This first risk algorithm for onset of major depression functions as well as similar risk algorithms for cardiovascular events and may be useful in prevention of depression.
BackgroundThere is evidence that the prevalence of common mental disorders varies across Europe.AimsTo compare prevalence of common mental disorders in general practice attendees in six European countries.MethodUnselected attendees to general practices in the UK, Spain, Portugal, Slovenia, Estonia and The Netherlands were assessed for major depression, panic syndrome and other anxiety syndrome. Prevalence of DSM–IV major depression, other anxiety syndrome and panic syndrome was compared between the UK and other countries after taking account of differences in demographic factors and practice consultation rates.ResultsPrevalence was estimated in 2344 men and 4865 women. The highest prevalence for all disorders occurred in the UK and Spain, and lowest in Slovenia and The Netherlands. Men aged 30–50 and women aged 18–30 had the highest prevalence of major depression; men aged 40–60 had the highest prevalence of anxiety, and men and women aged 40–50 had the highest prevalence of panic syndrome. Demographic factors accounted for the variance between the UK and Spain but otherwise had little impact on the significance of observed country differences.ConclusionsThese results add to the evidence for real differences between European countries in prevalence of psychological disorders and show that the burden of care on general practitioners varies markedly between countries.
We report results from the PREDICT-Gene case-control study nested in a prospective cohort designed to identify predictors of the onset of depression among adult primary-care attendees. We tested the potential gene-by-environment interaction between 5HTTLPR genotype at the serotonin transporter gene and previous exposure to threatening life events (TLEs) in depression. A total of 737 consecutively recruited participants were genotyped. Additional information was gathered on exposure to TLEs over a 6-month period, socio-demographic data and family history of psychological problems among first-degree relatives. Diagnoses of depression were ascertained using the Composite International Diagnostic Interview (CIDI) by trained interviewers. Two different depressive outcomes were used (ICD-10 depressive episode and ICD-10 severe depressive episode). Both the s/s genotype and exposure to increasing number of TLEs were significantly associated with depression. Moreover, the 5HTTLPR s/s genotype significantly modified the risk conferred by TLEs for both depressive outcomes. Thus, s/s homozygous participants required minimal exposure to TLE (1 TLE) to acquire a level of risk for depression that was only found among l/s or l/l individuals after significantly higher exposure to TLEs (two or more TLEs). The interaction was more apparent when applied to the diagnosis of ICD-10 severe depressive episode and after adjusting for gender, age and family history of psychological problems. Likelihood ratios tests for the interaction were statistically significant for both depressive outcomes (ICD-10 depressive episode: LR X 2 = 4.7, P = 0.09 (crude), LR-X 2 = 6.4, P = 0.04 (adjusted); ICD-10 severe depressive episode: LR X 2 = 6.9, P = 0.032 (crude), LR-X 2 = 8.1, P = 0.017 (adjusted)).
Previous reports and meta-analyses have yielded inconclusive results as to whether the s/s genotype at the 5-HTTLPR serotonin transporter polymorphism confers increased risk for depression. We tested the association between s/s genotype and depression in a large cohort (n = 737) of Spanish primary care consecutive attendees participating in a European study on predictors for depression in primary care (PREDICT study). Participants were administered the Composite International Diagnostic Interview (CIDI) depression subscale allowing diagnoses using ICD-10 criteria for depressive episodes. Participants were genotyped to establish 5HTTLPR genotype. Both univariable and multivariable associations between the s/s genotype and depression were tested twice using two different depressive outcomes (ICD-10 depressive episode and ICD-10 severe depressive episode). We found an association between the s/s genotype and both depressive outcomes that was independent of age, sex, family history of psychological problems among first degree relatives and presence of comorbid generalized anxiety disorder. When comparing s/s homozygous versus the rest, the adjusted odds ratio for any ICD-10 depressive episode and for severe ICD-10 depressive episode were 1.50 (95% CI: 1.0-2.2; P = 0.045) and 1.79 (95% CI: 1.1-2.8; P = 0.016), respectively. The association was significantly stronger with increasing severity of depression (chi2 for linear association=6.1; P = 0.013) suggesting a dose-dependent relationship. Our results are consistent with previous reports suggesting a small but independent effect by the s/s 5-HTTLPR genotype increasing the risk for depression.
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These findings suggest that several psychosocial factors might be considered factors of attrition in primary care cohorts and confirm that baseline characteristics are insufficient for analysing non-response in longitudinal studies, indicating that different retention strategies should be applied for patients interviewed at 6 and 12 months.
In our study, the HTR1A C(-1019)G polymorphism was found to be associated to the frequent clinical presentation of comorbid MD and GAD, suggesting a common genetic background for mixed depression and anxiety states. These findings should be considered as preliminary. Future replications in independent samples would be needed to confirm or discard such association.
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