Anna E. Prizment

Background: Processed meat is classified as a carcinogen and unprocessed red meat a probable carcinogen, but their associations with stomach cancer are not established. We evaluated intakes of these food groups and poultry, seafood, and eggs in relation to stomach cancer risk. Methods: Individual-level data for 1 100 370 females and 891 919 males from 20 cohorts were analysed. Diet was assessed at baseline by using food-frequency questionnaires or diet histories generally covering the past year and harmonized across studies. We used Cox regression to estimate multivariable-adjusted study- and sex-specific hazard ratios (HRs) and 95% confidence intervals (CIs) for associations with each food group and combined study-specific estimates by using random-effects meta-analysis. We repeated analyses using an aggregated dataset combining all studies. Results: During follow-up (mean = 8–23 years across studies), 8561 invasive gastric adenocarcinomas were diagnosed. Processed meat intake showed weak evidence of an overall association with stomach cancer risk (HR, 1.15 for ≥45 vs <3 g/day; 95% CI, 1.00–1.32 and HR, 1.03 per 25-g/day increment; 95% CI, 0.99–1.07). This association was limited to current smokers (Pinteraction = .01) and differed by geographic region, with evidence for an association in Australian and European studies and no association observed in Asian studies (Pinteraction = .02). Positive associations with stomach cancer were observed for egg intake; no association was found for unprocessed red meat, poultry, or seafood. Conclusion: Higher processed meat intake was associated with a modestly increased risk of stomach cancer among current smokers, although residual confounding by smoking dose remains possible. Findings for eggs warrant further investigation.

Background: Processed meat and unprocessed red meat are considered carcinogenic and ‘probably carcinogenic’ to humans, respectively, but findings for bladder cancer remain inconsistent. Objectives: We assessed associations between processed meat and unprocessed red meat intake and bladder cancer risk using data from the Pooling Project of Prospective Studies of Diet and Cancer. Methods: Associations with bladder cancer risk were assessed using individual-level data from 30 cohort studies from North America, Europe, Australia and Asia. Diet was assessed at enrolment using validated food frequency questionnaires or diet histories. Following a pre-specified analysis plan, study- and sex-specific hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox regression, adjusted for smoking status and duration and other potential confounders, and pooled using inverse-variance-weighted random-effects meta-analysis. Results: During median follow-up across cohorts of 8–29 years, among 2,575,971 participants, 20,780 were diagnosed with bladder cancer. Processed meat intake was associated with increased bladder cancer risk (HR comparing ≥40 with <5 g/day = 1.08; 95% CI: 1.02–1.15; HR per 20 g/day = 1.02; 95% CI: 1.00–1.03). Weaker evidence of association with increased risk was also observed for unprocessed red meat (HR comparing ≥100 with <20 g/day = 1.06; 95% CI: 1.00–1.13; HR per 50 g/day = 1.01; 95% CI: 0.99–1.03). There was no evidence of heterogeneity by study, sex, or region. Conclusions: Higher intakes of processed meat and unprocessed red meat were associated with a small increase in risk of bladder cancer. These findings are consistent with existing public health recommendations to limit consumption of red and processed meat.

Background: Stomach cancer presents complex etiological heterogeneity. Ethanol in alcoholic beverages and its metabolite acetaldehyde are carcinogens causally linked to several cancers, but their role in gastric carcinogenesis has not been established. We analyzed harmonized, individual-level prospective data to examine associations between alcohol intake and risk of stomach cancer and its subtypes. Methods: In total, 2 009 951 participants in 20 cohorts (mean follow-up = 9 to 29 years) within the Pooling Project of Prospective Studies of Diet and Cancer (n = 8357 incident invasive gastric adenocarcinomas) were included. We used Cox regression to assess associations between alcohol intake and risk of stomach cancer overall and by anatomical and histological subtype and population subgroup, adjusting for confounders. Results: Evidence for an association between alcohol intake and overall stomach cancer risk was weak (hazard ratio, HR, for ≥30 vs 0.1-<5 g/day: 1.06 [95% confidence interval, CI = 0.96 to 1.16], Pbetween-studies heterogeneity = .43). Positive associations with stomach cancer risk were observed in never smokers (HR, for ≥30 vs 0.1- .05). Conclusion: There was little evidence of an overall association between alcohol intake and stomach cancer risk, although modest positive associations were observed among never smokers and in Asian

Assessment of biological aging using proteomic clocks may enhance risk prediction and elucidate the molecular links between aging and chronic diseases. Here, among 17,473 participants of the European Prospective Investigation into Cancer and Nutrition, we examined associations of plasma SomaScan-based proteomic clocks, including organ-specific clocks, with risk factors, 24 incident chronic diseases and all-cause mortality, over up to 28 years of follow-up. Replication was conducted in the Whitehall II study. We show that the global age gap, an age acceleration score combining proteomic clocks, was associated with smoking, alcohol consumption, physical inactivity and higher risk of mortality, cardiovascular diseases, dementia and cancers of the liver, upper aero-digestive tract, lung and kidney. Lung, kidney and stomach cancers were more strongly associated with related organ-specific age gaps. Predictive performance of proteomic clocks for mortality was comparable to that of classical lifestyle risk factors. In summary, proteomic clocks appear promising biomarkers of generalized age-related disease risk.

Supplementary Figure S5: Natural logarithm hazard ratios of breast cancer for P-spline term scaled 313-SNP PRS with 4 degrees of freedom estimated by fully-adjusted Cox proportional hazards model stratified by alcohol consumption category among White women in ARIC (1990-2015)

Supplementary Figure S6: Natural logarithm hazard ratios of breast cancer for P-spline term scaled 313-SNP PRS with 4 degrees of freedom estimated by fully-adjusted Cox proportional hazards model stratified by alcohol consumption category among Black women in ARIC (1990-2015)

Supplementary Table S2: The association between 313-SNP PRS and breast cancer incidence stratified by maternal history of breast cancer and by race in ARIC (1990-2015)

Supplementary Figure S2: Time-dependent coefficients of current ethanol intake for breast cancer incidence estimated by fully adjusted Cox proportional hazards model in ARIC (1990-2015)

Supplementary Table S4: The association between current ethanol intake and breast cancer incidence restricted to those had a health insurance, stratified by race in ARIC (1990-2015)

Supplementary Figure S1: Time-dependent coefficients of scaled 313-SNP PRS for breast cancer incidence estimated by fully adjusted Cox proportional hazards model in ARIC (1990-2015)