Genetic Factors in Alcohol Dependence

2001 ◽  
2001 ◽  
Vol 178 (S40) ◽  
pp. s33-s40 ◽  
Author(s):  
A. C. Heath ◽  
P. A. F. Madden ◽  
K. K. Bucholz ◽  
L. J. Bierut ◽  
J. B. Whitfield ◽  
...  

BackgroundProgress in identifying genetic factors protective against alcohol dependence (AIcD) requires a paradigm shift in psychiatric epidemiology.AimsTo integrate analysis of research into the genetics of alcoholism.MethodData from prospective questionnaire and interview surveys of the Australian twin panel, and from a subsample who underwent alcohol challenge, were analysed.ResultsIn men, effects of alcohol dehydrogenase ADH2∗1/∗2 genotype or high alcohol sensitivity (risk-decreasing), and of history of childhood conduct disorder, or having monozygotic co-twin or twin sister with AIcD (risk-increasing) were significant and comparable in magnitude. Religious affiliation (Anglican versus other) was associated with the ADH2 genotype, but did not explain the associations with AIcD symptoms. No protective effect of the ADH2∗1/∗2 genotype was observed in women.ConclusionsThe early onset and strong familial aggregation of AIcD, and opportunity for within-family tests of genetic association to avoid confounding effects, make epidemiological family studies of adolescents and young adults and their families a priority.


2011 ◽  
Vol 17 (12) ◽  
pp. 1306-1315 ◽  
Author(s):  
K S Kendler ◽  
S H Aggen ◽  
C A Prescott ◽  
J Crabbe ◽  
M C Neale

2008 ◽  
Vol 154 (2) ◽  
pp. 275-287 ◽  
Author(s):  
R D Mayfield ◽  
R A Harris ◽  
M A Schuckit

2016 ◽  
Vol 18 (2) ◽  
pp. 120-128 ◽  
Author(s):  
Kimberly Goodyear ◽  
Mary R. Lee ◽  
Melanie L. Schwandt ◽  
Colin A. Hodgkinson ◽  
Lorenzo Leggio

1994 ◽  
Vol 9 (2) ◽  
pp. 63-69 ◽  
Author(s):  
P Gorwood ◽  
J Ades ◽  
J Feingold

SummaryPart of the familial factor of alcoholism is associated with the existence of genetic vulnerability. Genetic factors which interact with the pathogenesis of alcoholism are nevertheless complex, partial and for the moment partly unknown at the biological level. Recently, many association studies have been published concerning alcohol-dependence and genes coding for the second dopamine receptor. These associations, which have had positive replications, raise many questions. First of all, should the inheritance of alcoholism be regarded as a definitive fact? Secondly what is inherited? It could be alcoholism in general, a component of this disease (for instance, dependence on, sensitivity to or the seeking-process for alcohol), a specific pattern of drinking, presence of complications linked to alcohol abuse, or more general features, common to many addiction diseases. Thirdly, how could dopamine be linked to alcoholism? Furthermore, how should these positive associations be considered, given that two of these studies were negative, and that all linkage studies were negative. Lastly, are there other clues and ways of finding genetic vulnerability factors for alcohol abuse?


2016 ◽  
Vol 33 (S1) ◽  
pp. S320-S320
Author(s):  
J. Teixeira ◽  
G. Pereira ◽  
T. Mota ◽  
J. Cabral Fernandes

IntroductionAlcohol dependence is one of the psychiatric disorders for which hereditary influence is strongest. In fact, the importance of genetic factors in transmission of vulnerability to alcohol dependence was first described in literature many years ago by psychiatrists who dedicate to its study. That vulnerability may be explained by an epigenetic model in which biological hereditary factors associate with environmental factors to cause alcohol dependence.ObjectivesStudy the influence of genetic factors on alcohol dependence.MethodsDuring 4 consecutive months a sample of alcoholic patients was collected from the Alcohol Treatment Unit of CHPL (inpatients and outpatients). Biographic data, patient's psychiatric diagnosis and family history of alcohol dependence or of dependence of other drugs were recorded.ResultsInitial sample included 122 patients. After exclusion of patients who were also hospitalized in that period, the final sample included 102 patients (26% female), with a mean age of 48 years old. Main patients’ diagnosis was alcohol dependence but most of them (52%) presented psychiatric comorbidity. Most patients (55%) had family history of alcohol dependence or dependence of other substances, 26% did not have and 19% did not know. For 61% of patients, the father and/or mother were the affected relative. Most patients (61%) who had a family history of alcohol dependence or dependence of other substances had 2 or more affected relatives.ConclusionsMost patients with alcohol dependence have family history of alcohol dependence or dependence of other substances, usually in more than 1 relative, which must be taken in account during treatment.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2000 ◽  
Vol 15 (2) ◽  
pp. 123-128 ◽  
Author(s):  
F. Limosin ◽  
J. Adès ◽  
P. Gorwood

SummaryGenetic factors explain a non-negligible part of the vulnerability to alcohol dependence, the genetic influence in males being estimated at around 60%. The search for gene(s) potentially implicated in alcoholism is counteracted by the clinical heterogeneity of alcoholism, but also by heterogeneity of the etiologic factors involved. It is thus necessary to redefine more specific phenotypes with more simple determinism, and to focus on more specific subsets of candidate genes. In this view, the existence of co-occurrence (presence at the same time, whatever the cause) between antisocial personality and alcoholism is frequently reported. Three hypotheses have been previously proposed to explain this co-occurrence. Firstly, it could be a pure artefact or contamination, due to common items in diagnostic manuals widely used, such as the DSM or ICD. Secondly, antisocial personality and alcoholism could share common etiologic factor(s), and determine a ‘real’ co-morbidity. Finally, common genetic factors between these two disorders may exist, with the observation of a co-transmission of both disorders more often than expected by chance alone, meaning the existence of co-aggregation. Each of these three hypotheses will be reviewed and discussed.


2012 ◽  
Vol 57 (5) ◽  
pp. 1343-1348 ◽  
Author(s):  
Claudio Terranova ◽  
Marianna Tucci ◽  
Daniela Sartore ◽  
Fabiano Cavarzeran ◽  
Luisa Barzon ◽  
...  

2019 ◽  
Author(s):  
Audrey E. Padula ◽  
Jennifer A. Rinker ◽  
Fauzan Khan ◽  
Marcelo F. Lopez ◽  
Megan K. Mulligan ◽  
...  

AbstractAnxiety and mood disorders are often comorbid with alcohol use disorder (AUD) and are considered critical in the development, maintenance, and reinstatement of alcohol dependence and harmful alcohol-seeking behaviors. Because of this high comorbidity, it is necessary to determine shared and unique genetic factors driving heavy ethanol drinking and anxiety-related behaviors. We used a model of stress-induced escalation of drinking in ethanol dependent C57BL/6J mice to measure anxiety-like behaviors on the marble burying and novelty-suppressed feeding task (NSFT) during abstinence. In order to identify novel pharmacogenetic targets that may lead to more effective treatment, a targeted bioinformatics analysis was used to quantify the expression of K+ channel genes in the amygdala that covary with anxiety-related phenotypes in the well phenotyped and fully sequenced family of BXD strains. A pharmacological approach was used to validate the key bioinformatics finding in ethanol-dependent, stressed C57BL/6J mice during the NSFT. Amygdalar expression of Kcnn3 correlated significantly with just over 40 anxiety-associated phenotypes. Further examination of Kcnn3 expression revealed a strong eigentrait for anxiety-like behaviors in this family. Kcnn3 expression in the amygdala correlated negatively with binge-like and voluntary ethanol drinking. C57BL/6J mice treated with chronic intermittent ethanol exposure and repeated swim stress consumed more ethanol in their home cages and showed hypophagia on the NSFT during prolonged abstinence. Pharmacologically targeting KCNN3 protein with the KCa2 channel positive modulator 1-EBIO decreased ethanol drinking and reduced latency to approach food during the NSFT in ethanol-dependent, stressed mice. Collectively these validation studies provide central nervous system mechanistic links into to the covariance of stress, anxiety, and AUD in the BXD strains. Further this analytical approach is effective in defining targets for treating alcohol dependence and comorbid mood and anxiety disorders.


Sign in / Sign up

Export Citation Format

Share Document