Methodsmentioning

confidence: 99%

“…Familial influences accounted for 11% of the variance associated with remission in females (attributable to genetic influences shared with AUD) and 37% in males (attributable to environmental influences shared with the co-twin) which decreased the likelihood of remission (36). In the current study we used data from a high-risk family study, the Collaborative Study on the Genetics of Alcoholism (COGA), which has a high prevalence of lifetime AUD in the relatives of probands (19) and thus provides enough AUD-affected, and thus potentially remitted, proband-relative pairs to model persistent AUD, non-abstinent remission, and abstinent remission in both subjects. Greater AUD severity was associated with decreased likelihood of non-abstinent remission and increased likelihood of abstinent remission in population-based data and in previous work in COGA (10, 30, 37), consistent with other studies that found abstinent individuals had more severe AUD histories than non-abstinent individuals (27, 38, 39).…”

Section: Introductionmentioning

confidence: 99%

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Familial association of abstinent remission from alcohol use disorder in first‐degree relatives of alcohol‐dependent treatment‐seeking probands

et al. 2017

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BACKGROUND AND AIMS Studies that have included family history of alcohol use disorder (AUD) as a predictor of remission from AUD have yielded few significant results. The goals of this study were to estimate the association of persistent AUD, non-abstinent remission and abstinent remission (“AUD/remission status”) in a proband with AUD/remission status in a relative and to test whether this association differed in related and unrelated proband-relative pairs. DESIGN High-risk family study of alcohol dependence. Probands were recruited from treatment settings and relatives were invited to participate. Baseline assessments occurred between 1991–1998 with follow-up between 1996–2005. Half of probands were matched with a biological 1st-degree relative with lifetime AUD (related group) and half of probands were paired with an unrelated individual with lifetime AUD (unrelated group). SETTING Brooklyn, New York; Indianapolis, Indiana; Iowa City, Iowa; San Diego, California; Farmington, Connecticut; and St. Louis, Missouri, USA. PARTICIPANTS 606 probands (25.7% female, mean age 37.7) with baseline and follow-up data and 606 of their 1st degree relatives who had lifetime AUDs (45.8% female, mean age 36.2). MEASUREMENTS Persistent AUD, non-abstinent remission, and abstinent remission were based on self-report interview data on most recent AUD symptoms and alcohol consumption. Dependent variable was relatives’ AUD/remission status. Independent variable was probands’ AUD/remission status. FINDINGS 34.6% of probands and 20.6% of relatives were abstinent and 11.1% of probands and 22.8% of relatives were in non-abstinent remission. AUD/remission status was significantly correlated in related (r=.23, p=.0037) but not in unrelated pairs. A significant interaction of probands’ abstinent remission with a variable representing related (versus unrelated, p=.003) pairs suggested a familial association for abstinent remission. In related pairs, individuals with an abstinent proband were more likely to be abstinent themselves than were individuals whose proband had persistent AUD (relative risk ratio=3.27, 95% CI=1.56–6.85, p=.002); this association was not significant in unrelated pairs. CONCLUSIONS The likelihood of abstinent remission among people with alcohol use disorder (AUD) appears to be more than 3 times greater for individuals who are related to an abstinent proband versus those related to a proband with persistent AUD.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Familial association of abstinent remission from alcohol use disorder in first‐degree relatives of alcohol‐dependent treatment‐seeking probands

et al. 2017

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“…So far, a family history positive for alcohol abuse seems to be the best predictor of one's risk to develop an alcohol addiction [17]. Relatives of alcohol-addicted patients, for example, prefer higher levels of brain alcohol exposure [18] and are at a greater risk to develop an alcohol addiction [19]. …”

Section: Alcohol (Ab)use On the Threshold Of Adulthoodmentioning

confidence: 99%

How Do We ‘Learn' Addiction? Risk Factors and Mechanisms Getting Addicted to Alcohol

Hägele

Friedel²,

Kienast³

et al. 2014

Neuropsychobiology

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Background: Alcohol dependence is one of the leading contributors to the burden of disease in the world. A range of genetic and environmental risk factors has been identified to date, and preclinical and clinical studies including imaging studies have identified neuronal networks involved in the development of alcohol dependence. Methods: We review genetic and environmental risk factors for the development of alcohol addiction as well as structural and neuronal changes, including their transmitter systems, due to regular alcohol intake. Results: Stress as well as family background and, in juveniles, the peer group could be identified as environmental risk factors for alcohol dependence. Heritability is estimated at around 50%, and it seems to be comparable in women and men. There is ongoing research on a broad range of putative endophenotypes such as tolerance of the effects of alcohol intake or personal traits like ‘impulsivity'. On the neurobiological level, chronic alcohol intake seems to render mesolimbic circuits hypersensitive to alcohol and alter the motivational reward system including dopaminergic neurotransmission. Conclusion: Environmental and genetic risk factors, and especially their interaction, facilitate the development of alcohol dependence. Ongoing alcohol intake results in profound alterations of neuronal systems crucial for motivation, learning, memory and cognition control. Future studies should further combine the knowledge of neurobiological mechanisms and risk factors to develop new prevention strategies.

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“…Relatives of alcohol-dependent probands showed significant familial aggregation of ASPD in the Collaborative Study on the Genetics of Alcoholism (COGA) [Nurnberger et al, 2004]. A positive family history of alcoholism is associated with symptoms of ASPD [Grande et al, 1984; Alterman and Cacciola, 1998; Slutske et al, 1998; Jang et al, 2001] and evidence from family and twin studies supports a genetic contribution to the overlap in substance abuse and dependence, conduct disorder (CD), and ASPD [Stallings et al, 1997; Blonigen et al, 2005].…”

Section: Introductionmentioning

confidence: 99%

Ordered subsets linkage analysis of antisocial behavior in substance use disorder among participants in the collaborative study on the genetics of alcoholism

Jacobson¹,

Beseler²,

Lasky‐Su³

et al. 2008

American J of Med Genetics Pt B

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Heterogeneity in complex diseases such as Substance Use Disorder (SUD) reduces the power to detect linkage and makes replication of findings in other populations unlikely. It is therefore critical to refine the phenotype and use methods that account for genetic heterogeneity between families. SUD was operationalized as diagnosis of abuse or dependence to alcohol and/or any one of five illicit substances. Whole-genome linkage analysis of 241 extended pedigree families from the Collaborative Study on the Genetics of Alcoholism was performed in Merlin using an affected sibship design. An Ordered Subsets Analysis (OSA) using FLOSS sought to increase the homogeneity of the sample by ranking families by their density of childhood and adult antisocial behaviors, producing new maximum Nonparametric Lod (NPL) scores on each chromosome for each subset of families. Prior to OSA, modest evidence for linkage was found on chromosomes 8 and 17. Although changes in NPL scores were not statistically significant, OSA revealed possible evidence of linkages on chromosome 7, near markers D7S1795 and D7S821. NPL scores >3.0 were also observed on chromosomes 2, 3, 5, 9, and 14. However, the number of families used in these latter subsets for linkage may be too small to be meaningful. Results provide some evidence for the ability of OSA to reduce genetic heterogeneity, and add further support to chromosome 7 as a possible location to search for genes related to various SUD related processes. Nonetheless, replication of these results in other samples is essential.

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A Family Study of Alcohol Dependence

Cited by 227 publications

References 61 publications

Familial association of abstinent remission from alcohol use disorder in first‐degree relatives of alcohol‐dependent treatment‐seeking probands

Familial association of abstinent remission from alcohol use disorder in first‐degree relatives of alcohol‐dependent treatment‐seeking probands

How Do We ‘Learn' Addiction? Risk Factors and Mechanisms Getting Addicted to Alcohol

Ordered subsets linkage analysis of antisocial behavior in substance use disorder among participants in the collaborative study on the genetics of alcoholism

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