Search

[This corrects the article DOI: 10.3389/fnut.2022.1035580.]

Funding Information: This work was supported by Cancer Research UK (C33493/A29678), World Cancer Research Fund International (IIG_FULL_2020_033), and the Institut National du Cancer (INCa number 2021–138). The coordination of EPIC is financially supported by the IARC and the Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, which has additional infrastructure support provided by the UK National Institute for Health and Care Research Imperial Biomedical Research Centre. The national cohorts are supported by the Danish Cancer Society (Denmark); Ligue Contre le Cancer, Institut Gustave Roussy, Mutuelle Générale de l'Education Nationale, Institut National de la Santé et de la Recherche Médicale (INSERM; France); German Cancer Aid, German Cancer Research Center (DKFZ), German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Federal Ministry of Education and Research (BMBF; Germany); Associazione Italiana per la Ricerca sul Cancro-AIRC–Italy, Compagnia di SanPaolo and National Research Council (Italy); Dutch Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund, Statistics Netherlands (Netherlands); Health Research Fund (FIS)—Instituto de Salud Carlos III (ISCIII), Regional Governments of Andalucía, Asturias, Basque Country, Murcia and Navarra, and the Catalan Institute of Oncology (ICO; Spain); Swedish Cancer Society, Swedish Research Council and County Councils of Skåne and Västerbotten (Sweden); and Cancer Research UK (14136 to EPIC–Norfolk; C8221/A29017 to EPIC–Oxford) and Medical Research Council (1000143 to EPIC–Norfolk; MR/M012190/1 to EPIC–Oxford; UK). Where authors are identified as personnel of the International Agency for Research on Cancer or WHO, they are responsible for the views expressed in this Article and they do not necessarily represent the decisions, policy, or views of the International Agency for Research on Cancer or WHO. Publisher Copyright: © 2023 World Health Organization UPDATE NOTICE Correction to Lancet Planet Health 2023; 7: e219–32. The Lancet Planetary Health. 2023;7(5):e357. Scopus ID: 85158098931 Background: Food processing has been hypothesised to play a role in cancer development; however, data from large-scale epidemiological studies are scarce. This study investigated the association between dietary intake according to amount of food processing and risk of cancer at 25 anatomical sites using data from the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Methods: This study used data from the prospective EPIC cohort study, which recruited participants between March 18, 1991, and July 2, 2001, from 23 centres in ten European countries. Participant eligibility within each cohort was based on geographical or administrative boundaries. Participants were excluded if they had a cancer diagnosis before recruitment, had missing information for the NOVA food processing classification, or were within the top and bottom 1% for ratio of energy intake to energy requirement. Validated dietary questionnaires were used to obtain information on food and drink consumption. Participants with cancer were identified using cancer registries or during follow-up from a combination of sources, including cancer and pathology centres, health insurance records, and active follow-up of participants. We performed a substitution analysis to assess the effect of replacing 10% of processed foods and ultra-processed foods with 10% of minimally processed foods on cancer risk at 25 anatomical sites using Cox proportional hazard models. Findings: 521 324 participants were recruited into EPIC, and 450 111 were included in this analysis (318 686 [70·8%] participants were female individuals and 131 425 [29·2%] were male individuals). In a multivariate model adjusted for sex, smoking, education, physical activity, height, and diabetes, a substitution of 10% of processed foods with an equal amount of minimally processed foods was associated with reduced risk of overall cancer (hazard ratio 0·96, 95% CI 0·95–0·97), head and neck cancers (0·80, 0·75–0·85), oesophageal squamous cell carcinoma (0·57, 0·51–0·64), colon cancer (0·88, 0·85–0·92), rectal cancer (0·90, 0·85–0·94), hepatocellular carcinoma (0·77, 0·68–0·87), and postmenopausal breast cancer (0·93, 0·90–0·97). The substitution of 10% of ultra-processed foods with 10% of minimally processed foods was associated with a reduced risk of head and neck cancers (0·80, 0·74–0·88), colon cancer (0·93, 0·89–0·97), and hepatocellular carcinoma (0·73, 0·62–0·86). Most of these associations remained significant when models were additionally adjusted for BMI, alcohol and dietary intake, and quality. Interpretation: This study suggests that the replacement of processed and ultra-processed foods and drinks with an equal amount of minimally processed foods might reduce the risk of various cancer types. Funding: Cancer Research UK, l'Institut National du Cancer, and World Cancer Research Fund International. publishersversion publishersversion published

Funding Information: The Cancer Research UK and World Cancer Research Fund.This work was supported by Cancer Research UK C33493/A29678. Funding IIG_FULL_2020_033 was obtained from World Cancer Research Fund (WCRF UK), as part of the World Cancer Research Fund International grant programme. Where authors are identified as personnel of the International Agency for Research on Cancer / World Health Organization, the authors alone are responsible for the views expressed in this article and they do not necessarily represent the decisions, policy or views of the International Agency for Research on Cancer / World Health Organization. FR declares funding from The São Paulo Research Foundation (FAPESP) 16/14302-7 and 18/19820-1. This research has been conducted using the UK Biobank Resource under Application Number 29239. The authors would like to thank the participants of the UK Biobank study. Funding Information: This work was supported by Cancer Research UK C33493 / A29678 . Funding IIG_FULL_2020_033 was obtained from World Cancer Research Fund (WCRF UK), as part of the World Cancer Research Fund International grant programme. Where authors are identified as personnel of the International Agency for Research on Cancer / World Health Organization, the authors alone are responsible for the views expressed in this article and they do not necessarily represent the decisions, policy or views of the International Agency for Research on Cancer / World Health Organization. FR declares funding from The São Paulo Research Foundation (FAPESP) 16/14302-7 and 18/19820-1 . This research has been conducted using the UK Biobank Resource under Application Number 29239. The authors would like to thank the participants of the UK Biobank study. Publisher Copyright: © 2023 The Author(s) Background: Global dietary patterns are increasingly dominated by relatively cheap, highly palatable, and ready-to-eat ultra-processed foods (UPFs). However, prospective evidence is limited on cancer development and mortality in relation to UPF consumption. This study examines associations between UPF consumption and risk of cancer and associated mortality for 34 site-specific cancers in a large cohort of British adults. Methods: This study included a prospective cohort of UK Biobank participants (aged 40–69 years) who completed 24-h dietary recalls between 2009 and 2012 (N = 197426, 54.6% women) and were followed up until Jan 31, 2021. Food items consumed were categorised according to their degree of food processing using the NOVA food classification system. Individuals’ UPF consumption was expressed as a percentage of total food intake (g/day). Prospective associations were assessed using multivariable Cox proportional hazards models adjusted for baseline socio-demographic characteristics, smoking status, physical activity, body mass index, alcohol and total energy intake. Findings: The mean UPF consumption was 22.9% (SD 13.3%) in the total diet. During a median follow-up time of 9.8 years, 15,921 individuals developed cancer and 4009 cancer-related deaths occurred. Every 10 percentage points increment in UPF consumption was associated with an increased incidence of overall (hazard ratio, 1.02; 95% CI, 1.01–1.04) and specifically ovarian (1.19; 1.08–1.30) cancer. Furthermore, every 10 percentage points increment in UPF consumption was associated with an increased risk of overall (1.06; 1.03–1.09), ovarian (1.30; 1.13–1.50), and breast (1.16; 1.02–1.32) cancer-related mortality. Interpretation: Our UK-based cohort study suggests that higher UPF consumption may be linked to an increased burden and mortality for overall and certain site-specific cancers especially ovarian cancer in women. Funding: The Cancer Research UK and World Cancer Research Fund. publishersversion published

Funding Information: This work was supported by Cancer Research UK [Ref: C33493/A29678] and World Cancer Research Fund International [Ref: IIG_FULL_2020_033]. Publisher Copyright: © 2022, The Author(s), under exclusive licence to Springer Nature Limited. Ultra-processed foods (UPFs) have become increasingly dominant globally, contributing to as much as 60% of total daily energy intake in some settings. Epidemiological evidence suggests this worldwide shift in food processing may partly be responsible for the global obesity epidemic and chronic disease burden. However, prospective studies examining the association between UPF consumption and cancer outcomes are limited. Available evidence suggests that UPFs may increase cancer risk via their obesogenic properties as well as through exposure to potentially carcinogenic compounds such as certain food additives and neoformed processing contaminants. We identify priority areas for future research and policy implications, including improved understanding of the potential dual harms of UPFs on the environment and cancer risk. The prevention of cancers related to the consumption of UPFs could be tackled using different strategies, including behaviour change interventions among consumers as well as bolder public health policies needed to improve food environments. publishersversion published

Additional file 1: Supplementary information. Table S1. Number of metabolites included in each study population; Table S2. Metabolites associated with each anthropometric variable in the replication set; Table S3. Metabolites with the greatest contribution for each metabolic signature; Table S4. Correlations between the metabolic signatures and their corresponding anthropometric measure; Table S5. Metabolites that changed significantly from baseline to follow-up in the Intercept; Table S6. Metabolites significantly associated with weight loss in the Intercept; Table S7. Metabolites significantly associated with weight loss in the Intercept; Figure S1. Overall Rpartial2 and weighted Rpartial2 for each covariate and BMI in the discovery set; Figure S2. Overall Rpartial2 and weighted Rpartial2 for each covariate and WC in the discovery set; Figure S3. Overall Rpartial2 and weighted Rpartial2 for each covariate and WHR in the discovery set; Figure S4. Overall Rpartial2 and weighted Rpartial2 for each covariate and weight loss in the Intercept; Figure S5. Association of colorectal and endometrial cancers with the metabolic signatures further adjusted to C-peptide; Figure S6. Association of colorectal and endometrial cancers with the anthropometric measures of obesity; Figure S7. Smile plot of the associations between metabolites with weight loss in the Intercept.

Obesity has been associated with upper gastrointestinal cancers; however, there are limited prospective data on associations by subtype/subsite. Obesity can impact hormonal factors, which have been hypothesized to play a role in these cancers. We investigated anthropometric and reproductive factors in relation to esophageal and gastric cancer by subtype and subsite for 476,160 participants from the European Prospective Investigation into Cancer and Nutrition cohort. Multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox models. During a mean follow‐up of 14 years, 220 esophageal adenocarcinomas (EA), 195 esophageal squamous cell carcinomas, 243 gastric cardia (GC) and 373 gastric noncardia (GNC) cancers were diagnosed. Body mass index (BMI) was associated with EA in men (BMI ≥30 vs. 18.5–25 kg/m2: HR = 1.94, 95% CI: 1.25–3.03) and women (HR = 2.66, 95% CI: 1.15–6.19); however, adjustment for waist‐to‐hip ratio (WHR) attenuated these associations. After mutual adjustment for BMI and HC, respectively, WHR and waist circumference (WC) were associated with EA in men (HR = 3.47, 95% CI: 1.99–6.06 for WHR >0.96 vs. 98 vs. 0.82 vs. 84 vs. 2 vs. 0) and age at first pregnancy and GNC (HR = 0.54, 95% CI: 0.32–0.91; >26 vs., What's new? Obesity can change the body's hormone balance, and encourage the onset of cancer. Here, the authors investigated the relationship between obesity, hormones, and esophageal and gastric cancers. Using data from the EPIC cohort, they obtained information about anthropometric and reproductive factors for 476,160 participants. Excess fat around the waist, they found, was associated with esophageal adenocarcinoma and gastric cardia cancer, in women and men. In women, bearing children, as well as younger age at first pregnancy, had an inverse association with certain cancers. Ovariectomy was positively associated with gastric non‐cardia cancer, suggesting involvement of hormone pathways in these malignancies.

Descriptive data of the automaticity of each target behaviour (DOCX 18 kb)

CONSORT 2010 checklist of information to include when reporting a randomised trial* (DOC 218 kb)

Scree plot and Parallel analyses of the final 5 items retained in the â Internal Reliability and Factor Structure Studyâ . (DOCX 38Â kb)

Self-Regulation of Eating Behaviour Questionnaire. (DOCX 35Â kb)

Scree plot and Parallel analyses of the 14 items retained in the â Internal Reliability and Factor Structure Studyâ . (DOCX 43Â kb)

Dissertação (mestrado) - Universidade Federal de Santa Catarina, Centro de Ciências da Saúde. Programa de Pós-Graduação em Nutrição No Brasil, a rotulagem nutricional por porção e medida caseira em alimentos industrializados é considerada uma estratégia de promoção da alimentação saudável, em que a porção é apresentada como uma recomendação de consumo para a população. Ela deve fornecer informações padronizadas, precisas e compreensíveis, permitindo a comparabilidade entre alimentos similares e auxiliando a determinação do consumo. O presente estudo objetivou analisar como as porções e as medidas caseiras estão sendo definidas e declaradas na informação nutricional de rótulos de alimentos industrializados ultraprocessados comercializados no Brasil. Realizou-se um estudo transversal do tipo descritivo e analítico, no qual foram analisados todos os alimentos industrializados ultraprocessados à venda em um supermercado de Florianópolis (SC). Foram avaliados tanto os valores de referência quanto os valores declarados nos rótulos sobre porção, medida caseira, valor energético por porção e densidade energética. Além disso, foram analisadas a relação da porção com o valor energético e o peso total declarado nas embalagens, bem como a relação do fracionamento da medida caseira com o tamanho da porção e o tipo de medida caseira. Seguindo a legislação brasileira, os alimentos foram classificados em seis grupos e 34 subgrupos, sendo as variáveis categorizadas. Análises descritivas e analíticas foram conduzidas utilizando-se o programa estatístico Stata, versão 11.0. Foram analisados 2.072 alimentos industrializados, sendo encontrada variabilidade na declaração do tamanho da porção, com amplitude mínima de 21-30g, entre biscoitos salgados, e máxima de 55-420g, entre pratos preparados prontos e semiprontos. Os alimentos com porções menores e inadequadas em relação às porções recomendadas pela legislação apresentaram a menor densidade energética, o menor valor energético por porção e o maior peso total (p