G R Howe

Honolulu University, Honolulu, Hawaii, United States

Are you G R Howe?

Claim your profile

Publications (90)626.1 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The evidence for a protective effect of vegetables, fruits, and legumes against prostate cancer is weak and inconsistent. We examined the relationship of these food groups and their constituent foods to prostate cancer risk in a multicenter case-control study of African-American, white, Japanese, and Chinese men. Cases (n = 1619) with histologically confirmed prostate cancer were identified through the population-based tumor registries of Hawaii, San Francisco, and Los Angeles in the United States and British Columbia and Ontario in Canada. Controls (n = 1618) were frequency-matched to cases on ethnicity, age, and region of residence of the case, in a ratio of approximately 1:1. Dietary and other information was collected by in-person home interview; a blood sample was obtained from control subjects for prostate-specific antigen determination. Odds ratios (OR) were estimated using logistic regression, adjusting for age, geographic location, education, calories, and when indicated, ethnicity. Intake of legumes (whether total legumes, soyfoods specifically, or other legumes) was inversely related to prostate cancer (OR for highest relative to lowest quintile for total legumes = 0.62; P for trend = 0.0002); results were similar when restricted to prostate-specific antigen-normal controls or to advanced cases. Intakes of yellow-orange and cruciferous vegetables were also inversely related to prostate cancer, especially for advanced cases, among whom the highest quintile OR for yellow-orange vegetables = 0.67 (P for trend = 0.01) and the highest quintile OR for cruciferous vegetables = 0.61 (P for trend = 0.006). Intake of tomatoes and of fruits was not related to risk. Findings were generally consistent across ethnic groups. These results suggest that legumes (not limited to soy products) and certain categories of vegetables may protect against prostate cancer.
    Cancer Epidemiology Biomarkers & Prevention 09/2000; 9(8):795-804. · 4.13 Impact Factor
  • T E Rohan · Jain MG · G R Howe · AB Miller ·
    [Show abstract] [Hide abstract]
    ABSTRACT: To study the association between alcohol consumption and breast cancer risk. A case-cohort analysis was undertaken within the cohort of 56,837 women who were enrolled in the Canadian National Breast Screening Study (NBSS) and who completed a self-administered dietary questionnaire. (The NBSS is a randomized controlled trial of screening for breast cancer in women aged 40-59 at recruitment.) The cohort was recruited between 1980 and 1985, and during follow-up to the end of 1993 a total of 1469 women in the dietary cohort were diagnosed with biopsy-confirmed incident breast cancer. For comparative purposes a subcohort consisting of a random sample of 5681 women was selected from the full dietary cohort. After exclusions for various reasons the analyses were based on 1336 cases and 5238 noncases. When compared to nondrinkers the adjusted incidence rate ratios (95% confidence intervals) for those consuming > 0 and < or = 10 g of alcohol/day, > 10 and < or = 20 g/day, > 20 and < or = 30 g/day, > 30 and < or = 40 g/day, > 40 and < or = 50 g/day, and > 50 g/day were 1.01 (0.84-1.22), 1.16 (0.91-1.47), 1.27 (0.91-1.78), 0.77 (0.51-1.16), 1.00 (0.57-1.75), and 1.70 (0.97-2.98), respectively; the associated p value for the test for trend was 0.351. Similar findings were obtained when analyses were conducted separately in the screened and control arms of the NBSS, in premenopausal and postmenopausal women, for screen-detected and interval-detected breast cancer, and by levels of other breast cancer risk factors. The results of this study suggest that alcohol consumption might be associated with increased risk of breast cancer at relatively high levels of intake.
    Cancer Causes and Control 04/2000; 11(3):239-47. DOI:10.1023/A:1008933824645 · 2.74 Impact Factor
  • Source
    T E Rohan · M G Jain · G R Howe · A B Miller ·

    JNCI Journal of the National Cancer Institute 03/2000; 92(3):266-9. DOI:10.1093/jnci/92.3.266 · 12.58 Impact Factor
  • M G Jain · T E Rohan · G R Howe · A B Miller ·
    [Show abstract] [Hide abstract]
    ABSTRACT: To evaluate the role of nutritional factors in the etiology of endometrial cancer, we performed a case-cohort analysis using data from women enrolled in the National Breast Screening Study in Canada from 1980 to 1985. For this analysis, a subcohort was constructed by selecting a 10% random sample from the 56,837 women in the dietary cohort. Cases were the 221 women diagnosed with incident adenocarcinoma of the endometrium during follow-up to December 31, 1993 and ascertained by record linkage to the Canadian Cancer Database. Information on usual diet at enrollment and other epidemiological variables was collected by means of self-administered questionnaires. Hazard ratios were obtained from proportional hazards regression models, with estimation of robust standard errors. We found a strong association of endometrial cancer with body mass index > 25 kg/m2 (hazard ratio 2.72, 95% CI: 2.06-3.50). Endometrial cancer risk was not associated significantly with intakes of total energy, carbohydrates, proteins, total fat and major fatty acids, total dietary fiber and various types of fibers, vitamin C, E and A, folic acid, beta-carotene, lutein, or cryptoxanthin. Some decrease in risk was noted with relatively high intakes of saturated fat, animal fat or lycopene. The associations observed in the study were independent of total energy intake and most non-dietary risk factors. The study suggests that dietary intakes of energy and most major nutrients are not related to the risk of endometrial cancer among Canadian women.
    European Journal of Epidemiology 02/2000; 16(10):899-905. DOI:10.1023/A:1011012621990 · 5.34 Impact Factor
  • Source
    M G Jain · G R Howe · T E Rohan ·

    Cancer control: journal of the Moffitt Cancer Center 11/1999; 7(3):288-96. · 3.50 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: To assess the risk of invasive breast cancer associated with total and beverage-specific alcohol consumption and to evaluate whether dietary and nondietary factors modify the association. We included in these analyses 6 prospective studies that had at least 200 incident breast cancer cases, assessed long-term intake of food and nutrients, and used a validated diet assessment instrument. The studies were conducted in Canada, the Netherlands, Sweden, and the United States. Alcohol intake was estimated by food frequency questionnaires in each study. The studies included a total of 322647 women evaluated for up to 11 years, including 4335 participants with a diagnosis of incident invasive breast cancer. Pooled analysis of primary data using analyses consistent with each study's original design and the random-effects model for the overall pooled analyses. For alcohol intakes less than 60 g/d (reported by >99% of participants), risk increased linearly with increasing intake; the pooled multivariate relative risk for an increment of 10 g/d of alcohol (about 0.75-1 drink) was 1.09 (95% confidence interval [CI], 1.04-1.13; P for heterogeneity among studies, .71). The multivariate-adjusted relative risk for total alcohol intakes of 30 to less than 60 g/d (about 2-5 drinks) vs nondrinkers was 1.41 (95% CI, 1.18-1.69). Limited data suggested that alcohol intakes of at least 60 g/d were not associated with further increased risk. The specific type of alcoholic beverage did not strongly influence risk estimates. The association between alcohol intake and breast cancer was not modified by other factors. Alcohol consumption is associated with a linear increase in breast cancer incidence in women over the range of consumption reported by most women. Among women who consume alcohol regularly, reducing alcohol consumption is a potential means to reduce breast cancer risk.
    JAMA The Journal of the American Medical Association 02/1998; 279(7):535-40. · 35.29 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: 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. 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. 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. 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. 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.
    JNCI Journal of the National Cancer Institute 09/1997; 89(15):1132-8. DOI:10.1093/jnci/89.15.1132 · 12.58 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: 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.
    European Journal of Cancer Prevention 09/1997; 6(4):382-8. DOI:10.1097/00008469-199708000-00011 · 3.03 Impact Factor
  • Source
    W C Willett · G R Howe · L H Kushi ·
    [Show abstract] [Hide abstract]
    ABSTRACT: 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).
    American Journal of Clinical Nutrition 05/1997; 65(4 Suppl):1220S-1228S; discussion 1229S-1231S. · 6.77 Impact Factor
  • Source
    P Ghadirian · G.R. Howe · T.G. Hislop · P Maisonneuve ·
    [Show abstract] [Hide abstract]
    ABSTRACT: 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.
    International Journal of Cancer 04/1997; 70(6):679-81. DOI:10.1002/(SICI)1097-0215(19970317)70:6<679::AID-IJC9>3.0.CO;2-S · 5.09 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: 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 (age15 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.
    Cancer Causes and Control 12/1996; 8(1):49-56. DOI:10.1023/A:1018431104786 · 2.74 Impact Factor
  • Source
    H A Risch · L D Marrett · M Jain · G R Howe ·
    [Show abstract] [Hide abstract]
    ABSTRACT: 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.
    American Journal of Epidemiology 09/1996; 144(4):363-72. DOI:10.1093/oxfordjournals.aje.a008937 · 5.23 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: 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.
    Cancer Causes and Control 08/1996; 7(4):428-36. DOI:10.1007/BF00052669 · 2.74 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: 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. © 1996 Wiley-Liss, Inc.
    International Journal of Cancer 07/1996; 67(1):63 - 71. DOI:10.1002/(SICI)1097-0215(19960703)67:1<63::AID-IJC12>3.0.CO;2-D · 5.09 Impact Factor
  • Source
    M Jain · G R Howe · Rohan TE ·
    [Show abstract] [Hide abstract]
    ABSTRACT: 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.
    American Journal of Epidemiology 06/1996; 143(9):953-60. DOI:10.1093/oxfordjournals.aje.a008839 · 5.23 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Radioactive radon is an inert gas that can migrate from soils and rocks and accumulate in enclosed areas, such as homes and underground mines. Studies of miners show that exposure to radon decay products causes lung cancer. Consequently, it is of public health interest to estimate accurately the consequences of daily, low-level exposure in homes to this known carcinogen. Epidemiologic studies of residential radon exposure are burdened by an inability to estimate exposure accurately, low total exposure, and subsequent small excess risks. As a result, the studies have been inconclusive to date. Estimates of the hazard posed by residential radon have been based on analyses of data on miners, with recent estimates based on a pooling of four occupational cohort studies of miners, including 360 lung cancer deaths. To more fully describe the lung cancer risk in radon-exposed miners, we pooled original data from 11 studies of radon-exposed underground miners, conducted a comprehensive analysis, and developed models for estimating radon-associated lung cancer risk. We pooled original data from 11 cohort studies of radon-exposed underground miners, including 65,000 men and more than 2700 lung cancer deaths, and fit various relative risk (RR) regression models. The RR relationship for cumulative radon progeny exposure was consistently linear in the range of miner exposures, suggesting that exposures at lower levels, such as in homes, would carry some risk. The exposure-response trend for never-smokers was threefold the trend for smokers, indicating a greater RR for exposure in never-smokers. The RR from exposure diminished with time since the exposure occurred. For equal total exposure, exposures of long duration (and low rate) were more harmful than exposures of short duration (and high rate). In the miners, about 40% of all lung cancer deaths may be due to radon progeny exposure, 70% of lung cancer deaths in never-smokers, and 39% of lung cancer deaths in smokers. In the United States, 10% of all lung cancer deaths might be due to indoor radon exposure, 11% of lung cancer deaths in smokers, and 30% of lung cancer deaths in never-smokers. This risk model estimates that reducing radon in all homes exceeding the U. S. Environmental Protection Agency's recommended action level may reduce lung cancer deaths about 2%-4%. These estimates should be interpreted with caution, because concomitant exposures of miners to agents such as arsenic or diesel exhaust may modify the radon effect and, when considered together with other differences between homes and mines, might reduce the generalizability of findings in miners.
    JNCI Journal of the National Cancer Institute 07/1995; 87(11):817-27. DOI:10.1093/jnci/87.11.817 · 12.58 Impact Factor
  • Source
    HA Risch · G R Howe ·
    [Show abstract] [Hide abstract]
    ABSTRACT: Infertility is a common complication of pelvic inflammatory disease (PID) and may result in decreased parity. Low parity and possibly infertility are risk factors for ovarian cancer. We therefore examined the association between ovarian cancer and history of PID in a case-control study conducted during 1989-1992 in metropolitan Toronto and nearby areas of Southern Ontario, Canada. In total, 450 histologically verified new primary epithelial ovarian cancer cases ages 35-79 years were interviewed concerning their reproduction history. Over the same period, 564 randomly selected population controls, frequently matched to the cases according to three 15-year age groups, were interviewed similarly. Continuous unconditional logistic regression methods were used for analysis. It was found that cases were more likely than controls to report having had one or more episodes of PID; adjusted for age, parity, duration of oral contraceptive use, and other factors the odds ratio (OR) was 1.53 [95% confidence interval (CI), 1.10-2.13; P = 0.012]. Higher risk was present for women with recurrent PID (OR, 1.88; 95% CI, 1.13-3.12; P = 0.014). The elevated risk associated with PID was seen particularly among women < 60 years of age at interview (OR, 1.60; 95% CI, 1.09-2.35; P = 0.016), for women of parity 0 or 1 (OR, 2.40; 95% CI, 1.39-4.15; P = 0.0017), among women who had never ever had infertility (OR, 3.74; 95% CI, 1.28-10.9; P = 0.016), and for the small number of women who reported having PID before age 20 (OR, 3.08; 95% CI, 1.17-8.13; P = 0.023).(ABSTRACT TRUNCATED AT 250 WORDS)
    Cancer Epidemiology Biomarkers & Prevention 07/1995; 4(5):447-51. · 4.13 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: International and interethnic differences in prostate cancer incidence suggest an environmental, potentially modifiable etiology for the disease. We conducted a population-based case-control study of prostate cancer among blacks (very high risk), whites (high risk), and Asian-Americans (low risk) in Los Angeles, San Francisco, Hawaii, Vancouver, and Toronto. Our aim was to evaluate the roles of diet, physical activity patterns, body size, and migration characteristics on risk in these ethnic groups and to assess how much of the interethnic differences in risk might be attributed to interethnic differences in such lifestyle characteristics. We used a common protocol and questionnaire to administer personal interviews to 1655 black, white, Chinese-American, and Japanese-American case patients diagnosed during 1987-1991 with histologically confirmed prostate carcinoma and to 1645 population-based control subjects matched to case patients by age, ethnicity, and region of residence. Sera collected from 1127 control subjects were analyzed for levels of prostate-specific antigen (PSA) to permit comparison of case patients with control subjects lacking serological evidence of prostate disease. Odds ratios were estimated using conditional logistic regression. We estimated the proportion of prostate cancer attributable to certain risk factors and the proportion of interethnic risk differences attributable to interethnic differences in risk-factor prevalence. A positive statistically significant association of prostate cancer risk and total fat intake was found for all ethnic groups combined. This association was attributable to energy from saturated fats; after adjusting for saturated fat, risk was associated only weakly with monounsaturated fat and was unrelated to protein, carbohydrate, polyunsaturated fat, and total food energy. Saturated fat intake was associated with higher risks for Asian-Americans than for blacks and whites. In all ethnic groups combined, the risk tended to be higher when only case patients with advanced disease were compared with control subjects with normal PSA levels. Among foreign-born Asian-Americans, risk increased independently with years of residence in North America and with saturated fat intake. Crude estimates suggest that differences in saturated fat intake account for about 10% of black-white differences and about 15% of white-Asian-American differences in prostate cancer incidence. Risk was not consistently associated with intake of any micronutrients, body mass, or physical activity patterns. These data support a causal role in prostate cancer for saturated fat intake but suggest that other factors are largely responsible for interethnic differences in risk.
    JNCI Journal of the National Cancer Institute 06/1995; 87(9):652-61. DOI:10.1093/jnci/87.9.652 · 12.58 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Vasectomy, a widely used form of contraception, has been associated in some studies with increased prostate cancer risk. We assessed this association on the basis of data collected in a large multiethnic case-control study of prostate cancer that was conducted in the United States (Los Angeles, San Francisco, and Hawaii) and Canada (Toronto and Vancouver). In home interviews conducted with newly diagnosed prostate cancer case patients and population control subjects, we obtained information on the participants' medical history, including a history of vasectomy and the age at which the procedure was performed, as well as other potential risk factors. Blood samples were collected from control subjects only and were assayed for concentration of sex hormones and sex hormone-binding globulin. The present analysis was based on 1642 prostate cancer patients and 1636 control subjects. A history of vasectomy was not significantly associated with prostate cancer risk among all racial/ethnic groups combined (odds ratio [OR] = 1.1; 95% confidence interval [CI] = 0.83-1.3), whites (OR = 0.94; 95% CI = 0.69-1.3), blacks (OR = 1.0; 95% CI = 0.59-1.8), or Chinese-Americans (OR = 0.96; 95% CI = 0.42-2.2). Among Japanese-Americans, the OR was 1.8 (95% CI = 0.97-3.4), but the statistically nonsignificant elevation in risk was limited to more educated men and those with localized cancers. ORs did not vary significantly by age at vasectomy or years since vasectomy. We found a lower serum concentration of sex hormone-binding globulin and a higher ratio of dihydrotestosterone to testosterone among vasectomized control subjects than among nonvasectomized control subjects. The findings of this study do not support previous reports of increased prostate cancer risk associated with vasectomy. However, the altered endocrine profiles of vasectomized control subjects seen in this cross-sectional comparison warrant further evaluation in longitudinal studies.
    JNCI Journal of the National Cancer Institute 06/1995; 87(9):662-9. DOI:10.1093/jnci/87.9.662 · 12.58 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Increased risk of prostate cancer in men with a family history of the disease has been observed consistently in epidemiologic studies. However, most studies have been confined to white men; little is known about familial aggregation of prostate cancer in populations with unusually high incidence, such as African Americans, or in populations with low incidence, such as Asian-Americans. The authors report results from a population-based case-control study of prostate cancer among blacks, whites, and Asian-Americans in the United States and Canada. Controls were matched to cases on age (5-year groups), ethnicity (black, white, Chinese-American, Japanese-American), and region of residence (Los Angeles, San Francisco, Hawaii, Vancouver, Toronto). In the combined group of participants, 5% of controls and 13% of cases reported a father, brother, or son with prostate cancer. These prevalences were somewhat lower among Asian-Americans than among blacks or whites. A positive family history was associated with a statistically significant two- to threefold increase in risk in each of the three ethnic groups. The overall odds ratio associated with such a family history, adjusted for age and ethnicity, was 2.5 (95% confidence interval 1.9-3.3). This odds ratio varied by neither ethnicity nor age of the participants. Sera from 1,087 controls were used to examine the relations between family history and serum concentrations of androgens and prostate-specific antigen. The concentrations of sex hormone-binding globulin were slightly higher in men with than without a positive family history. Prostate-specific antigen concentrations were unrelated to family history.
    American Journal of Epidemiology 05/1995; 141(8):732-40. · 5.23 Impact Factor

Publication Stats

9k Citations
626.10 Total Impact Points


  • 2000
    • Honolulu University
      Honolulu, Hawaii, United States
  • 1996-2000
    • Columbia University
      • Department of Epidemiology
      New York, New York, United States
  • 1977-1996
    • University of Toronto
      • Faculty of Medicine
      Toronto, Ontario, Canada
  • 1995
    • Yale University
      • School of Medicine
      New Haven, Connecticut, United States
    • Stanford University
      • Department of Health Research and Policy
      Stanford, California, United States
  • 1992
    • University of Alberta
      Edmonton, Alberta, Canada
  • 1978
    • The University of Winnipeg
      Winnipeg, Manitoba, Canada