Burden of 30 cancers among men: Global statistics in 2022 and projections for 2050 using population-based estimates.

BACKGROUND: Men exhibit higher prevalence of modifiable risk factors, such as smoking and alcohol consumption, leading to greater cancer incidence and lower survival rates. Comprehensive evidence on global cancer burden among men, including disparities by age group and country, is sparse. To address this, the authors analyzed 30 cancer types among men in 2022, with projections estimated for 2050. METHODS: The 2022 GLOBOCAN estimates were used to describe cancer statistics for men in 185 countries/territories worldwide. Mortality-to-incidence ratios (MIRs) were calculated by dividing age-standardized mortality rates by incidence rates. RESULTS: In 2022, a high MIR (indicating poor survival) was observed among older men (aged 65 years and older; 61%) for rare cancer types (pancreatic cancer, 91%) and in countries with low a Human Development Index (HDI; 74%). Between 2022 and 2050, cancer cases are projected to increase from 10.3 million to 19 million (≥84%). Deaths are projected to increase from 5.4 million to 10.5 million (≥93%), with a greater than two-fold increase among men aged 65 years and older (≥117%) and for low-HDI and medium-HDI countries/territories (≥160%). Cancer cases and deaths are projected to increase among working-age groups (≥39%) and very-high-HDI countries/territories (≥50%). CONCLUSIONS: Substantial disparities in cancer cases and deaths were observed among men in 2022, and these are projected to widen by 2050. Strengthening health infrastructure, enhancing workforce quality and access, fostering national and international collaborations, and promoting universal health coverage are crucial to reducing cancer disparities and ensuring cancer equity among men globally.

Difference in Gastrointestinal Cancer Risk and Mortality by Dietary Pattern Analysis: A Systematic Review and Meta-Analysis.

CONTEXT: Several studies have demonstrated that dietary patterns identified by a posteriori and hybrid methods are associated with gastrointestinal (GI) cancer risk and mortality. These studies applied different methods for analyzing dietary data and reported inconsistent findings. OBJECTIVE: This systematic review and meta-analysis were aimed to determine the association between dietary patterns, derived using principal component analysis (PCA) and reduced rank regression (RRR), and GI cancer risk and GI cancer-caused mortality. DATA SOURCE: Articles published up to June 2023 in English were eligible for inclusion. The Medline, SCOPUS, Cochrane Library, CINHAL, PsycINFO, ProQuest, and Web of Sciences databases were used to identify prospective studies. The Preferred Reporting Item for Systematic Review and Meta-analysis Protocol 2020 was used to report results. DATA EXTRACTION: A total of 28 studies were eligible for inclusion. Varied approaches to deriving dietary patterns were used, including PCA (n = 22), RRR (n = 2), combined PCA and RRR (n = 1), cluster analysis (CA; n = 2) and combined PCA and CA (n = 1). DATA ANALYSIS: Two dietary patterns, "healthy" and "unhealthy," were derived using PCA and RRR. The healthy dietary pattern was characterized by a higher intake of fruits, whole grains, legumes, vegetables, milk, and other dairy products, whereas the unhealthy dietary pattern was characterized by a higher intake of red and processed meat, alcohol, and both refined and sugar-sweetened beverages. The findings indicated that the PCA-derived healthy dietary pattern was associated with an 8% reduced risk (relative risk [RR], 0.92; 95% CI, 0.87-0.98), and the unhealthy dietary pattern was associated with a 14% increased risk (RR, 1.14; 95% CI, 1.07-1.22) of GI cancers. Similarly, the RRR-derived healthy dietary pattern (RR, 0.83; 95% CI, 0.61-1.12) may be associated with reduced risk of GI cancers. In contrast, the RRR-derived unhealthy dietary pattern (RR, 0.93; 95% CI, 0.57-1.52) had no association with a reduced risk of GI cancers. Similarly, evidence suggested that PCA-derived healthy dietary patterns may reduce the risk of death from GI cancers, whereas PCA-derived unhealthy dietary patterns may increase the risk. CONCLUSION: Findings from prospective studies on the association of PCA-derived dietary patterns and the risk of GI cancers support the evidence of healthy and unhealthy dietary patterns as either protective or risk-increasing factors for GI cancers and for survivorship, respectively. The findings also suggest that the RRR-derived healthy dietary pattern reduces the risk of GI cancers (albeit with low precision), but no association was found for the RRR-derived unhealthy dietary pattern. Prospective studies are required to further clarify disparities in the association between PCA- and RRR-derived dietary patterns and the risk of GI cancers. Systematic review registration: PROSPERO registration no. CRD42022321644.

Plant-based and vegetarian diets are associated with reduced obstructive sleep apnoea risk.

Introduction: Obstructive sleep apnoea (OSA) and obesity commonly coexist. Weight loss and exercise are recommended management options for OSA. However, most of the current evidence on diet and OSA is focused on calorie restriction rather than diet quality. The aim of the present study was to determine the association of plant-based dietary indices (PDI) with OSA risk. Methods: Cross-sectional data from 14 210 participants of the National Health and Nutrition Examination Survey who provided dietary information using the 24-hour recall method were used. PDI - including healthy (hPDI), unhealthy (uPDI) and pro-vegetarian diet index (PVDI) - were determined. OSA risk was determined using the STOP-BANG questionnaire. Logistic regression was used to determine the relationship between dietary indices and OSA risk. Results: Higher adherence to PDI (odds ratio (OR)Q5 versus Q1=0.81; 95% confidence interval (CI): 0.66-1.00), hPDI (OR=0.83; 95% CI: 0.69-1.01) and PVDI (OR=0.84; 95% CI: 0.68-1.05) was inversely associated with OSA risk, whereas higher consumption of an unhealthy plant-based diet (OR=1.22; 95% CI: 1.00-1.49) was positively associated with OSA. Sex differences in estimates were observed for PDI in males (OR=0.71; 95% CI: 0.56-0.90) versus females (OR=0.93; 95% CI: 0.68-1.28), hPDI in males (OR=0.90; 95% CI: 0.68-1.18) versus females (OR=0.77; 95% CI: 0.54-1.09) and uPDI in males (OR=1.13; 95% CI: 0.89-1.44) versus females (OR=1.42; 95% CI: 1.03-1.97) but not for PVDI. Conclusions: Higher adherence to a healthy plant-based diet is associated with reduced OSA risk, while an unhealthy plant-based diet has a positive association. The magnitude of these associations differs by sex. Further longitudinal studies are warranted.

Ultra-processed food consumption and risk of chronic respiratory diseases mortality among adults: evidence from a prospective cohort study.

PURPOSE: The purpose of the study was to determine the relationships between ultra-processed food (UPF) consumption and risk of mortality due to chronic respiratory diseases (CRDs) overall, chronic obstructive pulmonary disease (COPD), and lung cancer. METHODS: A total of 96,607 participants aged 55 years and over were included from the Prostate, Lung, Colorectal and Ovarian (PLCO) cancer trial. Dietary intake was measured using food frequency questionnaire. Cox regression was fitted to estimate the risk of all-cause mortality and mortality due to CRDs overall, COPD and lung cancer associated with UPF intake. Competing risk regression was used to account for deaths from other causes and censoring. RESULTS: During the follow-up of 1,379,655.5 person-years (median 16.8 years), 28,700 all-cause, 4092 CRDs, 2015 lung cancer and 1,536 COPD mortality occurred. A higher intake of UPF increased the risk of mortality from CRDs overall by 10% (HR 1.10; 95% CI 1.01, 1.22) and COPD by 26% (HR 1.26; 95% CI 1.06, 1.49) but not associated with lung cancer mortality risk (HR 0.97; 95% CI 0.84, 1.12). However, the risk of lung cancer increased by 16% (HR 1.16; 95% CI 1.01, 1.34) in the highest UPF intake after multiple imputation. Dose-response relationships existed for CRDs and COPD mortality but not lung cancer. CONCLUSION: UPF consumption was associated with an increased risk of CRD mortality. The association between UPF consumption and lung cancer mortality is inconclusive and only significant when multiple imputation was applied.

Epidemiologic Factors in Relation to Colorectal Cancer Risk and Survival by Genotoxic Colibactin Mutational Signature.

BACKGROUND: The genotoxin colibactin causes a tumor single-base substitution (SBS) mutational signature, SBS88. It is unknown whether epidemiologic factors' association with colorectal cancer risk and survival differs by SBS88. METHODS: Within the Genetic Epidemiology of Colorectal Cancer Consortium and Colon Cancer Family Registry, we measured SBS88 in 4,308 microsatellite stable/microsatellite instability low tumors. Associations of epidemiologic factors with colorectal cancer risk by SBS88 were assessed using multinomial regression (N = 4,308 cases, 14,192 controls; cohort-only cases N = 1,911), and with colorectal cancer-specific survival using Cox proportional hazards regression (N = 3,465 cases). RESULTS: 392 (9%) tumors were SBS88 positive. Among all cases, the highest quartile of fruit intake was associated with lower risk of SBS88-positive colorectal cancer than SBS88-negative colorectal cancer [odds ratio (OR) = 0.53, 95% confidence interval (CI) 0.37-0.76; OR = 0.75, 95% CI 0.66-0.85, respectively, Pheterogeneity = 0.047]. Among cohort studies, associations of body mass index (BMI), alcohol, and fruit intake with colorectal cancer risk differed by SBS88. BMI ≥30 kg/m2 was associated with worse colorectal cancer-specific survival among those SBS88-positive [hazard ratio (HR) = 3.40, 95% CI 1.47-7.84], but not among those SBS88-negative (HR = 0.97, 95% CI 0.78-1.21, Pheterogeneity = 0.066). CONCLUSIONS: Most epidemiologic factors did not differ by SBS88 for colorectal cancer risk or survival. Higher BMI may be associated with worse colorectal cancer-specific survival among those SBS88-positive; however, validation is needed in samples with whole-genome or whole-exome sequencing available. IMPACT: This study highlights the importance of identification of tumor phenotypes related to colorectal cancer and understanding potential heterogeneity for risk and survival.

Genome-Wide Gene-Environment Interaction Analyses to Understand the Relationship between Red Meat and Processed Meat Intake and Colorectal Cancer Risk.

BACKGROUND: High red meat and/or processed meat consumption are established colorectal cancer risk factors. We conducted a genome-wide gene-environment (GxE) interaction analysis to identify genetic variants that may modify these associations. METHODS: A pooled sample of 29,842 colorectal cancer cases and 39,635 controls of European ancestry from 27 studies were included. Quantiles for red meat and processed meat intake were constructed from harmonized questionnaire data. Genotyping arrays were imputed to the Haplotype Reference Consortium. Two-step EDGE and joint tests of GxE interaction were utilized in our genome-wide scan. RESULTS: Meta-analyses confirmed positive associations between increased consumption of red meat and processed meat with colorectal cancer risk [per quartile red meat OR = 1.30; 95% confidence interval (CI) = 1.21-1.41; processed meat OR = 1.40; 95% CI = 1.20-1.63]. Two significant genome-wide GxE interactions for red meat consumption were found. Joint GxE tests revealed the rs4871179 SNP in chromosome 8 (downstream of HAS2); greater than median of consumption ORs = 1.38 (95% CI = 1.29-1.46), 1.20 (95% CI = 1.12-1.27), and 1.07 (95% CI = 0.95-1.19) for CC, CG, and GG, respectively. The two-step EDGE method identified the rs35352860 SNP in chromosome 18 (SMAD7 intron); greater than median of consumption ORs = 1.18 (95% CI = 1.11-1.24), 1.35 (95% CI = 1.26-1.44), and 1.46 (95% CI = 1.26-1.69) for CC, CT, and TT, respectively. CONCLUSIONS: We propose two novel biomarkers that support the role of meat consumption with an increased risk of colorectal cancer. IMPACT: The reported GxE interactions may explain the increased risk of colorectal cancer in certain population subgroups.