Biomedical subjects
Publications and source records attributed to R A Goldbohm.
We investigated whether smoking is associated with mutations in the Von Hippel-Lindau (VHL) gene in 337 cases of sporadic renal cell carcinoma (RCC) among 120 852 people followed for 11.3 years; the findings suggest that smoking causes RCC independently of VHL gene mutations.
BACKGROUND AND OBJECTIVE: To estimate the effects of reducing the prevalence of smoking in lower educated groups on educational differences in life expectancy. METHODS: A dynamic Markov-type multistate transition model estimated the effects on life expectancy of two scenarios. A "maximum scenario" where educational differences in prevalence of smoking disappear immediately, and a "policy target-scenario" where difference in prevalence of smoking is halved over a 20-year period. The two scenarios were compared to a reference scenario, where smoking prevalences do not change. Five Dutch cohort studies, involving over 67,000 participants aged 20 to 90 years, provided relative mortality risks by educational level, and smoking habits were assessed using national data of more than 120,000 persons. RESULTS: In the reference scenario, the difference in life expectancy at age 40 between highest and lowest educated groups was 5.1 years for men and 2.7 years for women. In the "maximum scenario" these differences were reduced to 3.6 years for men and 1.7 years for women (reduction approximately 30%), and in the "policy target-scenario" differences were 4.7 years for men and 2.4 years for women (reduction approximately 10%). CONCLUSION: Theoretically, educational differences in life expectancy would be reduced by 30% at maximum, if variations in smoking prevalence were eliminated completely. In practice, tobacco control policies that are targeted at the lower educated may reduce the differences in life expectancy by approximately 10%.
Alcohol has been hypothesized to promote ovarian carcinogenesis by its potential to increase circulating levels of estrogen and other hormones; through its oxidation byproduct, acetaldehyde, which may act as a cocarcinogen; and by depletion of folate and other nutrients. Case-control and cohort studies have reported conflicting results relating alcohol intake to ovarian cancer risk. We conducted a pooled analysis of the primary data from ten prospective cohort studies. The analysis included 529 638 women among whom 2001 incident epithelial ovarian cases were documented. After study-specific relative risks (RR) and 95% confidence intervals (CI) were calculated by Cox proportional hazards models, and then were pooled using a random effects model; no associations were observed for intakes of total alcohol (pooled multivariate RR=1.12, 95% CI 0.86-1.44 comparing > or =30 to 0 g day(-1) of alcohol) or alcohol from wine, beer or spirits and ovarian cancer risk. The association with alcohol consumption was not modified by oral contraceptive use, hormone replacement therapy, parity, menopausal status, folate intake, body mass index, or smoking. Associations for endometrioid, mucinous, and serous ovarian cancer were similar to the overall findings. This pooled analysis does not support an association between moderate alcohol intake and ovarian cancer risk.
Ovary cancer risk in relation to consumption of dairy products was investigated using a self-administered questionnaire on dietary habits and other risk factors for cancer, which was completed in 1986 by 62 573 postmenopausal women participating in the Netherlands Cohort Study. Follow-up for cancer was implemented by annual record linkage with the Netherlands Cancer Registry and a nationwide pathology registry. After 11.3 years of follow-up, data of 252 incident epithelial ovarian cancer cases and 2216 subcohort members were available for analysis. No association was seen between consumption of milk, yoghurt, cheese or fermented dairy products and ovarian cancer risk. The multivariable adjusted relative risk of epithelial ovarian cancer for women in the highest compared to the lowest quintile of intake of lactose or dairy fat was 0.93 (95% confidence interval (CI)=0.60-1.45; P(trend)=0.32) and 1.53 (95% CI=1.00-2.36; P(trend)=0.11), respectively. Lactose or dairy fat intakes were not associated with serous ovarian cancer risk. Our results do not support an association between consumption of dairy products or lactose intake and ovarian cancer.
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Case-cohort analyses were performed on meat and fish consumption in relation to K-ras mutations in 448 colon and 160 rectal cancers that occurred during 7.3 years of follow-up, excluding the first 2.3 years, and 2948 subcohort members of The Netherlands Cohort Study on diet and cancer. Adjusted incidence rate ratios and 95% confidence intervals were computed for colon and rectal cancer and for K-ras mutation status subgroups. Total fresh meat, most types of fresh meat and fish were not associated with colon or rectal cancer, neither overall nor with K-ras mutation status. However, several weak associations were observed for tumours with a wild-type K-ras, including beef and colon tumours, and an inverse association for pork with colon and rectal tumours; for meat products, an increased association was observed with wild-type K-ras tumours in the colon and possibly with G>A transitions in rectal tumours.
We reviewed 37 prospective cohort and four intervention studies on potential dietary risk factors for prostate cancer, published between 1966 and September 2003. Some studies were limited by small size, crude measurement of dietary exposure and limited control for confounders. Intervention and prospective cohort studies support a protective role against prostate cancer for selenium, and possibly for vitamin E, pulses and tomatoes/lycopene. Overall consumption of meat, eggs, vegetables, fruit, coffee, tea, carotenoids and vitamins A, C and D was not consistently related to prostate cancer risk. Intervention studies also indicate that supplementation with beta-carotene does not lower prostate cancer risk, except possibly in men with low beta-carotene status at baseline. For specific types of meat, alcoholic drinks, dairy products, fat and anthropometric measures, most cohort studies suggest either an increased risk or no relation with prostate cancer. For calcium, two cohort studies suggest an increased risk at very high calcium intakes (>2000 mg/day). In conclusion, prospective studies are consistent with a protective role for selenium, and possibly vitamin E, pulses and tomatoes/lycopene, in the aetiology of prostate cancer. Studies are inconclusive on the role of meat, dairy products, fat, vegetables, fruits, alcohol and anthropometric measures, whereas a very high calcium intake appears to be positively associated with prostate cancer risk.
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In the Netherlands Cohort Study among 120 852 subjects aged 55-69 years at baseline (1986), the association between vitamins and carotenoids intake, vitamin supplement use, and bladder cancer incidence was examined. Exposure status was measured with a food-frequency questionnaire. After 6.3 years of follow-up, data from 569 cases and 3123 subcohort members were available for case-cohort analyses. The age-, sex-, and smoking-adjusted relative risks (RRs) for retinol, vitamin E, folate, a-carotene, b-carotene, lutein and zeaxanthin, and lycopene were 1.04, 0.98, 1.03, 0.99, 1.16, 1.11, and 1.08, respectively, comparing highest to lowest quintile of intake. Only vitamin C (RR: 0.81, 95% CI: 0.61-1.07, P-trend = 0.08), and b-cryptoxanthin intake (RR: 0.74, 95% CI: 0.53-1.03, P-trend < 0.01) were inversely associated with bladder cancer risk. The association with vitamin C disappeared after adjustment for b-cryptoxanthin but not vice versa. The RRs for supplemental use of vitamin A, C or E compared to no use were around unity. We conclude that dietary or supplemental intake of vitamin A, vitamin C, vitamin E, and intake of folate, and most carotenoids are not associated with bladder cancer. In this study, only b-cryptoxanthin intake appeared to be inversely associated.
BACKGROUND: The aim of the current study was to evaluate the relation between physical activity and breast carcinoma risk with specific emphasis on interaction with other aspects of energy balance. METHODS: The Netherlands Cohort Study on diet and cancer was conducted among 62,537 women ages 55-69 years at baseline. Information regarding baseline recreational physical activity, history of sports participation, and occupational physical activity was collected with a questionnaire in 1986. After 7.3 years of follow-up, 1208 incident breast carcinoma cases were available for case-cohort analyses. RESULTS: A summed total of baseline recreational physical activity (including walking, cycling, gardening) showed an inverse association with breast carcinoma risk. Women who were active in the above-mentioned activities for > 90 minutes a day had a rate ratio (RR) of 0.76 (95% confidence interval [95% CI], 0.58-0.99) compared with women who were active < 30 minutes a day. Women who ever participated into sports before baseline had a RR of 1.13 (95% CI, 0.94-1.37) compared with women who never participated in sports. The relation between sports participation and breast carcinoma risk did not appear to be dependent on the time window of participation (before/after menarche, before/after birth of the first child, before/after age 20 years). No interaction was found between baseline recreational physical activity, body mass index (BMI) (kg/m(2)), energy intake, and weight gain/loss during adult life in relation to breast carcinoma, although in the subgroup of women with a high BMI we found a stronger inverse relation between recreational physical activity and breast carcinoma risk independent of energy intake. Occupational physical activity was not found to be related to breast carcinoma risk. CONCLUSIONS: The current study findings support the hypothesis that recreational physical activity is associated inversely with breast carcinoma risk.
This study investigated the association between prostate cancer risk and energy restriction during childhood. The authors examined the hypothesis among 58,279 men aged 55-69 years enrolled in the Netherlands Cohort Study on Diet and Cancer. Information on diet and risk factors was collected by questionnaire in 1986. Additional information was collected on residence during the Dutch Hunger Winter (1944-1945) and the World War II years (1940-1944) and father's employment status during the economic depression of 1932-1940, used as indicators of exposure. A case-cohort approach was used. After 7.3 years of follow-up (through December 1993), 903 prostate cancer cases were available for analysis. Analyses were carried out for all prostate cancer cases. The prostate cancer rate ratio for men who had lived in a western Netherlands city in 1944-1945 was 1.15 (95% confidence interval (CI): 0.80, 1.31), and the rate ratio for men who had lived in a western rural area in 1944-1945 was 1.30 (95% CI: 0.97, 1.73). Residence during the war years (1940-1944) and father's employment in 1932-1940 showed no relation to prostate cancer risk. In subgroup analyses in which exposure before, during, and after the adolescent growth spurt was evaluated, the same pattern as that of the overall data was shown. The authors found no evidence for the hypothesis that energy restriction early in life decreases prostate cancer risk later in life.
Recently, there has been interest in whether intakes of specific types of fat are associated with breast cancer risk independently of other types of fat, but results have been inconsistent. We identified 8 prospective studies that met predefined criteria and analyzed their primary data using a standardized approach. Holding total energy intake constant, we calculated relative risks for increments of 5% of energy for each type of fat compared with an equivalent amount of energy from carbohydrates or from other types of fat. We combined study-specific relative risks using a random effects model. In the pooled database, 7,329 incident invasive breast cancer cases occurred among 351,821 women. The pooled relative risks (95% confidence intervals [CI]) for an increment of 5% of energy were 1.09 (1.00-1.19) for saturated, 0.93 (0.84-1.03) for monounsaturated and 1.05 (0.96-1.16) for polyunsaturated fat compared with equivalent energy intake from carbohydrates. For a 5% of energy increment, the relative risks were 1.18 (95% CI 0.99-1.42) for substituting saturated for monounsaturated fat, 0.98 (95% CI 0.85-1.12) for substituting saturated for polyunsaturated fat and 0.87 (95% CI 0.73-1.02) for substituting monounsaturated for polyunsaturated fat. No associations were observed for animal or vegetable fat intakes. These associations were not modified by menopausal status. These data are suggestive of only a weak positive association with substitution of saturated fat for carbohydrate consumption; none of the other types of fat examined was significantly associated with breast cancer risk relative to an equivalent reduction in carbohydrate consumption.
CONTEXT: Some epidemiologic studies suggest that elevated fruit and vegetable consumption is associated with a reduced risk of breast cancer. However, most have been case-control studies in which recall and selection bias may influence the results. Additionally, publication bias may have influenced the literature on associations for specific fruit and vegetable subgroups. OBJECTIVE: To examine the association between breast cancer and total and specific fruit and vegetable group intakes using standardized exposure definitions. DATA SOURCES/STUDY SELECTION: Eight prospective studies that had at least 200 incident breast cancer cases, assessed usual dietary intake, and completed a validation study of the diet assessment method or a closely related instrument were included in these analyses. DATA EXTRACTION: Using the primary data from each of the studies, we calculated study-specific relative risks (RRs) that were combined using a random-effects model. DATA SYNTHESIS: The studies included 7377 incident invasive breast cancer cases occurring among 351 825 women whose diet was analyzed at baseline. For comparisons of the highest vs lowest quartiles of intake, weak, nonsignificant associations were observed for total fruits (pooled multivariate RR, 0.93; 95% confidence interval [CI], 0.86-1.00; P for trend =.08), total vegetables (RR, 0.96; 95% CI, 0.89-1.04; P for trend =.54), and total fruits and vegetables (RR, 0.93; 95% CI, 0.86-1.00; P for trend =.12). No additional benefit was apparent in comparisons of the highest and lowest deciles of intake. No associations were observed for green leafy vegetables, 8 botanical groups, and 17 specific fruits and vegetables. CONCLUSION: These results suggest that fruit and vegetable consumption during adulthood is not significantly associated with reduced breast cancer risk.
Although several epidemiologic studies have been conducted on alcohol consumption and bladder cancer risk, the risk according to quantity and type of alcohol consumed is not clear. The authors investigated these associations in a large prospective cohort study on diet and cancer among 120,852 subjects in the Netherlands aged 55-69 years at baseline (1986). Subjects completed a questionnaire on risk factors for cancer, including alcohol consumption. Follow-up for incident cancer was established by record linkage to cancer registries. The case-cohort analysis was restricted to a follow-up period of 6.3 years and was based on 594 cases with bladder cancer and 3,170 subcohort members. The authors corrected for age and smoking in multivariable analyses. The incidence rate ratios for men who consumed <5, 5-<15, 15-<30, and > or =30 grams of alcohol per day were 1.49, 1.52, 1.16, and 1.63 compared with nondrinkers, respectively (p for trend = 0.13). Alcohol consumed from beer, wine, and liquor was associated with moderately elevated risks, although most were not statistically significant. The incidence rate ratios for women varied around unity. The results of this study do not suggest an important association between alcohol consumption and bladder cancer risk.
OBJECTIVES: Coffee, tea, and fluid consumption have been thought to influence bladder cancer incidence. In a large prospective study, these associations were investigated. METHODS: In 1986, cohort members (55-69 years) completed a questionnaire on cancer risk factors. Follow-up was established by linkage to cancer registries until 1992. The multivariable case-cohort analysis was based on 569 bladder cancer cases and 3,123 subcohort members. RESULTS: The incidence rate ratios (RR) for men consuming <2 cups of coffee/day was 0.89 (95% CI 0.51-1.5) using the median consumption category (4-<5 cups/day) as reference. This RR increased to 1.3 (95% CI 0.94-1.9) for men consuming >7 cups/day, although no clear dose response association was found. The RRs decreased from 1.2 (95% CI 0.56-2.7) for women consuming <2 cups of coffee/day to 0.36 (95% CI 0.18-0.72) for women consuming >5 cups/day compared to the median consumption category (3-<4 cups/day). Men and women who abstained from drinking tea had a RR of 1.3 (95% Cl 0.97-1.8) compared to those consuming 2-<3 cups of tea per day (median consumption category). The RR for men and women comparing highest to lowest quintile of total fluid consumption was 0.87 (95% CI 0.63 1.2). CONCLUSION: The data suggest a possible positive association between coffee consumption and bladder cancer risk in men and a probable inverse association in women. Tea consumption was inversely associated with bladder cancer. Total fluid consumption did not appear to be associated with bladder cancer.
BACKGROUND: Determining folate intake is difficult because existing folate data in food-composition tables are scarce and unreliable. OBJECTIVE: The purposes of this study were first to analyze 125 of the most important foods that contribute to folate intake in the Netherlands and second to estimate the folate intake of a representative sample of the population. DESIGN: We analyzed the folate content of foods by using a newly developed HPLC trienzyme method combined with an affinity chromatography cleanup step. These results were then used to estimate the folate intake of persons aged 1-92 y who participated in the second Dutch National Food Consumption Survey (DNFCS) in 1992 (n = 6218). RESULTS: For 35 important folate-containing foods, the mean relative folate contents measured by HPLC were 66%, 80%, and 77% of values for comparable foods included in the British food-composition table; the Ministry of Agriculture, Fisheries and Food table; and the US Department of Agriculture database, respectively. P values for comparison of relative values with 100% were 0.001, 0.171, and 0.144, respectively. The mean dietary folate intake of the DNFCS participants was 182 +/- 119 microg/d. Intake of supplement users (n = 86) was 344 microg/d, with 147 microg/d from supplements. On the basis of these findings, 42% of men and 54% of women do not meet current Dutch recommendations of 60 microg/d for children and 200 microg/d for adults. CONCLUSIONS: Total folate quantities in foods, analyzed by HPLC, are approximately 25% lower than amounts listed in recent food-composition tables estimated by use of the microbiological method. On the basis of these new data, approximately 50% of a representative Dutch population sample does not meet the current recommendations for folate intake.
BACKGROUND: Plant sterols in vegetable foods might prevent colorectal cancer. OBJECTIVE: The objective was to study plant sterol intakes in relation to colorectal cancer risk in an epidemiologic study. DESIGN: The study was performed within the framework of the Netherlands Cohort Study on Diet and Cancer in 120852 subjects who completed a baseline questionnaire in 1986. After 6.3 y of follow-up, 620 colon and 344 rectal cancer cases were detected. A case-cohort approach was used to calculate confounder-adjusted rate ratios (RRs) and their 95% CIs for quintiles of plant sterol intake. RESULTS: The total mean (+/-SD) intake of campesterol, stigmasterol, beta-sitosterol, campestanol, and beta-sitostanol was 285 +/- 97 mg/d. Major contributors to plant sterol intake were bread (38%), vegetable fats (26%), and fruit and vegetables (21%). For men, there was no clear association between intake of any of the plant sterols and colon cancer risk when age, smoking, alcohol use, family history of colorectal cancer, education level, and cholecystectomy were controlled for. Adjustment for energy did not alter the result. For rectal cancer, adjustment for energy resulted in positive associations between risk and campesterol and stigmasterol intakes. For women, there was no clear association between intake of any of the plant sterols and colorectal cancer risk. CONCLUSION: A high dietary intake of plant sterols was not associated with a lower risk of colon and rectal cancers in the Netherlands Cohort Study on Diet and Cancer.