Intervention targeted at physicians' treatment of musculoskeletal disorders and sickness certification: an interrupted time series analysis.

OBJECTIVE: An intervention was carried out at the occupational healthcare services (OHS) of the City of Helsinki beginning in 2016. We investigated the association between the intervention and employee sick leaves using interrupted time series analysis. DESIGN: Register-based cohort study with a quasi-experimental study design. SETTING: Employees of the City of Helsinki. PARTICIPANTS: We analysed individual-level register-based data on all employees who were employed by the city for any length of time between 2013 and 2018 (a total 86 970 employees and 3 014 075 sick leave days). Sick leave days and periods that were OHS-based constituted the intervention time series and the rest of the sick leave days and periods contributed to the comparison time series. INTERVENTION: Recommendations provided to physicians on managing pain and prescribing sick leave for low back, shoulder and elbow pain. OUTCOME MEASURES: Number of sick leave days per month and sick leave periods per year. RESULTS: For all sick leave days prescribed at OHS, there was no immediate change in sick leave days, whereas a gradual change showing decreasing number of OHS-based sick leave days was detected. On average, the intervention was estimated to have saved 2.5 sick leave days per year per employee. For other sick leave days, there was an immediate increase in the level of sick leave days after the intervention and a subsequent gradual trend showing decreasing number of sick leave days. CONCLUSIONS: The intervention may have reduced employee sick leaves and therefore it is possible that it had led to direct cost savings. However, further evidence for causal inferences is needed.

Socioeconomic inequalities in impairment associated with depressive symptoms: Evidence from the National Survey on Drug Use and Health.

OBJECTIVE: Individuals with low socioeconomic status have higher rates of depression, but it is unknown whether the socioeconomically disadvantaged also have more disabling depressive symptoms. We examined (1) the associations of three indicators of socioeconomic status with depression-related severe role impairment, and (2) whether socioeconomic factors moderate the association between individual depression symptoms and depression-related severe role impairment. METHODS: We used data from the National Survey on Drug Use and Health (NSDUH). Depressive symptoms, role impairment and socioeconomic indicators (poverty, participation in workforce, educational attainment) were self-reported by participants. The analytic sample consisted of participants who screened positive for a depressive episode during past 12 months (n = 32 661). We used survey-weighted logistic models to examine the associations of depressive symptoms with severe role impairment and the modifying effects of socioeconomic indicators. RESULTS: The association between depression symptom count and severe role impairment was stronger among those not in workforce (OR = 1.12[1.02-1.23]). The association between specific depression symptoms and severe role impairment was stronger for conditions of poverty (fatigue, OR = 2.97 [1.54-5.73]; and anhedonia, OR = 1.93[1.13-3.30]), workforce non-participation (inability to concentrate/indecisiveness, OR = 1.54[1.12-2.12]), and lower educational attainment (anhedonia, OR = 0.77 [0.59-0.99]). Feelings of worthlessness was the only symptom with independent associations for all socioeconomic groups (adjusted OR = 1.91[1.35-2.70]). CONCLUSION: Depression was more frequent and also more disabling for socioeconomically disadvantaged groups, especially when assessed with workforce participation. Additionally, some specific symptoms showed socioeconomic differences. Our findings highlight the need to prioritize population groups with more severe impairment associated with depressive symptoms.

Explaining the association between anxiety disorders and alcohol use disorder: A twin study.

BACKGROUND: It is unknown whether social anxiety disorder (SAD) has a unique association with alcohol use disorder (AUD) over and beyond that of other anxiety disorders, how the associations develop over time, and whether the associations are likely to be causal. METHODS: Diagnoses of AUD, SAD, generalized anxiety disorder, panic disorder, agoraphobia, and specific phobias were assessed twice using the Composite International Diagnostic Interview among 2,801 adult Norwegian twins. The data were analyzed using logistic regression analyses and multivariate biometric structural equation modeling. RESULTS: SAD had the strongest association with AUD, and SAD predicted AUD over and above the effect of other anxiety disorders. In addition, SAD was prospectively associated with AUD, whereas other anxiety disorders were not. AUD was associated with a slightly elevated risk of later anxiety disorders other than SAD. Biometric modeling favored a model where SAD influenced AUD compared to models where the relationship was reversed or due to correlated risk factors. Positive associations between AUD and other anxiety disorders were fully explained by shared genetic risk factors. CONCLUSIONS: Unlike other anxiety disorders, SAD plausibly has a direct effect on AUD. Interventions aimed at prevention or treatment of SAD may have an additional beneficial effect of preventing AUD, whereas interventions aimed at other anxiety disorders are unlikely to have a similar sequential effect on AUD.

Stability and change in etiological factors for alcohol use disorder and major depression.

Alcohol use disorder (AUD) and major depressive disorder (MDD) are often comorbid. It is not understood how genetic risk factors for these disorders relate to each other over time and to what degree they are stable. Age-dependent characteristics of the disorders indicate that different genetic factors could be relevant at different stages of life, and MDD may become increasingly correlated with AUD over time. DSM-IV diagnoses of AUD and MDD were assessed by interviews of 2,801 young adult twins between 1999 and 2004 (T1) and 2,284 of the same twins between 2010 and 2011 (T2). Stability, change, and covariation were investigated in longitudinal biometric models. New genetic factors explained 56.4% of the genetic variance in AUD at T2. For MDD, there was full overlap between genetic influences at T1 and T2. Genetic risk factors for MDD were related to AUD, but their association with AUD did not increase over time. Thus, genetic risk factors for AUD, but not MDD, vary with age, suggesting that AUD has age-dependent heritable etiologies. Molecular genetic studies of AUD may therefore benefit from stratifying by age. The new genetic factors in AUD were not related to MDD. Environmental influences on the 2 disorders were correlated in middle, but not in young adulthood. The environmental components for AUD correlated over time (r = .27), but not for MDD. Environmental influences on AUD can have long-lasting effects, and the effects of preventive efforts may be enduring. Environment influences seem to be largely transient. (PsycINFO Database Record