Use of computerized record linkage in cohort studies.
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Canada↗
Biomedical subjects
G R Howe
Publications and source records attributed to G R Howe.
Some statistical considerations in the analysis of dietary epidemiologic studies.
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Diet↗
Epidemiologic aspects of gallbladder cancer: a case-control study of the SEARCH Program of the International Agency for Research on Cancer.
BACKGROUND: There are few previous epidemiologic studies of gallbladder cancer, a rare but nearly always lethal gastrointestinal cancer with a demonstrated greater frequency in adult women and older subjects of both sexes, and also in the members of populations throughout central and eastern Europe and certain racial groups such as native American Indians. Unfortunately, the prospects for the prevention of this form of cancer are poor. PURPOSE: Our purpose in conducting this study was to investigate possible new risk factors for gallbladder cancer and to strengthen our understanding of established causal agents that may be involved in this disease. METHODS: A large, collaborative, multicenter, case-control study of cancer of the gallbladder was conducted in five centers located in Australia (Adelaide), Canada (Montreal and Toronto), The Netherlands (Utrecht), and Poland (Opole) from January 1983 through July 1988. Case subjects with gallbladder cancer were accrued by the centers from hospital pathology records and from reports to regional cancer registries. Cancer diagnosis was confirmed by either biopsy, cholecystectomy, or at the time of autopsy. Control subjects were randomly assigned at each center from the population. The pooled analysis included 196 case subjects and 1515 control subjects (who did not report previous cholecystectomy). Ninety-eight percent of the subjects were white. Personal interviews of case subjects, control subjects, and surrogates (spouse or next of kin) were conducted by trained personnel. RESULTS: After adjusting for potential confounding factors (age, sex, center, type of interview, years of schooling, alcohol intake, and lifetime cigarette smoking), a history of gallbladder symptoms requiring medical attention (e.g., reduced bile secretion from the gallbladder into the small intestine due to obstructions of the common bile or cystic ducts) was the major risk factor associated with this form of cancer (odds ratio [OR] = 4.4; 95% confidence interval [CI] = 2.6-7.5). This association was present even in subjects who had their first gallbladder examination because of symptoms present more than 20 years earlier (OR = 6.2; 95% CI = 2.8-13.4). Other variables associated with gallbladder cancer risk included an elevated body mass index, high total energy intake, high carbohydrate intake (after adjustment for total energy intake), and chronic diarrhea. All of these risk factors have been previously associated with gallstone disease. CONCLUSIONS: These findings are consistent with a major role of gallstones, or risk factors for gallstones, in the cause of gallbladder cancer. Additional information on whether or not screening high-risk subjects for gallstones or gallbladder cancer is needed.
Adult↗
Family history of prostate cancer: a multi-center case-control study in Canada.
In a population-based case-control study of prostate cancer conducted in Montreal, Toronto and Vancouver between 1989 and 1993, a total of 640 newly incident cases and 639 aged-matched population controls were interviewed as to their family history of prostate cancer as well as nutritional and other lifestyle and environmental factors. In total, 94 cases (15%) reported at least one blood relative with a family history, as compared with 32 (5%) of controls, giving a relative risk of 3.32 (95% confidence interval 2.18-5.05). The association was very consistent across all 3 centers, and was similar for each specific type of relative considered (fathers or brothers). Thus, this study provides further evidence of familial aggregation of prostate cancer, and suggests the possibility that part or all of such clustering could be related to inherited genetic patterns; if so, the availability of screening procedures for the disease offers the possibility of useful early intervention in individuals with such inherited susceptibility.
Aged↗
Non-dietary factors as risk factors for breast cancer, and as effect modifiers of the association of fat intake and risk of breast cancer.
To assess more precisely the relative risks associated with established risk factors for breast cancer, and whether the association between dietary fat and breast cancer risk varies according to levels of these risk factors, we pooled primary data from six prospective studies in North America and Western Europe in which individual estimates of dietary fat intake had been obtained by validated food-frequency questionnaires. Based on information from 322,647 women among whom 4,827 cases occurred during follow-up: the multivariate-adjusted risk of late menarche (age 15 years or more compared with under 12) was 0.72 (95 percent confidence interval [CI] = 0.62-0.82); of being postmenopausal was 0.82 (CI = 0.69-0.97); of high parity (three or more births compared with none) was 0.72 (CI = 0.61-0.86); of late age at first birth (over 30 years of age compared with 20 or under) was 1.46 (CI = 1.22-1.75); of benign breast disease was 1.53 (CI = 1.41-1.65); of maternal history of breast cancer was 1.38 (CI = 1.14-1.67); and history of a sister with breast cancer was 1.47 (CI = 1.27-1.70). Greater duration of schooling (more than high-school graduation compared with less than high-school graduation) was associated significantly with higher risk in age-adjusted analyses, but was attenuated after controlling for other risk factors. Total fat intake (adjusted for energy consumption) was not associated significantly with breast cancer risk in any strata of these non-dietary risk factors. We observed a marginally significant interaction between total fat intake and risk of breast cancer according to history of benign breast disease; with fat intake being associated nonsignificantly positively with risk among women with a previous history of benign breast disease; no other significant interactions were observed. Risks for reproductive factors were similar to those observed in case-control studies; relative risks for family history of breast cancer were lower. We found no clear evidence in any subgroups of a major relation between total energy-adjusted fat intake and breast cancer risk.
Breast Neoplasms↗
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 intake of dietary fat upon colorectal cancer risk in a combined analysis of data from 13 case-control studies previously conducted in populations with differing colorectal cancer rates and dietary practices. Original data records for 5,287 cases of colorectal cancer and 10,470 controls were combined. 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 13 studies. However, there was little, if any, evidence of any energy-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 (P trend = 0.39). The analysis suggests that, among these case-control studies, there is no energy-independent association between dietary fat intake and risk of colorectal cancer. It also suggests that simple substitution of fat by other sources of calories is unlikely to reduce meaningfully the risk of colorectal cancer.
Adult↗
Adjustment for total energy intake in epidemiologic studies.
In epidemiologic studies, total energy intake is often related to disease risk because of associations between physical activity or body size and the probability of disease. In theory, differences in disease incidence may also be related to metabolic efficiency and therefore to total energy intake. Because intakes of most specific nutrients, particularly macronutrients, are correlated with total energy intake, they may be noncausally associated with disease as a result of confounding by total energy intake. In addition, extraneous variation in nutrient intake resulting from variation in total energy intake that is unrelated to disease risk may weaken associations. Furthermore, individuals or populations must alter their intake of specific nutrients primarily by altering the composition of their diets rather than by changing their total energy intake, unless physical activity or body weight are changed substantially. Thus, adjustment for total energy intake is usually appropriate in epidemiologic studies to control for confounding, reduce extraneous variation, and predict the effect of dietary interventions. Failure to account for total energy intake can obscure associations between nutrient intakes and disease risk or even reverse the direction of association. Several disease-risk models and formulations of these models are available to account for energy intake in epidemiologic analyses, including adjustment of nutrient intakes for total energy intake by regression analysis and addition of total energy to a model with the nutrient density (nutrient divided by energy).
Coronary Disease↗
Cigarette smoking and risk of prostate cancer: a population-based case-control study in Ontario and British Columbia, Canada.
The relationship between cigarette smoking and risk of prostate cancer was examined in a case-control study conducted in Ontario and British Columbia, Canada. In each centre, cases were men with a histologically confirmed diagnosis of adenocarcinoma of the prostate notified to the provincial cancer registry. In Ontario, controls were selected randomly from assessment lists maintained by the Ontario Ministry of Revenue and were frequency matched to the cases on age. In British Columbia, controls were also frequency matched to the cases on age and were selected randomly from a roster maintained by the Medical Services Plan of British Columbia. The study in Ontario was conducted between April 1990 and April 1992, and that in British Columbia was conducted between January 1989 and December 1991. In all, the study included 408 cases (207 in Ontario and 201 in British Columbia) and 407 controls (207 in Toronto and 200 in British Columbia (one case was unmatched). Overall, there was little variation in risk of prostate cancer with pack-years of cigarette consumption (filter and non-filter cigarettes combined), and there was no evidence for an effect confined to filter or non-filter cigarettes. There was some evidence for a positive association with non-filter cigarettes in British Columbia, but on formal testing for heterogeneity, this finding was not inconsistent with the absence of an association in Ontario. There was also little variation in risk by years since first smoked or (for ex-smokers) by years since quitting. These data provide little support for an association between cigarette smoking and prostate cancer risk.
Adenocarcinoma↗
Differences in risk factors for epithelial ovarian cancer by histologic type. Results of a case-control study.
A case-control study of associations between dietary and reproductive factors and cancer of the ovary was conducted during 1989-1992 in metropolitan Toronto and nearby areas of southern Ontario, Canada. In total, 450 women aged 35-79 years with histologically verified new primary epithelial ovarian cancers were interviewed concerning their reproductive history and dietary practices. Over the same time period, 564 randomly selected population controls, frequency-matched to the cases according to three 15-year age groups, were also interviewed. Continuous unconditional logistic regression methods were used for analysis. It was found that childbearing and use of oral contraceptives were associated with significant decreasing trends in the risk of epithelial ovarian cancer of all principal histologic types except mucinous tumors. For each full-term pregnancy, the odds ratio was 0.76 (95% confidence interval (CI) 0.69-0.85) for nonmucinous tumors and 1.03 (95% CI 0.88-1.21) for mucinous tumors; for each year of oral contraceptive use, the odds ratio was 0.89 (95% CI 0.85-0.93) for nonmucinous tumors and 0.98 (95% CI 0.93-1.04) for mucinous tumors (p = 0.00051 and p = 0.0040, respectively, for the difference in odds ratios between mucinous and nonmucinous tumors). Saturated fat intake also appeared to convey greater increased risk for women with mucinous tumors than for women with neoplasms of other histologic types (p = 0.029). Among women with nonmucinous tumors, increasing trends in risk of invasive serous cancer (p = 0.018), and particularly endometrioid cancer (p = 0.0041), were seen with use of noncontraceptive estrogens. Otherwise, borderline-malignant neoplasms seemed to have a similar spectrum of risk factor associations as invasive cancers. On the basis of this study and a number of others, the authors suggest that mucinous ovarian tumors may be etiologically unrelated to other types of epithelial tumors, and thus should be considered separately in studies of ovarian cancer.
Adult↗
Cigarette smoking and pancreas cancer: a case control study of the search programme of the IARC.
A multi-centre case-control study of pancreas cancer, designed to be population-based, to use a random sample of local populations as controls and to use a common protocol and core questionnaire, was conducted as the first study of the SEARCH programme of the International Agency for Research on Cancer. "Ever-smokers" were found to be at increased risk for pancreas cancer compared with "never-smokers" consistently in all strata of gender, response status and centre. Risk of pancreas cancer was found to increase with increasing lifetime consumption of cigarettes, the relative risk rising to 2.70 (95% C.I. 1.95 to 3.74) in the highest intake category. The overall trend in risk was highly significant and the association was found consistently in each stratum of gender, response status and centre. Fifteen years had to pass from quitting cigarette smoking until the risk fell to a level compatible with that in never-smokers among the heaviest group of smokers; among the 2 lowest tertiles this happened within 5 years. Further, reported smoking habits more than 15 years before diagnosis appeared to have no influence on pancreas-cancer risk, irrespective of amount smoked. The results are consistent with a causal role for cigarette smoking in the aetiology of pancreas cancer and illustrate that ceasing to smoke cigarettes can lead to reductions in the elevated risk of pancreas cancer produced by this habit.
Case-Control Studies↗
Anthropometric and reproductive factors and the risk of pancreatic cancer: a case-control study in Shanghai, China.
To examine the possible role of body size and reproductive factors in pancreatic cancer, data were analyzed from a population-based case-control study conducted in Shanghai, China. Cases (n = 451) were permanent residents of Shanghai, 30-74 years of age, newly diagnosed with pancreatic cancer between October 1, 1990, and June 30, 1993. Deceased cases (19%) were excluded from the study. Controls (n = 1,552) were randomly selected from permanent Shanghai residents and frequency-matched to cases by gender and age. Information on body size and reproductive and other possible risk factors was collected through personal interviews. After adjustment for age, income, smoking and other confounders, a positive dose-response relation between body mass index and risk of pancreatic cancer was observed in both sexes. Among women, the risk of pancreatic cancer was significantly associated with number of pregnancies and live births. Compared with 0-2 pregnancies or live births, the odds ratio (OR) for 8 or more pregnancies was 1.90, while that for 5 or more births was 1.88. A modest elevation in risk, independent of parity, was associated with early age at first birth. Risk increased over 40% among women with a first birth at or before age 19 years relative to those at age 26 years or older. Ever use of oral contraceptives was associated with excess risk, though based on small numbers of users. Our findings suggest that, in Shanghai, obesity, gravidity, parity and perhaps use of oral contraceptives are associated with moderate increases in risk of pancreatic cancer, indicating that hormonal determinants deserve further investigation.
Aged↗
Dietary assessment in epidemiology: comparison on food frequency and a diet history questionnaire with a 7-day food record.
The validity of two types of diet assessment methods, a self-administered food frequency questionnaire and and interviewer-administered detailed diet history, was assessed relative to a 7-day food record on a population- based sample of 95 men and 108 women in Toronto, Canada, between May 1989 and July 1990. Each study subject completed both questionnaire methods, a food frequency questionnaire and an interviewer-administered diet history, as well as a 7-day food record in a crossover design. Data were analyzed for both unadjusted and energy-adjusted nutrients to estimate Pearson's and intraclass correlations and agreement within the categories. Mean values for the intake of most nutrients assessed by the two questionnaire methods were similar. Average, energy-adjusted Pearson's correlation coefficients for men between a food frequency questionnaire and a 7-day food record were 0.55 for macronutrients and 0.48 for micronutrients compared with 0.47 for macro- and 0.48 for micronutrients between an interviewer-administered diet history and a 7-day food record. For women, they were 0.48 for macro- and 0.54 for micronutrients between a food frequency questionnaire and a 7-day food record and 0.46 and 0.49, respectively, between an interviewer-administered diet history and a 7-day food record. The energy-adjusted Pearson correlations were generally higher than were the energy-unadjusted Pearson correlations and the intraclass correlations. The present study suggests that a food frequency questionnaire is comparable with an interviewer-administered diet history as a predictor of nutrients as estimated form a 7-day food record.
Adult↗
Cohort studies of fat intake and the risk of breast cancer--a pooled analysis.
BACKGROUND: Experiments in animals, international correlation comparisons, and case-control studies support an association between dietary fat intake and the incidence of breast cancer. Most cohort studies do not corroborate the association, but they have been criticized for involving small numbers of cases, homogeneous fat intake, and measurement errors in estimates of fat intake. METHODS: We identified seven prospective studies in four countries that met specific criteria and analyzed the primary data in a standardized manner. Pooled estimates of the relation of fat intake to the risk of breast cancer were calculated, and data from study-specific validation studies were used to adjust the results for measurement error. RESULTS: Information about 4980 cases from studies including 337,819 women was available. When women in the highest quintile of energy-adjusted total fat intake were compared with women in the lowest quintile, the multivariate pooled relative risk of breast cancer was 1.05 (95 percent confidence interval, 0.94 to 1.16). Relative risks for saturated, monounsaturated, and polyunsaturated fat and for cholesterol, considered individually, were also close to unity. There was little overall association between the percentage of energy intake from fat and the risk of breast cancer, even among women whose energy intake from fat was less than 20 percent. Correcting for error in the measurement of nutrient intake did not materially alter these findings. CONCLUSIONS: We found no evidence of a positive association between total dietary fat intake and the risk of breast cancer. There was no reduction in risk even among women whose energy intake from fat was less than 20 percent of total energy intake. In the context of the Western lifestyle, lowering the total intake of fat in midlife is unlikely to reduce the risk of breast cancer substantially.
Adult↗
Nutritional factors and prostate cancer: a case-control study of French Canadians in Montreal, Canada.
The relationship between the risk of prostate cancer and dietary intake of energy, fat, vitamin A, and other nutrients was investigated in a case-control study conducted in Montreal (Quebec), Canada. French Canadians aged 35 to 84 years with a recent, histologically confirmed diagnosis of adenocarcinoma of the prostate were identified through the admission offices of five major francophone teaching-hospitals in Montreal from 1989 to 1993. Population-based controls matched for age (+/- five years), language, and place of residence were selected by a modified random-digit dialing method. The study included 232 cases and 231 controls. Information on dietary intake was collected by means of a quantitative dietary history. No association was evident between energy intake and the risk of prostate cancer. In contrast, there was some evidence of an inverse association with intake of total fat, animal fat, monounsaturated fat, and particularly saturated fat (odds ratio = 0.69, 95 percent confidence interval = 0.40-1.18, P = 0.05), while a nonsignificant positive association was found with polyunsaturated fat. In addition, high intake of retinol and vegetable protein (highest cf lowest quartile) was associated with reduced risk, but was not statistically significant. No associations were established between intake of other nutrients and risk. These patterns persisted after adjustment for a number of potential confounding factors.
Adenocarcinoma↗
Nutrition and pancreatic cancer.
Epidemiologic evidence on the relation between nutrition and pancreatic cancer is reviewed. A number of epidemiologic studies of diet and cancer of the pancreas have been reported including descriptive, case-control, and cohort studies. Overall, fairly consistent patterns of positive associations with the intake of meat, carbohydrates, and dietary cholesterol have been observed. Consistent inverse relationships with fruit and vegetable intakes and, in particular, with two markers of such foods, namely fiber and vitamin C, also have been noted. However, the methodologic limitations of these studies, particularly the descriptive and case-control studies, are such that causal inferences regarding these empirical associations currently are not warranted. Future follow-up of existing dietary cohorts should enable more precise assessment of the possible role of diet in the etiology of cancer of the pancreas.
Animals↗
Breast cancer mortality between 1950 and 1987 after exposure to fractionated moderate-dose-rate ionizing radiation in the Canadian fluoroscopy cohort study and a comparison with breast cancer mortality in the atomic bomb survivors study.
The relationship between exposure to low-linear energy transfer ionizing radiation and subsequent breast cancer mortality risk is reported based on a further 7 years of follow-up in the Canadian fluoroscopy study. Amongst 31,917 women first treated for tuberculosis in a Canadian institution between 1930 and 1952, a total of 688 breast cancer deaths were observed between 1950 and 1987. There is a strong linear trend of increasing risk with increasing dose (P < 0.0001), with the excess relative risk per sievert decreasing with age at exposure (P = 0.0003). The excess relative risk is approximately constant between 5 and 39 years after exposure, with a suggestion of a decrease between 40 and 57 years after exposure, though this could be a chance effect (P = 0.22). Combined analyses of the Canadian fluoroscopy data and the data for the atomic bomb survivors with respect to breast cancer mortality are also reported. In general the two studies are reasonably consistent, the only distinct difference being the much greater excess relative risk per sievert amongst women exposed to very high doses in the province of Nova Scotia (P, heterogeneity <0.0001). Based on the combined data sets a simple relative risk (RR) model for the effect of a dose of D sieverts at age A years is developed: RR(D) = 1.0 + 0.52D exp[-0.10(A-15)]. This model fits the combined data well, and is used to predict excess lifetime risks of breast cancer mortality after radiation exposure from routine annual mammography.
Adolescent↗
Risk of lung cancer mortality after exposure to radon decay products in the Beaverlodge cohort based on revised exposure estimates.
Exposures to radon decay products have been re-estimated for 65 men who died of lung cancer between 1950 and 1980, and 126 matched controls selected from the Beaverlodge cohort of 8,487 workers at the Beaverlodge mine in Northern Saskatchewan. The revised exposure estimates were based on a more thorough review of individual employment records for the study subjects than originally conducted, together with historic data from area-specific measurements of exposure rates in the mine. The revised cumulative exposures are approximately 60% higher than the original exposure estimates, which were based on mine-wide averages for those exposures incurred prior to 1967, and which used geometric rather than arithmetic means for area exposure rates. Despite the increase in estimated exposures using the revised estimates, the excess relative risk per 100 working level months has increased from 2.70 to 3.25, most likely due to a substantial reduction in random exposure measurement error. The new data show similar modifying effects of risk by time since exposure and age at risk as other studies of underground miners, but provide no evidence of an inverse exposure-rate effect, in contrast to a strong effect seen in the analyses based on the original exposure estimates.
Case-Control Studies↗
Radiation-related health risks. Future directions for research.
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Financing, Government↗