Prostate cancer and prediagnostic levels of serum vitamin D metabolites (Maryland,United States)

An hypothesis has been forwarded linking prostate cancer to low serum levels of vitamin D metabolites. We sought to test this hypothesis using sera obtained in a large, prospective cohort study. A serum bank in Washington County, Maryland (United States) has stored sera obtained from 20,305 county residents during a blood collection campaign undertaken in August through November 1974. We studied sera obtained from 61 residents who were diagnosed with prostate cancer during the period 1980 through 1992. Each prostate cancer case was matched to two controls on age (±1 yr) and race. Controls had donated blood in the same blood-collection campaign and had not been diagnosed with prostate cancer through 1992. Serum levels of vitamin D metabolites did not differ significantly between cases and controls. Mean 25-hydroxyvitamin D (25-D) levels were 34.3 ng/ml and 33.2 ng/ml, and mean 1,25-dihydroxyvitamin D (1,25-D) levels were 41.0 pg/ml and 40.1 pg/ml, in cases and controls, respectively. No statistically significant trends or differences between cases and controls were found in an analysis by quintile of serum level. We also did not observe the association of vitamin D metabolites with prostate cancer to be strongest among older men with more severe disease, as previously has been reported. In summary, although our study's power was limited, our findings provide little support for the hypothesis that vitamin D metabolite levels are associated strongly with subsequent risk for prostate cancer.Dr Braun is with the Epidemiology and Biostatistics Program, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Authors are also affiliated with the Department of Epidemiology, Johns Hopkins University School of Hygiene and Public Health, Baltimore, MD, USA (Drs Helzlsouer and Comstock), and the Department of Pediatrics, Medical University of South Carolina, Charleston, SC, USA (Dr Hollis). Address correspondence to Dr Braun, Epidemiology and Biostatistics Program, National Cancer Institute, EPN 443, Bethesda, MD 20892-7374, USA.     

Calcium, vitamin D, sunshine exposure, dairy products and colon cancer risk (United States)

Objective: Epidemiologic studies on calcium, vitamin D and colon cancer are inconsistent, whereas experimental studies more regularly show a protective effect. To evaluate potential sources of inconsistencies, data from a large case–control study were analyzed, stratifying on potential effect modifiers. Methods: Data were collected by certified interviewers in Northern California, Utah and Minnesota. Analyses included 1993 incident colon cancer cases and 2410 population-based controls. Multivariate logistic regression models included age, sex, BMI, family history, physical activity, intake of energy, dietary fiber, aspirin and NSAIDs. Results: Dietary calcium was inversely associated with colon cancer risk in men (OR highest vs lowest quintile = 0.6, 95% CI = 0.5–0.9) and women (OR = 0.6, 95% CI = 0.4–0.9). No statistically significant associations were observed for dietary vitamin D or sunshine exposure. Consumption of total low-fat dairy products was associated with a statistically significantly decreased risk in men and women (ORs highest vs lowest category of intake = 0.8 and 0.7 respectively). Calcium supplement use was inversely associated with risk in both sexes (ORs use vs non-use = 0.8). Vitamin D supplements were inversely associated with risk in men (OR = 0.5) and women (OR = 0.6) but confidence limits included 1.0. Conclusions: These data provide additional support of an inverse association between high levels of calcium intake and colon cancer risk.     

Serum levels of vitamin D metabolites and the subsequent risk of colon and rectal cancer in Finnish men

Experimental and human epidemiologic data suggest a protective rolefor vitamin D in large bowel cancer. To investigate this association, weconducted a nested case-control study within a Finnish clinical trial cohort.Cases (n = 146) were participants diagnosed with primary adenocarcinoma ofthe large bowel. Controls were matched (2:1) to cases on age, date ofbaseline blood draw, and study clinic. Prediagnostic serum levels of thevitamin D metabolites, 25-hydroxyvitamin D (25-OH D), and1,25-dihydroxyvitamin D (1,25-DIOHD) were used as primary exposure measures.The baseline geometric-mean serum level of 25-OH D was 11.6 percent lower incases than in controls (12.2 cf 13.8 ug/l, P = 0.01) while serum levels of1,25-DIOH D did not differ by case-control status. No association was seenbetween serum levels of 1,25-DIOH D and large bowel cancer risk. However, theestimated relative risk (RR) of large bowel cancer decreased with increasinglevel of serum 25-OH D and the associa tion was more pronounced for rectalcancer (55 cases; RR by quartile = 1.00, 0.93, 0.77, 0.37; trend P = 0.06).Neither exclusion of early cases nor multivariate adjustment for potentialconfounders materially altered these estimates. There was no evidence ofeffect modification by level of 1,25-dihydroxyvitamin D or with other knownrisk-factors for large bowel cancer.     

The epidemiology of vitamin D and cancer incidence and mortality: A review (United States)

In vitro and animal studies indicate that vitamin D may have anti-cancer benefits, including against progression and metastasis, against a wide spectrum of cancers. Supporting an anti-cancer effect of vitamin D is the ability of many cells to convert 25(OH)D, the primary circulating form of vitamin D, into 1,25(OH)₂D, the most active form of this vitamin. No epidemiologic studies have directly measured vitamin D concentrations or intakes on risk of total cancer incidence or mortality. However, higher rates of total cancer mortality in regions with less UV-B radiation, and among African-Americans and overweight and obese people, each associated with lower circulating vitamin D, are compatible with a benefit of vitamin D on mortality. In addition, poorer survival from cancer in individuals diagnosed in the months when vitamin D levels are lowest suggests a benefit of vitamin D against late stages of carcinogenesis. The only individual cancer sites that have been examined directly in relation to vitamin D status are colorectal, prostate and breast cancers. For breast cancer, some data are promising for a benefit from vitamin D but are far too sparse to support a conclusion. The evidence that higher 25(OH)D levels through increased sunlight exposure or dietary or supplement intake inhibit colorectal carcinogenesis is substantial. The biologic evidence for an anti-cancer role of 25(OH)D is also strong for prostate cancer, but the epidemiologic data have not been supportive. Although not entirely consistent, some studies suggest that higher circulating 1,25(OH)₂D may be more important than 25(OH)D for protection against aggressive, poorly-differentiated prostate cancer. A possible explanation for these divergent results is that unlike colorectal tumors, prostate cancers lose the ability to hydroxylate 25(OH)D to 1,25(OH)₂D, and thus may rely on the circulation as the main source of 1,25(OH)₂D. The suppression of circulating 1,25(OH)₂D levels by calcium intake could explain why higher calcium and milk intakes appear to increase risk of advanced prostate cancer. Given the potential benefits from vitamin D, further research should be a priority.     

Serum concentrations of organochlorine compounds and endometrial cancer risk (United States)

Objectives: Endogenous and exogenous estrogens are important in the development of endometrial cancer. Several organochlorine compounds, such as o,p-DDT, have estrogenic properties. The objective of this case-control analysis was to examine serum concentrations of organochlorine compounds and risk of endometrial cancer.Methods: Analyses were based on a sample of 90 endometrial cancer cases and 90 individually matched community controls from a multicenter case-control study in five geographic regions of the United States. Information on potential confounders, including menstrual and reproductive factors, cigarette smoking, diet, and weight, was obtained by interview.Results: The adjusted relative risk of endometrial cancer in the highest quartile of exposure compared with women in the lowest quartile was 0.7 (95 percent confidence interval [CI] = 0.2-2.0) for p,p-DDE, and 0.9 for total polychlorinated biphenyls (PCBs) (CI = 0.4-2.5).Conclusions: These findings do not support the hypothesis that organochlorine compounds are linked to the development of endometrial cancer.     

Prostate cancer screening (United States)

In 1995, there will be 244,000 new cases of prostate cancer, and 40,400 deaths from prostate cancer, among men in the United States. The American Cancer Society reports that the incidence rate of prostate cancer is increasing at an accelerated pace, and was 21 percent higher in 1994 than in 1993. The major reason for this steep rise is likely to be due to increased popularity of prostate cancer screening which, by identifying latent, asymptomatic cases, may convert them into clinical cases. Is screening—an important means of cancer control for many sites—a reasonable approach for prostate cancer control? The answer is not straightforward because prostate cancer is not one, but three diseases: a latent form which will cause no harm; a progressive form which will become symptomatic and can kill; and a rapidly progressive form so malignant that it is likely to kill, whether detected early or late. Screen-detection may be worthwhile only for the second form, as tumors of the first form need never be detected, and tumors of the third form progress so rapidly that timely screen-detection is nearly impossible and, if accomplished, may be valueless. As there is no way to differentiate among the three diseases when screening, the possible deleterious effects of screen-detection must be weighed against the benefits.Dr Waterbor is with the Department of Epidemiology, School of Public Health, University of Alabama at Birmingham, AL, USA. Dr Bueschen is with the Division of Urology, Department of Surgery, School of Medicine, University of Alabama at Birmingham. Address correspondence to Dr Waterbor, University of Alabama at Birmingham, Department of Epidemiology, Tidwell Hall 201, 720 S 20th Street, Birmingham, AL 35924-0008, USA.     

Diabetes mellitus and risk of prostate cancer (United States)

A lower risk of prostate cancer among diabetics has been suggested by several but not all studies. However, the studies have not always accounted for time since diagnosis of diabetes mellitus, or have not examined confounding factors such as diet and diagnostic bias. We thus examined this relationship in the Health Professionals Follow-Up Study from 1986 and 1994, in which 1,369 new cases of non-stage A1 prostate cancer were documented in 47,781 men. A prior history of a diagnosis of diabetes (mostly adult-onset) was associated with a reduced risk of prostate cancer (multivariate relative risk [RR] = 0.75; 95 percent confidence interval [CI] = 0.59-0.95) controlling for age, body mass index (wt/ht2) at age 21, and, in 1986, race, vasectomy, and intakes of total energy, total fat, calcium, fructose, and lycopene. After excluding the first year of follow-up after the diagnosis of diabetes, the RR was 0.63 (CI = 0.54-0.89). Prostate cancer was not reduced in the first five years after diagnosis (RR = 1.24, CI = 0.87-1.77), but was lower in the next five years (RR = 0.66, CI = 0.39-1.10) and lowest after 10 years (RR = 0.54, CI = 0.37-0.78); P-value for trend across time = 0.004. Similar associations were noted for advanced cases. Detection bias was unlikely to account for our findings. The basis of this relationship is unclear but may reflect hormonal changes related to diabetes, perhaps low testosterone levels.     

Serum vitamin D,vitamin D binding protein,and lung cancer survival

ObjectivesVitamin D may prolong cancer survival by inhibiting tumor progression and metastasis, however, there are limited epidemiologic studies regarding the association between circulating 25-hydroxyvitamin D (25(OH)D) and lung cancer survival. The aim of this study was to examine the relationship between serum 25(OH)D and lung cancer specific survival and to evaluate whether vitamin D binding protein (DBP) concentration modified this association.Materials and methods25(OH)D and DBP were measured in fasting serum samples from 500 male lung cancer cases in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Cox proportional hazards regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CI) for lung cancer related death according to quartiles of season-specific 25(OH)D, DBP, and the molar ratio of 25(OH)D:DBP, a proxy for free circulating 25(OH)D.ResultsComparing highest to lowest quartiles, serum 25(OH)D (HR = 1.18; 95% CI: 0.89–1.56) and DBP (HR = 0.95; 95% CI: 0.71–1.26) were not associated with lung cancer survival and DBP concentration did not modify the association with 25(OH)D (p for interaction = 0.56). There was suggestion of an association between higher serum 25(OH)D and better survival from adenocarcinoma (HR = 0.64; 95% CI: 0.17–2.45) and small cell carcinoma (HR = 0.55; 95% CI: 0.21–1.45), but these estimates were based on a relatively small number of cases.ConclusionSerum 25(OH)D was not associated with overall lung cancer survival regardless of DBP concentration, however, these findings should be examined in other studies that include women and subjects with higher 25(OH)D levels.     

Early body size and subsequent weight again as predictors of breast cancer incidence (Iowa,United States)

We examined whether associations of adult weight gain with the risk of postmenopausal breast cancer vary by stature, waist-hip ratio (WHR), and early adult size in a cohort of 37,105 Iowa (United States) women. Both low body mass index (kg/m²) (BMI) at age 18 and high subsequent weight-gain were associated independently with increased risk of incident postmenopausal breast cancer. After stratifying on BMI at age 18, high weight gain was associated with increased risk irrespective of whether early BMI was low (relative risk [RR]=1.92, 95 percent confidence interval [CI]=1.45–2.53) or high (RR=1.59, Ci=1.19–2.12). Women with lower BMI at 18 were at a higher risk at all levels of weight change, but having low BMI at age 18 and low subsequent weight gain conferred no significantly excess risk over those with high BMI at 18 and low gain. An inconsistent increase in risk was associated with taller stature; there was no additional risk associated with high WHR. Part of the observed risk from lower early size may reflect greater weight gain by lighter women. Limiting adult weight gain thus may be a feasible method to avoid increasing an individual's risk of breast cancer. Reasons for different effects of early cf late weight gain are not established, but benefits of a greater size at age 18 are likely to be offset by increased risks of other weight-related diseases at older ages.This work was supported by grant R01-CA 39724 from the US National Cancer Institute. Dr Barnes-Josiah was supported by a US Public Health Service Award (5 T32 CA 09607).     

Risk of endometrial cancer following cessation of menopausal hormone use (Washington, United States)

While there are a number of benefits to the health of postmenopausal women from use of unopposed estrogens, the increased risk of endometrial cancer related to these hormones has led many women to use combined estrogen-progestogen therapy instead, or not to use hormones at all. Most women who take hormones do so only in the early portion of their postmenopausal years, so the risk of endometrial cancer following cessation of use might bear heavily on the overal risk/benefit evaluation. We analyzed data from a case-control study of women in western Washington (United States) to assess the magnitude of excess risk of endometrial cancer following discontinuation of estrogen use. Cases (n=661) consisted of women aged 45 to 74 diagnosed between 1985 and 1991 who resided in one of three counties in Washington State. Controls (n=865) were identified by random-digit dialing. Subjects were interviewed in-person to ascertain current and prior hormone use. The analysis was restricted to women who had not received combined estrogen-progestin therapy. Among women who had used unopposed estrogens at some time, risk of endometrial cancer declined as time since last use increased. Nonetheless, even among women who used these hormones for just a few years, the risk remained elevated by 30 to 70 percent almost a decade after cessation. These results, combined with those of most (but not all) other studies of this issue, suggest that a woman who has discontinued unopposed estrogen therapy may retain a small increased risk of endometrial cancer for a long period of time.Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, the Department of Epidemiology, University of Washington Department of Biostatistics University of Washington, Seattle, WA. Department of Epidemiology, University of Washington, Seattle, WA 98195, USA. This research was supported by US National Cancer Institute contracts R01 CA47749 and R35 CA39779.     

Calcium,vitamin D,and risk of adenoma recurrence (United States)

Objective: Few data exist regarding the association between calcium intake and adenoma recurrence, and no data exist for vitamin D. We investigated the role of dietary and supplemental sources of calcium and vitamin D in the etiology of adenoma recurrence. Methods: Analyses were conducted among 1304 male and female participants in the Wheat Bran Fiber (WBF) trial of adenoma recurrence. Multiple logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). Results: In the fully adjusted multivariate model, the OR for participants with dietary calcium intake above 1068 versus those with intake below 698 mg/day was 0.56 (95% CI = 0.39–0.80; p-trend = 0.007). Calcium supplementation at doses above 200 mg/day did not affect risk of recurrence. Although a borderline inverse association between dietary vitamin D and recurrence was observed after adjustment for age and gender, the association weakened in the fully adjusted model (OR = 0.78 for individuals in the upper compared to the lower quartile; 95% CI = 0.54–1.13). No association was shown for supplemental sources of vitamin D. Conclusions: Results of this study indicate that a higher intake of calcium decreases the risk of adenoma recurrence by approximately 45%, whereas vitamin D has no significant effect on recurrence rates.     

Recent oral contraceptive use and risk of breast cancer (United States)

We examined the association between recent oral contraceptive (OC) use and the risk of breast cancer in data from a large population-based case-control study in the United States. Cases (n=6,751) were women less than 75 years old who had breast cancer identified from statewide tumor registries in Wisconsin, Massachusetts, Maine, and New Hampshire. Controls (n=9,311) were selected randomly from lists of licensed drivers (if aged under 65 years) and from lists of Medicare beneficiaries (if aged 65 through 74 years). Information on OC use, reproductive experiences, and family and medical history was obtained by telephone interview. After adjustment for parity, age at first delivery, and other risk factors, women who had ever used OCs were at similar risk of breast cancer as never-users (relative risk [RR]=1.1, 95 percent confidence interval [CI]=10–1.2). Total duration of usealso was not related to risk. There was a suggestion that more recent use was associated with an increased risk of breast cancer; use less than two years ago was associated with an RR of 1.3 (CI=0.9–1.9). However, only among women aged 35 to 45 years at diagnosis was the increase in risk among recent users statistically significantly elevated (RR=2.0, CI=1.1–3.9). Use prior to the first pregnancy or among nulliparous women was not associated with increased risk. Among recent users of OCs, the risk associated with use was greatest among non-obese women, e.g., among women with body mass index (kg/m²) less than 20.4, RR=1.7, CI=1.1–2.8. While these results suggest that, in general, breast cancer risk is not increased substantially among women who have used OCs, they also are consistent with a slight increased risk among subgroups of recent users.Authors are with the University of Wisconsin Comprehensive Cancer Center, Madison, WI, USA (Dr Newcomb, Ms Trentham Dietz); NIEHS Epidemiology Branch, Research Triangle Park, NC (Dr Longnecker); Fred Hutchinson Cancer Research Center, Seattle, WA (Dr Surer); Department of Obstetrics and Gynecology, Pritzker School of Medicine, The University of Chicago, Chicago, IL (Dr Mittendorf); Department of Community and Family Medicine, Dartmouth Medical School, Hanover, NH (Dr Baron); Boston University, School of Public Health, Boston, MA (Dr Clapp); Department of Epidemiology and Department of Nutrition, Harvard School of Public Health, and Channing Laboratory, Harvard Medical School and Department of Medicine, Brigham and Women's Hospital, Boston, MA (Dr Willett). Address correspondence to: Dr Polly A. Newcomb, University of Wisconsin-Madison Comprehensive Cancer Center, 1300 University Ave., #4780, Madison, WI 53706, USA. Supported by Public Health Service (National Cancer Institute) grants R01 CA 47147 and R01 CA 47305.     

Dairy products, calcium, phosphorous, vitamin D, and risk of prostate cancer (Sweden)

Objectives: Dairy products consistently have been associated with an increased risk of prostate cancer, yet the mechanism of this relationship remains unknown. Recent hypotheses propose that 1,25 dihydroxyvitamin D (1,25 D) is protective for prostate cancer. One study in the United States found that calcium consumption, which can lower circulating 1,25 D, was associated with higher risk of advanced prostate cancer, and we sought to address this hypothesis in a distinct population.Methods: We analyzed data from a population-based case- control study of prostate cancer conducted in Örebro, Sweden, with 526 cases and 536 controls. Using unconditional logistic regression models, we examined the relationship of dairy products, dietary calcium, phosphorous, and vitamin D with risk of total, extraprostatic, and metastatic prostate cancer.Results: Calcium intake was an independent predictor of prostate cancer (relative risk (RR)=1.91, 95 percent confidence interval (CI) 1.23-2.97 for intake 1183 vs. <825mg/day), especially for metastatic tumors (RR=2.64, 95 percent CI 1.24-5.61), controlling for age, family history of prostate cancer, smoking, and total energy and phosphorous intakes. High consumption of dairy products was associated with a 50 percent increased risk of prostate cancer.Conclusions: Our results support the hypothesis that high calcium intake may increase risk of prostate cancer, and this relation may underlie previously observed associations between dairy products and prostate cancer.     

The accuracy of prostate cancer staging in a population-based tumor registry and its impact on the Black-White stage difference (Connecticut,United States)

Stage at diagnosis of prostate cancer is a major determinant of survival. Among Blacks, prostate cancer is diagnosed at a later stage of disease than among Whites. This study examined the accuracy of routine coding of prostate cancer stage in the Connecticut (United States) Tumor Registry (CTR) and its effect on the Black/White stage difference. Medical records were collected for 115 Black and 136 White men with prostate cancer diagnosed between 1987 and 1990. Stage at diagnosis was determined by a panel of two of the study members and compared with the stage in the CTR file. According to the panel, 32 percent of Blacks, but only 15 percent of Whites, were diagnosed with distant stage disease. Fifty-eight cases (26 percent of Whites and 20 percent of Blacks) were staged incorrectly by the CTR. Two-fifths of the errors were due to incomplete medical records at the CTR and three-fifths were due to CTR coding or data management errors. The more accurate staging did not have an appreciable impact on the Black/White stage difference. Further work is needed to characterize the accuracy of routinely coded cancer registry stage data for different cancer sites, to devise ways of improving accuracy, and to determine the impact of staging inaccuracies on research that utilizes these data.This study was supported by grant 5-PO1-CA42101 from the US National Cancer Institute. Dr Dubrow received support from an NCI Preventive Oncology Academic Award, K07-CA01463.     

Physical activity in usual occupation and risk of breast cancer (United States)

We have used data from a large population-based case-control study inthe United States to evaluate the effect of occupational physical activity onbreast cancer risk. Women diagnosed with breast cancer identified from fourstate cancer registries, and controls randomly selected from lists oflicensed drivers or Medicare beneficiaries, were interviewed by telephone forinformation on usual occupation and other factors. We classified usualoccupation into one of four categories of physical activity. After excludingsubjects for whom a strength rating could not be assigned, we had a finalsample size of 4,863 cases and 6,783 controls. Using conditional logisticregression models, we calculated adjusted odds ratios (OR) and 95 percentconfidence intervals (CI) for occupations having light, medium, and heavyactivity compared with sedentary ones. Women with heavy-activity occupationshad a lower risk of breast cancer than women with sedentary jobs (OR = 0.82,CI = 0.63-1.08), as di d women with jobs with medium activity (OR = 0.86, CI= 0.77-0.97) or light activity (OR = 0.92, CI = 0.84-1.01). There was asignificant decreasing trend in the ORs from sedentary to heavy work (P =0.007). Although limited by exposure misclassification, these data areconsistent with the hypothesis that physical activity reduces the risk ofbreast cancer.     

UV, latitude, and spatial trends in prostate cancer mortality: All sunlight is not the same (United States)

Objective We showed previously that Caucasian mortality rates from prostate cancer for 1970–1979 are significantly inversely correlated with ultraviolet (UV) radiation. We now present the analysis of prostate cancer mortality data over a 45-year period (1950–1994) in order to examine the persistence of this pattern. Furthermore, because vitamin D synthesis does not occur during winter months at latitudes higher than 40° N, we examined this relationship above and below 40° N latitude. Methods We used trend surface and linear regression analyses to characterize the relationship between prostate cancer mortality and UV radiation for U.S. counties at northern and southern latitudes. Results For U.S. Caucasians, prostate cancer mortality rates at the county and SEA levels followed a significant north–south spatial trend that is the inverse of UV radiation. We found significant inverse correlations between UV radiation and prostate cancer mortality at all time points over this 45-year period. These correlations were significantly more pronounced at locations north of 40° N latitude. Conclusions Our analyses confirm and extend our findings that the geographic distribution of prostate cancer mortality is the inverse of that of UV radiation. This effect is strongest in counties north of 40° N latitude, where vitamin D synthesis is limited to non-winter months. These findings add additional support for the hypothesis that vitamin D insufficiency increases risk for prostate cancer.     

Strenuous physical activity in young adulthood and risk of breast cancer (United States)

The epidemiologic data on the relation between strenuous physical activity and breast cancer are limited and inconsistent. Because risk of breast cancer may be influenced by ovarian function which, in turn, is modulated by physical activity, the hypothesis that exercise may be associated with a reduced risk of breast cancer merits further investigation. We, therefore, conducted a large case-control study in 1988–91, and interviewed 6,888 women (17 to 74 years of age) with breast cancer in Maine, Massachusetts, New Hampshire, and Wisconsin (United States). Interviewed controls (9,539 women, 18 to 74 years of age) were selected randomly from lists of licensed drivers (for younger women) or from a roster of Medicare enrollees (for older women). We used multivariate adjusted odds ratios (OR) and 95 percent confidence intervals (CI) from logistic regression models to estimate relative risks between self-reported physical activity when 14 to 22 years of age and breast cancer. When compared with sedentary controls, women who reported any strenuous physical activity during ages 14 to 22 years had a modest reduction in the risk of breast cancer (OR=0.95, CI=0.93–0.97). However, those who exercised vigorously at least once a day had a 50 percent reduction in risk of breast cancer (OR=0.5, CI=0.4–0.7). These data support the hypothesis that women who are physically active have a reduced risk of breast cancer.This project is funded by grants (R01 CA 47147 and R01 CA 47305) from the US Public Health Service.Dr Mittendorf was also supported by National Research Service Award No. 5 T32 ES07069.     

Marijuana use and cancer incidence (California, United States)

The purpose of this retrospective cohort study was to examine therelationship of marijuana use to cancer incidence. The study populationconsisted of 64,855 examinees in the Kaiser Permanente multiphasic healthcheckup in San Francisco and Oakland (California, United States), between1979-85, aged 15 to 49 years, who completed self-ad-ministered questionnairesabout smoking habits, including marijuana use. Follow-up for cancer incidencewas conducted through 1993 (mean length 8.6 years). Compared withnonusers/experimenters (lifetime use of less than seven times), ever- andcurrent use of marijuana were not associated with increased risk of cancer ofall sites (relative risk [RR] = 0.9, 95 percent confidence interval [CI] =0.7-1.2 for ever-use in men; RR = 1.0, CI = 0.8-1.1 in women) in analysesadjusted for sociodemographic factors, cigarette smoking, and alcohol use.Marijuana use also was not associated with tobacco-related cancers or withcancer of the following sites: co lorectal, lung, melanoma, prostate, breast,cervix. Among nonsmokers of tobacco cigarettes, ever having used marijuanawas associated with increased risk of prostate cancer (RR = 3.1, CI =1.0-9.5) and nearly significantly increased risk of cervical cancer (RR =1.4, CI = 1.0-2.1). We conclude that, in this relatively young study cohort,marijuana use and cancer were not associated in overall analyses, but thatassociations in nonsmokers of tobacco cigarettes suggested that marijuana usemight affect certain site-specific cancer risks.     

Incomplete pregnancies and risk of ovarian cancer (Washington, United States)

Because of the reduced risk of ovarian cancer related to prior full-term pregnancies, we sought to determine whether there was any association with a history of one or more incomplete pregnancies. White female residents of three counties in Washington State (United States) diagnosed with ovarian cancer during 1986–88 (n=322), and a random sample of control women selected from these same counties (n=426), were interviewed regarding their pregnancy and childbearing histories. Among women who had given birth to at least one child, an additional incomplete pregnancy was not associated with the risk of ovarian cancer (relative risk [RR]=1.1, 95 percent confidence interval [CI]=0.8–1.6, adjusting for age, oral contraceptive use, and number of births). For those who had never given birth, a somewhat smaller proportion of cases had a history of incomplete pregnancy than controls (RR=0.8, CI=0.4–1.7). In an analysis restricted to ever-pregnant women, a prior induced or spontaneous abortion was not found to be associated with the incidence of ovarian tumors (RR=1.0, CI=0.6–1.7, and RR=1.3, CI=0.8–1.9, respectively). Other studies of the possible relation between incomplete pregnancies and ovarian cancer generally have observed either a weak negative association or no association at all. It is possible that if incomplete pregnancies do affect the risk of ovarian cancer, their impact might be too small to be identified reliably through epidemiologic studies.This research was supported in part by a grant from the US National Cancer Institute (R35 CA39779), and by the Cancer Surveillance System of the Fred Hutchinson Cancer Research Center, which is funded by Contract No. N01-CN-05230 from the Surveillance, Epidemiology and End Results (SEER) program of the National Cancer Institute with additional support from the Fred Hutchinson Cancer Research Center.     

Diet diversity, diet composition, and risk of colon cancer (United States)

In this study, we evaluate diet diversity, diet composition, and risk of colon cancer in an incident population-based study of 1,993 cases and2,410 controls in the Kaiser Permanente Medical Care Program of Northern California, eight counties in Utah, and the Twin Cities area of Minnesota(United States). Ninety-one and one-half percent of the population were non-Hispanic White. Dietary intake was obtained using an adaptation of the CARDIA diet-history questionnaire. Diet diversity was defined as the number of unique food items reported; diversity also was explored within six major food groups. Composition of the diet was described by estimating the proportion of total number of food items contributed by major food groups. Younger individuals, higher educated individuals, and those who lived in larger households reported eating the most diverse diet. Total diet diversity was not associated with colon cancer. However, eating a diet with greater diversity of meats, poultry, fish, and eggs, was associated with a50 percent increase in risk among all men (95 percent confidence interval[CI] = 1.1-2.0; P trend = 0.01), with slightly stronger associations for younger men and men with distal tumors. A diet with a greater number of refined grain products also was associated with increased risk among men(odds ratio [OR] = 1.7, CI = 1.3-2.3). Women who ate a diet with a more diverse pattern of vegetables were at approximately a 20 percent lower risk than women who had the least diverse diet in vegetables. Assessment of diet composition showed that men who consumed a large proportion of their food items from meat, fish, poultry, and eggs were at an increased risk, with the most marked association being for distal tumors (OR = 1.7, CI = 1.2-2.5).Women who consumed the largest percentage of their food items in the form of plant foods (fruits, vegetables, or whole grains) were at a reduced risk of developing colon cancer (OR = 0.7, CI = 0.5-1.0). This revised version was published online in July 2006 with corrections to the Cover Date.