Reliability of a lifetime history of major depression: 
implications for heritability and co-morbidity

Foley, Debra L.; Neale, Michael C.; Kendler, Kenneth S.

doi:10.1017/s0033291798006977

Cited by 71 publications

(75 citation statements)

References 44 publications

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“…Heritability estimates obtained from cross-sectional twin studies are also problematic as they do not allow measurement error to be estimated, resulting in inflation of the E component. In a longitudinal twin study that overcame this problem, heritability was estimated at 66% (95% CI: 53-78%) [Foley et al, 1998], which is compatible with the heritability of 75% reported in the largest clinical sample of twins with unipolar depression [McGuffin et al, 1996]. …”

Section: Gele Demonstrationsupporting

confidence: 63%

“…However, we are going to assume that the disease pedigree is for the rarer phenotype of being clinically depressed. We will approximate clinical caseness to meeting diagnosis at two-time points five years apart, what Foley et al [1998] refer to as reliably diagnosed depression. Using Table I in Foley et al [1998] the prevalence of reliably diagnosed depression is approximately 60% of the prevalence for meeting criteria at one (or more) of two-time points.…”

Section: Gele Demonstrationmentioning

confidence: 99%

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Software for generating liability distributions for pedigrees conditional on their observed disease states and covariates

Campbell

Sham

Knight

et al. 2009

Genetic Epidemiology

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For many multifactorial diseases, aetiology is poorly understood. A major research aim is the identification of disease predictors (environmental, biological, and genetic markers). In order to achieve this, a two-stage approach is proposed. The initial or synthesis stage combines observed pedigree data with previous genetic epidemiological research findings, to produce estimates of pedigree members' disease risk and predictions of their disease liability. A further analysis stage uses the latter as inputs to look for associations with potential disease markers. The incorporation of previous research findings into an analysis should lead to power gains. It also allows separate predictions for environmental and genetic liabilities to be generated. This should increase power for detecting disease predictors that are environmental or genetic in nature. Finally, the approach brings pragmatic benefits in terms of data reduction and synthesis, improving comprehensibility, and facilitating the use of existing statistical genetics tools. In this article we present a statistical model and Gibbs sampling approach to generate liability predictions for multifactorial disease for the synthesis stage. We have implemented the approach in a software program. We apply this program to a specimen disease pedigree, and discuss the results produced, comparing its results with those generated under a more naïve model. We also detail simulation studies that validate the software's operation.

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Section: Gele Demonstrationsupporting

confidence: 63%

Section: Gele Demonstrationmentioning

confidence: 99%

Software for generating liability distributions for pedigrees conditional on their observed disease states and covariates

Campbell

Sham

Knight

et al. 2009

Genetic Epidemiology

View full text Add to dashboard Cite

show abstract

“…Another limitation is that test-retest data were not available for our samples, which made it impossible to estimate the reliability of the lifetime interviews. In studies in which unreliability of measurement was taken into account, heritability estimates were around 50% for phobias and 66% for MDD (Foley et al, 1998). These studies demonstrate that in our study the effect of familial influences might be underestimated.…”

Section: Discussionmentioning

confidence: 99%

Familial Clustering of Major Depression and Anxiety Disorders in Australian and Dutch Twins and Siblings

et al. 2005

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T he aim of this study was to investigate familial influences and their dependence on sex for panic disorder and/or agoraphobia, social phobia, generalized anxiety disorder and major depression. Data from Australian (N = 2287) and Dutch (N = 1185) twins and siblings who were selected for a linkage study and participated in clinical interviews to obtain lifetime Diagnostic and Statistical Manual of Mental Disorders (4th ed.; DSM-IV) diagnoses were used. In a liability model, tetrachoric correlations were estimated in sibling pairs and sex differences between sibling correlations were tested. For each diagnosis, the sibling correlations could be constrained to be equal across the Australian and Dutch samples. With the exception of panic disorder and/or agoraphobia, all sibling correlations were the same for brother, sister and opposite-sex sibling pairs and were around .20. For panic disorder and/or agoraphobia, the correlation was .23 in brother and sister pairs, but absent in opposite-sex sibling pairs. From these results it can be concluded that upper heritability estimates, based on twice the correlations in the sibling pairs, vary between 36% (major depression) and 50% (social phobia). Furthermore, different genetic risk factors appear to contribute to the vulnerability for panic disorder and/or agoraphobia in men and women. No other sex differences were found.Anxiety disorders and major depression (MDD) are common disorders. In epidemiological studies, lifetime prevalences in women are found to be around 30% for some kind of anxiety disorders and around 20% for MDD (Bijl et al., 1998;Kessler et al., 1994). Although these prevalences are lower in men, they are still high with figures ranging between 14% and 19% for anxiety disorders and between 11% and 13% for MDD (Bijl et al., 1998;Kessler et al., 1994). These prevalences may be even higher as cross-sectional surveys are biased by recall problems. When recall bias is considered, the prevalence of lifetime MDD is estimated at 30% in men and 40% in women (Kruijshaar et al., 2005). These disorders constitute a huge public health problem, mainly due to the chronic and disabling course, but in the case of MDD, also as a result of the increased risk for other major diseases such as cardiac mortality (Musselman et al., 1998;Penninx et al., 2001).Consequently, the etiology of these disorders is an important topic of research. Over the last 20 years, several family and twin studies have been performed to investigate the influence of familial factors on anxiety and depression. In the description of the results, we will focus on MDD, panic disorder and/or agoraphobia, social phobia and generalized anxiety disorder (GAD). Sullivan et al. (2000) and Hettema, Neale, et al. (2001) discussed the results of family and twin studies on lifetime diagnoses of MDD and anxiety disorders respectively and performed a metaanalysis when possible. They included studies in which the disorders were defined by operationalized diagnostic criteria, such as the Diagnostic and Statistical Man...

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“…This diathesis may be consistent with the relatively high comorbidity of panic disorder and major depression in the clinical literature. 112,113 However, it is noteworthy that panic disorder and major depression are both associated with reductions in cortical GABA level, while atypical depression, a form of depression associated with heightened mood reactivity and panic attacks, is not (Sanacora G et al, unpublished data). In this regard, atypical depression and bipolar depression are similar.…”

Section: Cortical Gaba Deficits In Mood Disordersmentioning

confidence: 99%

Glutamate and GABA systems as targets for novel antidepressant and mood-stabilizing treatments

et al. 2002

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Glutamate and ␥-amino butyric acid (GABA) systems are emerging as targets for development of medications for mood disorders. There is increasing preclinical and clinical evidence that antidepressant drugs directly or indirectly reduce N-methyl-D-aspartate glutamate receptor function. Drugs that reduce glutamatergic activity or glutamate receptor-related signal transduction may also have antimanic effects. Recent studies employing magnetic resonance spectroscopy also suggest that unipolar, but not bipolar, depression is associated with reductions in cortical GABA levels. Antidepressant and mood-stabilizing treatments also appear to raise cortical GABA levels and to ameliorate GABA deficits in patients with mood disorders. The preponderance of available evidence suggests that glutamatergic and GABAergic modulation may be an important property of available antidepressant and mood-stabilizing agents. Future research will be needed to develop and evaluate new agents with specific glutamate and GABA receptor targets in the treatment of mood disorders. Molecular Psychiatry (2002) 7, S71-S80.

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Reliability of a lifetime history of major depression: implications for heritability and co-morbidity

Abstract: Background. In unselected samples, the diagnosis of major depression (MD) is not highly reliable. It is not known if occasion-specific influences on reliability index familial risk factors for MD, or how reliability is associated with risk for co-morbid anxiety disorders.

Cited by 71 publications

References 44 publications

Software for generating liability distributions for pedigrees conditional on their observed disease states and covariates

Software for generating liability distributions for pedigrees conditional on their observed disease states and covariates

Familial Clustering of Major Depression and Anxiety Disorders in Australian and Dutch Twins and Siblings

Glutamate and GABA systems as targets for novel antidepressant and mood-stabilizing treatments

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