Diet is regarded as one of the most important environmental factors associated with colorectal cancer (CRC) risk. A recent report comprehensively concluded that total energy intake does not have a simple relationship with CRC risk, and that the data were inconsistent for carbohydrate, cholesterol and protein. The objective of this study was to identify the associations of CRC risk with dietary intakes of total energy, protein, fat, carbohydrate, fiber, and alcohol using data from a large case-control study conducted in Newfoundland and Labrador (NL) and Ontario (ON), Canada.
Incident colorectal cancer cases (n = 1760) were identified from population-based cancer registries in the provinces of ON (1997-2000) and NL (1999-2003). Controls (n = 2481) were a random sample of residents in each province, aged 20-74 years. Family history questionnaire (FHQ), personal history questionnaire (PHQ), and food frequency questionnaire (FFQ) were used to collect study data. Logistic regression was used to evaluate the association of intakes of total energy, macronutrients and alcohol with CRC risk.
Total energy intake was associated with higher risk of CRC (OR: 1.56; 95% CI: 1.21-2.01, p-trend = 0.02, 5th versus 1st quintile), whereas inverse associations emerged for intakes of protein (OR: 0.85, 95%CI: 0.69-1.00, p-trend = 0.06, 5th versus 1st quintile), carbohydrate (OR: 0.81, 95%CI: 0.63-1.00, p-trend = 0.05, 5th versus 1st quintile) and total dietary fiber (OR: 0.84, 95% CI:0.67-0.99, p-trend = 0.04, 5th versus 1st quintile). Total fat, alcohol, saturated fatty acids, monounsaturated fatty acids, polyunsaturated fatty acids, and cholesterol were not associated with CRC risk.
This study provides further evidence that high energy intake may increase risk of incident CRC, whereas diets high in protein, fiber, and carbohydrate may reduce the risk of the disease.
Previous epidemiological studies have been suggestive but inconclusive in demonstrating inverse associations of calcium, vitamin D, dairy product intakes with risk of colorectal cancer (CRC). We conducted a large population-based comparison of such associations in Newfoundland and Labrador (NL) and Ontario (ON).
A case control study design was used. Colorectal cancer cases were new CRC patients aged 20-74 years. Controls were a sex and age-group matched random sample of the population in each province. 1760 cases and 2481 controls from NL and ON were analyzed. Information on dietary intake and lifestyle was collected using self-administered food frequency and personal history questionnaires.
Controls reported higher mean daily intakes of total calcium and total vitamin D than cases in both provinces. In ON, significant reduced CRC risk was associated with intakes of total calcium (OR of highest vs. lowest quintiles was 0.57, 95% CI 0.42-0.77, p(trend) = 0.03), total vitamin D (OR = 0.73, 95% CI 0.54-1.00), dietary calcium (OR = 0.76, 95% CI 0.60-0.97), dietary vitamin D (OR = 0.77, 95% CI 0.61-0.99), total dairy products and milk (OR = 0.78, 95% CI 0.60-1.00), calcium-containing supplements use (OR = 0.76). In NL, the inverse associations of calcium, vitamin D with CRC risk were most pronounced among calcium- or vitamin D-containing supplement users (OR = 0.67, 0.68, respectively).
Results of this study add to the evidence that total calcium, dietary calcium, total vitamin D, dietary vitamin D, calcium- or vitamin D-containing supplement use may reduce the risk of CRC. The inverse associations of CRC risk with intakes of total dairy products and milk may be largely due to calcium and vitamin D.
Few studies have investigated associations between nonoccupational exposure to ambient volatile organic compounds and lung cancer. We conducted a case-control study of 445 incident lung cancers and 948 controls (523 hospital, 425 general population) in Toronto, Ontario, Canada, between 1997 and 2002. Participants provided information on several risk factors, including tobacco use, secondhand exposure to cigarette smoke, obesity, and family history of cancer. Exposure to benzene, hydrocarbons, and nitrogen dioxide was estimated using land-use regression models. Exposures were linked to residential addresses to estimate exposure at the time of interview, 10 years before interview, and across past residences (time-weighted average). Logistic regression was used to estimate adjusted odds ratios. Analyses involving the population-based controls found that an interquartile-range increase in the time-weighted average benzene concentration (0.15 µg/m(3)) across previous residences was associated with lung cancer (odds ratio = 1.84, 95% confidence interval: 1.26, 2.68). Similarly, an interquartile-range increase in the time-weighted average nitrogen dioxide concentration (4.8 ppb) yielded an odds ratio of 1.59 (95% confidence interval: 1.19, 2.12). Our study suggests that long-term exposure to ambient volatile organic compounds and nitrogen dioxide at relatively low concentrations is associated with lung cancer. Further work is needed to evaluate joint relationships between these pollutants, smoking, and lung cancer.
Comment In: Am J Epidemiol. 2014 Feb 15;179(4):455-624287469
Comment In: Am J Epidemiol. 2014 Feb 15;179(4):452-424287471
To evaluate the influence of dietary fibre on menarche in a cohort of pre-menarcheal girls.
Prospective cohort study.
Free-living pre-menarcheal girls (n = 637), 6 to 14 years of age.
Information on dietary intake, physical activity and date of menarche was collected at baseline and was updated annually by self-administered questionnaires for three years. Cox proportional hazards models were used to evaluate the association between dietary fibre and menarche, adjusting for age at entry to the study and potential confounders.
A higher intake of energy-adjusted dietary fibre was associated with a lower risk of (i.e. a later age at) menarche (relative hazard 0.54, 95% confidence interval (CI) 0.31-0.94 for highest vs. lowest quartile, P for trend = 0.027). At the fibre component level, a higher intake of energy-adjusted cellulose was associated with a lower risk of menarche (relative hazard 0.45, 95% CI 0.26-0.76, P for trend = 0.009).
The findings are consistent with the hypothesis that pre-menarcheal dietary intake can influence menarche.
Lynch syndrome is a cancer predisposition syndrome which includes colon cancer. It is caused by inherited defects in DNA mismatch repair genes. Sporadic colon cancers are influenced by exogenous hormones (e.g., postmenopausal hormones); we hypothesized that polymorphisms which influence endogenous hormones would therefore modify age at colon cancer onset among Lynch syndrome mutation carriers.
We genotyped 146 Caucasian Lynch syndrome mutation carriers for a 5'-untranslated region polymorphism in cytochrome P450 17A1 (CYP17; c.-34T-->C) and an exon 4 polymorphism in catechol O-methyltransferase (COMT; c.472G-->A); 50 mutation carriers had developed colon or rectal cancer at last contact. We used chi(2) tests to assess differences in counts. Kaplan-Meier survival curves and Cox proportional hazard models assessed age at onset of colorectal cancer stratified by CYP17 and COMT genotypes.
Homozygous carriers of the CYP17 C allele were diagnosed with colorectal cancer 18 years earlier than homozygous carriers of the T allele. Hazard ratios identified that, relative to homozygous carriers of the T allele (T/T), carriers of one copy (T/C) and two copies (C/C) of the rare allele were, respectively, at 1.9-fold and 2.9-fold increased the risk of colon cancer at any age. The COMT rare allele suggested a nonstatistically significant trend of decreased colon cancer risk.
This study showed that a polymorphism in CYP17 (c.-34T-->C) modifies age at onset of Lynch syndrome. Because of the high risk of colorectal cancer among this group, knowledge of the CYP17 genotype is warranted for genetic counseling and risk assessment. Future work should assess polymorphisms associated with steroid hormones in Lynch syndrome mutation carriers.
Several N-nitroso compounds (NOC) have been shown to be carcinogenic in a variety of laboratory animals, but evidence of their carcinogenicity in humans is lacking. We aimed to examine the association between NOC intake and colorectal cancer (CRC) risk and possible effect modification by vitamins C and E and protein in a large case-control study carried out in Newfoundland and Labrador and Ontario, Canada. A total of 1760 case patients with pathologically confirmed adenocarcinoma and 2481 population controls were asked to complete a self-administered FFQ to evaluate their dietary intakes 1 year before diagnosis (for cases) or interview (for controls). Adjusted OR and 95 % CI were calculated across the quintiles of NOC (measured by N-nitrosodimethylamine (NDMA)) intake and relevant food items using unconditional logistic regression. NDMA intake was found to be associated with a higher risk of CRC (highest v. lowest quintiles: OR 1·42, 95 % CI 1·03, 1·96; P for trend = 0·005), specifically for rectal carcinoma (OR 1·61, 95 % CI 1·11, 2·35; P for trend = 0·01). CRC risk also increased with the consumption of NDMA-containing meats when the highest tertile was compared with the lowest tertile (OR 1·47, 95 % CI 1·03, 2·10; P for trend = 0·20). There was evidence of effect modification between dietary vitamin E and NDMA. Individuals with high NDMA and low vitamin E intakes had a significantly increased risk than those with both low NDMA and low vitamin E intakes (OR 3·01, 95 % CI 1·43, 6·51; P for interaction = 0·017). The present results support the hypothesis that NOC intake may be positively associated with CRC risk in humans. Vitamin E, which inhibits nitrosation, could modify the effect of NDMA on CRC risk.
The relationship between major dietary patterns and colorectal cancer (CRC) in other populations largely remains consistent across studies. The objective of the present study is to assess if dietary patterns are associated with the risk of CRC in the population of Newfoundland and Labrador (NL).
Data from a population based case-control study in the province of NL were analyzed, including 506 CRC patients (306 men and 200 women) and 673 controls (400 men and 273 women), aged 20-74 years. Dietary habits were assessed by a 169-item food frequency questionnaire (FFQ). Logistic regression analyses were performed to investigate the association between dietary patterns and the CRC risk.
Three major dietary patterns were derived using factor analysis, namely a Meat-diet pattern, a Plant-based diet pattern and a Sugary-diet pattern. In combination the three dietary patterns explained 74% of the total variance in food intake. Results suggest that the Meat-diet and the Sugary-diet increased the risk of CRC with corresponding odds ratios (ORs) of 1.84 (95% CI: 1.19-2.86) and 2.26 (95% CI: 1.39-3.66) for people in the highest intake quintile compared to those in the lowest. Whereas plant-based diet pattern decreases the risk of CRC with a corresponding OR of 0.55 (95% CI: 0.35-0.87). Even though odds ratios (ORs) were not always statistically significant, largely similar associations across three cancer sites were found: the proximal colon, the distal colon, and the rectum.
The finding that Meat-diet/Sugary-diet patterns increased and Plant-based diet pattern decreased the risk of CRC would guide the promotion of healthy eating for primary prevention of CRC in this population.
Data on susceptibility to kidney stone disease are sparse in individuals of nonEuropean ancestry residing in North America. We determined the relative risk of calcium nephrolithiasis among people of different ethnic backgrounds living in the same geographic region.
Using a cross-sectional design 1,128 consecutive patients with idiopathic calcium nephrolithiasis 18 to 50 years old were recruited from a population based Kidney Stone Center in Toronto. Age and gender adjusted odds ratios and 95% confidence intervals were calculated by logistic regression using the 2001 Canada Census population data.
Compared to Europeans the relative risk of calcium nephrolithiasis was significantly higher in individuals of Arabic (OR 3.8, 2.7-5.2), West Indian (OR 2.5, 1.8-3.4), West Asian (OR 2.4, 1.7-3.4) and Latin American (OR 1.7, 1.2-2.4) origin, and significantly lower in those of East Asian (OR 0.4, 0.3-0.5) and African (OR 0.7, 0.5-0.9) background. Several ethnic groups had kidney stone risk factors that were significantly different from those of the European group including higher urinary uric acid, urea excretion and estimated protein intake, and lower urinary citrate, potassium, magnesium and phosphate excretion. However, none was consistent with the variation in relative risk of stone disease overall.
The propensity for the development of calcium nephrolithiasis differed markedly among ethnic groups in North America. While environmental factors could not be completely ruled out, this variability may reflect the influence of genetic susceptibility because there was no dominant environmental factor to account for the differences in relative risk of stone disease.