Lyndsey F. Watson

The relationship between dietary fat intake and risk of colorectal cancer: evidence from the combined analysis of 13 case-control studies

The objective of this study was to examine the effects of the intakeof dietary fat upon colorectal cancer risk in a combined analysis of datafrom 13 case-control studies previously conducted in populations withdiffering colorectal cancer rates and dietary practices. Original datarecords for 5,287 cases of colorectal cancer and 10,470 controls werecombined. Logistic regression analysis was used to estimate odds ratios (OR)for intakes of total energy, total fat and its components, and cholesterol.Positive associations with energy intake were observed for 11 of the 13studies. However, there was little, if any, evidence of anyenergy-independent effect of either total fat with ORs of 1.00, 0.95, 1.01,1.02, and 0.92 for quintiles of residuals of total fat intake (P trend =0.67) or for saturated fat with ORs of 1.00, 1.08, 1.06, 1.21, and 1.06 (Ptrend = 0.39). The analysis suggests that, among these case-control studies,there is no energy-independent association between dietary fat intake andrisk of colorectal cancer. It also suggests that simple substitution of fatby other sources of calories is unlikely to reduce meaningfully the risk ofcolorectal cancer.

Body weight and physical activity as predictors of colorectal cancer risk.

The associations between colorectal cancer and body weight (expressed as body mass index) and between colorectal cancer and physical activity were examined in 715 histologically confirmed cases of colorectal adenocarcinoma and 727 age- and sex-matched controls. The data were obtained from a large, population-based study, The Melbourne Colorectal Cancer Study, which was conducted in Melbourne, Australia. There was a statistically significant increase in the risk of rectal cancer but not of colon cancer in overweight and obese males but not in females. This association for males remained statistically significant after adjustment was made for dietary risk factors previously established for this study (Nutr Cancer 9, 21-42, 1987), with the exception of sodium intake, which produced a downward modification of the relative risk close to unity. The increased risk of rectal cancer in overweight and obese males was modified by beer intake, which was previously found to be a risk for rectal cancer in males in this study. Various levels of physical activity were not statistically significantly associated with the risk of colorectal cancer in either males or females. Also, the colorectal cancer risks associated with the body mass index were not significantly altered by adjustment for the physical activity level.

Diet, alcohol, smoking, serum β‐carotene, and vitamin A in male nonmelanocytic skin cancer patients and controls

A case-control study was conducted in Melbourne, Australia of 88 consecutive males admitted for the surgical removal of a nonmelanocytic skin cancer (histologically confirmed basal cell carcinoma and squamous cell carcinoma) and of 88 male control patients admitted for small elective surgical procedures. In both cases and controls, previous diet, alcohol consumption, and smoking habit were investigated and serum beta-carotene and vitamin A levels were measured. A statistically significant inverse relationship was found between the risk of skin cancer and a high intake of fish (p = 0.05); vegetables in general (p < 0.001); beans, lentils, or peas (p < 0.001), carrots, silverbeet (Swiss chard), or pumpkin (p < 0.001); cruciferous vegetables (cabbage, brussel sprouts, or broccoli) (p < 0.001); and beta-carotene- and vitamin C-containing foods (p = 0.004). Cases had a lower mean serum level of beta-carotene (p < 0.001) and vitamin A (p = 0.02) than controls. The incidence of skin cancer in the study was inversely related to the level of serum beta-carotene (p < 0.0001). The correlation coefficient between dietary beta-carotene/vitamin C and serum beta-carotene was 0.22 (p = 0.04). Smoking and alcohol consumption showed no statistically significant association with the risk of nonmelanocytic skin cancer. The results were similar for both cell types. A high intake of vegetables including cruciferous vegetables, beta-carotene- and vitamin C-containing foods, and fish appears to be protective for nonmelanocytic skin cancer, and this deserves further study, as does the possible etiologic relevance of the low serum levels of beta-carotene and vitamin A.

Colorectal polyps, diet, alcohol, and family history of colorectal cancer: A case‐control study

A case-control study was conducted in Melbourne, Australia. Cases (n = 49) were patients who had one or more histologically confirmed adenomatous polyps larger than 1 cm in diameter previously removed by endoscopy. In both the cases and the community controls (n = 727), previous diet, alcohol consumption, and family history of colorectal cancer in near relatives were investigated. The family history rate of colorectal cancer was similar in the two groups. Those with adenomatous polyps were found to have a low fiber/vegetable intake (p = 0.04); in males, there was a high intake of beef (p = 0.04), milk drinks (p = 0.01), and beer (p = 0.05). This study provides further evidence for the hypothesis that dietary factors and alcohol consumption may play a role in the development of adenomatous colorectal polyps and that these factors are similar to dietary risk factors for colorectal cancer.

Oral and pharyngeal cancer, diet, smoking, alcohol, and serum vitamin A and β-carotene levels: A case-control study in men

A case-control study was conducted in Melbourne, Australia. Forty-one men with histologically confirmed squamous cell oral or pharyngeal cancer were compared with 398 male community controls. A statistically significant increase in risk was found for alcohol (ethanol) consumption and for smoking, and there was a synergistic effect for these two exposures. Statistically significant protection was noted with increasing intake of dietary vitamin C, dietary beta-carotene, fruit, vegetables, and dietary fiber. The mean serum levels of beta-carotene and vitamin A were statistically significantly lower when the cases were compared with another set of 88 male controls of a similar age who were hospitalized for minor surgical operations. This study confirms a causal effect of smoking and alcohol and a protective role for a high dietary intake of fruit, vegetables, cereals, and, particularly, beta-carotene- and vitamin C-containing foods.

Dietary and Alcohol Intake, Smoking Pattern, Occupational Risk, and Family History in Lung Cancer Patients: Results of a Case-Control Study in Males

In a case-control study of 71 consecutive new male cases of lung cancer and 71 male hospital control patients, previous dietary and alcohol intake, smoking pattern, occupation, dust exposure, and family history of lung cancer were investigated. The cases and controls were similar in age, country of origin, area of residence, and marital status. Using a frequency-based assessment of previous dietary intake, broad food groups were similar for cases and controls. Cases had a significantly lower intake of fish than controls did (odds ratio = 0.5, confidence interval = 0.2-1.0, p = 0.05). A protective effect for fish consumption in lung cancer has not been previously reported. The dietary intake of foods containing retinol and beta-carotene and the intake of alcohol were not significantly different between cases and controls. For cases, smoking duration was longer and the time since cessation for exsmokers was shorter, cigarette pack years were longer, and the number of cigarettes smoked per day was greater. The factors of occupation, dust exposure, and family history of cancer (including lung cancer) were similarly distributed between cases and controls.

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

From the data obtained in a large comprehensive population-based case-control study of colorectal cancer (The Melbourne Colorectal Cancer Study), attributable risk was calculated for a family history of colorectal cancer in near relatives for diet (when > or = 5 of the 11 previously determined dietary risk factors were present) and for beer consumption (for rectal cancer only). The attributable risk was 11% in the presence of a family history of colorectal cancer and 46% in the presence of five or more dietary risk factors. The attributable risk for rectal cancer in the presence of beer consumption was 31% in males and 11% in females. These data are relevant in the consideration of primary prevention of colorectal cancer in Australia, but their general application needs to be approached with caution in view of major differences in the genetic background and the dietary practices in various regions of the world and in view of the uncertainty of what is achievable change, especially for dietary practices.

The Nutritional Causes of Large Bowel Cancer

Colorectal cancer is one of the commonest cancers in developed countries and worldwide, there are over 500,000 new cases each year [1] and over 300,000 deaths are directly attributable to this cancer. An understanding of the causes and the possibilities for prevention of this cancer are therefore of global interest and importance. This communication outlines “The Melbourne Colorectal Cancer Study” and the major findings of the study so far, focuses in detail on the nutritional findings of the study and then compares these to an overview of the literature during the previous 25 years, to conclude with our current understanding of the nutritional causes of large bowel cancer.