Observational studies suggest that dietary patterns may impact mental health outcomes, although biologically plausible pathways are yet to be tested. We aimed to elucidate the longitudinal relationship between dietary patterns, adiposity, inflammation and mental health including depressive symptoms in a population-based cohort of adolescents. Data were provided from 843 adolescents participating in the Western Australian Pregnancy Cohort (Raine) Study at 14 and 17 years (y) of age. Structural equation modelling was applied to test our hypothesised models relating dietary patterns, energy intake and adiposity (body mass index) at 14 y to adiposity and the pro-inflammatory adipokine (leptin) and inflammation (high sensitivity C-reactive protein - hs-CRP) at 17 y, and these inflammatory markers to depressive symptoms (Beck Depression Inventory) and Internalising and Externalising Behavioral Problems (Child Behavior Check List Youth Self- Report) at 17 y. We further tested a reverse hypothesis model, with depression at 14 y as a predictor of dietary patterns at the same time-point. The tested models provided a good fit to the data. A 'Western' dietary pattern (high intake of red meat, takeaway, refined foods, and confectionary) at 14 y was associated with higher energy intake and BMI at 14 y, and with BMI and biomarkers of inflammation at 17 y (all p < .05). A 'Healthy' dietary pattern (high in fruit, vegetables, fish, whole-grains) was inversely associated with BMI and inflammation at 17 y (p < .05). Higher BMI at 14 y was associated with higher BMI (p < .01), leptin (p < .05), hs-CRP (p < .05), depressive symptoms (p < .05) and mental health problems (p < .05), all at 17 y. A 'Western' dietary pattern associates with an increased risk of mental health problems including depressive symptoms in adolescents, through biologically plausible pathways of adiposity and inflammation, whereas a 'Healthy' dietary pattern appears protective in these pathways. Longitudinal modelling into adulthood is indicated to confirm the complex associations of dietary patterns, adiposity, inflammation and mental health problems, including depressive symptoms.

Background: Chronic musculoskeletal pain has been linked to dementia; however, chronic pain typically occurs in multiple sites; therefore, this study was to investigate whether greater number of chronic pain sites is associated with a higher risk of dementia and its subtypes. Methods: Participants (N = 356,383) in the UK Biobank who were dementia-free at baseline were included. Pain in the hip, knee, back, and neck/shoulder or ‘all over the body’ and its duration were assessed. Participants were categorised into six groups: no chronic pain; chronic pain in 1, 2, 3, and 4 sites, and ‘all over the body’. All-cause dementia and its subtypes were ascertained using hospital inpatient and death registry records. Cox regression was used to investigate the associations between the number of chronic pain sites and the incidence of all-cause dementia and its subtypes. Results: Over a median follow-up of 13 years, 4959 participants developed dementia. After adjustment for sociodemographic, lifestyle, comorbidities, pain medications, psychological problems, and sleep factors, greater number of chronic pain sites was associated with an increased risk of incident all-cause dementia (hazard ratio [HR] = 1.08 per 1 site increase, 95% CI 1.05–1.11) and Alzheimer’s disease (AD) (HR = 1.09 per 1-site increase, 95% CI 1.04–1.13) in a dose–response manner but not vascular and frontotemporal dementia. No significant association was found between the number of chronic pain sites and the risk of incident all-cause dementia among a subsample that underwent a fluid intelligence test. Conclusions: Greater number of chronic pain sites was associated with an increased risk of incident all-cause dementia and AD, suggesting that chronic pain in multiple sites may contribute to individuals’ dementia risk and is an underestimated risk factor for dementia.