International journal of epidemiology最新文献

Background: The association between dairy intake and mortality remains unclear, particularly in populations with low dairy consumption, such as the Japanese population. Thus, we investigated the associations between dairy intake and mortality in a pooled analysis of 10 Japanese cohorts.

Methods: We analysed data from 180 267 males and 218 423 females aged ≥35 years at baseline (1983-2014) without a history of cardiovascular disease (CVD) or cancer. Dairy consumption (milk, yogurt, cheese, and total dairy intakes) was assessed through self-reported food frequency questionnaires. Multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated for each study and pooled by using random-effects models to evaluate the associations with all-cause and cause-specific mortality.

Results: Over 11.5-24.4 years of follow-up, 41 218 males and 28 659 females died. In males, compared with consuming milk

Conclusion: Dairy intake, particularly daily milk intake, may reduce mortality risk, especially cerebrovascular disease mortality risk, in Japanese males and females.

Background: Renal cell carcinoma (RCC) histological subtypes clear cell RCC (ccRCC; >75% of cases) and papillary RCC (papRCC; ∼15%) exhibit distinct molecular and genetic profiles, patient demographics, and prognoses. Previous epidemiologic studies have identified several risk factors for overall RCC, although few have explored differences in etiology across subtypes.

Methods: For this study, we applied two-sample Mendelian randomization (MR) to findings from a genome-wide association study of RCC (27 213 cases, 488 019 controls) to investigate the effects of RCC risk factors with ccRCC (15 507 cases) and papRCC (2103 cases). We also conducted case-only MR analyses contrasting ccRCC and papRCC cases to test for heterogeneity in risk factor effects across subtypes.

Results: MR for overall RCC confirmed associations with obesity, blood pressure, smoking, and several other suspected risk factors. In subtype-specific analyses, we observed stronger associations with ccRCC than for papRCC for anthropometric measures such as body mass index [ccRCC odds ratio (ORccRCC) = 1.58 per standard deviation increase, 95% confidence interval (CI) = 1.50-1.68; papRCC odds ratio (ORpapRCC) = 1.24, 95% CI = 1.07-1.42; Pheterogeneity = 2.7 × 10-4], while stronger associations with papRCC were observed for chronic kidney disease (ORccRCC = 1.07, 95% CI = 0.99-1.15; ORpapRCC = 1.39, 95% CI = 1.16-1.66; Pheterogeneity = 5.42 × 10-5), creatinine-based estimated glomerular filtration rate (ORccRCC = 0.96, 95% CI = 0.92-1.01; ORpapRCC = 0.71, 95% CI = 0.64-0.79; Pheterogeneity = 7.76 × 10-5), and telomere length (ORccRCC = 1.98, 95% CI = 1.93-2.06; ORpapRCC = 2.50, 95% CI = 2.28-2.72; Pheterogeneity = 6.2 × 10-3). Further analysis identified the colocalization of significant RCC risk loci and 20 risk factors along with potential target genes through transcriptomic analysis.

Conclusion: These results highlight the heterogeneous nature of RCC etiology and the importance of considering histologic subtypes in etiologic and genetic studies.

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.