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Background Positive psychological characteristics in people with type 2 diabetes (T2D) are associated with better health and longevity, and one plausible physiological mechanism involves lower markers of inflammation. Positive affect is related to lower basal inflammatory markers and smaller inflammatory responses to acute stress, but this association in people with T2D remains to be examined. Purpose To examine the relationship between happiness and inflammatory markers at baseline and in response to acute stress in people with T2D. Methods One hundred forty people with T2D took part in laboratory-based stress testing. We aggregated daily happiness ratings over 7 days before stress testing. During the laboratory session, participants underwent two mental stress tasks—the mirror tracing and the Stroop task. Blood was sampled at baseline and post-stress (up to 75 min post-stress) to detect plasma interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL-1Ra), and monocyte chemoattractant protein-1 (MCP-1). Associations between happiness and inflammatory markers and responses were analyzed using multivariable linear regressions. Results Greater daily happiness significantly predicted lower baseline and post-stress IL-6 concentrations, and lower baseline MCP-1, after adjusting for covariates. The association between happiness and reduced basal IL-6 maintained after further controlling for daily sadness. We did not find significant associations between daily happiness and inflammatory responses to acute stress. No associations were detected for IL-1Ra. Conclusions Happier individuals with T2D have lower inflammatory markers before and after acute stress, albeit independent of stress responsivity. Findings could provide a protective physiological pathway linking daily happiness with better health in people with T2D., Happier individuals with type 2 diabetes have lower inflammatory factors before and after acute stress. Inflammatory stress responses did not vary between those reporting higher or lower happiness.

People with Type 2 diabetes (T2D) show dysregulated inflammatory responses to acute stress, but the effect of sex on inflammatory responses in T2D remains unclear. The purpose of this study was to investigate differences in interleukin (IL)‐6 stress responses between older men and women with T2D. One hundred and twenty‐one people (76 men; mean age = 64.09, SD = 7.35, 45 women; mean age = 63.20, SD = 6.70) with doctor‐verified T2D took part in this laboratory‐based stress testing study. Participants carried out acute mental stress tasks, and blood was sampled at baseline, immediately poststress, 45 min poststress, and 75 min poststress to detect plasma IL‐6 concentrations. IL‐6 change scores were computed as the difference between the baseline measurement and the three time points poststress. Main effects and interactions were tested using mixed model analysis of covariance. We found a significant main effect of time on IL‐6 levels, and a significant Sex × Time interaction. In adjusted analyses including the three change scores and all the covariates, the significant Sex × Time interaction was maintained; IL‐6 responses were greater in women at 45 and 75 min poststress compared with men, adjusting for age, body mass index, smoking, household income, glycated hemoglobin, oral antidiabetic medication, insulin/other injectable antidiabetic medication, depressive symptoms, and time of day of testing. Different inflammatory stress response pathways are present in men and women with T2D, with women producing larger IL‐6 increases. The long‐term implications of these differences need to be elucidated in future studies., This laboratory study is the first to examine sex differences in inflammatory stress responsivity in people with Type 2 diabetes (T2D). Older women with T2D have higher rates of some inflammatory‐related conditions compared to their male counterparts, including coronary heart disease and stroke. Notably, these conditions are leading causes of premature mortality in this population. IL‐6 is adversely involved in diabetes progression, and we found evidence of sex differences in IL‐6 stress responses. This study contributes to the understanding of the mechanisms that may explain, to some extent, the different levels of disease vulnerability in this a priori high‐risk population.

Introduction Children with long-term physical health conditions (pLTCs) are at increased risk of mental health conditions but less is known about time trends in the mental health of this group of children. Methods We used data from three comparable, population-based surveys of children conducted in 1999, 2004, and 2017. We examined whether the proportion of children aged 5–15 years old with comorbid mental health conditions (measured using the multi-informant Development and Well-being Assessment tool) and pLTCs (measured using parental report) in England increased from 1999 to 2017 using linear regression analysis. Results Our analysis used data from 8662 (1999), 6401 (2004) and 6219 (2017) children, respectively. The proportion of children with comorbid pLTCs and psychiatric disorders was 0.050 (95% CI = 0.045, 0.055) in 1999, 0.054 (95% CI = 0.049, 0.060) in 2004, and 0.059 (95% CI = 0.053, 0.065) in 2017. The linear regression model revealed a non-significant effect of time on the proportion of children with comorbid pLTCs and psychiatric disorders from 1999 to 2017 (B = 0.0004785; SE = 0.0001256; p = 0.163). Conclusion The estimated prevalence of school-aged children with comorbid pLTCs and mental health conditions in England remained stable since 1999, highlighting the need to prioritize mental health resources for children with physical health comorbidities.

BACKGROUND: Inflammatory dysregulation may be linked with mental health disturbances in people with Type 2 Diabetes (T2D), however no previous studies have examined longitudinal associations between inflammatory stress responses and mental health outcomes in T2D. PURPOSE: To better understand the biological mechanisms that might predispose people with T2D to poor mental health in the future. METHODS: At baseline, 140 participants with T2D participated in a laboratory stress testing study (mean age = 64 years). Participants underwent two mental stress tasks and blood was sampled before and up to 45 min post-stress to detect plasma interleukin (IL)-6. The Center for Epidemiological Studies-Depression scale and the Short Form-36 Health Survey were completed at baseline and 7.5 years later. We tested associations between IL-6 stress responses and a) depression symptoms and b) mental health-related quality of life (QoL) at baseline and at follow-up using linear regression analyses adjusting for age, sex, and body mass index (BMI). Results: Up to 66 participants provided follow-up data. In cross-sectional analyses, increased IL-6 stress responses immediately post-task were associated with lower mental health-related quality of life (B = -21.73, p = 0.005, 95% CI [-36.82, -6.63]) adjusting for age, sex, and BMI. In longitudinal analyses, increased IL-6 stress responses at 45 min post-task were associated with increased depressive symptoms (B = 10.31 p = 0.048, 95% CI [0.10, 20.51]) and decreased mental health-related QoL (B = -21.18 p = 0.031, 95% CI [-40.34, -2.02]) adjusting for age, sex, and BMI. The association between the 45-min IL-6 response and depressive symptoms at follow-up was diminished after further adjustment for physical health-related QoL and baseline depressive symptoms (B = 10.14, p = 0.055, 95% CI [-0.21,20.48]). CONCLUSIONS: This study supports the link between inflammatory stress responsivity and future mental health outcomes in people with T2D. Further research involving a larger sample size is required.