International journal of epidemiology最新文献

Background: Dementia risk is influenced by metabolic and lifestyle factors, including hyperinsulinemia, chronic inflammation, and type 2 diabetes. Glycemic index (GI) and glycemic load (GL) reflect the quality and quantity of dietary carbohydrates and their impact on glucose metabolism and systemic health. However, their associations with the risk of dementia subtypes remain unclear. This study examined the associations between dietary GI and GL and the risk of all-cause and different dementia subtypes, such as Alzheimer's disease (AD), vascular dementia (VD), and frontotemporal dementia.

Methods: A prospective analysis was conducted by using data from 202 302 dementia-free participants in the UK Biobank cohort. Dietary GI and GL were estimated by using the Oxford WebQ 24-hour web-based dietary questionnaire. Cox proportional hazards regressions with restricted cubic splines were used to evaluate nonlinear relationships. Two-piece Cox models were used to identify inflection points, which served as reference values to estimate hazard ratios (HRs).

Results: Dementia incidence was 0.89 per 1000 person-years. GI (mean±SD: 48.71 ± 7.68) showed an inverse J-shaped association with dementia risk, while GL (121.49 ± 39.00) showed a J-shaped pattern, with inflection points at 49.30 and 111.01, respectively. After adjusting for potential confounders, GI values of <49.30 were inversely associated with dementia risk [HR, 0.838; 95% confidence interval (CI), 0.758-0.926], while GL values of >111.01 were associated with higher dementia risk (HR, 1.145; 95% CI, 1.048-1.251). Similar findings were observed for AD and VD.

Conclusion: Low-GI diets may offer protective effects against all-cause dementia, AD, and VD, whereas high-GL diets may increase the risk. These findings underscore the importance of considering both carbohydrate quality and quantity in dementia prevention and management strategies.

Background: Despite an incidence increase in recent decades, the etiology of testicular germ cell tumors (TGCT) remains poorly understood. The hypothesis of a two-stage development, combining initial alteration in utero followed by malignant transformation later in life, has been suggested. This study examined the association between cumulative lifetime occupational and para-occupational solvent exposure and TGCT risk.

Methods: The French multicenter case-control study TESTIS included 454 cases and 670 controls. Participants provided information on their occupational history; participants' mothers (N = 547) provided information on their own and the father's occupational history. Solvent exposure was assessed by using the Matgéné job-exposure matrices. The influence of the parental and subject's occupational exposures over the lifetime and at different periods (i.e. fetal life/infancy; childhood; adolescence; subject's exposure) on TGCT was examined. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by using conditional logistic regression models.

Results: An OR for TGCT of 1.03 (95% CI 0.59-1.79) was found for the lifetime solvent exposure. When each period was examined individually, the results showed an increased TGCT risk in adult males who were occupationally exposed to trichloroethylene (OR = 3.09; 95% CI 1.25-7.65); fuels and petroleum-based solvents (OR = 1.91; 95% CI 1.21-3.02); diesel, kerosene, and fuel oil (OR = 2.26; 95% CI 1.16-4.41); and ketones and esters (OR = 1.66; 95% CI 1.02-2.71), and suggested a positive association with solvent exposure during adolescence (OR = 1.77; 95% CI 0.95-3.31).

Conclusion: Overall, this study did not suggest a substantial role of cumulative lifetime solvent exposure and TGCT risk. The results showed an increased TGCT risk associated with solvent exposure during adulthood. Indirect exposure to certain solvents during adolescence might also promote TGCT development.

Background: Sleep-related problems exhibit strong social patterning and are associated with pain; however, their mediating role in socio-economic inequities in pain remains largely unknown. We aim to assess the extent to which life course socio-economic inequities in pain experience and severity are mediated through sleep quality and duration.

Methods: We used data from 1719 individuals [52.0% women; mean age 60.1 years (SD 9.1)] from the Swiss CoLaus|PsyCoLaus study, with both sleep measures at baseline (2009-2012) and pain measures at follow-up (2014-2017). Life course socio-economic conditions were assessed by using the father's and individual's occupational position, educational level, and income. Potential mediators included self-reported sleep quality (measured by using the Pittsburgh Sleep Quality Index, ranging from 0 to 21, with high scores indicating poorer sleep quality) and duration (short <6 h/night; normal 6-8.5 h/night; long >8.5 h/night). Presence of pain, chronic pain, and pain severity were assessed by using a self-administered questionnaire. We estimated age, sex, and country of birth with adjusted β coefficient, odds ratio, and proportion mediated by using counterfactual mediation analyses.

Results: Pain and chronic pain were reported by 47% and 40.8% of the participants, respectively. Among 699 participants with reported pain severity data, the mean pain severity score was 3.6 (SD 1.7) (scale ranging from 0 = no to 10 = worst imaginable pain). Sleep quality explained 30% of the educational, 21% of the occupational, and 45% of the income inequities in pain; 20% of the occupation and 51% of the income inequities in chronic pain; and 15%, 9%, and 16% of the father's occupation, educational, and income inequities in pain severity, respectively. Short sleep duration explained 31% of the education inequities in pain and 37% of the education and income inequities in chronic pain.

Conclusion: This study suggests poor sleep quality and short sleep duration partially mediate socio-economic inequities in pain. The role of other potential mediators at individual and societal levels should be further investigated.