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Biomedical subjects

H O Adami

Publications and source records attributed to H O Adami.

At least 127 records · Page 7Linked to original sources
PubMed1997

Diet and risk of renal cell cancer: a population-based case-control study.

In a few previous studies on diet and renal cell cancer, an inconsistent positive association with meat, milk, and protein and a negative association with vegetable and fruit consumption have been found. Whereas earlier studies have dealt with recent diet only, our study explored the effect of foods consumed both during the usual adult lifetime and 20 years prior to interview. The study included 379 individuals with incident histologically verified renal cell cancer and 350 control subjects residing in eight counties in Sweden between June 1989 and December 1991. Usual adult dietary intake and dietary habits 20 years prior to interview were assessed by a structured face-to-face interview and a self-administered questionnaire, respectively. Odds ratios were estimated through unconditional logistic regression. We have not observed an association of renal cell cancer with milk or total meat consumption per se; however, frequent intake of fried/sautéed meat increased the risk of renal cell cancer by about 60%; frequent consumption of poultry was also associated with an increased risk (P for trend, 0.05). A significantly protective effect on risk of renal cell cancer was observed with increasing consumption of fruit (P for trend, 0.05). When analyzed by smoking status, total fruit and especially citrus fruit consumption among nonsmokers showed an even stronger protective effect; the highest quartiles of total fruit, apple, and citrus fruit consumption entailed a 50-60% reduction in risk of renal cell cancer compared with the lowest quartiles. There was a suggestion of a protective effect of high total vegetable consumption. A protective effect of vitamin C and alpha-tocopherol was also more pronounced in nonsmokers (P for trend, 0.004 and 0.007, respectively). Our study adds to the evidence that diet may have an important role in the etiology of renal cell cancer.

Aged↗
PubMed1996

Energy, nutrient intake and prostate cancer risk: a population-based case-control study in Sweden.

The role of diet in the etiology of prostate cancer remains unclear, because results from several case-control and cohort studies on fat intake and risk of prostate cancer have been inconsistent; few of the studies have adjusted the results for caloric intake. To examine the relationship between energy, intake of several nutrients and risk of prostate cancer (all stages combined and advanced stages separately), we conducted a population-based case-control study in Orebro County, Sweden, from 1989 through 1994. A total of 526 patients with newly diagnosed prostate cancer and 536 controls, randomly selected from the population register and frequency-matched by age, were included in the analyses. Information about dietary intake was obtained from a self-administered semi-quantitative food frequency questionnaire. Odds ratios with 95% confidence intervals were estimated by unconditional logistic regression. In age-adjusted analyses, there were positive associations of prostate cancer (all stages combined) risk with total energy intake as well as intake of total fat (saturated and monounsaturated), protein, retinol and zinc. The positive association with energy intake was stronger for advanced cancer, with an excess risk of 70% for the highest quartile vs. the lowest. After adjustment for energy intake, there was no apparent association of prostate cancers (all stages combined) with any of the investigated nutrients. However, a weak positive association between intake of retinol and advanced cancer was observed. We conclude that our results provide some evidence that total energy intake is a risk factor for prostate cancer.

Adult↗
PubMed1996

Excess risk of primary liver cancer in patients with diabetes mellitus.

BACKGROUND: Chronic infection with hepatitis B virus, alcohol consumption, and cirrhosis of the liver are recognized risk factors for primary liver cancer. A few, but not all, studies have suggested that diabetes mellitus also increases risk for this cancer. PURPOSE: We conducted a population-based cohort study to analyze the risk of developing primary liver cancer and biliary tract (gallbladder, extrahepatic bile ducts, and ampulla of Vater) cancers among patients with diabetes. METHODS: A cohort of 153 852 patients with a hospital discharge diagnosis of diabetes in the period from 1965 through 1983 was identified by use of the Swedish In-patient Register. Follow-up for these patients extended from the date of cohort entry through December 31, 1989. Incident cases of cancer during follow-up were identified through the Swedish Cancer Registry. To minimize the impact of selection bias, we excluded from the analysis patients who were diagnosed with liver and biliary tract cancers during the first year of follow-up. Standardized incidence ratios (SIRs) and their 95% confidence intervals (CIs) were computed by use of nationwide rates of liver and biliary tract cancers, adjusted for age, sex, and calendar year, for comparison. RESULTS: During 1-24 years of follow-up, 819 incident cancers in the combined category of primary liver (n = 533) and biliary tract (n = 286) were identified in the cohort, yielding an overall SIR of 2.5 (95% CI = 2.3-2.6). The risk was higher in men (SIR = 3.2; 95% CI = 2.9-3.6) than in women (SIR = 2.0; 95% CI = 1.8-2.2). The incidence of primary liver cancer alone was increased fourfold (SIR = 4.1; 95% CI = 3.8-4.5); again, the risk was higher in men (SIR = 4.7; 95% CI = 4.2-5.2) than in women (SIR = 3.4; 95% CI = 2.9-3.9). Smaller increases in risk were seen for cancers of the gallbladder, the extrahepatic bile ducts, and the ampulla of Vater. After exclusion of diabetic patients with concomitant diseases that predispose to primary liver cancer, such as alcoholism, cirrhosis, and hepatitis, the persistence of an approximately threefold excess risk was observed. CONCLUSIONS: Our findings suggest that patients with diabetes are at increased risk of developing primary liver cancer and perhaps cancers of the biliary tract. The mechanisms involved in the association of diabetes and liver cancer remain to be clarified. Additional studies are needed to determine whether patients with insulin-dependent diabetes mellitus and those with non-insulin-dependent diabetes mellitus differ in their risk for primary liver cancer or whether the risk is affected by the type of diabetes treatment.

Adult↗
PubMed1996

Smoking and colorectal cancer: a 20-year follow-up study of Swedish construction workers.

BACKGROUND: Although cigarette smoking has consistently been shown to be positively related to the risk of adenomatous polyp development (benign neoplastic growth of epithelial tissue in the colon), most studies of cigarette smoking and the risk of colorectal cancer have been negative. However, in two large prospective studies in women and men, a statistically significant association between cigarette smoking and an increased risk of colorectal cancer was found, but only after more than 35 years of smoking. PURPOSE: To shed further light on the alleged relationship between long-term smoking and colorectal cancer risk, we performed a retrospective cohort study among Swedish construction workers, with many long-term smokers, complete long-term follow-up, and a large number of observed cases. METHODS: We analyzed the association of smoking with colon cancer and with rectal cancer, using data on a cohort of approximately 135000 male construction workers. High-quality exposure information was collected with the use of a comprehensive questionnaire filled out at the time of enrollment in the cohort, from 1971 through 1975. Complete follow-up was achieved through 1991 and the subjects were observed for an average of 17.6 years, thereby contributing approximately 2375000 person-years of follow-up. We calculated age-adjusted rate ratios (RRs) with the use of Poisson-based multiplicative multivariate models followed by further multivariate modeling that adjusted for other variables. RESULTS: A total of 713 incident colon cancers and 505 rectal cancers were observed. There was no statistically significant association between current smoking status, number of cigarettes smoked or number of years smoking, and risk of colorectal cancer. The age-adjusted RRs were 0.98 (95% confidence interval [CI] = 0.82-1.17) and 1.16 (95% CI = 0.94-1.44) for colon and rectal cancers, respectively, among current smokers, and 1.07 (95% CI = 0.63-1.82) and 1.08 (95% CI = 0.58-2.03) among smokers of 25 or more cigarettes per day, relative to nonsmokers. Among smokers for more than 30 years at the start of follow-up, the age-adjusted RRs were 1.03 (95% CI = 0.85-1.25) and 1.21 (95% CI = 0.96-1.53) for colon and rectal cancers, respectively, relative to nonsmokers. Heavy smokers of cigars and pipes had a statistically nonsignificant tendency toward excess risk for colon cancer, but there was no clear dose-risk trend. CONCLUSION: Our large cohort study did not indicate any excess risk of colon cancer in males who were long-term heavy smokers and provided only weak support for an association with rectal cancer. Our data are thus consistent with the majority of previous reports. The reasons for the discrepancies in comparison with recent U.S. data have yet to be identified.

Adult↗
PubMed1996

A prospective study of smoking and risk of prostate cancer.

We evaluated the hypothesis that smoking increases the incidence of and mortality from prostate cancer. High-quality smoking information was collected in 1971-1975 in a nation-wide cohort of 135,006 male construction workers in Sweden. We achieved virtually complete follow-up through record linkages and ascertained as of December 1991 2,368 incident cases of prostate cancer and 709 deaths due to this disease. Rate ratios (RR) of prostate cancer incidence and mortality, with 95% confidence intervals (CI), were estimated in Poisson-based age-adjusted models, with amount and duration of smoking as independent variables. We found no convincing association between current smoking status, number of cigarettes smoked or years since onset and risk of prostatic cancer. The age-adjusted incidence RR among previous smokers was 1.09 and among current smokers 1.11 compared with non-smokers. Weak and inconsistent trends were seen with increasing number of cigarettes smoked per day and increasing duration among current smokers. Smokers of 15 or more cigarettes daily for at least 30 years experienced an incidence RR of 1.30. Mortality in ex-smokers was similar to that in never-smokers; it was, however, slightly increased among current smokers without any trend with amount smoked or duration. The weak and inconsistent associations between smoking and prostate cancer could easily have arisen due to bias or confounding. We therefore conclude that smoking is most likely not causally linked to the occurrence of prostate cancer.

Adult↗
PubMed1996

Trends in non-epithelial cancer incidence in Denmark, Finland, and Sweden, 1961-1990.

Trends in the incidence of non-epithelial cancers are particularly likely to reflect environmental carcinogens, since these malignancies are not commonly the targets of screening efforts, and have generally not been closely associated with life style factors such as cigarette smoking and diet. We used data from nation-wide cancer registries in Denmark, Finland, and Sweden to examine trends in non-epithelial cancers over the period 1961-1990. Linear regression analysis of age-standardized rates, and age-period-cohort models were fit to assess the temporal patterns within each country. Within each of the 3 countries, there was a similarly increasing incidence of both hematological malignancies and nervous system/bone/soft-tissue neoplasms. The increases were smallest in children and adolescents (ages 0-14), moderate among young and middle aged adults (ages 15-64), and most pronounced among the elderly (ages 65+). Age-period-cohort modeling suggested that the dominant factor in the increases were birth cohort effects. It is not clear what factors underlie this increase in incidence; it seems most likely that increases both in diagnostic efficiency and in exposure to environmental carcinogens play a role.

Adolescent↗
PubMed1996

Trends in prostate cancer survival in Sweden, 1960 through 1988: evidence of increasing diagnosis of nonlethal tumors.

BACKGROUND: The incidence of prostate cancer has increased during the past 30 years but has been paralleled by increases in survival rates from this disease, despite the absence of documented major improvement in curative treatment. Since a high prevalence of microscopic prostate cancer has been observed in autopsied men and because many prostate cancers may never surface clinically, increased diagnostic activities might have led to increased detection of less aggressive tumors. PURPOSE: This study was conducted to elucidate whether the trends in prostate cancer incidence and patient survival may be due to increasing diagnoses of nonlethal tumors. METHODS: We analyzed a population-based cohort comprising all cases of prostate cancer (n = 80,901) detected in Sweden during the period of 1960 through 1988. Five hundred eighteen patients (0.64% of the total number) who could not be followed because of emigration or an incomplete national registration number were excluded. Observed and relative survival rates were calculated for the entire cohort of 80,383 assessable patients per 5-year age group in 5-year periods of diagnosis and according to diagnostic method and were compared between geographic areas with differences in incidence rates. To estimate the independent effects of these determinants, multivariate analyses were performed. RESULTS: For the 80,383 patients with complete follow-up, the 10- and 20-year observed survival rates were 17.5% (95% confidence interval [CI] = 17.2%-17.9%) and 3.5% (95% CI = 3.2%-3.7%), and the relative survival rates were 41.1% (95% CI = 40.3%-41.9%) and 28.6% (95% CI = 26.5%-30.1%), respectively. Relative survival rates improved markedly over time; 10-year relative survival rates increased from 29% (95% CI = 27%-31%) among case patients diagnosed in 1960 through 1964 to 45% (95% CI = 43%-46%) among those diagnosed in 1975 through 1979. Relative survival rates leveled off after about 18 years at 18% (95% CI = 15%-20%) among patients diagnosed in 1960 through 1964 and at 31% (95% CI = 28%-34%) among those diagnosed in 1970 through 1974. An even more favorable outlook was observed in those case patients diagnosed later. In areas with a high or low incidence of prostate cancer, the 10-year relative survival rates were 45% (95% CI = 44%-47%) and 36% (95% CI = 34%-38%), respectively. In the early 1960s, the calculated loss of life expectancy after diagnosis varied from about 68% (95% CI = 61%-75%) of the expected length of life in the youngest age group to about 48% (95% CI = 46%-50%) in the oldest age group. From 1960 through 1964 to 1985 through 1988, the loss of life expectancy decreased by more than 50% in all age groups. The differences in relative survival rates between age groups were small, with a gradual decrease in age groups more than 60-64 years of age. CONCLUSIONS: Most of the great temporal improvement and geographic variation in survival rates are quantitatively consistent, with likely increases in the rate of detection of nonlethal tumors. IMPLICATIONS: The increase in relative survival rates must be taken into consideration when evaluating the outcome of treatment of prostate cancer, since nonrandomized comparisons may be confounded by time trends. Diagnosis of nonlethal tumors raises concerns because the individual would suffer from the psychologic burden of a cancer diagnosis without any therapeutic benefit.

Age Distribution↗
PubMed1996

Perinatal characteristics in relation to incidence of and mortality from prostate cancer.

OBJECTIVE: To test the hypothesis that factors causing morbidity and mortality from prostate cancer may operate in utero. DESIGN: Matched case-control study of singleton men born between 1874 and 1946 at one hospital. SETTING: Uppsala University Hospital. SUBJECTS: 250 patients with prostate cancer and 691 controls, including 80 patients who died from prostate cancer and their 196 matched controls. MAIN OUTCOME MEASURES: Mother's age at menarche, parity, pre-eclampsia or eclampsia before delivery, age at delivery and socioeconomic status; case or control's birth length and weight, placental weight, prematurity derived from gestational age, and presence of jaundice. RESULTS: Both pre-eclampsia (odds ratio 0, 95% confidence interval 0 to 0.71) and prematurity (0.31, 0.09 to 1.04) were inversely associated with incidence of prostate cancer. Among subjects born full term, placental weight, birth weight, and ponderal index (weight/height 3) showed non-significant positive associations with prostate cancer incidence, and stronger associations with mortality. CONCLUSION: Prenatal exposures that are likely correlates of pregnancy hormones and other growth factors are important in prostate carcinogenesis and influence the natural course as well as the occurrence of this cancer.

Age Factors↗
PubMed1996

The risk of stomach cancer in patients with gastric or duodenal ulcer disease.

BACKGROUND: Helicobacter pylori infection, now considered to be a cause of gastric cancer, is also strongly associated with gastric and duodenal ulcer disease. The discovery of these relations has brought the long-controversial connection between peptic ulcers and gastric cancer into focus. METHODS: We estimated the risk of stomach cancer in a large cohort of hospitalized patients with gastric or duodenal ulcers, as recorded in the Swedish Inpatient Register between 1965 and 1983. Altogether, 57,936 patients were followed through 1989, for an average of 9.1 years. The standardized incidence ratio--the ratio of the observed number of cancers to the number expected on the basis of the incidence in the Swedish population at large--was used as a measure of relative risk. RESULTS: After peaking in the first 3 years of follow-up, the standardized incidence ratio for gastric cancer among 29,287 patients with gastric ulcers leveled off at 1.8 (95 percent confidence interval, 1.6 to 2.0) and remained significantly increased throughout follow-up, which was as long as 24 years for some patients. Prepyloric ulcer, diagnosed in 8646 patients, was not associated with a significant excess risk (standardized incidence ratio, 1.2; 95 percent confidence interval, 0.8 to 1.6). In the cohort of patients with duodenal ulcers (24,456 patients), the incidence of gastric cancer was significantly lower than expected. After the second year of follow-up, the standardized incidence ratio was only 0.6 (95 percent confidence interval, 0.4 to 0.7) and remained stable thereafter. CONCLUSIONS: Gastric ulcer disease and gastric cancer have etiologic factors in common. A likely cause of both is atrophic gastritis induced by H. pylori. By contrast, there appear to be factors associated with duodenal ulcer disease that protect against gastric cancer.

Adult↗
PubMed1996

Predictors of late mortality in cutaneous malignant melanoma--a population-based study in Sweden.

We determined risk factors for late deaths from cutaneous malignant melanoma (CMM) based on clinical characteristics at diagnosis, initial surgical treatment, histopathologic features of the primary tumor and type of eventual recurrences during follow-up. We examined deaths from CMM 8 or more completed years after the initial diagnosis in a case-control study nested in a nationwide cohort comprising all 8,838 patients with CMM diagnosed in Sweden during 1960-1978 with complete follow-up through 1986. There were 285 case patients and 285 control patients, individually matched by sex, age and follow-up time. Conditional logistic regression was used to obtain odds ratios (OR) as estimates of the relative risk. The risk of late mortality increased stepwise, almost 19-fold, with increasing tumor thickness from < or = 0.75 to > or = 7.00 mm. Besides the thickest tumors (> or = 7.00 mm), those of intermediate thickness (1.50-2.49 mm) had the highest risk (OR 8.5). After adjustment for tumor thickness, non-radical primary surgical treatment increased the risk of late mortality almost 3-fold while prophylactic lymph node dissection entailed a significantly reduced risk of late mortality (OR 0.5); the histopathologic features increasing level of invasion and vertical growth phase also remained significantly associated with a poor outcome. In a multivariate model, non-radical primary surgical treatment, prophylactic lymph node dissection, vertical growth phase, level of invasion and lymphocyte reaction were independent predictors of late mortality.

Adult↗
PubMed1996

Testicular nonseminoma and seminoma in relation to perinatal characteristics.

BACKGROUND: Testicular cancer incidence peaks during the third decade of life, and an increasing trend in the occurrence of this disease has been seen in many countries. Few risk factors have been established for testicular cancer, but evidence suggests that causal factors operate early in life, perhaps even in utero. PURPOSE: We performed a case-control study to evaluate specific perinatal characteristics as risk factors for the two main histopathologic types of testicular cancer: seminomas and nonseminomas. METHODS: Two hundred thirty-two case patients with invasive testicular cancer and 904 individually matched control subjects (all singleton births), nested in a cohort of men born at 10 hospitals in Sweden from 1920 through 1978, were included in the study. Perinatal information about the study subjects and their parents was obtained from birth records. For the mothers, information was recorded concerning age at menarche, marital status, parity, age at delivery, maternal weight at delivery and at first visit to a maternal-care center, education and/or profession, and any medical problems encountered during pregnancy or after delivery. For the fathers, information was obtained concerning age at delivery and education and/or profession. For the study subjects, information was recorded about the following: gestational age, birth length and weight, placental weight, method of delivery (normal, cesarean section, or with forceps or vacuum extractor), medical problems during hospital stay, presence of jaundice, method of feeding at discharge, and duration of hospital stay after birth. Individuals diagnosed with testicular cancer were identified through the Swedish National Cancer Registry and the Uppsala Regional Cancer Registry. The data were analyzed by use of conditional logistic regression modeling. RESULTS: When testicular cancer was modeled as a single entity, significantly elevated risks were associated with neonatal jaundice (adjusted odds ratio [OR] = 2.30; 95% confidence interval [CI] = 1.07-4.94) and with either low (< 2500 g) or high (> or = 4000 g) birth weight (OR = 2.59; 95% CI = 1.05-6.38 and OR = 1.58; 95% CI = 1.10-2.29, respectively). When seminomas and nonseminomas were analyzed separately, high maternal socioeconomic status (OR = 2.54; 95% CI = 1.05-6.12), neonatal jaundice (OR = 3.96; 95% CI = 1.47-10.69), and low birth weight (OR = 7.62; 95% CI = 1.59-36.60) were associated with nonseminomas, whereas high placental weight (OR = 3.50; 95% CI = 0.97-12.62) suggested increased risk for seminomas. CONCLUSIONS AND IMPLICATIONS: Perinatal exposures appear to influence the risk of testicular cancer, and seminomas and nonseminomas may have somewhat different risk profiles. Future epidemiologic studies should consider the possibility of etiologic heterogeneity in the development of seminomas and nonseminomas.

Birth Weight↗
PubMed1996

Increase in testicular cancer incidence in six European countries: a birth cohort phenomenon.

BACKGROUND: For unknown reasons, the age-standardized incidence of testicular cancer has shown a rapid increase in virtually all countries (mostly Western) studied. For populations with a sufficiently long period of cancer registration, this development can be traced back to the first half of this century. PURPOSE: By evaluating data from six countries with long periods of cancer registration (Denmark, Norway, Sweden, the former German Democratic Republic [East Germany], Finland, and Poland), we sought to determine whether the increase in testicular cancer risk follows a birth cohort pattern and, if so, to quantify and compare any birth cohort effects. METHODS: A total of 30,908 incident cases of testicular cancer, diagnosed from 1945 through 1989 in men who were 20-84 years of age, were identified in population-based cancer registries in the six countries. In addition to performing simple trend analyses, we fitted several Poisson regression models (with the explanatory variables age, time period [calendar time], and birth cohort) to the data. Individual models were estimated by the maximum likelihood method. RESULTS: The age-standardized incidence of testicular cancer was found to vary among the six populations and, on the basis of total registration data, increased annually at rates ranging from 2.3% (in Sweden) to 5.2% (in East Germany). A comparison of several regression models indicated that birth cohort was a stronger determinant of testicular cancer risk than was calendar time for all six populations. Within each population, little variation in testicular cancer risk was observed for men born between 1880 and 1920; thereafter, the risk began to increase. Among men born in Denmark, Norway, and Sweden between 1930 and 1945 (the period encompassing the Second World War), the increasing trend in risk was interrupted (i.e., a leveling in risk occurred). After 1945, an uninterrupted increase in risk was observed for all six populations. With men born around 1905 as the reference group, the relative risk of testicular cancer for those born around 1965 varied from 3.9 (95% confidence interval [CI] = 2.7-5.6) in Sweden to 11.4 (95% CI = 8.3-15.5) in East Germany. CONCLUSIONS AND IMPLICATIONS: The increasing trend in testicular cancer risk observed for these six populations follows a birth cohort pattern. This distinct risk pattern provides a framework for the identification of specific etiologic factors.

Adult↗
PubMed1996

Risk of cancer following splenectomy.

Only 2 small population-based studies have previously evaluated cancer risk in splenectomized patients. Our objective was thus to investigate cancer incidence following splenectomy for external trauma or for surgical treatment of non-malignant conditions of adjacent organs. Using the unique personal identification number assigned to each Swedish resident, we linked centralized hospitalization records with nationwide total population and cancer incidence data. We excluded cancers diagnosed within the first 12 months after splenectomy and computed standardized incidence ratios for 1,295 patients (contributing 14,390 person-years) splenectormized for external trauma and for 985 patients (contributing 8,91 1 person-years) whose splenectomy accompanied surgical treatment of non-malignant conditions of adjacent organs (mostly peptic ulcers), using age-, sex- and period-specific rates for cancer incidence derived from the entire Swedish population. Patients undergoing splenectomy for external trauma had no significant excess of total or site-specific cancers. Individuals splenectormized in conjunction with surgery for non-malignant conditions of adjacent organs had a non-significant 40% elevated risk of total cancer, with significant increases of lung and ovarian cancers. The excesses of lung and ovarian cancers may be due to chance, but we could not exclude the conditions for which the surgery was performed, other treatments or common predisposing factors (such as cigarette smoking, which has been linked with both peptic ulcer and lung cancer).

Adult↗
PubMed1996

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↗
PubMed1996

Iodine supplementation in Sweden and regional trends in thyroid cancer incidence by histopathologic type.

We studied regional patterns of thyroid cancer incidence in relation to iodine intake and iodinization in Sweden using 5,838 incident cases diagnosed in the period 1958-1981. Region was defined either by iodine status, urban-rural status or health-care region (internal controls). Age, period and cohort models were fitted to evaluate trends and regional variation in incidence by histopathologic type. In iodine-deficient areas, the relative risk (RR) of developing thyroid cancer was 0.92 for all histologic types combined, 0.80 for papillary cancer and 0.87 for anaplastic carcinoma. Residence in iodine-deficient regions was associated with a 2-fold increased risk of follicular cancer in men (RR 1.98) and a 17% increase in risk in women (RR 1.17). Regional differences in iodine intake fell after iodinization of the food supply, which was started in 1936 and enhanced in 1966. Nevertheless, incidence of both papillary and follicular carcinoma increased during the study period, with largely similar trends in iodine-deficient and iodine-sufficient areas. Overall, residence in urban or rural areas was not an important determinant of incidence, though trends in the incidence of papillary, follicular and anaplastic cancer did vary between urban and rural areas. The occurrence of thyroid cancer differed only marginally between the 6 health-care regions in Sweden, suggesting that the observations in regions defined by iodine intake were unlikely to be artifactual. Our data suggest that iodinization of the food supply is not associated with adverse trends in the occurrence of thyroid cancer.

Adenocarcinoma, Follicular↗