High Red Meat Diet Research Articles

Spatial metabolomics using mass-spectrometry imaging to decipher the impact of high red meat diet on the colon metabolome in rat

Colorectal cancer (CRC) is the third most common cancer in the world with a higher prevalence in the developed countries, mainly caused by environmental and lifestyle factors such as diet, particularly red meat consumption. The metabolic impact of high red meat consumption on the epithelial part of the colon was investigated using Matrix-Assisted Laser Desorption/Ionization Mass Spectrometry Imaging (MSI), to specifically analyze the epithelial substructure. Ten colons from rats fed for 100 days high red or white meat diet were subjected to untargeted MSI analyses using two spatial resolutions (100 μm and 10 μm) to evaluate metabolite changes in the epithelial part and to visualize the distribution of metabolites of interest within the epithelium crypts. Our results suggest a specific effect of red meat diet on the colonic epithelium metabolism, as evidenced by an increase of purine catabolism products or depletion in glutathione pool, reinforcing the hypothesis of increased oxidative stress with red meat diet. This study also highlighted cholesterol sulfate as another up-regulated metabolite, interestingly localized at the top of the crypts. Altogether, this study demonstrates the feasibility and the added value of using MSI to decipher the effect of high red meat diet on the colonic epithelium.

Burden of ischemic stroke attributable to a high red meat diet in China, 1990-2019: analysis based on the 2019 Global Burden of Disease Study.

The burden of ischemic stroke (IS) linked to high consumption of red meat is on the rise. This study aimed to analyze the mortality and disability-adjusted life years (DALYs) trends for IS attributed to high red meat intake in China between 1990 and 2019 and to compare these trends with global trends. This study extracted data on IS attributed to diets high in red meat in China from 1990 to 2019 from the Global Burden of Disease Study (GBD) database. Key measures, including mortality, DALYs, age-standardized mortality rates (ASMR), and age-standardized DALYs rates (ASDR), were used to estimate the disease burden. The estimated annual percentage change and joinpoint regression models were employed to assess the trends over time. An age-period-cohort analysis was used to assess the contribution of a diet high in red meat to the age, period, and cohort effects of IS ASMR and ASDR. Between 1990 and 2019, deaths and DALYs from IS attributed to a diet high in red meat in China, along with corresponding age-standardized rates, significantly increased. The overall estimated annual percentage change for the total population and across sex categories ranged from 1.01 to 2.08. The average annual percentage changes for overall ASDR and ASMR were 1.4 and 1.33, respectively, with male ASDR and ASMR average annual percentage changes at 1.69 and 1.69, respectively. Contrastingly, female ASDR and ASMR average annual percentage changes were 1.07 and 0.87, respectively. Except for a few periods of significant decrease in females, all other periods indicated a significant increase or nonsignificant changes. Incidence of IS linked to a diet high in red meat rose sharply with age, displaying increasing period and cohort effects in ASDR. Female ASMR period and cohort effect ratios initially increased and then decreased, whereas the male ratio showed an upward trend. This study comprehensively analyzed epidemiological characteristics that indicated a marked increase in mortality and DALYs from IS attributable to high red meat consumption, contrasting with a global downtrend. This increase was more pronounced in males than females. This research provides valuable insights for enhancing IS prevention in China.

Urinary Metabolome Analysis Reveals Potential Microbiota Alteration and Electrophilic Burden Induced by High Red Meat Diet: Results from the French NutriNet-Santé Cohort and an In Vivo Intervention Study in Rats.

High red and processed meat consumption is associated with several adverse outcomes such as colorectal cancer and overall global mortality. However, the underlying mechanisms remain debated and need to be elucidated. Urinary untargeted Liquid Chromatography-Mass Spectrometry (LC-MS) metabolomics data from 240 subjects from the French cohort NutriNet-Santé are analyzed. Individuals are matched and divided into three groups according to their consumption of red and processed meat: high red and processed meat consumers, non-red and processed meat consumers, and at random group. Results are supported by a preclinical experiment where rats are fed either a high red meat or a control diet. Microbiota derived metabolites, in particular indoxyl sulfate and cinnamoylglycine, are found impacted by the high red meat diet in both studies, suggesting a modification of microbiota by the high red/processed meat diet. Rat microbiota sequencing analysis strengthens this observation. Although not evidenced in the human study, rat mercapturic acid profile concomitantly reveals an increased lipid peroxidation induced by high red meat diet. Novel microbiota metabolites are identified as red meat consumption potential biomarkers, suggesting a deleterious effect, which could partly explain the adverse effects associated with high red and processed meat consumption.

The Association with Dietary Patterns and Risk of Anemia in Japanese Elderly.

Anemia is a risk factor for frailty. Although various factors can reduce the risk of anemia, information on dietary contributions is limited. This study aimed to evaluate the association between anemia and eating patterns in Japanese elderly. Our study included 6,864 elderly individuals, aged ≥65 y, whose data were obtained from the 2010-2015 National Health and Nutritional Survey, Japan. Anemia was defined as whole blood hemoglobin concentrations <13 g/dL in men, and <12 g/dL in women. We classified eating patterns into 33 food groups, using food items obtained from dietary records, and identified three dietary patterns using principal component analysis method. Participants were assigned and divided into quartiles according to pattern-specific factor scores. We calculated adjusted odds ratios (ORs) for anemia using multivariate logistic regression, and assigned the first quartile (minimum) as the reference. The overall prevalence of anemia was 17.1%. The meats and vegetables eating pattern was characterized by red meat and other vegetables, the Japanese eating pattern by rice and salted or pickled vegetables, and the fruits and vegetables eating pattern by fruits and green-yellow vegetables. Participants in the highest meats and vegetables eating pattern quartile had a 20% lower risk of anemia than those in the lowest quartile (OR 0.81; 95% confidence interval (CI) 0.66-1.00); the Japanese eating pattern participants had a 20% higher risk of anemia (OR 1.28; 95% CI 1.06-1.53). The fruits and vegetables eating pattern participants had no significant change in their risk of anemia. This study may indicate that consuming a high red meat diet prevents anemia in elderly Japanese individuals.

A systems biology approach to identifying genetic factors affected by aging, lifestyle factors, and type 2 diabetes that influences Parkinson's disease progression

The underlying causes of Parkinson's disease (PD) remain unclear, making it difficult to determine how particular aspects of a patient's health may affect PD development and their treatment response. One alternative approach of investigating interactions between PD and co-morbidities (or other health factors) is to compare the dysregulated cellular or gene pathways they share with affected tissues. To achieve this, we developed a quantitative framework to reveal significant interactions between PD and other significant health factors that may be impacted. In this study, we analyzed gene expression microarray data from tissues affected by PD, type II diabetes (T2D), aging (AG), sedentary lifestyle (SL), high dietary fat (HFD), hypercholesterolemia (HC), high body fat (HBF), high red meat diet (RMD), high alcohol consumption (AC), smoking (SM) and control datasets. We have developed genetic associations of these factors with PD, based on the neighborhood-based benchmarking and multilayer network topology. We identified 1323 differentially expressed genes (DEGs) in the PD patients compared to healthy controls, 779 genes with down-regulated expression and 544 genes up-regulated. 69 dysregulated genes were common to PD and AC datasets; PD datasets also shared, respectively, 51, 45, 43 and 42 DEGs with the T2D, AG, HFD and HBF datasets. Ontological and pathway analyses identified significant gene ontology and molecular pathways with the potential to enhance our understanding of the fundamental molecular factors associated with PD progression. Moreover, we employed a validation gene expression dataset along with Mendelian Inheritance in Man (OMIM) and dbGaP as gold benchmark databases to validate the identified PD associated genes and molecular pathways. Our formulated methodologies used a network-based approach and identified a number of significant genes and pathways that may particularly affect PD, signifying how PD incidence and development may be influenced by the risk factors that may indicate avenues to new therapeutic approaches.

Butyrylated starch intake can prevent red meat-induced O6-methyl-2-deoxyguanosine adducts in human rectal tissue: a randomised clinical trial.

Epidemiological studies have identified increased colorectal cancer (CRC) risk with high red meat (HRM) intakes, whereas dietary fibre intake appears to be protective. In the present study, we examined whether a HRM diet increased rectal O(6)-methyl-2-deoxyguanosine (O(6)MeG) adduct levels in healthy human subjects, and whether butyrylated high-amylose maize starch (HAMSB) was protective. A group of twenty-three individuals consumed 300 g/d of cooked red meat without (HRM diet) or with 40 g/d of HAMSB (HRM+HAMSB diet) over 4-week periods separated by a 4-week washout in a randomised cross-over design. Stool and rectal biopsy samples were collected for biochemical, microbial and immunohistochemical analyses at baseline and at the end of each 4-week intervention period. The HRM diet increased rectal O(6)MeG adducts relative to its baseline by 21% (P < 0.01), whereas the addition of HAMSB to the HRM diet prevented this increase. Epithelial proliferation increased with both the HRM (P < 0.001) and HRM + HAMSB (P < 0.05) diets when compared with their respective baseline levels, but was lower following the HRM + HAMSB diet compared with the HRM diet (P < 0.05). Relative to its baseline, the HRM + HAMSB diet increased the excretion of SCFA by over 20% (P < 0.05) and increased the absolute abundances of the Clostridium coccoides group (P < 0.05), the Clostridium leptum group (P < 0.05), Lactobacillus spp. (P < 0.01), Parabacteroides distasonis (P < 0.001) and Ruminococcus bromii (P < 0.05), but lowered Ruminococcus torques (P < 0.05) and the proportions of Ruminococcus gnavus, Ruminococcus torques and Escherichia coli (P < 0.01). HRM consumption could increase the risk of CRC through increased formation of colorectal epithelial O(6)MeG adducts. HAMSB consumption prevented red meat-induced adduct formation, which may be associated with increased stool SCFA levels and/or changes in the microbiota composition.

Dietary manipulation of oncogenic microRNA expression in human rectal mucosa: a randomized trial.

High red meat (HRM) intake is associated with increased colorectal cancer risk, while resistant starch is probably protective. Resistant starch fermentation produces butyrate, which can alter microRNA (miRNA) levels in colorectal cancer cells in vitro; effects of red meat and resistant starch on miRNA expression in vivo were unknown. This study examined whether a HRM diet altered miRNA expression in rectal mucosa tissue of healthy volunteers, and if supplementation with butyrylated resistant starch (HRM+HAMSB) modified this response. In a randomized cross-over design, 23 volunteers undertook four 4-week dietary interventions; an HRM diet (300 g/day lean red meat) and an HRM+HAMSB diet (HRM with 40 g/day butyrylated high amylose maize starch), preceded by an entry diet and separated by a washout. Fecal butyrate increased with the HRM+HAMSB diet. Levels of oncogenic mature miRNAs, including miR17-92 cluster miRNAs and miR21, increased in the rectal mucosa with the HRM diet, whereas the HRM+HAMSB diet restored miR17-92 miRNAs, but not miR21, to baseline levels. Elevated miR17-92 and miR21 in the HRM diet corresponded with increased cell proliferation, and a decrease in miR17-92 target gene transcript levels, including CDKN1A. The oncogenic miR17-92 cluster is differentially regulated by dietary factors that increase or decrease risk for colorectal cancer, and this may explain, at least in part, the respective risk profiles of HRM and resistant starch. These findings support increased resistant starch consumption as a means of reducing risk associated with an HRM diet.

Accumulation of promutagenic DNA adducts in the mouse distal colon after consumption of heme does not induce colonic neoplasms in the western diet model of spontaneous colorectal cancer

Red meat is considered a risk factor for colorectal cancer (CRC). Heme is considered to promote colonic hyperproliferation and cell damage. Resistant starch (RS) is a food that ferments in the colon with studies demonstrating protective effects against CRC. By utilizing the western diet model of spontaneous CRC, we determined if feeding heme (as hemin chloride) equivalent to a high red meat diet would increase colonic DNA adducts and CRC and whether RS could abrogate such effects. Four groups of mice: control, heme, RS and heme + RS were fed diets for 1 or 18 months. Colons were analyzed for apoptosis, proliferation, DNA adducts "8-hydroxy-2-deoxyguanosine" and "O(6) -methyl-2-deoxyguanosine" (O(6) MeG), and neoplasms. In the short term, heme increased cell proliferation (p < 0.05). Changes from 1 to 18 months showed increased cell proliferation (p < 0.01) and 8-hydroxy-2-deoxyguanosine adducts (p < 0.05) in all groups, but only heme-fed mice showed reduced apoptosis (p < 0.01) and increased O(6) MeG adducts (p < 0.01). The incidence of colon neoplasms was not different between any interventions. We identified heme to increase proliferation in the short term, inhibit apoptosis over the long term, and increase O(6) MeG adducts in the colon over time although these changes did not affect colonic neoplasms within this mouse model.

Dietary Heme Alters Microbiota and Mucosa of Mouse Colon without Functional Changes in Host-Microbe Cross-Talk

Colon cancer is a major cause of cancer deaths in Western countries and is associated with diets high in red meat. Heme, the iron-porphyrin pigment of red meat, induces cytotoxicity of gut contents which injures surface cells leading to compensatory hyperproliferation of crypt cells. This hyperproliferation results in epithelial hyperplasia which increases the risk of colon cancer. In humans, a high red-meat diet increases Bacteroides spp in feces. Therefore, we simultaneously investigated the effects of dietary heme on colonic microbiota and on the host mucosa of mice. Whole genome microarrays showed that heme injured the colonic surface epithelium and induced hyperproliferation by changing the surface to crypt signaling. Using 16S rRNA phylogenetic microarrays, we investigated whether bacteria play a role in this changed signaling. Heme increased Bacteroidetes and decreased Firmicutes in colonic contents. This shift was most likely caused by a selective susceptibility of Gram-positive bacteria to heme cytotoxic fecal water, which is not observed for Gram-negative bacteria, allowing expansion of the Gram-negative community. The increased amount of Gram-negative bacteria most probably increased LPS exposure to colonocytes, however, there is no appreciable immune response detected in the heme-fed mice. There was no functional change in the sensing of the bacteria by the mucosa, as changes in inflammation pathways and Toll- like receptor signaling were not detected. This unaltered host-microbe cross-talk indicates that the changes in microbiota did not play a causal role in the observed hyperproliferation and hyperplasia.

Synthesis of deuterium and C‐13‐labelled ethyl glycolate and their subsequent use in the synthesis of labelled analogues of the DNA adduct O6‐carboxymethyl‐2′‐deoxyguanosine

The adduct O6‐carboxymethyl‐2′‐deoxyguanosine (O6CMdG) is of importance as it has been previously linked to high red meat diet in humans, and as yet, a liquid chromatography‐mass spectrometry (LC‐MS) method has not been developed due to lack of appropriate standards. The synthesis of the deuterated and C‐13 analogues required the use of [2H2]‐ and [13C2]ethyl glycolate to label the carboxymethyl moiety of O6CMdG. [2H2]Ethyl glycolate was synthesised via acid hydrolysis of ethyl diazoacetate using deuterated solvents (59% yield), whilst [13C2]ethyl glycolate was synthesised from [13C2]glycine in a three‐step procedure (35% yield). The labelled ethyl glycolates were then used to synthesise [2H2]‐ and [13C2]O6CMdG for future use as internal standards in the LC‐MS analysis of biological samples. Copyright © 2011 John Wiley &amp; Sons, Ltd.

Urinary Biomarkers of Meat Consumption

Meat intake has been positively associated with incidence and mortality of chronic diseases, including diabetes, heart disease, and several different cancers, in observational studies by using self-report methods of dietary assessment; however, these dietary assessment methods are subject to measurement error. One method to circumvent such errors is the use of biomarkers of dietary intake, but currently there are no accepted biomarkers for meat intake. We investigated four analytes (creatinine, taurine, 1-methylhistidine, and 3-methylhistidine) specifically found in meat and excreted in urine. Twenty-four-hour urine samples were collected from 17 individuals on controlled diets containing varying levels of meat: vegetarian (0 g/d), low red meat (60 g/d), medium red meat (120 g/d), and high red meat (420 g/d), as part of two randomized crossover feeding studies. When compared with the low red meat diet or the vegetarian diet, the urinary levels of all four analytes were significantly higher in urine samples collected after 15 days of a high red meat diet (P < 0.0001). Only urinary 1-methylhistidine and 3-methylhistidine were statistically significantly different for every diet type, increasing as the amount of meat in the diet increased (P < 0.01 for 1-methylhistidine and P < 0.05 for 3-methylhistidine). Furthermore, urinary excretion of 1-methylhistidine and 3-methylhistidine elevated with increasing meat intake in every individual. Urinary 1-methylhistidine and 3-methylhistidine may be good biomarkers of meat intake. To determine the public health impact of red meat on cancer risk, biomarkers are crucial to estimate true intake; these potential biomarkers should be further investigated in free-living populations.

Moderate energy restriction-induced weight loss affects circulating IGF levels independent of dietary composition

Obesity is associated with major changes in the circulating IGF system. However, it is not clear to what extent the IGF system is normalized following diet, and the possible role of different types of diet is also unknown. To compare changes in the circulating IGF system following 12 weeks of moderate energy restriction (7000 kJ/day) in overweight or obese males on a high protein high red meat diet (HP) or a high carbohydrate diet (HC). Seventy-six men (mean age, 51+/-1.0 years; body mass index, 32.8+/-0.5 kg/m(2)) were allocated to matched groups treated with isocaloric diets of HP (n=34) or HC (n=42). Outcome measures were weight, body composition, IGF-related peptides, homoeostasis model assessment of insulin resistance (HOMA1-IR) and adipokines. Weight loss did not differ between diets (HP 8.5+/-0.6 kg; HC 8.2+/-0.6 kg, P>0.05). IGF-related peptides increased total IGF1 (HP 23%; HC 18%, P<0.0001), bioactive IGF1 (HP 18%; HC 15%, P<0.002), IGF1:IGF-binding protein-3 (IGFBP-3; HP 29%; HC 22%, P<0.0001) and IGFBP-1 (HP 24%; HC 25%, P<0.01). By contrast, decreases were observed in IGFBP-3 (HP -4%; HC -3%, P<0.01), pro-IGF2 (HP -3%; HC -6%, P=0.001), total IGF2 (HP -7%; HC -3%, P=0.001) and sIGF2R (HP -10%; HC -6%, P<0.005). Only IGFBP-2 increased differentially by diet (HP 34%; HC 50%, P<0.0001, diet P<0.05). Adiponectin increased in both diets, but leptin and HOMA-IR decreased (P<0.001). Weight loss induced by moderate energy restriction modulated the IGF system independent of dietary protein or red meat content. The effect of diet on IGFBP-2 appeared to have limited biological effect as total IGF2 and pro-IGF2 did not change.

Diet-induced endogenous formation of nitroso compounds in the GI tract

Red or processed meat, but not white meat or fish, is associated with colorectal cancer. The endogenous formation of nitroso compounds is a possible explanation, as red or processed meat—but not white meat or fish—causes a dose-dependent increase in fecal apparent total N-nitroso compounds (ATNC) and the formation of nitroso-compound-specific DNA adducts. Red meat is particularly rich in heme and heme has also been found to promote the formation of ATNC. To investigate the underlying mechanism of ATNC formation, fecal and ileal samples of volunteers fed a high red meat or a vegetarian diet were analyzed for nitrosyl iron, nitrosothiols, and heme. To simulate the processes in the stomach, food homogenates and hemoglobin were incubated under simulated gastric conditions. Nitrosyl iron and nitrosothiols were significantly ( p < 0.0001) increased in ileal and fecal samples after a high red meat diet compared with a vegetarian diet; significantly more nitrosyl iron than nitrosothiols was detectable in ileal ( p < 0.0001) and fecal ( p < 0.001) samples. The strong correlation between fecal nitrosyl iron and heme (0.776; p < 0.0001) suggested that nitrosyl heme is the main source of nitrosyl iron, and ESR confirmed the presence of nitrosyl heme in fecal samples after a high red meat diet. Under simulated gastric conditions, mainly nitrosothiols were formed, suggesting that acid-catalyzed thionitrosation is the initial step in the endogenous formation of nitroso compounds. Nitrosyl heme and other nitroso compounds can then form under the alkaline and reductive conditions of the small and large bowel.

Red Meat Enhances the Colonic Formation of the DNA Adduct O6-Carboxymethyl Guanine: Implications for Colorectal Cancer Risk

Red meat is associated with increased risk of colorectal cancer and increases the endogenous formation of N-nitrosocompounds (NOC). To investigate the genotoxic effects of NOC arising from red meat consumption, human volunteers were fed high (420 g) red meat, vegetarian, and high red meat, high-fiber diets for 15 days in a randomized crossover design while living in a volunteer suite, where food was carefully controlled and all specimens were collected. In 21 volunteers, there was a consistent and significant (P < 0.0001) increase in endogenous formation of NOC with the red meat diet compared with the vegetarian diet as measured by apparent total NOC (ATNC) in feces. In colonic exfoliated cells, the percentage staining positive for the NOC-specific DNA adduct, O(6)-carboxymethyl guanine (O(6)CMG) was significantly (P < 0.001) higher on the high red meat diet. In 13 volunteers, levels were intermediate on the high-fiber, high red meat diet. Fecal ATNC were positively correlated with the percentage of cells staining positive for O(6)CMG (r(2) = 0.56, P = 0.011). The presence of O(6)CMG was also shown in intact small intestine from rats treated with the N-nitrosopeptide N-acetyl-N'-prolyl-N'-nitrosoglycine and in HT-29 cells treated with diazoacetate. This study has shown that fecal NOC arising from red meat include direct acting diazopeptides or N-nitrosopeptides able to form alkylating DNA adducts in the colon. As these O(6)CMG adducts are not repaired, and if other related adducts are formed and not repaired, this may explain the association of red meat with colorectal cancer.

Effect of Vegetables, Tea, and Soy on Endogenous N-Nitrosation, Fecal Ammonia, and Fecal Water Genotoxicity During a High Red Meat Diet in Humans

Red meat increases colonic N-nitrosation, and this may explain the positive epidemiological relationship between red meat intake and colorectal cancer risk. Vegetables, tea, and soy have been shown to block N-nitroso compound (NOC) formation and are associated with protection against colorectal cancer. To determine whether these supplements affect fecal NOC excretion during consumption of a high red meat (420 g/day) diet, 11 male volunteers were studied over a randomized series of 15-day dietary periods. Seven of these subjects completed a further dietary period to test the effects of soy (100 g/day). Soy significantly suppressed fecal apparent total NOC (ATNC) concentration (P = 0.02), but supplements of vegetables (400 g/day as 134 g broccoli, 134 g brussels sprouts, and 134 g petits pois) and tea extract (3 g/day) did not affect mean levels of fecal ATNC, nitrogen and ammonia excretion, and fecal water genotoxicity. However, fecal weight was increased (P < 0.001) and associated with reduced transit time (r = 0.594, P < 0.0001), so that contact between ATNC, nitrite, and ammonia and the large bowel mucosa would have been reduced. Longer transit times were associated with elevated fecal ATNC concentrations (r = 0.42, P = 0.002). Fecal nitrite was significantly suppressed during the tea supplement compared with the meat-only (P = 0.0028) and meat + vegetables diets (P = 0.005 for μg NO2/g).

Does increased endogenous formation of N-nitroso compounds in the human colon explain the association between red meat and colon cancer?

High red meat diets have been linked with risk of sporadic colorectal cancer; but their effects on mutations which occur in this cancer are unknown. G-->A transitions in K-ras occur in colorectal cancer and are characteristic of the effects of alkylating agents such as N-nitroso compounds (NOC). We studied th effect of red meat consumption on faecal NOC levels in eight male volunteers who consumed diets low or high in meat (60 or 600 g/day), as beef, lamb or pork, whilst living in a metabolic suite. Increased intake of red meat induced a significant (P<0.024) 3-fold increase from 40 + or - 7 to ab average of 113 + or - 25 microgram/day NOC, a range of exposure in faeces similar to that from tobacco-specific NOC in cigarette smoke. THe diets were isoenergetic and contained equal amounts of fat, but concentrations of heterocyclic amines were low. Faecal excretion of the promotor ammonia was significantly increased to 6.5 + or - 1.08 mmol/day. When the high red meat diets were supplemented with 20 g phytate-free wheat bran in six volunteers there was no reduction in NOC levels (mean 138 + or - 41 microgram/day NOC), but faecal weight increased. Higher starch and non-starch polysaccharide intakes reduced intraluminal cross-linking in microcapsules (r=-0.77) and reduced faecal pH (r=-0.64). In two volunteers there was no effect of 600 g white meat and fish o faecal NOC (mean low white meat diet 68 + or - 10 microgram/day, high white meat 56 + or -6 microgram/day nor on faecal nitrate, nitrite and iron. Faecal nitrite levels increased on changing from a white to red meat diet (mean high white meat diet 46 + or - 7 mg/day, high red meat diet mean 80 + or - 7 mg/day.) Increased endogenous production of NOC and precursors from increased red meat, but not white meat and fish, consumption may be relevant to the aetiology of colorectal cancer.