Alcohol Problems in Adoptees Raised Apart From Alcoholic Biological Parents

Goodwin, Donald W.; Schulsinger, Fini; Hermansen, Leif; Guze, Samuel B.; Winokur, George

doi:10.1001/archpsyc.1973.01750320068011

Cited by 821 publications

(235 citation statements)

References 18 publications

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“…These include the influence of shared risk factors, including genetic vulnerabilities, that act to increase the risks of both MDD and AUDs. Specifically, family psychiatric history has been shown to be a stronger predictor of co-morbid depression and alcohol dependence than of either condition in isolation (Dawson & Grant, 1998), and a number of twin, adoption and extended family studies have reported significant genetic correlations between MDD and AUD (Cloninger et al 1979 ;Wender et al 1986 ;Coyrell et al 1992 ;Kendler et al 1993 ;Prescott et al 2000), although such correlations have not been universally reported (Goodwin et al 1973(Goodwin et al , 1977Gershon et al 1982 ;Merikangas et al 1985) and, more recently, it has been suggested that the genetic correlation between MDD and AUD can be explained by the shared genetic influence of antisocial personality disorder (Fu et al 2002). Other explanations for the observed comorbidity between MDD and AUD include the possibility that AUDs may induce MDD (Brown & Schuckit, 1988 ;Brook et al 2002 ;Ramsey et al 2004 ;Schuckit, 2006) or conversely that MDD may induce AUDs through processes such as self-medication (Deykin et al 1987 ;Khantzian, 1997 ;Kuo et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Differential criterion functioning of alcohol use symptomatology in major depressive disorder?

Lynskey

Agrawal

2007

Psychol. Med.

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Background. Major depressive disorder (MDD) and alcohol use disorders (AUDs) are among the most prevalent psychiatric disorders and are frequently co-morbid. However, some component of this co-morbidity may be artifactual and arise from the influence of current mental state on self-reports of AUD.Method. This study examined whether past-year MDD is associated with differential criterion functioning (DCF) in reports of AUD symptomatology in male and female participants in the National Epidemiological Survey on Alcohol and Related Conditions (NEASRC).Results. Reports of past-year AUD symptomatology were adequately summarized by a single-factor model in which each of the 11 abuse and dependence criteria had high factor loadings (0.71-0.93) and did not vary between men and women after allowing for threshold differences. Co-morbid MDD was associated with higher AUD mean scores. There was some evidence for DCF with past-year MDD being associated with a lower endorsement of use in hazardous situations among men whereas women with MDD were more likely to endorse both social/interpersonal problems and emotional/physical problems.Conclusions. Several items assessing AUD display DCF in the presence of MDD. While these findings highlight the need to consider the possibility that mental state can influence reporting of psychiatric symptoms and potentially inflate estimates of co-morbidity, they suggest that only a negligible component of the co-morbidity between MDD and AUDs can be attributed to over-reporting of alcohol symptomatology conditional on current MDD.

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Section: Discussionmentioning

confidence: 99%

Differential criterion functioning of alcohol use symptomatology in major depressive disorder?

Lynskey

Agrawal

2007

Psychol. Med.

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“…Twin studies with adoption have provided strong evidence for an important genetic influence on the risk of becoming an alcoholic in both men and women (Heath et al 1997a). Twin studies in Scandinavia and the United States have shown consistently higher rates of alcoholism in monozygotic compared to dizygotic twins of male alcoholics (Hrubec and Omenn 1981; Kaij 1960; Koskenvuo et al 1984), and adoption studies have shown consistently higher rates of alcoholism in the adopted-away sons of alcoholic biological parents than in control adoptees (Cadoret et al 1994;Goodwin et al 1973). While a genetic influence on alcoholism in women generally has been considered weaker, recent analyses suggest that this may be the result of low statistical power due to the low base rate of alcoholism in women (Heath et al 1997b; Kessler et al 1994).…”

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confidence: 99%

Drug Addiction, Dysregulation of Reward, and Allostasis

Koob

Moal

2001

Neuropsychopharmacology

2,541

1,962

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This paper reviews recent developments in the neurocircuitry and neurobiology of addiction from a perspective of allostasis. A model is proposed for brain changes that occur during the development of addiction that explain the persistent vulnerability to relapse long after drug-taking has ceased. Addiction is presented as a cycle of spiralling dysregulation of brain reward systems that progressively increases, resulting in the compulsive use and loss of control over drug-taking. The development of addiction recruits different sources of reinforcement, different neuroadaptive mechanisms, and different neurochemical changes to dysregulate the brain reward system. Counteradaptive processes such as opponent-process that are part of normal homeostatic limitation of reward function fail to return within the normal homeostatic range and are hypothesized to form an allostatic state. Allostasis from the addiction perspective is defined as the process of maintaining apparent reward function stability by changes in brain reward mechanisms. The allostatic state represents a chronic deviation of reward set point and is fueled not only by dysregulation of reward circuits per se, but also by the activation of brain and hormonal stress responses. The manifestation of this allostatic state as compulsive drugtaking and loss of control over drug-taking is hypothesized to be expressed through activation of brain circuits involved in compulsive behavior such as the cortico-striatal-thalamic loop. The view that addiction is the pathology that results from an allostatic mechanism using the circuits established for natural rewards provides a realistic approach to BACKGROUNDDrug addiction is a chronically relapsing disorder that is defined by two major characteristics: a compulsion to take the drug with a narrowing of the behavioral repertoire toward excessive drug intake, and a loss of control in limiting intake (American Psychiatric Association 1994; World Health Organization 1992). An important challenge for neurobiological research is to understand the neuroadaptive differences between controlled drug use and loss of control, and by extension, the molecular, cellular and system processes that lead to addiction (Koob and Le Moal 1997).Animal models are critical for understanding the neuropharmacological mechanisms involved in the development of addiction. While there are no complete animal models of addiction, animal models do exist for many elements of the syndrome. These elements can be derived from symptoms or diagnostic criteria for addiction or conceptual frameworks such as different sources of reinforcement (American Psychiatric Association 1994; World Health Organization 1992). Linking neu- 24 , NO . 2 ropharmacological events to animal models can occur at multiple levels of analysis -molecular, cellular and system -and it will only be the integration of these changes across dimensions of analysis that will allow a full understanding of the neurobiology of drug addiction.Advances in neuroscience research are rapidly unr...

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“…Firstdegree relatives of affected individuals are at a 2-to 8-fold increased risk for alcohol dependence (5,6). Adoption studies and twin studies have clarified that this familial clustering of alcohol dependence is attributable largely to genetic factors (7)(8)(9)(10)(11). In most recent studies, these heritable influences explain ≈50-80% of the individual differences in liability to alcohol dependence (12,13).…”

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confidence: 99%

A genome-wide association study of alcohol dependence

Bierut

Agrawal

Bucholz

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

413

466

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Excessive alcohol consumption is one of the leading causes of preventable death in the United States. Approximately 14% of those who use alcohol meet criteria during their lifetime for alcohol dependence, which is characterized by tolerance, withdrawal, inability to stop drinking, and continued drinking despite serious psychological or physiological problems. We explored genetic influences on alcohol dependence among 1,897 European-American and African-American subjects with alcohol dependence compared with 1,932 unrelated, alcohol-exposed, nondependent controls. Constitutional DNA of each subject was genotyped using the Illumina 1M beadchip. Fifteen SNPs yielded P < 10 −5 , but in two independent replication series, no SNP passed a replication threshold of P < 0.05. Candidate gene GABRA2 , which encodes the GABA receptor α2 subunit, was evaluated independently. Five SNPs at GABRA2 yielded nominal (uncorrected) P < 0.05, with odds ratios between 1.11 and 1.16. Further dissection of the alcoholism phenotype, to disentangle the influence of comorbid substance-use disorders, will be a next step in identifying genetic variants associated with alcohol dependence.

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Alcohol Problems in Adoptees Raised Apart From Alcoholic Biological Parents

Cited by 821 publications

References 18 publications

Differential criterion functioning of alcohol use symptomatology in major depressive disorder?

Differential criterion functioning of alcohol use symptomatology in major depressive disorder?

Drug Addiction, Dysregulation of Reward, and Allostasis

A genome-wide association study of alcohol dependence

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