Attributable risk for diet, alcohol, and family history in the Melbourne colorectal cancer study

Kune, Gabriel A.; Bannerman, Susan; Watson, Lyndsey F.

doi:10.1080/01635589209514223

Cited by 33 publications

(9 citation statements)

References 15 publications

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“…As such, the role of diet as a contributing factor in colorectal cancer (CRC) development has been examined in hundreds of scientific studies. Some researchers have speculated that in western cultures, dietary factors may contribute to up to 50% of new CRC cases (Kune et al, 1992;Willett, 2001); however, there is controversy regarding the specific nutrients, individual foods, or food combinations thought to contribute to CRC. A prominent source of this controversy has been variability in the results of epidemiologic studies examining CRC and a variety of 'exposures', including dietary patterns, broad food groups, individual food items, and micronutrients.…”

Section: Introductionmentioning

confidence: 99%

Meta-analysis of prospective studies of red meat consumption and colorectal cancer

Alexander

Weed²,

Cushing³

et al. 2011

European Journal of Cancer Prevention

121

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The relationship between red meat consumption and colorectal cancer (CRC) has been the subject of scientific debate. To estimate the summary association between red meat intake and CRC and to examine sources of heterogeneity, a meta-analysis of prospective studies was conducted. Thirty-four prospective studies of red meat and CRC were identified, of which 25 represented independent nonoverlapping study populations. Summary relative risk estimates (SRREs) for high versus low intake and dose-response relationships were calculated. In the high versus low intake meta-analysis, the SRRE was 1.12 (95% CI: 1.04-1.21) with significant heterogeneity (P=0.014). Summary associations were modified by tumor site and sex. The SRREs for colon cancer and rectal cancer were 1.11 (95% CI: 1.03-1.19) and 1.19 (95% CI: 0.97-1.46), respectively. The SRREs among men and women were 1.21 (95% CI: 1.04-1.42) and 1.01 (95% CI: 0.87-1.17), respectively. The available epidemiologic data are not sufficient to support an independent and unequivocal positive association between red meat intake and CRC. This conclusion is based on summary associations that are weak in magnitude, heterogeneity across studies, inconsistent patterns of associations across the subgroup analyses, and the likely influence of confounding by other dietary and lifestyle factors.

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Section: Introductionmentioning

confidence: 99%

Meta-analysis of prospective studies of red meat consumption and colorectal cancer

Alexander

Weed²,

Cushing³

et al. 2011

European Journal of Cancer Prevention

121

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show abstract

“…It was estimated that dietary factors may contribute to more than 50% of all colorectal cases in Western cultures (Kune et al, 1992;Willett, 2001). However, if this estimate is accurate, evidence for specific dietary nutrients or contaminants, individual foods, or food combinations has not been elucidated.…”

Section: Introductionmentioning

confidence: 99%

Processed meat and colorectal cancer: a quantitative review of prospective epidemiologic studies

Alexander

Miller

Cushing

et al. 2010

European Journal of Cancer Prevention

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A tremendous amount of scientific interest has been generated regarding processed meat consumption and cancer risk. Therefore, to estimate the association between processed meat intake and colorectal cancer (CRC), a meta-analysis of prospective studies was conducted. Twenty-eight prospective studies of processed meat and CRC were identified, of which 20 represented independent nonoverlapping study populations. Summary relative risk estimates (SRREs) for high versus low intake and dose-response relationships were calculated. The SRRE for high (vs. low) processed meat intake and CRC was 1.16 [95% confidence interval (CI): 1.10-1.23] for all studies. Summary associations were modified considerably by sex; the SRRE for men was 1.23 (95% CI: 1.07-1.42) and the SRRE for women was 1.05 (95% CI: 0.94-1.16), based on nine and 13 studies, respectively. Sensitivity analyses did not indicate appreciable statistical variation by tumor site, processed meat groups, or study location. The SRRE for each 30-gram increment of processed meat and CRC was 1.10 (95% CI: 1.05-1.15) based on nine studies, and the SRRE for each incremental serving of processed meat per week was 1.03 (95% CI: 1.01-1.05) based on six studies. Overall, summary associations were weak in magnitude (i.e. most less than 1.20), processed meat definitions and analytical comparisons were highly variable across studies, and isolating the independent effects of processed meat intake is difficult, given the likely influence of confounding by other dietary and lifestyle factors. Therefore, the currently available epidemiologic evidence is not sufficient to support a clear and unequivocal independent positive association between processed meat consumption and CRC.

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“…Multiple factors, such as high consumption of red meats and insufficient intake of fibers and folate, are associated with the etiology of CRC. Alcohol consumption is also recognized as one of the major risk factors for CRC development [14,15,16]. According to the data from the Korean Multi-Center Cancer Cohort study, longer duration and higher average amount of alcohol consumption account for elevated risk of CRC in men (HR 1.93 [1.17–3.18] for ≥30 years of consumption compared to non-drinkers; HR 2.24 [1.31–3.84] for ≥30 g/day) [17].…”

Section: Introductionmentioning

confidence: 99%

Molecular Basis of Alcohol-Related Gastric and Colon Cancer

Lee

2017

IJMS

117

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Many meta-analysis, large cohort studies, and experimental studies suggest that chronic alcohol consumption increases the risk of gastric and colon cancer. Ethanol is metabolized by alcohol dehydrogenases (ADH), catalase or cytochrome P450 2E1 (CYP2E1) to acetaldehyde, which is then further oxidized to acetate by aldehyde dehydrogenase (ALDH). Acetaldehyde has been classified by the International Agency for Research on Cancer (IARC) as a Group 1 carcinogen to humans. The acetaldehyde level in the stomach and colon is locally influenced by gastric colonization by Helicobacter pylori or colonic microbes, as well as polymorphisms in the genes encoding tissue alcohol metabolizing enzymes, especially ALDH2. Alcohol stimulates the uptake of carcinogens and their metabolism and also changes the composition of enteric microbes in a way to enhance the aldehyde level. Alcohol also undergoes chemical coupling to membrane phospholipids and disrupts organization of tight junctions, leading to nuclear translocation of β-catenin and ZONAB, which may contributes to regulation of genes involved in proliferation, invasion and metastasis. Alcohol also generates reactive oxygen species (ROS) by suppressing the expression of antioxidant and cytoprotective enzymes and inducing expression of CYP2E1 which contribute to the metabolic activation of chemical carcinogens. Besides exerting genotoxic effects by directly damaging DNA, ROS can activates signaling molecules involved in inflammation, metastasis and angiogenesis. In addition, alcohol consumption induces folate deficiency, which may result in aberrant DNA methylation profiles, thereby influencing cancer-related gene expression.

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Attributable risk for diet, alcohol, and family history in the Melbourne colorectal cancer study

Cited by 33 publications

References 15 publications

Meta-analysis of prospective studies of red meat consumption and colorectal cancer

Meta-analysis of prospective studies of red meat consumption and colorectal cancer

Processed meat and colorectal cancer: a quantitative review of prospective epidemiologic studies

Molecular Basis of Alcohol-Related Gastric and Colon Cancer

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