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Biomedical subjects

E Negri

Publications and source records attributed to E Negri.

At least 199 records · Page 11Linked to original sources
PubMed1998

Family history of cancer and risk of colorectal cancer in Italy.

Subjects with a family history of colorectal cancer (CRC) are at increased risk of CRC, but quantification of the risk in different populations, the possible differences in risk according to localization of the cancer and the association of family history of other cancers with CRC risk are still open issues. We have therefore analysed data from a multicentric case-control study conducted in six Italian areas between 1992 and 1996 of 1225 incident cases of colon cancer, 728 cases of rectal cancer and 4154 controls admitted for acute conditions to the same network of hospitals as the cases. Unconditional logistic regression models including terms for gender, age, study centre, years of education and number of siblings were used to estimate the odds ratios (ORs) of CRC according to various aspects of history of CRC and other cancers in first-degree relatives. The OR for family history of CRC was 3.2 (95% confidence interval, CI, 2.5-4.1) for colon cancer and 2.2 (95% CI 1.6-3.1) for rectal cancer. Colon cancer was significantly associated with a family history of stomach (OR 1.4), bone (OR 2.1) and kidney (OR 2.3) cancers, while rectal cancer was significantly associated with a family history of lymphomas (OR 2.8). There was a 30% higher risk of colon and rectal cancer in subjects with a family history of any cancer, excluding intestine. The ORs for family history of CRC were 5.2 for colon and 6.3 for rectum when the proband's age was below 45 years. The ORs were similar when the affected relative was a parent or a sibling and in different strata of age of relative(s). For subjects with two or more first-degree relatives with CRC, the risk was 6.9 for the right colon, 5.8 for the transverse and descending colon, 3.8 for the sigma, 3.2 for the rectosigmoid junction and 1.9 for the rectum. This study confirms that a family history of CRC in first-degree relatives increases the risk of both colon and rectal cancer, the association being stronger at younger ages and for right colon.

Adult↗
PubMed1998

Meal frequency and coffee intake in colon cancer.

Several studies suggested that frequent eating may increase colon cancer risk. To further clarify this issue, a case-control study was carried out in six areas of Italy on 1,225 incident cases < 75 years of age with histologically confirmed colon cancer and 4,154 control subjects. The controls were hospitalized for acute, nonneoplastic conditions unrelated to long-term dietary modifications. After allowance for education, physical activity, intake of vegetables, and major energy sources, there was a trend of increasing risk with increasing eating frequency (odds ratio for > or = 4 vs. < or = 2 daily meals = 1.24). Coffee intake, which was inversely associated with cancer risk, exerted a modification effect, with an odds ratio of 1.89 for frequent eaters who drank fewer than two cups of coffee per day. Frequent eating increases, whereas high coffee intake decreases, the excretion of bile acids, which are suspected to be carcinogenic to the colon. Thus, it is conceivable that frequent coffee intake may counterbalance the effect of frequent eating.

Adult↗
PubMed1998

Liver cirrhosis and the risk of primary liver cancer.

The relationship between liver cirrhosis and hepatocellular carcinoma is recognized, but quantification of risk is still uncertain. Therefore, we analysed data from a case-control study conducted in Italy between 1984 and 1997 on 499 cases of incident, histologically confirmed hepatocellular carcinoma and 1,552 controls in hospital with acute, non-neoplastic disease. Overall, 87 (17.4%) cases vs 10 (0.6%) controls reported clinical history of liver cirrhosis. The corresponding odds ratio (OR) was 27.5 (95% confidence interval (CI), 14.3-15.2) after allowance for sociodemographic factors, and 16.2 (95% CI, 7.9-32.9) after simultaneous allowance for all identified confounding factors, including alcohol consumption and clinical history of hepatitis. The association was of similar magnitude for subjects whose cirrhosis was diagnosed < 55 years (OR = 14.8) or at age 55 or over (OR = 20.0), and the multivariate OR was 33.7 < 5 years after diagnosis of cirrhosis, 37.3 between 5 and 9 years, and 7.6 (95% to 2.7-21.3) > or = 10 years since diagnosis of cirrhosis. The association was stronger in males (OR = 23.4) than in females (OR = 5.9), similar in various age groups, and somewhat stronger in more educated subjects (OR = 53.7), with history of hepatitis (OR = 33.1), reporting heavy alcohol consumption (OR = 24.9) or high body mass index (OR = 58.1), although the interaction term was significant only for sex. In terms of population attributable risk, 17% of hepatocellular carcinomas in this population can be attributed to clinical history of liver cirrhosis.

Adult↗
PubMed1998

Diet, alcohol, coffee and pancreatic cancer: final results from an Italian study.

The relation between selected indicator foods, alcohol and coffee intake, and the risk of pancreatic cancer was evaluated in a case-control study conducted between 1983 and 1992 in northern Italy on 362 patients with histologically confirmed, incident cancers of the pancreas, and 1,552 controls in hospital for acute, non-neoplastic diseases. Odds ratios (ORs) for subsequent tertiles of intake were computed after allowance for sociodemographic factors and tobacco smoking. Pancreatic cancer risk was directly associated with consumption of meat (OR for the highest frequency tertile = 1.43), liver (OR = 1.43) and ham and sausages (OR = 1.64), and inversely with consumption of fresh fruit (OR = 0.59), fish (OR = 0.65) and olive oil (OR = 0.58). No appreciable association was found with coffee (OR = 1.21) and alcohol consumption (OR = 1.20). A summary score was derived by summing the six related food items; compared to the lowest level, the OR was 2.7 for the highest quintile, and the population attributable risk was 36% (95% confidence interval, 15-57%), indicating the scope of diet for the prevention of this common neoplasm in the Italian population.

Adult↗
PubMed1998

Hormone replacement therapy and risk of colon and rectal cancer.

The hypothesis that sex hormones may influence colorectal cancer risk was formulated in the early 1980s, but epidemiological studies on a relationship between colorectal cancer risk and hormone replacement therapy (HRT) have only accumulated over the last few years. To investigate the relationship between HRT and colon and rectal cancer and the role of other covariates that might modify it, we analyzed combined data from two case-control studies conducted in Italy between 1985 and 1996, including 994 women with incident colon cancer, 542 with rectal cancer, and 3110 controls with acute, non-neoplastic, nondigestive, non-hormone-related disorders. Odds ratios (ORs) and 95% confidence intervals (CIs) were derived from unconditional multiple logistic regression equations including terms for age, center/study period, education, family history of colorectal cancer, status and age at menopause, parity, use of oral contraceptives, total energy intake, and body mass index. Ever use of HRT was inversely associated with cancer of the colon (OR = 0.64, 95% CI = 0.46-0.88) and of the rectum (OR = 0.46, 95% CI = 0.29-0.72). Increasing duration of use of HRT was related to decreasing risk for colon and rectal cancers (P for trend < 0.01). No interaction emerged, and the inverse association persisted across separate strata of other risk factors. This study, one of the largest case-control investigations on exogenous female hormones and colorectal cancer thus far, provides further evidence that women who have ever used HRT are at lower risk of colon and rectal cancer. Because colorectal cancer is the second most common neoplasm and cause of death among nonsmoking women in developed countries, these results may have a major public health impact.

Aged↗
PubMed1998

Trends in cancer mortality in Argentina, 1966-91.

Trends in death certification rates for 12 major cancer sites and total cancer mortality in Argentina were analysed for the period 1966-91 on the basis of the World Health Organization database. In the late 1960s, total cancer mortality rates in Argentina (184/100,000 men, 117/100,000 women, world standard) were among the highest in the world. Over the 25-year period considered, however, cancer mortality in Argentina declined by 15% in both sexes, to reach 157/100,000 in men and 99/100,000 in women, for 1990-91. These rates were somewhat lower than those of North America and, particularly for women, relatively low on a worldwide scale. The favourable trends, observed mostly between the 1960s and the 1980s, reflect the steady decline in gastric cancer rates in both sexes, together with some decline in oesophageal, lung and other tobacco-related neoplasms, mostly in men, following some decline in tobacco consumption over the last two decades. The fall in oesophageal cancer may be related to decreased consumption of hot maté, too. Colorectal cancer rates were high in the 1960s, but declined by 17% in men and 35% in women. An approximately 50% decline was observed for skin cancer mortality, which was among the lowest in the world in the early 1990s, and some decline was observed also for leukaemias and uterine cancer, while breast and prostate neoplasms showed a general stability. The two major unfavourable features of cancer mortality in Argentina were the persistently high rates for oesophageal in men, and for uterine cancer mortality in women. These are likely a result of hot maté drinking for oesophageal cancer and inadequate screening for cervical cancer.

Age Distribution↗
PubMed1998

Oral contraceptive use and risk of colorectal cancer.

To evaluate the relation between oral contraceptives and colon and rectal cancer, we analyzed combined data from two case-control studies conducted in six Italian regions between 1985 and 1996. The studies included 803 women with incident colon cancer, 429 with rectal cancer, and 2,793 controls with acute, nonneoplastic, nondigestive, non-hormone-related disorders. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) from unconditional multiple logistic regression equations, including terms for age, center/study period, education, family history of colorectal cancer, menopausal status, age at menopause, parity, use of hormone replacement therapy, body mass index [weight (kg) per height squared (m2)], and total energy intake. Ever-use of oral contraceptives was inversely associated with colon cancer (OR = 0.63; 95% CI = 0.45-0.87) and rectal cancer (OR = 0.66; 95% CI = 0.43-1.01). Duration of use of oral contraceptives was inversely related to risk of colon but not rectal cancer. This study suggests that women who have ever used oral contraceptives are at lower risk of colon and rectal cancer.

Adult↗
PubMed1998

Role of different types of vegetables and fruit in the prevention of cancer of the colon, rectum, and breast.

We compared the effect of 26 types or groups of vegetables and fruit on the risk of cancer using data from two case-control studies that included 1,225 cases of cancer of the colon, 728 cases of cancer of the rectum, 2,569 cases of cancer of the breast, and 5,155 hospital controls interviewed between 1991 and 1996 in six Italian areas. Most vegetables were inversely associated with cancer of the colon and rectum, whereas only carrots and raw vegetables lowered breast cancer risk. High fruit intake was associated only with a reduction of rectal cancer. Different contents of sugar, fiber, carotenoids, and folic acid in fruits vs vegetables plus the concurrent consumption of oil with vegetables may partly explain these findings.

Breast Neoplasms↗
PubMed1998

Fiber intake and risk of colorectal cancer.

The relationship between various types of fiber and colorectal cancer risk was investigated using data from a case-control study conducted between January 1992 and June 1996 in Italy. The study included 1953 cases of incident, histologically confirmed colorectal cancers (1225 colon cancers and 728 rectal cancers) admitted to the major teaching and general hospitals in the study areas and 4154 controls with no history of cancer admitted to hospitals in the same catchment areas for acute nonneoplastic diseases. Dietary habits were investigated using a validated food frequency questionnaire. Odds ratios (ORs) were computed after allowance for age, sex, and other potential confounding factors, including physical activity and protein, fat, and carbohydrate intake. Fiber was analyzed both as a continuous variable and in quintiles. For most types of fiber, the OR of colon and rectal cancers was significantly below 1, and no appreciable differences emerged between the two. When the unit was set at the difference between the upper cutpoints of the fourth and first quintile, i.e., the 80th and 20th percentiles, the ORs for colorectal cancer were 0.68 for total fiber (determined by the Englyst method as nonstarch polysaccharides), 0.67 for soluble noncellulose polysaccharides (NCPs), 0.71 for total insoluble fiber, 0.67 for cellulose, 0.82 for insoluble NCPs, and 0.88 for lignin. When fiber was classified according to the source, the OR was 0.75 for vegetable fiber, 0.85 for fruit fiber, and 1.09 for cereal fiber. The ORs were similar for the two sexes and the strata of age, education, physical activity, family history of colorectal cancer, and energy intake. Likewise, no appreciable differences emerged when subsites of the colon and rectum were investigated separately. This study provides additional support for a protective and independent effect of fiber on colorectal cancer, particularly for cellulose and soluble NCPs, and of fiber of vegetable or fruit origin.

Adult↗
PubMed1998

Impact of inherited polymorphisms in glutathione S-transferase M1, microsomal epoxide hydrolase, cytochrome P450 enzymes on DNA, and blood protein adducts of benzo(a)pyrene-diolepoxide.

The benzo(a)pyrene (BaP) metabolite benzo(a)pyrenediolepoxide (BPDE) is strongly implicated as a causative agent of lung cancer. To assess the risk of exposure to BaP, we made a combined analysis of levels of BPDE adducts to hemoglobin (Hb), serum albumin (SA), and lymphocyte DNA in 44 patients with incident lung cancer, as a prototype of a population mainly exposed to tobacco-derived BaP. We also investigated whether genetic polymorphisms of cytochrome P450IA1 (CYPIA1), microsomal epoxide hydrolase (mEH), and glutathione S-transferase M1 (GSTM1), which are involved in BaP metabolism, can be determinants of adduct formation. BPDE-Hb, BPDE-SA, and BPDE-DNA adducts were quantified as BaP tetrols released from hydrolysis of macromolecules and measured by high-resolution gas chromatography-negative ion chemical ionization-mass spectrometry to achieve high specificity and sensitivity. Individuals with detectable Hb adducts were positive for SA adducts but not vice versa, suggesting that BPDE-Hb adducts are less informative indicators of BaP exposure. Using PCR methods on DNA, we characterized GSTM1 deletion, CYPIA1 MspI and exon 7 valine variants, and mEH polymorphisms at amino acid positions 113 (EH3) and 139 (EH4). Levels of BPDE adducts were no different among CYPIA1, mEH, and GSTM1 genotypes. However, individuals with measurable BPDE-SA adducts were CYPIA1 variant carriers more frequently (P = 0.03). There was a slightly higher percentage of DNA detectable adducts in subjects with CYPIA1 exon 7 valine polymorphism. When subjects were classified by both polymorphisms on the mEH gene, those with two slow alleles (EH3 homozygous mutated) and no fast alleles (EH4 homozygous wild type) had a lower frequency of BPDE-SA adducts and no DNA adducts (P = 0.06). These results are based on a small number of observations thus far, but this exploratory study suggests that CYPIA1 and mEH variants might have an impact on BPDE exposure markers such as BPDE-SA adducts. Chemical specificity in adduct measurements is important to identify the biomarkers that reflect BaP exposure more accurately.

Aged↗
PubMed1997

Intake of selected micronutrients and risk of colorectal cancer.

The relationship between various micronutrients and colorectal cancer risk was investigated using data from a case-control study conducted between January 1992 and June 1996 in Italy. Cases were 1,953 incident, histologically confirmed colorectal cancers (1,225 of the colon and 728 of the rectum), admitted to the major teaching and general hospitals in the study areas, and 4,154 controls with no history of cancer, admitted to hospitals in the same catchment areas for acute, non-neoplastic diseases unrelated to the digestive tract and requiring no long-term modifications of the diet. Dietary habits were investigated using a validated food-frequency questionnaire. Odds ratio (ORs) were computed after allowance for age, sex and other potential confounding factors, including physical activity, total energy and fibre intake. For most micronutrients, ORs were below unity with increasing quintile of intake. The most consistent protective effects were for carotene, riboflavin and vitamin C (Multivariate ORs from the continuous model, with unit set as the difference between the upper cut-point of the 4th quintile and that of the 1st one, were 0.65, 0.73 and 0.80, respectively). Inverse relationships were observed also for calcium and vitamin D (ORs of 0.85 and 0.93, respectively). When the combined effect of calcium and vitamin D and selected anti-oxidants was considered, the OR reached 0.46 in subjects reporting high calcium/vitamin D and high anti-oxidant intake compared to those reporting low intake of both groups of micronutrients. Most results were apparently stronger for colon cancer and among females. Our results provide further support for a protective effect of several micronutrients on colorectal cancer risk and some indications for a specific and stronger effect of selected anti-oxidants.

Adult↗
PubMed1997

Coffee and tea intake and risk of cancers of the colon and rectum: a study of 3,530 cases and 7,057 controls.

The relationship between coffee, decaffeinated coffee and tea intake and risk of cancers of the colon and rectum was considered combining data from 2 case-control studies, one conducted between 1985 and 1991 in Northern Italy and the other between 1991 and 1996 in 6 Italian centers. Cases were patients below age 80, with histologically confirmed cancer of the colon (n = 2,166) or rectum (n = 1,364), and controls were 7,057 patients admitted to hospital for a wide spectrum of acute, non-neoplastic, non-digestive tract diseases. Compared with coffee non-drinkers, the risk of colon cancer was reduced in drinkers of 4 or more cups/day [multivariate odds ratios (ORs) 0.73; 95% confidence intervals 0.60-0.89), with a significant trend in risk with dose; no significant association emerged between coffee drinking and risk of rectal cancer (OR 1.00 for drinkers of 4 or more cups/day). Decaffeinated coffee was consumed in small amounts by about 4% of cases and controls and the OR was 0.92 for colon and 0.88 for rectal cancers. Tea consumption was generally limited to 1 cup/day or to occasional intake and did not substantially modify the risk of colon and rectal cancers. No significant heterogeneity was found for the inverse relationship between coffee intake and colon cancer risk across strata of age at diagnosis, sex, smoking status, total alcohol and meat and vegetable intake, while the protection of coffee was stronger in people eating 3 or more meals/day. Thus, our results confirm that coffee intake has a quantifiable protective effect on colon cancer risk.

Adult↗
PubMed1997

Diabetes mellitus and the risk of primary liver cancer.

The relationship between diabetes mellitus and primary liver cancer was investigated in a case-control study conducted in Italy between 1984 and 1996 on 428 cases with incident, histologically confirmed hepatocellular carcinoma, 59 with gallbladder and bile duct cancer, and 1,502 control subjects in the hospital for acute non-neoplastic diseases. Sixty-four cases of hepatocellular carcinoma vs. 87 controls reported a history of diabetes, corresponding to an odds ratio (OR) of 2.3 after allowance for age, sex and area of residence, and of 2.1 [95% confidence interval (CI) = 1.4-3.2] after further allowance for alcohol and tobacco consumption, history of hepatitis and liver cirrhosis, body mass index and history of liver cancer in first-degree relatives. The ORs were similar both for subjects diagnosed with diabetes below age 45, who most likely had insulin-dependent diabetes, and for those diagnosed later, who were likelier to have non-insulin-dependent diabetes. The OR was 2.3 for subjects whose diabetes was diagnosed <5 years before diagnosis of liver cancer, 1.9 for those diagnosed 5-9 years in advance and 2.2 for those diagnosed since 10 years or more. Five cases of gallbladder and bile duct cancer reported a history of diabetes: the corresponding OR was 1.2 (95% CI 0.5-2.9). The OR of hepatocellular carcinoma was 2.4 for males and 2.0 for females, 3.0 for subjects diagnosed with liver cancer under age 60 and 1.8 for those diagnosed at age 60 or over. None of the other covariates considered, including education, history of hepatitis, liver cirrhosis and alcohol drinking showed any meaningful modifying effect or interaction. The potential pathogenic mechanisms include liver alteration-and consequent cell proliferation-in subjects with diabetes. Thus a history of diabetes mellitus could explain about 8% (95% CI 5-11) of cases of liver cancer in this population.

Adult↗
PubMed1997

Family history of cancer and risk of breast cancer.

The relationship between breast cancer risk and family history of cancer in first-degree relatives was investigated using data from a multicentric case-control study conducted in Italy between June 1991 and April 1994 on 2,569 women aged less than 75 years, with histologically confirmed incident breast cancer, and 2,588 control women admitted to hospital for acute, non-neoplastic, non-gynaecological conditions. Relative to women with no history, those with a family history of breast cancer had an odds ratio (OR) of 2.4 [95% confidence interval (CI) 1.9-3.0], and those with family history of intestinal cancer had an OR of 1.3 (95% CI 1.0-1.7). No significant relations emerged between breast cancer risk and family history of prostate (OR 1.1), ovarian (OR 1.3), cervical or endometrial (OR 1.2) or other cancers, except gallbladder (OR 8.6). The OR for family history of any type of cancer except breast cancer was 1.1. For family history of breast cancer the ORs were similar across strata of age of the proband, being 2.4 below age 45, 2.2 at age 45-59 and 2.7 above age 60, and whether the relative affected was the mother, sister(s) or both, while the risk appeared higher if the age at onset of breast cancer in the relative was lower than 40 years (OR 3.5), rather than higher (OR 2.2). Thus, our results, based on the investigation of all neoplasms in first-degree relatives, confirm that breast cancer risk is increased in women with a family history of breast cancer, while there was no material association with family history of cancer in general, excluding breast cancer.

Adult↗
PubMed1997

Frequency of family history of acute myocardial infarction in patients with acute myocardial infarction. Argentine FRICAS (Factores de Riesgo Coronario en America del Sur) Investigators.

The relation between family history of acute myocardial infarction (AMI) and the risk of AMI was analyzed using data of a case-control study conducted in Argentina between 1992 and 1994. Case patients were 1,060 subjects with AMI admitted to 35 coronary care units, and controls were 1,071 subjects admitted to the same network of hospitals where cases had been identified, for a wide spectrum of acute conditions unrelated to known or likely risk factors for AMI: 31% of cases versus 15% of controls reported > or = 1 first-degree relative with history of AMI. Compared with subjects without family history of AMI, the odds ratio (OR) of AMI, after allowance for age, sex, cholesterolemia, smoking, diabetes, hypertension, body mass index, education, social class, and physical exercise, was 2.18 (95% confidence interval [CI] 1.74 to 2.74) for those with family history of AMI. The OR was 2.04 (95% CI 1.60 to 2.60) for subjects with 1 relative, and 3.18 (95% C 1.86 to 5.44) for those reporting > or = 2 relatives with AMI. In women the OR for any family history of AMI was 2.83, and in men 2.01. The association was of similar magnitude if the mother (OR 1.98), the father (OR 2.13), or a sibling (OR 2.48) had had an AMI. The association with family history was stronger at a younger age because the OR for subjects reporting > or = 2 more relatives with a history of AMI was 4.42 for subjects aged < 55 years, and 3.00 for those aged > or = 55 years. The association between AMI and family history of AMI was consistent across separate strata of education, social class, smoking, and serum cholesterol, but was less strong in subjects with history of diabetes and hypertension. When the interaction of known risk factors with family history of AMI was analyzed, hypercholesterolemia, hypertension, and smoking had approximately multiplicative effects on the relative risk. The OR was 4.50 for subjects with family history and cholesterol > or = 240 ml/dl, 4.52 for those with hypertension, and 5.77 for current smokers with family history of AMI. Thus, this study confirms that a family history of AMI is a strong and independent risk factor for AMI. In this population from Argentina, family history accounted for 14% of all cases of AMI in men and 26% in women.

Adult↗
PubMed1997

Case-control study of oestrogen replacement therapy and risk of cervical cancer.

OBJECTIVE: To examine the relation between use of oestrogen replacement therapy and risk of cervical cancer. DESIGN: Case-control study. SETTING: Northern Italy. SUBJECTS: 645 women aged 40-75 years with cervical cancer admitted between 1981 and 1993 to university and general hospitals. The control group consisted of 749 women aged 40-75 years admitted to the same hospitals with acute conditions judged to be unrelated to any of the known or suspected risk factors for cervical cancer. MAIN OUTCOME MEASURES: Use of oestrogen replacement therapy and risk of cervical cancer. RESULTS: 40 cases versus 86 controls had ever used oestrogens, and the corresponding multivariate odds ratio was 0.5 (95% confidence interval 0.3 to 0.8). The odds ratios of cervical cancer decreased with duration of use, being 0.6 (0.4 to 1.1) for less than 12 months' use and 0.5 (0.2 to 1.0) for use for 12 months or more compared with never users. The protection tended to be somewhat stronger for women reporting first oestrogen use before age 50. The odds ratio was 0.9 (0.5 to 1.7) for women who had taken oestrogens within the past 10 years and 0.4 (0.2 to 0.7) for those who had taken them 10 or more years ago. CONCLUSION: These findings suggest that exogenous oestrogens do not increase the risk of cervical cancer and may decrease the risk.

Adenocarcinoma↗
PubMed1997

Food groups and risk of colorectal cancer in Italy.

The proportion of colorectal cancer attributed to dietary habits is high, but several inconsistencies remain, especially with respect to the influence of some food groups. To further elucidate the role of dietary habits, 1,225 subjects with cancer of the colon, 728 with cancer of the rectum and 4,154 controls, hospitalized with acute non-neoplastic diseases, were interviewed between 1992 and 1996 in 6 different Italian areas. The validated food-frequency questionnaire included 79 questions on food items and recipes, categorised into 16 food groups. After allowance for non-dietary confounding factors and total energy intake, significant trends of increasing risk of colorectal cancer with increasing intake emerged for bread and cereal dishes (odds ratio [OR] in highest vs. lowest quintile = 1.7), potatoes (OR = 1.2), cakes and desserts (OR = 1.1), and refined sugar (OR = 1.4). Intakes of fish (OR = 0.7), raw and cooked vegetables (OR = 0.6 for both) and fruit other than citrus fruit (OR = 0.7) showed a negative association with risk. Consumption of eggs and meat (white, red or processed meats) seemed uninfluential. Most findings were similar for colon and rectum, but some negative associations (i.e., coffee and tea, and fish) appeared stronger for colon cancer. Our findings lead us to reconsider the role of starchy foods and refined sugar in light of recent knowledge on the digestive physiology of carbohydrates and the insulin/colon cancer hypothesis. The beneficial role of most vegetables is confirmed, with more than 20% reduction in risk of colorectal cancer from the addition of one daily serving.

Adult↗