Co-morbidity and familial aggregation of alcoholism and anxiety disorders

1998 ◽  
Vol 28 (4) ◽  
pp. 773-788 ◽  
Author(s):  
K. R. MERIKANGAS ◽  
D. E. STEVENS ◽  
B. FENTON ◽  
M. STOLAR ◽  
S. O'MALLEY ◽  
...  

Background. This study examined the patterns of familial aggregation and co-morbidity of alcoholism and anxiety disorders in the relatives of 165 probands selected for alcoholism and/or anxiety disorders compared to those of 61 unaffected controls.Methods. Probands were either selected from treatment settings or at random from the community. DSM-III-R diagnoses were obtained for all probands and their 1053 first-degree relatives, based on direct interview or family history information.Results. The findings indicate that: (1) alcoholism was associated with anxiety disorders in the relatives, particularly among females; (2) both alcoholism and anxiety disorders were highly familial; (3) the familial aggregation of alcoholism was attributable to alcohol dependence rather than to alcohol abuse, particularly among male relatives; and (4) the pattern of co-aggregation of alcohol dependence and anxiety disorders in families differed according to the subtype of anxiety disorder; there was evidence of a partly shared diathesis underlying panic and alcoholism, whereas social phobia and alcoholism tended to aggregate independently.Conclusions. The finding that the onset of social phobia tended to precede that of alcoholism, when taken together with the independence of familial aggregation of social phobia and alcoholism support a self-medication hypothesis as the explanation for the co-occurrence of social phobia and alcoholism. In contrast, the lack of a systematic pattern in the order of onset of panic and alcoholism among subjects with both disorders as well as evidence for shared underlying familial risk factors suggests that co-morbidity between panic disorder and alcoholism is not a consequence of self-medication of panic symptoms. The results of this study emphasize the importance of examining co-morbid disorders and subtypes thereof in identifying sources of heterogeneity in the pathogenesis of alcoholism.

2011 ◽  
Vol 42 (7) ◽  
pp. 1449-1459 ◽  
Author(s):  
F. S. Goes ◽  
M. G. McCusker ◽  
O. J. Bienvenu ◽  
D. F. MacKinnon ◽  
F. M. Mondimore ◽  
...  

BackgroundCo-morbidity of mood and anxiety disorders is common and often associated with greater illness severity. This study investigates clinical correlates and familiality of four anxiety disorders in a large sample of bipolar disorder (BP) and major depressive disorder (MDD) pedigrees.MethodThe sample comprised 566 BP families with 1416 affected subjects and 675 MDD families with 1726 affected subjects. Clinical characteristics and familiality of panic disorder, social phobia, specific phobia and obsessive-compulsive disorder (OCD) were examined in BP and MDD pedigrees with multivariate modeling using generalized estimating equations.ResultsCo-morbidity between mood and anxiety disorders was associated with several markers of clinical severity, including earlier age of onset, greater number of depressive episodes and higher prevalence of attempted suicide, when compared with mood disorder without co-morbid anxiety. Familial aggregation was found with co-morbid panic and OCD in both BP and MDD pedigrees. Specific phobia showed familial aggregation in both MDD and BP families, although the findings in BP were just short of statistical significance after adjusting for other anxiety co-morbidities. We found no evidence for familiality of social phobia.ConclusionsOur findings suggest that co-morbidity of MDD and BP with specific anxiety disorders (OCD, panic disorder and specific phobia) is at least partly due to familial factors, which may be of relevance to both phenotypic and genetic studies of co-morbidity.


1990 ◽  
Vol 20 (2) ◽  
pp. 311-319 ◽  
Author(s):  
Kenneth S. Kendler

SynopsisAll major psychiatric disorders aggregate in families. For most disorders, both genes and environmental factors play an important role in this aggregation. While recent work has tended to concentrate on the importance of genetic factors, this report focuses on the potential importance of environmental risk factors which themselves aggregate in families. In particular, this article examines how much of the familial aggregation of a psychiatric disorder may result from the familial aggregation of a risk factor. The model is illustrated and then applied to putative familial risk factors for schizophrenia and depression. The results of the model suggest that if parental loss and exposure to pathogenic rearing practices are true risk factors for depression, then they could account for a significant proportion of the familial aggregation of depression. By contrast, the model predicts that even if obstetric injury and low social class are true risk factors for schizophrenia, they together would account for only a very small proportion of the tendency for schizophrenia to aggregate in families.


2006 ◽  
Vol 36 (8) ◽  
pp. 1153-1162 ◽  
Author(s):  
PO-HSIU KUO ◽  
CHARLES O. GARDNER ◽  
KENNETH S. KENDLER ◽  
CAROL A. PRESCOTT

Background. Although alcohol dependence (AD) and major depression (MD) are highly co-morbid, their causal relationship is unclear. In this longitudinal study, we used a genetically informative population-based twin sample to examine the age-at-onset distributions and the temporal relationship of AD and MD.Method. Our sample included 7477 twins, whose diagnoses of AD and MD and age-at-onset information were obtained from structured interviews. Individual-level survival analyses were conducted based on 2603 monozygotic (MZ) twins, and co-twin diagnosis was included in models as an index of familiar liability to AD and MD.Results. The age-at-onset distributions of AD and MD differed substantially. Most onsets of AD were in young adulthood, whereas MD had a flatter distribution across age. Most subjects, especially women, had an onset of MD preceding AD. Prior MD significantly affected risk for developing AD, and this risk decreased over time. By contrast, preceding AD had negligible effects on the risk for future MD. Familial risk was transmitted within disorders but there was little evidence of additional familial liability shared across disorders.Conclusions. Risk for developing AD was substantially increased by a prior episode of MD. The association was only partially accounted for by familial factors, providing support for a direct causal effect such as self-medication. The etiologic path from AD to MD was insignificant.


2010 ◽  
Vol 41 (1) ◽  
pp. 97-105 ◽  
Author(s):  
T. Frisell ◽  
P. Lichtenstein ◽  
N. Långström

BackgroundEtiological theory and prior research with small or selected samples suggest that interpersonal violence clusters in families. However, the strength and pattern of this aggregation remains mostly unknown.MethodWe investigated all convictions for violent crime in Sweden 1973–2004 among more than 12.5 million individuals in the nationwide Multi-Generation Register, and compared rates of violent convictions among relatives of violent individuals with relatives of matched, non-violent controls, using a nested case–control design.ResultsWe found strong familial aggregation of interpersonal violence among first-degree relatives [e.g. odds ratio (OR)sibling 4.3, 95% confidence interval (CI) 4.2–4.3], lower for more distant relatives (e.g. ORcousin 1.9, 95% CI 1.9–1.9). Risk patterns across biological and adoptive relations provided evidence for both genetic and environmental influences on the development of violent behavior. Familial risks were stronger among women, in higher socio-economic strata, and for early onset interpersonal violence. There were crime-specific effects (e.g. ORsibling for arson 22.4, 95% CI 12.2–41.2), suggesting both general and subtype-specific familial risk factors for violent behavior.ConclusionsThe observed familiality should be accounted for in criminological research, applied violence risk assessment, and prevention efforts.


2004 ◽  
Vol 3 (3) ◽  
pp. 323-341
Author(s):  
Hélène Poissant ◽  
Cameron Montgomery

This article is a literature review of studies on attention deficit and hyperactivity disorder (ADHD) and Depression (Depression). Domains evaluated in our review include co-morbidity in proband and family in relation to ADHD and Depression, longitudinal studies concerning outcomes of ADHD in relation to Depression, and familial risk factors related to ADHD and Depression. The studies that were examined established a link between ADHD and Depression in probands as well as in their families. Studies addressing the question of the primary or secondary status of Depression in ADHD do not reveal any clear link between an initial diagnosis of ADHD and a Depression outcome, suggesting that childhood diagnosis of ADHD alone usually does not evolve into adult Depression. The long-term evolution of ADHD into Depression seems to be related more to the presence of an initial comorbidity condition in ADHD children and adolescents. Family factors seem to influence the genesis of ADHD and Depression. There also seems to be a direct link between Major Depression in mothers and ADHD in their children.


2011 ◽  
Vol 42 (6) ◽  
pp. 1239-1248 ◽  
Author(s):  
Y. Li ◽  
S. Shi ◽  
F. Yang ◽  
J. Gao ◽  
Youhui Li ◽  
...  

BackgroundStudies conducted in Europe and the USA have shown that co-morbidity between major depressive disorder (MDD) and anxiety disorders is associated with various MDD-related features, including clinical symptoms, degree of familial aggregation and socio-economic status. However, few studies have investigated whether these patterns of association vary across different co-morbid anxiety disorders. Here, using a large cohort of Chinese women with recurrent MDD, we examine the prevalence and associated clinical features of co-morbid anxiety disorders.MethodA total of 1970 female Chinese MDD patients with or without seven co-morbid anxiety disorders [including generalized anxiety disorder (GAD), panic disorder, and five phobia subtypes] were ascertained in the CONVERGE study. Generalized linear models were used to model association between co-morbid anxiety disorders and various MDD features.ResultsThe lifetime prevalence rate for any type of co-morbid anxiety disorder is 60.2%. Panic and social phobia significantly predict an increased family history of MDD. GAD and animal phobia predict an earlier onset of MDD and a higher number of MDD episodes, respectively. Panic and GAD predict a higher number of DSM-IV diagnostic criteria. GAD and blood-injury phobia are both significantly associated with suicidal attempt with opposite effects. All seven co-morbid anxiety disorders predict higher neuroticism.ConclusionsPatterns of co-morbidity between MDD and anxiety are consistent with findings from the US and European studies; the seven co-morbid anxiety disorders are heterogeneous when tested for association with various MDD features.


1992 ◽  
Vol 41 (4) ◽  
pp. 261-273 ◽  
Author(s):  
J.L. Hopper

AbstractFamilial aggregation for disease is important; strong familial risk factors must exist even if the increased risk to a relative of an affected individual is modest. It is in practice difficult, however, to conduct studies in genetic epidemiology which conform to strict epidemiological principles. For twin studies there are two major questions: Are twins ‘no different’ from the population on which inference is to be made? Are study twins ‘no different’ to twins in the population? The importance of each question of bias depends on the scientific question, the trait(s) studied, and sampling issues. The strength of the twin design is its ability to refute the null hypothesis that genetic factors do not explain variation in a trait. Following the Popperian paradigm, alternate hypotheses should be considered in depth (both theoretically and empirically), with a design and sample size sufficient to exclude not just naive explanations. More sophisticated statistical techniques are now being applied, so the philosophy, assumptions, and limitations of statistical modelling must be appreciated. The concept of ‘heritability’ has, in the past, been misunderstood and misused. New advances in DNA technology promise to revolutionise epidemiological thinking, and so case-control-pedigree designs may well become standard tools. The strengths and limitations of studies based on related individuals as the sampling unit are discussed.


1993 ◽  
Vol 8 (4) ◽  
pp. 179-191
Author(s):  
I Jalenques ◽  
AJ Coudert

SummaryThis review studies the epidemiology of anxiety disorders of childhood and adolescence, including prevalence rates, comorbidity patterns, risk factors and course. Comorbidity is very important: most children with anxiety disorders also have one or several other anomalies, usually anxiety or mood disorders. The authors point out the main evidence suggesting that a number of risk factors are associated with childhood anxiety disorders: age, sex, low socioeconomic setting; child's personality, and lastly, familial risk factors which have a very strong influence: children of parents with current or past anxiety disorders are more at risk of having anxiety disorders. Concerning the course of disorders, we have tentatively defined subsets of children or adolescents with anxiety disorders, and tried to clarify the recovery rate of these subsets. Future directions for research are suggested.


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