Cohort studies suggest that the relationship between major depression (MD) and Type 2 diabetes (T2DM) is bidirectional. However, this association may be confounded by shared genetic or environmental factors. The objective of this study was to use a twin design to investigate the association between MD and T2DM.
Data come from the Screening Across the Lifespan Twin Study, a sample of monozygotic and dizygotic twins 40 years or older sampled from the Swedish Twin Registry (n = 37,043). MD was assessed by using the Composite International Diagnostic Inventory. Structural equation twin modeling and Cox proportional hazards modeling were used to assess the relationship between MD and T2DM.
Approximately 19% of respondents had a history of MD and 5% had a history of T2DM. MD was associated with 32% increased likelihood of T2DM (95% confidence interval = 1.00-1.80) among twins aged 40 to 55 years, even after accounting for genetic risk, but was not associated with T2DM among twins older than 55 years. T2DM was associated with 33% increased likelihood of MD (95% confidence interval = 1.02-1.72) among younger, but not older twins. Cholesky decomposition twin modeling indicated that common unique environmental factors contribute to the association between MD and T2DM.
Environmental factors that are unique to individuals (i.e., not shared within families) but common to both MD and T2DM contribute to their co-occurrence in midlife. However, we cannot exclude the possibility of bidirectional causation as an alternate explanation. It is likely that multiple processes are operating to effect the relation between psychiatric and medical conditions in midlife.
Cites: Am J Public Health. 2010 May;100(5):933-919846689
The aim of this study was to analyze whether exposure to workplace bullying among 5701 female employees in the Danish eldercare sector increases the risk of onset of a major depressive episode (MDE).
Participants received questionnaires in 2004-2005 and again in 2006-2007. MDE was assessed with the Major Depression Inventory. We examined baseline bullying as a predictor of onset of MDE at follow-up using multiple logistic regression. We further conducted a cross-sectional analysis at the time of follow-up among participants who at baseline were free of bullying, MDE, and signs of reduced psychological health. Finally, we analyzed reciprocal effects, by using baseline bullying and baseline MDE as predictors for bullying and MDE at follow-up.
Onset rates of MDE in the groups of no, occasional, and frequent bullying were 1.5%, 3.4%, and 11.3%, respectively. Odds ratios (OR) for onset of MDE were 2.22 [95% confidence interval (95% CI) 1.31-3.76] for occasional bullying and OR 8.45 (95% CI 4.04-17.70) for frequent bullying, after adjustment for covariates. In the cross-sectional analysis, OR were 6.29 (95% CI 2.52-15.68) for occasional bullying and 20.96 (95% CI 5.80-75.80) for frequent bullying. In the analyses on reciprocal effects, both baseline bullying [occasional: OR 2.12 (95% CI 1.29-3.48) and frequent: OR 6.39 (95% CI 3.10-13.17)] and baseline MDE [OR 7.18 (95% CI 3.60-14.30] predicted MDE at follow-up. However, only baseline bullying [occasional: OR 7.44 (95% CI 5.94-9.31) and frequent: OR 11.91 (95% CI 7.56-18.77)] but not baseline MDE [OR 0.93 (95% CI 0.47-1.84)] predicted bullying at follow-up.
Workplace bullying increased the risk of MDE among female eldercare workers. MDE did not predict risk of bullying. Eliminating bullying at work may be an important contribution to the prevention of MDE.
Comorbid mood and anxiety disorders are commonly seen in clinical practice. The goal of this article is to review the available literature on the epidemiologic, etiologic, clinical, and management aspects of this comorbidity and formulate a set of evidence- and consensus-based recommendations. This article is part of a set of Canadian Network for Mood and Anxiety Treatments (CANMAT) Comorbidity Task Force papers.
We conducted a PubMed search of all English-language articles published between January 1966 and November 2010. The search terms were bipolar disorder and major depressive disorder, cross-referenced with anxiety disorders/symptoms, panic disorder, agoraphobia, generalized anxiety disorder, social phobia, obsessive-compulsive disorder, and posttraumatic stress disorder. Levels of evidence for specific interventions were assigned based on a priori determined criteria, and recommendations were developed by integrating the level of evidence and clinical opinion of the authors.
Comorbid anxiety symptoms and disorders have a significant impact on the clinical presentation and treatment approach for patients with mood disorders. A set of recommendations are provided for the management of bipolar disorder (BD) with comorbid anxiety and major depressive disorder (MDD) with comorbid anxiety with a focus on comorbid posttraumatic stress disorder, use of cognitive-behavioral therapy across mood and anxiety disorders, and youth with mood and anxiety disorders.
Careful attention should be given to correctly identifying anxiety comorbidities in patients with BD or MDD. Consideration of evidence- or consensus-based treatment recommendations for the management of both mood and anxiety symptoms is warranted.
Using a representative longitudinal cohort consisting of more than 8,000 community residents, this study sought to evaluate patterns of interaction between childhood adversity and adult stressors in relation to MDE. The goal was to interpret the interactions using epidemiologic theory.
A Canadian longitudinal study called the National Population Health Survey (NPHS) was the data source. This NPHS began in 1994 and the cohort has subsequently been interviewed every 2 years. Childhood adversities were assessed retrospectively and adult stressors and MDE were evaluated during follow-up. Interactions between various potential MDE risk factors were assessed on an additive scale using linear regression and on a multiplicative scale using logistic regression.
Hypothesized interactions between negative childhood experiences and more recent stressors were apparent in statistical models adopting an additive (linear regression), but not multiplicative (logisitic), perspective. According to the component-cause model of etiology, this pattern suggests shared causal mechanisms. There was no general tendency for such interactions to occur with other risk factors.
Biological mechanisms responsible for early life calibration of stress response systems may generate persistent sensitization to stressors, thereby increasing the risk of MDE following exposure to stressful events later in life. Reliance on multiplicative models such as logistic regression and log-binomial regression in psychiatric epidemiological studies may render etiologically important interactions more difficult to identify.
This study investigated the associations of cigarette smoking and alcohol intoxication with major depressive episode.
Major depressive episode during the past 12 months was assessed in a national representative cross sectional study using the Short Form of the University of Michigan version of the Composite International Diagnostic Interview (the UM-CIDI Short Form).
A random sample of 5993 non-institutionalised Finnish people aged 15-75 years was interviewed as a part of the 1996 Finnish Health Care Survey.
In logistic regression models the factors associated with major depressive episode in the past 12 months were smoking 10 or more cigarettes daily (odds ratio (OR) 2.26; 95% confidence intervals (95% CI) 1.68, 3.04) and alcohol intoxication at least once a week (OR 2.99; 95%CI 1.70, 5.25). Their effects were independent of each other, and remained significant even after adjusting for other major risk factors (marital status, education, unemployment and chronic diseases). The attributable proportion (a measure of the impact of the risk factors of the disease on the population) for daily smoking of 10 or more cigarettes was 0.15, and for alcohol intoxication at least once a week 0.04.
Cigarette smoking and alcohol intoxication seem to be important risk factors for major depressive episode. In this population the impact of smoking was greater.
To investigate whether job strain interacts with psychosocial factors outside of the workplace in relation to the risk of major depression and to examine the roles of psychosocial factors outside of the workplace in the relationship between job strain and the risk of major depression.
Data from the longitudinal cohort of the Canadian National Population Health Survey (NPHS) were used. Major depressive episode (MDE) in the past 12 months was assessed by the Composite International Diagnostic Interview-Short Form. Participants who were working and who were between the ages of 18 and 64 years old in 2000/2001 (n = 6,008) were followed to 2006/2007. MDE that occurred from 1994/1995 to 2000/2001 were excluded from the analysis.
High job strain, negative life events, chronic stress and childhood traumatic events were associated with the increased risk of MDE. There was no evidence that job strain interacted with psychosocial factors outside of the workplace in relation to the risk of MDE. The incidence proportion in participants who reported having exposed to none of the stressors, one type of stressor, two types of stressors and three or more types of stressors was 2.6, 4.3, 6.6 and 14.2%, respectively. The odds of developing MDE in participants who were exposed to three or four types of stressors was more than four times higher than the reference group.
MDE may be facilitated by simultaneous exposure to various stressors. There is a dose-response relationship between the risk of MDE and the number of stressors.
We assessed the impact of changes in dimensions of the psychosocial work environment on risk of depression in a longitudinal cohort of Canadian workers who were free of depression when work conditions were initially reported.
Using a sample (n = 3735) from the Canadian National Population Health Survey, we examined the effects of changes in job control, psychological demands, and social support over a 2-year period on subsequent depression. We adjusted models for a number of covariates, including personal history of depression.
Respondents with increased psychological demands were more likely to have depression over the following 2 years (odds ratio = 2.36; 95% confidence interval = 1.14, 4.88). This risk remained statistically significant after adjustment for age, gender, marital status, presence of children, level of education, chronic health conditions, subclinical depression when work conditions were initially assessed, family history of depression, and personal history of depression.
These results demonstrate that changes in psychological demands have a stronger influence than changes in job control on the onset of depression, highlighting the importance of not assuming an interaction between these 2 components of job strain when assessing health outcomes.
OBJECTIVE: To investigate whether patients with a diagnosis of affective disorder are at an increased risk of developing Parkinson's disease compared with medically ill control groups. METHOD: By linkage of public hospital registers from 1977 to 1993, three study cohorts were identified: patients with affective disorder episodes (mania or depression) and patients with osteoarthritis or diabetes. Time to the first diagnosis of Parkinson's disease was estimated with the use of survival analysis. RESULTS: A total of 164 385 patients entered the study base. The risk of being given a diagnosis of Parkinson's disease was significantly increased for patients with affective disorder, odds ratio 2.2 (CI 95% 1.7-2.8) compared with osteoarthritis, and depressive disorders, odds ratio 2.2 (CI 95% 1.7-2.9) compared with osteoarthritis. CONCLUSION: This study supports the hypothesis of a common aetiology for major affective disorder and Parkinson's disease.
This study tests the hypothesis that gender differences in depression diminish after menopause (around the age of 55). Methods Using the 1994 National Population Health Survey, we examine the relationship between age and gender on major depressive disorder in relation to sociodemographic and social covariates using contingency table analyses and multivariate logistic regression.
Contingency table and multivariate analyses identify significantly higher rates of depression among women before and after the age period associated with menopause. A series of multivariate analyses controlling for a broad array of social factors also does not lead to any convergence in differences of rates of depression between males and females. Hormone replacement therapy (HRT) does not have a significant impact on these observed relationships.
These findings are at odds with a recent study that has identified menopause as a point where gender differences in depression diminish. Further research is required to address this inconsistency.
Depression is a common psychiatric condition in Parkinson's disease (PD), yet the burden of depression on health-related quality of life (HRQL) has not been clearly delineated in this patient population.
To evaluate the impact of depression and life stress on HRQL in the Canadian community dwelling population with PD.
A total of 259 respondents from the Canadian Community Health Survey (CCHS 1.1) with self-reported PD were interviewed. Measures included Health Utilities Index Mark 3 (HUI3), Composite International Diagnostic Interview Short Form for Major Depression and a single question regarding the amount of stress in their lives most days. Adjusted HUI3 scores were compared according to depression and life stress using ANCOVA models.
Respondents without depression had overall HUI3 scores that were 0.29 units higher than respondents with depression [adjusted mean (95% CI) 0.49 (0.39-0.59) vs. 0.20 (0.03-0.37)]. The difference in overall HUI3 scores between respondents who reported high levels of stress as those who did not was 0.19 [adjusted mean (95% CI) 0.42 (0.29-0.55) vs. 0.23 (0.10-0.36)].
Substantial impact of depression and life stress, two modifiable factors, on HRQL is seen in PD. HRQL may be improved by clinical management of these nonmotor symptoms in PD.