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Adverse psychosocial working environments characterized by job strain (the combination of high demands and low control at work) are associated with an increased risk of depressive symptoms among employees, but evidence on clinically diagnosed depression is scarce. We examined job strain as a risk factor for clinical depression.
We identified published cohort studies from a systematic literature search in PubMed and PsycNET and obtained 14 cohort studies with unpublished individual-level data from the Individual-Participant-Data Meta-analysis in Working Populations (IPD-Work) Consortium. Summary estimates of the association were obtained using random-effects models. Individual-level data analyses were based on a pre-published study protocol.
We included six published studies with a total of 27 461 individuals and 914 incident cases of clinical depression. From unpublished datasets we included 120 221 individuals and 982 first episodes of hospital-treated clinical depression. Job strain was associated with an increased risk of clinical depression in both published [relative risk (RR) = 1.77, 95% confidence interval (CI) 1.47–2.13] and unpublished datasets (RR = 1.27, 95% CI 1.04–1.55). Further individual participant analyses showed a similar association across sociodemographic subgroups and after excluding individuals with baseline somatic disease. The association was unchanged when excluding individuals with baseline depressive symptoms (RR = 1.25, 95% CI 0.94–1.65), but attenuated on adjustment for a continuous depressive symptoms score (RR = 1.03, 95% CI 0.81–1.32).
Job strain may precipitate clinical depression among employees. Future intervention studies should test whether job strain is a modifiable risk factor for depression.
This study examined two competing hypotheses concerning the association between diabetes and treatment for depression: (1) the detection/ascertainment bias hypothesis suggesting that those with diabetes are more likely to be diagnosed with and treated for depression because of increased medical attention and (2) a hypothesis assuming that diabetes and depression share common underlying pathophysiological pathways.
The study population included all persons aged 35–65 years in Finland with any record of type 2 diabetes in the national health and population registers from 1999 to 2002 and for whom register-based data on depression treatment (antidepressant medication use and hospitalizations for depression) were available at least 2 years before and after the diagnosis of diabetes (n = 18 217). Sociodemographic data were individually linked to the study population. Associations between diabetes diagnosis and time and indicators of depression care were assessed with population-averaged multilevel logistic models.
Within the year following diagnosis diabetes, there was a 5% increase in antidepressant medication use but not in hospitalization for depression. The longitudinal change in antidepressant use over time was less steep after the diabetes diagnosis, and hospitalization risk decreased after the diagnosis. These associations between diabetes diagnosis and depression treatment were not modified by the participant's socio-economic position (SEP).
These findings support the common cause hypothesis that treatment for diabetes is beneficial to the prevention of depression rather than the detection/ascertainment hypothesis that individuals with diabetes have higher rates of depression because they receive more medical attention in general.
The anti-emetic efficacy of prophylactic ondansetron and tropisetron in combination with a low dose of droperidol in patients with high probability for post-operative nausea and vomiting undergoing gynaecological laparoscopy was compared. Patients were randomly allocated in a double-blind manner to receive either ondansetron 8 mg (n=45) or tropisetron 5 mg (n=43) at the end of surgery. A standardized general anaesthetic technique was used, including droperidol 0.75 mg. The incidence of nausea was 36% and 49% (P=0.28), and vomiting occurred in 13% and 14% of the patients in the ondansetron and tropisetron groups, respectively. The onset time for rescue medication was significantly sooner after tropisetron than ondansetron (3 h 18min vs. 6 h 25min; P=0.007). There were no statistically significant differences in efficacy between prophylactic ondansetron and tropisetron combined with droperidol in a high-risk population. However, ondansetron appeared to be more effective in preventing post-operative nausea and vomiting in the early hours after surgery compared with tropisetron.
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