Depression and change in occupational functioning in type 2 diabetes.

BACKGROUND: The effect of depression on both employment and productivity in type 2 diabetes (T2D) is poorly understood. AIMS: We tested whether depressive symptoms at diagnosis of T2D are associated with change in employment status and productivity over 2-year follow-up. METHODS: In a prospective analysis of working-age (18-63 years) people with newly diagnosed T2D recruited from primary care, we tested the association between depressive symptoms at diagnosis of T2D (baseline) and employment rates over 2 years. Using the Patient Health Questionnaire-9, depressive symptoms were measured categorically (depression caseness score ≥10) and continuously. In those employed, we measured changes in presenteeism and absenteeism using the World Health Organization (WHO) Health and Work Performance Questionnaire in univariate and multivariate models, respectively, including and excluding part-time workers. RESULTS: Of 1202 people aged 18-63 at baseline, 982 (82%) provided employment information; the mean age was 50.3 (SD 8.1) years, 44% were female, 59% of non-white ethnicity and 16% had depression. After adjustment for age, sex, ethnicity, socio-economic status, diabetes control and depression treatment, depression caseness was associated with worsening unemployment over 2 years only in full-time workers (odds ratio 0.43 (95% CI 0.20, 0.96), P < 0.05). In those employed full-time or part-time, total depressive symptoms were associated with worsening presenteeism over 2 years after full adjustment (ß = -2.63 (95% CI -4.81, -0.45), P < 0.05), despite no association with worsening absenteeism. CONCLUSIONS: In newly diagnosed T2D, depressive symptoms demonstrate an association with worsening employment rate and decline in work productivity over 2-year follow-up.

Depressive symptoms in inflammatory bowel disease: an extraintestinal manifestation of inflammation?

Depressive symptoms are reported by more than 20% of people with inflammatory bowel disease (IBD), while sleep difficulties and fatigue are even more common. Co-morbid depressive symptoms predict a poor IBD course, including increased risk of relapse and surgery, which is inconsistently improved by psychological treatments. Rather than being distinct systems, there is compelling evidence for bidirectional communication between gut and brain, driven by neural, metabolic, endocrine and inflammatory mediators. An emerging concept is that depressive symptoms may be mechanistically linked to excess inflammation and dysregulation of the gut-brain axis. Given the close link between the intestinal microbiota and host immune responses, patients prone to shifts in their intestinal microbiome, including smokers, those with poor diet and early life stress, may be exposed to exaggerated immune responses. Excess inflammation is associated with brain changes (depressive symptoms, fatigue, sleep difficulties) and worsening gastrointestinal symptoms, which are exacerbated by psychological distress. Equally, treatments both for depressive symptoms and IBD provide opportunities to break this cycle by reducing the causes and effects of inflammation. As well as addressing potential risk factors such as smoking and diet, treatments to alter the microbiome may reduce depressive symptoms. Observational evidence suggests that anti-inflammatory treatments for IBD may improve co-morbid depressive symptoms correlating with reduction in inflammation. With a growing range of treatments targeting inflammation centrally, peripherally and in the gut, IBD provides a unique model to understand the interplay between brain and gut in the pathogenesis of depressive symptoms, both in IBD and in the whole population.

Investigating incretin-based therapies as a novel treatment for depression in type 2 diabetes: Findings from the South London Diabetes (SOUL-D) Study.

We aimed to investigate the association between incretin-based therapies and 1-year change in depressive symptoms in a cohort of 1735 patients with newly diagnosed type 2 diabetes. The incretin group experienced significant reduction in depressive symptoms compared to controls. This was independent of HbA1c and may be mediated by an anti-inflammatory mechanism.