High intake of processed and red meat is associated with increased risk of colorectal cancer

2002 ◽  
Vol 3 (4) ◽  
pp. 146-147
Author(s):  
Stewart Truswell
2010 ◽  
Vol 105 (3) ◽  
pp. 384-392 ◽  
Author(s):  
Ossama Allam ◽  
Diane Bahuaud ◽  
Sylviane Taché ◽  
Nathalie Naud ◽  
Denis E. Corpet ◽  
...  

Red meat intake is associated with an increased risk of colorectal cancer. We have previously shown that haemin, Hb and red meat promote carcinogen-induced preneoplastic lesions, aberrant crypt foci (ACF), in the colon of rats. We have also shown that dietary calcium phosphate inhibits haemin-induced promotion and normalises faecal lipoperoxides and cytotoxicity. Unexpectedly, high-calcium phosphate control diet-fed rats had more preneoplastic lesions in the colon than low-Ca control diet-fed rats. The present study was designed to find a Ca supplementation with no adverse effect, by testing several doses and types of Ca salts. Onein vitrostudy and two short-term studies in rats identified calcium carbonate as the most effective Ca salt to bind haemin vitroand to decrease faecal biomarkers previously associated with increased carcinogenesis: faecal water cytotoxicity and thiobarbituric acid-reactive substances. A long-term carcinogenesis study in dimethylhydrazine-injected rats demonstrated that a diet containing 100 μmol/g calcium carbonate did not promote ACF, in contrast with a previously tested calcium phosphate diet. The results suggest that calcium carbonate, and not calcium phosphate, should be used to reduce haem-associated colorectal cancer risk in meat eaters. They support the concept that the nature of the associated anion to a protective metal ion is important for chemoprevention.


2022 ◽  
Vol 29 ◽  
pp. 107327482110566
Author(s):  
Anna Lewandowska ◽  
Grzegorz Rudzki ◽  
Tomasz Lewandowski ◽  
Aleksandra Stryjkowska-Góra ◽  
Sławomir Rudzki

Background Colorectal cancer defined as cancer of the colon or rectum, is the third most frequently diagnosed cancer in men and the second in women, and, according to the World Health Organization database GLOBOCAN, it accounts for nearly 1.4 million new cases annually worldwide. The occurrence of colorectal cancer is associated with nonmodifiable risk factors, including age and hereditary factors, as well as with modifiable environmental and lifestyle factors. Methods The study included 800 patients, 400 diagnosed with colorectal cancer and 400 within the control group, who gave their written informed consent to participate in the study. Patients with cancer other than colorectal cancer were randomly selected for control group I, and patients with no cancer diagnosis were selected for control group II. The method used was a case-control study – an observational and analytical study with a control group, conducted among patients of the Clinical Oncology Centre and the Provincial Hospital in the years 2019–2020. The study comparing the exposure was carried out in a group of people who developed the endpoint, that is colorectal cancer, with the exposure in a well-matched group of controls who did not reach the endpoint. Assessment of activity and BMI was used according to WHO recommendations, as well as the expert system. The data were tested for the distribution and the homogeneity of variance was validated before applying the parameter tests. Comparison of quantitative variables between groups was performed using ANOVA. Results The mean age of the patients was 64.53 ± 8.86 years, of the control group I – 59.64 ± 9.33 and the control group II – 57.5 (7.83). There was a strong positive association between the incidence of ulcerative colitis and the risk of colorectal cancer ( P < .01). Among obese subjects, the risk of developing colorectal cancer was 1.27 (95% CI, 1.06–1.53) compared with nonobese subjects. A strong positive relationship was found between low physical activity converted to metabolic equivalent of MET effort per week and the risk of colorectal cancer ( P < .001). The relative risk for current smokers was 2.17 (95% CI 1.79–2.66). There was an association between higher fat consumption and higher red meat consumption and the risk of developing colorectal cancer ( P < .01). Conclusions Obesity, low physical activity, active and passive smoking and high salt and red meat consumption have been associated with an increased risk of colorectal cancer. These findings provide further evidence of the importance of maintaining a healthy lifestyle.


2007 ◽  
Vol 35 (5) ◽  
pp. 1355-1357 ◽  
Author(s):  
G.G.C. Kuhnle ◽  
S.A. Bingham

Colorectal cancer is the third most common cancer in developed countries such as the U.K., but incidence rates around the world vary approx. 20-fold. Diet is thought to be a key factor determining risk: red and processed meat, but not white meat or fish, are associated with an increased risk of colorectal cancer. The endogenous formation of N-nitroso compounds is a possible explanation because red and processed meat, but not white meat or fish, cause a dose-dependent increase in faecal ATNCs (apparent total N-nitroso compounds) and the formation of nitroso-compound-specific DNA adducts in humans. Red meat is particularly rich in haem which has been found to promote the endogenous formation of ATNC. Nitrosyl haem and nitroso thiols have been identified as major constituents of both faecal and ileal ATNC with a significant increase in the formation of these compounds following a diet rich in red meat. In vitro incubations show that, under simulated gastric conditions, nitroso thiols are the main species of nitroso compound formed, suggesting that acid-catalysed thionitrosation is the initial step in the endogenous formation of nitroso compounds. Nitrosyl haem and other nitroso compounds can then form under the alkaline and reductive conditions of the small and large bowel.


2008 ◽  
Vol 99 (5) ◽  
pp. 1000-1006 ◽  
Author(s):  
Fabrice Pierre ◽  
Raphaëlle Santarelli ◽  
Sylviane Taché ◽  
Françoise Guéraud ◽  
Denis E. Corpet

Red meat consumption is associated with increased risk of colorectal cancer. We have previously shown that haemin, Hb and red meat promote carcinogen-induced preneoplastic lesions: aberrant crypt foci (ACF) and mucin-depleted foci (MDF) in rats. We have also shown that dietary Ca, antioxidant mix and olive oil inhibit haemin-induced ACF promotion, and normalize faecal lipoperoxides and cytotoxicity. Here we tested if these strategies are effective also against red meat promotion in dimethylhydrazine-induced rats. Three diets with 60 % beef meat were supplemented with calcium phosphate (31 g/kg), antioxidant agents (rutin and butylated hydroxyanisole, 0·05 % each) and olive oil (5 %). ACF, MDF, faecal water cytotoxicity, thiobarbituric acid reactive substances (TBARS) and urinary 1,4-dihydroxynonane mercapturic acid (DHN-MA) were measured. Beef meat diet increased the number of ACF (+30 %) and MDF (+100 %) (P < 0·001), which confirms our previous findings. Promotion was associated with increased faecal water TBARs ( × 4) and cytotoxicity ( × 2), and urinary DHN-MA excretion ( × 15). Ca fully inhibited beef meat-induced ACF and MDF promotion, and normalized faecal TBARS and cytotoxicity, but did not reduce urinary DHN-MA. Unexpectedly, high-calcium control diet-fed rats had more MDF and ACF in the colon than low-Ca control diet-fed rats. Antioxidant mix and olive oil did not normalize beef meat promotion nor biochemical factors. The results confirm that haem causes promotion of colon carcinogenesis by red meat. They suggest that Ca can reduce colorectal cancer risk in meat-eaters. The results support the concept that toxicity associated with the excess of a useful nutrient may be prevented by another nutrient.


2014 ◽  
Vol 146 (5) ◽  
pp. S-408
Author(s):  
Yezaz A. Ghouri ◽  
Sachin Batra ◽  
Nirav C. Thosani ◽  
Sushovan Guha

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 407
Author(s):  
Reetta Holma ◽  
Reijo Laatikainen ◽  
Helena Orell ◽  
Heikki Joensuu ◽  
Katri Peuhkuri ◽  
...  

Chemotherapy-induced mucosal injury of the small intestine may interfere with the enzymes and transporters responsible for the hydrolysis and absorption of dietary carbohydrates causing diarrhoea, abdominal discomfort and pain. The aim of this study was to investigate the association between the consumption of foods rich in FODMAPs (fermentable oligo-, di- and monosaccharides and polyols) and gastrointestinal symptoms in patients receiving adjuvant therapy for colorectal cancer. The patients (n = 52) filled in a 4-day food diary at baseline and during therapy and kept a symptom diary. The intakes of FODMAP-rich foods were calculated as portions and the intakes were divided into two consumption categories. Patients with high consumption of FODMAP-rich foods had diarrhoea more frequently than those with low consumption (for lactose-rich foods the odds ratio (OR) was 2.63, P = 0.03; and for other FODMAP-rich foods 1.82, P = 0.20). Patients with high consumption of both lactose-rich and other FODMAP-rich foods had an over 4-fold risk of developing diarrhoea as compared to those with low consumption of both (OR, 4.18; P = 0.02). These results were confirmed in multivariate models. Conclusion: Consumption of lactose-rich foods results in an increased risk of diarrhoea during adjuvant therapy for colorectal cancer, especially when the consumption of other FODMAP-rich foods is also high.


2021 ◽  
Vol 43 (1) ◽  
Author(s):  
Loïc Le Marchand

AbstractSince Dr. Sugimura’s discovery of heterocyclic aromatic amines (HAA) in broiled fish, many epidemiological studies have been conducted to investigate their role in human cancers, often focusing on colorectal cancer. The difficulty in measuring HAA exposure from meat and fish intake in these studies has resulted in inconsistent findings. Because studying individuals who may be particularly susceptible to the carcinogenic effects of HAA might facilitate the demonstration of a link with cancer, multiple studies have focused on individuals with the high activity phenotype for CYP1A2 and/or NAT2, the two main metabolic enzymes involved in the bioactivation of HAA. These investigations have also yielded inconsistent results. Two recent large pooled analyses of colorectal cancer studies have helped clarify the overall evidence. One was conducted in whites and reported no interaction of red meat intake and NAT2 genotype on risk in Whites. The other was conducted in Japanese and African Americans, two populations with high rates of the disease and a prevalence of the at-risk rapid NAT2 phenotype 10- and 2-fold greater than in whites, respectively. In those groups, a significant interaction was found, with the association of red meat with colorectal cancer being strongest among individuals with the rapid NAT2 phenotype, intermediate among those with the intermediate phenotype and not significant among those with the slow NAT2 phenotype. Recent research on biomarkers has focused on PhIP hair content, as a marker of exposure to HAA, and on DNA adducts using new sensitive quantitative methods, as markers of early biological effects. These advances, when brought to bear, may contribute greatly to the further elucidation of the carcinogenicity of HAA in humans.


2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A38-A38
Author(s):  
Shilpa Ravindran ◽  
Heba Sidahmed ◽  
Harshitha Manjunath ◽  
Rebecca Mathew ◽  
Tanwir Habib ◽  
...  

BackgroundPatients with inflammatory bowel disease (IBD) have increased risk of developing colorectal cancer (CRC), depending on the duration and severity of the disease. The evolutionary process in IBD is driven by chronic inflammation leading to epithelial-to-mesenchymal transition (EMT) events in colonic fibrotic areas. EMT plays a determinant role in tumor formation and progression, through the acquisition of ‘stemness’ properties and the generation of neoplastic cells. The aim of this study is to monitor EMT/cancer initiating tracts in IBD in association with the deep characterization of inflammation in order to assess the mechanisms of IBD severity and progression towards malignancy.Methods10 pediatric and 20 adult IBD patients, admitted at Sidra Medicine (SM) and Hamad Medical Corporation (HMC) respectively, have been enrolled in this study, from whom gut tissue biopsies (from both left and right side) were collected. Retrospectively collected tissues (N=10) from patients with malignancy and history of IBD were included in the study. DNA and RNA were extracted from fresh small size (2–4 mm in diameter) gut tissues using the BioMasher II (Kimble) and All Prep DNA/RNA kits (Qiagen). MicroRNA (miRNA; N=700) and gene expression (N=800) profiling have been performed (cCounter platform; Nanostring) as well as the methylation profiling microarray (Infinium Methylation Epic Bead Chip kit, Illumina) to interrogate up to 850,000 methylation sites across the genome.ResultsDifferential miRNA profile (N=27 miRNA; p<0.05) was found by the comparison of tissues from pediatric and adult patients. These miRNAs regulate: i. oxidative stress damage (e.g., miR 99b), ii. hypoxia induced autophagy; iii. genes associated with the susceptibility to IBD (ATG16L1, NOD2, IRGM), iv. immune responses, such as TH17 T cell subset (miR 29). N=6 miRNAs (miR135b, 10a196b, 125b, let7c, 375) linked with the regulation of Wnt/b-catenin, EM-transaction, autophagy, oxidative stress and play role also in cell proliferation and mobilization and colorectal cancer development were differentially expressed (p<0.05) in tissues from left and right sides of gut. Gene expression signature, including genes associated with inflammation, stemness and fibrosis, has also been performed for the IBD tissues mentioned above. Methylation sites at single nucleotide resolution have been analyzed.ConclusionsAlthough the results warrant further investigation, differential genomic profiling suggestive of altered pathways involved in oxidative stress, EMT, and of the possible stemness signature was found. The integration of data from multiple platforms will provide insights of the overall molecular determinants in IBD patients along with the evolution of the disease.Ethics ApprovalThis study was approved by Sidra Medicine and Hamad Medical Corporation Ethics Boards; approval number 180402817 and MRC-02-18-096, respectively.


2021 ◽  
pp. 1-38
Author(s):  
Ala Al Rajabi ◽  
Geraldine Lo Siou ◽  
Alianu K. Akawung ◽  
Kathryn L McDonald ◽  
Tiffany R. Price ◽  
...  

ABSTRACT Current cancer prevention recommendations advise limiting red meat intake to <500g/week and avoiding consumption of processed meat, but do not differentiate the source of processed meat. We examined the associations of processed meat derived from red vs. non-red meats with cancer risk in a prospective cohort of 26,218 adults who reported dietary intake using the Canadian Diet History Questionnaire. Incidence of cancer was obtained through data linkage with Alberta Cancer Registry with median (IQR) follow-up of 13.3 (5.1) years. Multivariable Cox proportional hazards regression models were adjusted for covariates and stratified by age and gender. The median (IQR) consumption (g/week) of red meat, processed meat from red meat and processed meat from non-red meat were 267.9 (269.9), 53.6 (83.3), and 11.9 (31.8), respectively. High intakes (4th Quartile) of processed meat from red meat was associated with increased risk of gastro-intestinal cancer Adjusted Hazard Ratio (AHR) (95% CI): 1.68 (1.09 – 2.57) and colorectal cancers AHR (95% CI): 1.90 (1.12 – 3.22), respectively in women. No statistically significant associations were observed for intakes of red meat or processed meat from non-red meat. Results suggests that the carcinogenic effect associated with processed meat intake may be limited to processed meat derived from red meats. The findings provide preliminary evidence toward refining cancer prevention recommendations for red and processed meat intake.


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