Lifetime Panic-Depression Comorbidity in the National Comorbidity Survey

Harvard University, Cambridge, Massachusetts, United States
Archives of General Psychiatry (Impact Factor: 14.48). 10/1998; 55(9):801-8. DOI: 10.1001/archpsyc.55.9.801
Source: PubMed


The National Comorbidity Survey is a nationally representative survey of the prevalences and correlates of DSM-III-R disorders in the US household population.
Retrospective age-at-onset reports were used to study predictive relationships between lifetime panic and depression.
Strong associations were found between the lifetime prevalences of panic and major depressive episodes (odds ratios: for panic attacks with depression, 6.2; for panic disorder with depression, 6.8). These associations were not significantly influenced by the inclusion or exclusion of respondents with mania. Temporally primary depression predicted a first onset of subsequent panic attacks but not of panic disorder. Temporally primary panic attacks, with or without panic disorder and whether or not the panic was persistent, predicted a first onset of subsequent major depression. The associations between panic attack and depression were attenuated in models that controlled for prior traumatic life experiences and histories of other DSM-III-R disorders.
Lifetime panic-depression comorbidity characterizes most community respondents with panic disorder and a substantial few of those with major depression. The absence of a dose-response relationship suggests that primary panic attack is a marker, rather than a causal risk factor, of subsequent depression. Primary depression, in comparison, appears to be a genuine risk factor for secondary panic attacks. That primary depression predicts panic attacks but not panic disorder suggests that secondary panic is a severity marker of depression rather than a comorbid condition. These results are far from definitive because they are based on retrospective reports, lay-administered diagnostic interviews, and only 1 survey. However, they raise important questions that could lead to a fundamental rethinking of panic-depression comorbidity if they are replicated in future epidemiological and clinical studies.

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Available from: Tevfik Bedirhan Ustun, Aug 19, 2015
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    • "In a retrospective analysis of longitudinal data, in individuals who had met criteria for both GAD and major depressive episode (Wittchen et al. 2003b), the depression diagnosis followed that of GAD in 52% of individuals and preceded GAD in only 29%. In a further study which relied on participants' recall in a population who had experienced depression and panic attacks, a first depressive episode was recalled as occurring after the first panic attack in 43% of cases and preceding it in 31% (Kessler et al. 1998). However, in a subsample who had had a diagnosis of panic disorder, which has a higher threshold, 22% recalled that panic disorder preceded the first depressive episode whereas 48% reported that a depressive episode began first. "
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    ABSTRACT: Generalized anxiety disorder (GAD) and panic disorder (PD) differ in their biology and co-morbidities. We hypothesized that GAD but not PD symptoms at the age of 15 years are associated with depression diagnosis at 18 years. Using longitudinal data from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort we examined relationships of GAD and PD symptoms (measured by the Development and Well-Being Assessment) at 15 years with depression at 18 years (by the Clinical Interview Schedule - Revised) using logistic regression. We excluded adolescents already depressed at 15 years and adjusted for social class, maternal education, birth order, gender, alcohol intake and smoking. We repeated these analyses following multiple imputation for missing data. In the sample with complete data (n = 2835), high and moderate GAD symptoms in adolescents not depressed at 15 years were associated with increased risk of depression at 18 years both in unadjusted analyses and adjusting for PD symptoms at 15 years and the above potential confounders. The adjusted odds ratio (OR) for depression at 18 years in adolescents with high relative to low GAD scores was 5.2 [95% confidence interval (CI) 3.0-9.1, overall p < 0.0001]. There were no associations between PD symptoms and depression at 18 years in any model (high relative to low PD scores, adjusted OR = 1.3, 95% CI 0.3-4.8, overall p = 0.737). Missing data imputation strengthened the relationship of GAD symptoms with depression (high relative to low GAD scores, OR = 6.2, 95% CI 3.9-9.9) but those for PD became weaker. Symptoms of GAD but not PD at 15 years are associated with depression at 18 years. Clinicians should be aware that adolescents with GAD symptoms may develop depression.
    Psychological Medicine 08/2015; -1:1-13. DOI:10.1017/S003329171500149X · 5.94 Impact Factor
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    • "Seventy-three percent of persons with major depression have comorbid lifetime anxiety disorders, whereas 27–77% of those with a principal diagnosis of an anxiety disorder develop a lifetime diagnosis of depression (Brown, Campbell, Lehman, Grisham, & Mancill, 2001). In comparison to those with pure diagnoses, individuals with comorbid anxiety and depressive disorders experience greater chronicity and severity of each diagnosis; poorer work and psychosocial functioning; lower perceived quality of life; and a heightened risk of suicide (Brown, Schulberg, Madonia, Shear, & Houck, 1996; Kessler et al., 1998; Olfson et al., 1997; Pfeiffer, Ganoczy, Ilgen, Zivin, & Valenstein, 2009; Sherbourne, Wells, Meredith, Jackson, & Camp, 1996). Hence, a greater understanding of the mechanisms behind this comorbidity is imperative. "
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    ABSTRACT: Anxiety and depression are often highly correlated with each other. To explain this connection, the present study examined the longitudinal relationship between earlier anxiety and later depression, using avoidance as a mediator and trauma as a moderator. Participants (N = 6,504 adolescents) completed baseline measures of anxiety and depression, a measure of avoidance one year later, a measure of trauma six to eight years later, and a measure of depression 12 to 14 years later. Analyzed with structural equation models, the results showed that anxiety predicted later depression, and this relationship was partially mediated by avoidance. The relationship between avoidance and depression was not moderated by trauma. Together, these findings suggest that anxiety may influence later depression through avoidance, and this relationship remains unaffected by experiencing a traumatic experience.
    Journal of Anxiety Disorders 06/2014; DOI:10.1016/j.janxdis.2014.03.007 · 2.96 Impact Factor
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    • "At the least, their behaviors suggest that LH hypoactivity is a common underlying pathology. This is also suggested by the observations that PD is frequently comorbid with depression (Leckman et al., 1983; Gorman and Coplan, 1996; Kessler et al., 1998), and this comorbidity is more likely after LH stroke (Bhogal et al., 2004; Barker-Collo, 2007; for review). In keeping with the evidence suggesting that negative emotions in particular are shared between the hemispheres, the nature of each hemisphere's involvement may be that the RH mediates the subjective affect and the LH regulates it. "
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    ABSTRACT: Presented is a model suggesting that the right hemisphere (RH) directly mediates the identification and comprehension of positive and negative emotional stimuli, whereas the left hemisphere (LH) contributes to higher level processing of emotional information that has been shared via the corpus callosum. RH subcortical connections provide initial processing of emotional stimuli, and their innervation to cortical structures provides a secondary pathway by which the hemispheres process emotional information more fully. It is suggested that the LH contribution to emotion processing is in emotional regulation, social well-being, and adaptation, and transforming the RH emotional experience into propositional and verbal codes. Lastly, it is proposed that the LH has little ability at the level of emotion identification, having a default positive bias and no ability to identify a stimulus as negative. Instead, the LH must rely on the transfer of emotional information from the RH to engage higher-order emotional processing. As such, either hemisphere can identify positive emotions, but they must collaborate for complete processing of negative emotions. Evidence presented draws from behavioral, neurological, and clinical research, including discussions of subcortical and cortical pathways, callosal agenesis, commissurotomy, emotion regulation, mood disorders, interpersonal interaction, language, and handedness. Directions for future research are offered.
    Frontiers in Human Neuroscience 04/2014; 8(1):230. DOI:10.3389/fnhum.2014.00230 · 2.99 Impact Factor
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