The purpose of this study was to investigate the risk of transitional cell carcinoma among subjects with an intake of acetaminophen, aspirin, some other drugs and with some intercurrent diseases. The source person-time ('study base') included subjects living in Stockholm in 1985-1987. The study included 325 subjects with a transitional cell carcinoma of the urinary tract and 393 controls randomly selected from the source person-time. Data were obtained by a postal questionnaire supplemented by a telephone interview. A relative risk (with a 95% confidence interval) of 1.6 (1.1-2.3) was obtained after an intake of acetaminophen, adjusted for age, aspirin, gender and smoking. Conversely, a 30% decrease in risk was obtained after an intake of aspirin. No details in the exposure substantiated the finding for acetaminophen. The inherent validity problems of observational studies, and the weak evidence in this and previous studies of the association between acetaminophen and transitional cell carcinoma, makes available epidemiological evidence insufficient to regulate the use of this commonly ingested analgesic. Increased risks were, in addition, found for tetracyclines, nitrofurantoin and a history of allergic asthma and a decreased risk found for rheumatic symptoms. The findings stress the nonepidemiological data concerning the potential carcinogenicity of acetaminophen and may be a foundation for future research of some other drugs and diseases.
PURPOSE: To study adult height in children that grew up with asthma before inhaled steroids became first-line therapy. METHODS: Data from the Swedish Medical Birth Register (self-reported asthma) and the Hospital Discharge Register (first hospitalization for asthma) were used, to compare adult height for asthmatic and non-asthmatic pregnant women. The analysis was restricted to women in their first full-term pregnancy, born in Sweden between 1960-1974 and of Swedish citizenship. RESULTS: The mean height of all the women in the study population was 166.7 cm (SD = 8.8, n = 287,750) and of the women who reported asthma 166.5 cm (SD = 6.1, n = 13,059, p
The association between alcohol intake and colorectal cancer was examined in a population-based case-control study performed in Stockholm in 1986-88. The study included 352 cases of colon cancer, 217 cases of rectal cancer, and 512 controls. Relative risks, with 95% confidence intervals, were calculated for total alcohol intake and for different alcoholic beverages. Total alcohol intake (> or = 30 g 100% ethanol per day) was not associated with colon cancer (relative risk = 0.9, confidence intervals = 0.4-1.8) or rectal cancer (1.0, 0.4-2.1). There was no evidence supporting beverage specificity (for colorectal cancer and > or = 10 g 100% ethanol per day: beer 1.1, 0.6-2.0, wine 1.0, 0.4-2.7, spirits 1.0, 0.6-1.6). The associations did not vary according to gender or site within the large bowel. These analyses were adjusted for year of birth and gender (when appropriate). Further adjustments for diet, body mass or physical activity had little or no influence on the results. The present study does not support the hypothesis that alcohol plays an important role in the aetiology of cancer of the colon and rectum in a population with a relatively low alcohol intake.
BACKGROUND AND PURPOSE: Since stroke is a principal cause of death in elderly people, we analyzed the association between alcohol and stroke mortality in a cohort of 15,077 middle-aged and older men and women. METHODS: Data on alcohol habits were obtained from a questionnaire in 1967. The subsequent 20 years yielded 769 deaths from stroke, of which 574 were ischemic. Relative mortality risks (RR) were estimated from logistic regression analyses with lifelong alcohol abstainers as a reference group. Adjustments were made for age and smoking. RESULTS: No association was found between alcohol intake and hemorrhagic stroke. An elevated risk of ischemic stroke was found for men who drank infrequently, that is, a few times a year or less often (RR, 2.0; 95% confidence interval [CI], 1.3 to 3.2), for those who were intoxicated now and then (RR, 1.8; 95% CI, 1.1 to 2.8), and for those who reported "binge" drinking a few times in the year or less often (RR, 1.6; 95% CI, 1.1 to 2.5). Among women only ex-drinkers had an elevated risk of dying of ischemic stroke (RR, 3.3; 95% CI, 1.5 to 7.2). The risk was reduced for women who had an estimated average consumption of 0 to 5 g pure alcohol per day (RR, 0.6; 95% CI, 0.5 to 0.8); for those who did not drink every day (RR, 0.7; 95% CI, 0.5 to 0.9); and for those who never "went on a binge" (RR, 0.6; 95% CI, 0.5 to 0.8) or became intoxicated (RR, 0.7; 95% CI, 0.5 to 0.9). CONCLUSIONS: Drinking habits were associated only with deaths from ischemic stroke, and the risk patterns were different for men and women. In analyses, ex-drinkers should not be included with lifelong abstainers, since the former tend to run high health risk.
In the early 1980s, Doll and Peto estimated that about 35% of all deaths from cancer in the United States were attributable to dietary factors, with a margin of uncertainty ranging from 10 to 70%. Since then, several dietary factors, e.g. fat and meat, have been suggested to increase the risk for cancer, while other factors, e.g. fibre, fruit and vegetables, have been suggested to decrease the risk. The case-control and cohort studies have, however, given ambiguous results, and the overall evidence is far from conclusive. The major findings on dietary factors that increase risk have been reported from case-control studies, but have not been confirmed in large population-based cohort studies. Although the research in this area indicates that diet is important in cancer prevention, current knowledge does not allow reliable estimates of the numbers and proportions of cancers that could be avoided through well-described modifications of dietary habits. During the last 10 years, low physical activity has been pinpointed as a risk factor for cancers at various sites, especially the colon; however, the causal mechanism is still unknown. Obesity, defined as a body mass index of 30 or more, is consistently associated with endometrial and gall-bladder cancers in women and renal-cell cancer in both men and women. As the prevalence of obesity was between 5 and almost 20% in the Nordic populations in 1995, 625 cancer cases (310 endometrial cancers, 270 renal-cell cancers in men and women and 45 gall-bladder and bile-duct cancers among women) can be predicted in the Nordic countries around the year 2000 to be caused by obesity. This implies that about 1% of all cancers in Nordic women and less than 1% of those in Nordic men could be avoided around the year 2000 if a healthy body weight could be maintained by all inhabitants.
The impact of tobacco use and coffee and tea intake on the risk of colorectal cancer is unclear. Previous research has suggested that coffee may be protective against these cancers, and investigation regarding tea or cigarette smoking has yielded inconsistent results. To clarify these issues, we evaluated coffee and tea intake and tobacco smoking as risk factors for cancer of the colon and rectum in a population-based case-control study from Stockholm, Sweden. Cases were ascertained from the regional cancer registry, and controls identified through population registers. Subjects completed a questionnaire requesting information regarding foods and beverages consumed, exercise, tobacco use, and personal characteristics. Logistic regression modelling was used to compute odds ratios. A total of 352 cases of colon cancer, 217 cases of rectal cancer, and 512 controls took part. High coffee intake was negatively associated with the risk of colon cancer: the odds ratio for those drinking 6 or more cups per day was 0.55 (95% confidence interval, 0.31-0.96) compared to those drinking one or fewer. There was no association with rectal cancer. For tea, the associations were the opposite: there was no association with colon cancer risk, but the odds ratio for rectal cancer was 0.56 (95% confidence interval, 0.34-0.90) for those drinking 2 or more cups per day compared with those drinking none. Smokers of 11 or more cigarettes per day had a 20 to 30% reduction in the risk of colon and rectal cancer, but these findings were consistent with chance. There was no association of long-term cigarette smoking with risk.
To explore the relationships between C-reactive protein (CRP), metabolic syndrome (MetS) and incidence of severe knee or hip osteoarthritis (OA) in a prospective study.
A population-based cohort (n=5171, mean age 57.5+/-5.9 years) was examined between 1991 and 1994. Data was collected on lifestyle habits, measures of overweight, blood pressure as well as high-density lipoprotein (HDL) cholesterol, triglycerides, glucose and CRP measured with high-sensitive methods. Incidence of severe OA, defined as arthroplasty due to knee or hip OA, was monitored over 12 years of follow-up, in relation to CRP levels and presence of the MetS according to the adult treatment panel III-national cholesterol education program (ATPIII-NCEP) definition.
A total of 120 participants had severe hip OA and 89 had knee OA during the follow-up. After adjustment for age, sex, smoking, physical activity and CRP, presence of MetS was associated with significantly increased risk of knee OA (relative risk [RR]: 2.1, 95% confidence interval [CI]: 1.3-3.3). However, this relationship was attenuated and non-significant after adjustment for body mass index (BMI) (RR: 1.1, 95% CI: 0.7-1.8). MetS was not significantly associated with incidence of hip OA. In women, CRP was associated with knee OA in the age-adjusted analysis. However, there was no significant relationship between CRP and incidence of knee or hip OA after risk factor adjustments.
The increased incidence of knee OA in participants with the MetS was largely explained by increased BMI. CRP was not associated with incidence of knee or hip OA when possible confounding factors were taken into account.
The epidemiology of large bowel cancer suggests an etiological role for dietary factors. Although the evidence is inconsistent, several studies have suggested an inverse association between dietary vitamin D or calcium and colorectal cancer risk. We conducted a population-based case-control study to examine the relationship between dietary vitamin D and calcium and colorectal cancer among residents of Stockholm, Sweden. Between January 1986 and March 1988, 352 cases of colon cancer and 217 cases of rectal cancer diagnosed among living persons residing in Stockholm County were identified via a cancer surveillance network established among all the hospitals in Sweden and the Stockholm Regional Cancer Registry. Controls (512) were randomly selected from a computerized population registry. Dietary intake was assessed using a quantitative food frequency questionnaire focusing on average consumption during the preceding 5 years. Supplemental intake of vitamin D and calcium was not ascertained. Logistic regression was used to calculate odds ratios (ORs) as the measure of association between the exposure of interest (vitamin D or calcium) and cancer risk. Increasing levels of dietary vitamin D were inversely associated with the risk of colorectal cancer. The association was somewhat more pronounced for cancers of the rectum [OR, 0.5; 95% confidence interval (CI), 0.3-0.9 between the highest and lowest quartiles] than for cancers of the colon (OR, 0.6; 95% CI, 0.4-1.0) after adjustment for age, sex, and total caloric and protein intake. Dietary calcium was not associated with the adjusted risk of colon (OR, 1.2; 95% CI, 0.7-2.1) or rectal cancer (OR, 1.0; 95% CI, 0.5-1.9). Further adjustments for fat and dietary fiber intake, body mass index, and physical activity had little or no effect on the results. These results suggest that dietary vitamin D may reduce the risk of large bowel cancer, particularly rectal cancer. In addition, although some of the previous data suggested a protective effect for calcium against cancers of the large bowel, we could not document such an effect.
Three population-based case-control studies in Sweden have found an association between fried foods and pancreatic cancer, urothelial cancer and colorectal cancer, respectively. Only one of these studies included questions about the preferred method of frying the meat surface. This study was performed in Stockholm in 1986-88 and included 347 cases of colon cancer, 212 cases of rectal cancer and 505 controls. Total meat intake, frequent consumption of brown gravy, and a preference for a heavily browned meat surface each independently increased the risk for colorectal cancer. The relative risks (RRs) were higher for frequent intake of boiled meat (RR colon = 1.7, RR rectum = 2.7) than for frequent intake of meat fried with a medium or lightly browned surface (RR colon = 0.8, RR rectum = 1.1), but the highest risks were for frequent intake of meat fried with a heavily browned surface (RR colon = 2.8, RR rectum = 6.0). The analyses were adjusted for year of birth, gender and fat intake. Further adjustments for total energy, dietary fiber intake, body mass and physical activity had little or no influence on the relative risks. These results indicate that the cooking method is a neglected risk factor for cancer, but also that the measurements of exposure, used so far, are inadequate. First, the agents (exposure) of interest have to be identified in laboratory studies; secondly, accurate methods to measure the exposure in epidemiologic studies have to be established; and thirdly, these methods have to be used in well-designed epidemiologic studies.
The associations between methods of cooking meats and colorectal cancer were examined in a population-based case-referent study performed in Stockholm in 1986-1988. The study included 559 cases and 505 referents. Total meat intake, frequent consumption of brown gravy, and a preference for a heavily browned meat surface each independently increased the risk for colorectal cancer. The relative risks (RR) were higher for rectal than for colon cancer, and for boiled meat (RR colon = 1.7, RR rectum = 2.7) than for meat fried with a medium or lightly browned surface (RR colon = 0.8, RR rectum = 1.1), but the highest risks were for meat fried with a heavily browned surface (RR colon = 2.8, RR rectum = 6.0). The analyses were adjusted for year of birth, gender and fat intake. Further adjustments for total energy, dietary fiber intake, body mass and physical activity had little or no influence on the results. The findings suggest that, in addition to frequent meat intake, a heavily browned meat surface formed when frying meat at high temperatures is important in the etiology of colorectal cancer.