In recent years, there has been increasing interest in the potential role of industrial food processing in the etiology of diseases. The NOVA classification system (not an abbreviation) developed by Monteiro et al. classifies foods into four groups based on their degree and purpose of processing: (1) unprocessed or minimally processed foods, (2) processed culinary ingredients, (3) processed foods, and (4) ultra-processed foods (UPF).
Ultra-processed foods (UPF) are complexly manufactured industrial formulations using ingredients not normally found in kitchens (e.g., maltodextrin, hydrogenated oils, modified starches) and cosmetic additives (e.g., emulsifiers, flavors, colors, artificial sweeteners). ). They are typically cheap, very tasty and widely available ready-to-eat products that are often consumed in large quantities, replacing more nutritious, unprocessed or minimally processed foods in the diet .
Examples of ultra-processed foods (UPF) include soft drinks, packaged sweet or savory snacks, candy, packaged breads and rolls, reconstituted meat products, and frozen or shelf-stable ready meals.
Several studies have shown that UPF consumption may be associated with an increased risk of cancer. In the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, Kliemann et al. found positive associations between higher UPF intake and risk of head and neck cancer (HNC; hazard ratio [HR] = 1.14 per one standard deviation [SD] higher UPF intake, confidence interval [CI] 95%: 1.06–1.24) and esophageal adenocarcinoma (OAC; HR = 1.21 per 1 SD higher UPF intake, 95% CI: 1.05 to 1.39). They also found an inverse association between UPF consumption and the risk of esophageal squamous cell carcinoma (HR = 0.79 per 1 SD higher UPF intake, 95% CI 0.64-0.96), although this did not hold up. additional adjustments for alcohol consumption and body mass index (BMI) and various dietary factors (HR = 0.90 per 1 SD higher UPF intake, 95% CI: 0.72 to 1.11).
UPF consumption has also been positively associated with higher adiposity (i.e., BMI, fat mass, waist circumference, and waist-to-hip ratio (WHR). Since body fat (measured by BMI, hip circumference waist circumference and WHR) is an established modifiable risk factor for OCA, and visceral adiposity (i.e., waist circumference and WHR) has been positively associated with HNC risk, it is plausible that positive associations between consumption of UPF and these cancers of the upper aerodigestive tract are mediated by adiposity.
The aim of this study was to re-evaluate and further investigate the associations between UPF consumption and the risk of HNC and OAC in the EPIC study. Complementing the study by Kliemann et al., this study explored the associations between UPF consumption and the risk of HNC and its subtypes (i.e., oral cavity, oropharynx, hypopharynx, larynx, and unspecified/overlapping cancers) as defined the International Head and Neck Cancer Epidemiology (INHANCE) consortium. We also investigated effect modification by smoking, alcohol consumption, sex, physical activity, and educational level in the associations between UPF consumption and the risk of upper aerodigestive tract cancers. Additionally, this study assessed the possibility of residual confounding using accidental death as a negative control outcome. Finally, the role of BMI and WHR in the associations between UPF consumption and the risk of HNC and OA was examined using mediation analysis.
Aim
To investigate the role of adiposity in the associations between ultra-processed food (UPF) consumption and head and neck cancer (HNC) and esophageal adenocarcinoma (OAC) in the European Prospective Investigation into Cancer and Nutrition cohort ( EPIC).
Methods
Our study included 450,111 participants from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. We used Cox regressions to investigate the associations between UPF consumption and the risk of HNC and OAC.
Mediation analysis was performed to evaluate the role of body mass index (BMI) and waist-to-hip ratio (WHR) in these associations. In sensitivity analyses, we investigated accidental death as a negative control outcome.
Results
During a mean follow-up of 14.13 ± 3.98 years, 910 and 215 participants developed head and neck cancer (HNC) and esophageal adenocarcinoma (OAC), respectively.
A 10% g/day higher intake of UPF was associated with an increased risk of HNC (hazard ratio [HR] = 1.23, 95% confidence interval [CI]: 1.14–1.34) and OAC (HR = 1.24, 95% CI: 1.05– 1.47).
The waist-hip ratio (WHR) mediated 5% (95% CI 3-10%) of the association between UPF consumption and the risk of HNC, while BMI and WHR, respectively, mediated 13% (CI 95% 6-53%) and 15% (95% CI 6-53%). CI 8-72%) of the association between UPF consumption and the risk of OAC.
UPF consumption was positively associated with accidental death in the negative control analysis.
Figure : Associations between consumption of ultra-processed foods (in %g/d) and head and neck cancer subtypes. Risk ratios for every 10% g/d of increased intake of ultra-processed foods. Entry time was defined as age at recruitment, while exit time was defined as age at first cancer diagnosis (excluding non-melanoma skin cancer) or age at last follow-up. (i.e., death, emigration, loss to follow-up, or end to follow-up). tracking), whichever comes first. Model 1 was stratified by age at recruitment into 1-year, sex, and subcenter categories. Model 2 was additionally adjusted for education, physical activity, height, and smoking. Model 3 was additionally adjusted for alcohol consumption. N = 450,111, of whom 234, 235, 66, 310, and 65 had cancer of the oral cavity, oropharynx, hypopharynx, larynx, and unspecified/overlapping regions of the oral cavity and pharynx, respectively. Abbreviations: CI, confidence interval; UPF, ultra-processed foods
Conclusions
In conclusion, we reaffirm that UPF intake is associated with an increased risk of HNC and OA in the EPIC study. Since BMI and WHR explain little of the associations between UPF consumption and upper aerodigestive tract cancers, more research is required to investigate other mechanisms that may be at play (if indeed there is any causal effect of UPF consumption). UPF in these cancers).
Our results are likely influenced by residual confounders, as indicated by the negative control analysis. Therefore, our findings should be considered cautiously until they are replicated in other settings (i.e., in populations with different underlying confusion structures) or triangulated with evidence obtained using other methodological approaches.
Final message We reaffirm that higher consumption of ultra-processed foods (UPF) is associated with a higher risk of HNC and OA in EPIC. The proportion mediated by adiposity was small. More research is required to investigate other mechanisms that may be at play (if there really is any causal effect of UPF consumption on these cancers). |
