Obesity is a well‐known risk factor for postmenopausal breast cancer. In contrast, the relationship between obesity and stage of breast cancer at diagnosis is less clear. We hypothesized that increased breast size in obese women may delay discovery of breast tumors. Thus, the purpose of our study was to examine whether there is an association between body mass and stage of breast cancer at diagnosis using hospital medical records. Newly diagnosed breast cancer cases ( n = 966) in the Baltimore metropolitan area from 1991 to 1997 were included in our study. Patient information including age, ethnicity, weight, height and pathology data were obtained from hospital medical records. High body mass was significantly associated with late stage of breast cancer at diagnosis. Women who were obese (body mass index [BMI] ≥ 27.3) were more likely to be at an advanced stage at diagnosis compared with women with a BMI of < 27.3 (multivariate‐adjusted odds ratio [OR] 1.57, 95% confidence interval [CI] 1.15–2.14). The association between body mass and stage at diagnosis was stronger among women younger than 50 years (OR 2.34, 95% CI 1.34–4.08) compared with women 50 years or older (OR 1.30, 95% CI 0.89–1.91). Our study suggests that higher body mass is associated with advanced stage of breast cancer at diagnosis. This finding may be of considerable concern, given the increasing prevalence of obesity in women in the United States and the poor prognosis associated with late‐stage tumors. © 2001 Wiley‐Liss, Inc.

OBJECTIVEBlack women are more likely to be diagnosed at a more advanced stage of breast cancer than are white women. Traditionally, this has been attributed in part to social or cultural factors. Given that black women are more likely to be obese than white women and that being obese is associated with a more advanced stage at diagnosis, this study aims to assess to what extent the racial difference in stage at diagnosis can be explained by racial differences in obesity.METHODSIncident cases of breast cancer between 1991 and 1997 (white, n = 585; black, n = 381) were identified from hospitals in the Baltimore metropolitan area. Information, including age, race, weight, height, and pathology reports, was obtained from hospital medical records.RESULTSBlack women were more likely than white women to be diagnosed with breast cancer at tumor-node-metastasis (TNM) stage II or greater (age-adjusted odds ratio [OR] = 1.51, 95% confidence interval [CI] 1.15-1.99). Further, black women were more likely than white women to be overweight or obese. A high body mass index (BMI) was significantly associated with an advanced stage of breast cancer at diagnosis. Adjustment for the higher prevalence of obesity in black women attenuated the risk estimate of more advanced stage of breast cancer at diagnosis in black women compared with white women by approximately 30%.CONCLUSIONSOur results suggest that the higher prevalence of obesity among black women plays an important role in explaining their relative disadvantage in stage at diagnosis of breast cancer. Nonetheless, a racial difference in stage of breast cancer at diagnosis persists after adjustment for obesity.

Science is the process of discovering truth, and "truth" is sampled each time we do a study. The results from all of our studies will be distributed around the truth, and different study designs give different amounts and different qualities of sampled material. Truth is ascertained only when sufficient numbers of appropriate studies are conducted, and no one study or one study design has a monopoly on truth. Currently, the randomized clinical trial is considered the penultimate study design and the ultimate test of the hypothesis, but only if it is double-blinded, placebo-controlled, and analyzed by an intention-to-treat protocol.The study design most similar to the randomized controlled trial is the prospective cohort study. In this observational approach, a cohort (group of individuals) is assembled and followed in real time while end points (e.g. breast cancers, heart attacks, fractures) accrue. This is contrasted to the randomized controlled trial, where a group of individuals is assembled, intervened upon, and followed in real time while end points accrue. The major advantage of the randomized controlled trial over an observational study is that the randomization process should eliminate any "bias" in the exposure of interest. However, the randomized controlled trial, like all study designs, has other limitations.Major limitations of the randomized controlled trial include significant financial and other costs, problems with external generalizability, the placebo effect, external monitoring, multi-center differences, and the (frequently problematic) intention-to-treat analysis rule. Many of these limitations do not occur in prospective cohort studies. For example, since a placebo is not administered in an observational study, there is no placebo effect, and since the study is not monitored by a data and safety monitoring board, abrupt truncation of the study duration is not usually seen in observational cohort studies.These limitations of randomized controlled trials are discussed, with specific references to several recently published randomized controlled trials in women (HERS, NSABP P-1, and the Royal Marsden Hospital trials). The HERS trial is significant because despite overwhelming observational evidence that menopausal estrogen therapy prevents heart disease, HERS found no overall difference in heart disease events in women assigned to an estrogen-plus-progestin intervention. The NSABP P-1 and the Royal Marsden Hospital trials are significant in that they were testing the same hypothesis (whether tamoxifen can prevent breast cancer), but came to entirely different conclusions.Two major questions will be posed from this specific review:One: Given conflicting evidence by study design (observational vs. randomized clinical trial), does menopausal estrogen therapy protect against heart disease?Two: Given conflicting evidence within study design (conflicting randomized clinical trials), does tamoxifen prevent breast cancer?.

OBJECTIVE:To describe long-term mortality trends by ethnicity, sex, and age for selected cancers and to assess the effect of age-adjustment using different standard populations on rate ratios and rate differences comparing black to white cancer mortality. DESIGN:Mortality rates for selected cancers were obtained from published reports of the Vital Statistics of the United States (1950-1992). All ethnic- and sex-specific cancer rates were directly age-adjusted to the total 1970 US standard population and to a subset of the 1970 US standard population 40 years and older. RESULTS:Over a 42-year period, lung cancer mortality increased in all population subgroups. Colorectal cancer mortality declined in whites, but increased in blacks. Prostate cancer mortality increased slightly in white men, but dramatically increased in black men. Breast cancer mortality stabilized in white women, but increased markedly in black women. Uterine cancer mortality declined for both ethnicities, while ovarian cancer mortality rates increased for both ethnicities. As expected, the ratios of the age-adjusted cancer mortality rates comparing blacks to whites were the same regardless of the age structure used as the standard population. In contrast, the differences in the age-adjusted rates between blacks and whites were greater when the age-truncated standard population was used. CONCLUSIONS:There are unexplained ethnic differences in the long-term mortality trends of selected cancers. Of particular concern are the increasing death rates in black individuals from colorectal, prostate, breast, and ovarian cancers. Since almost all deaths from these cancers occur in persons over 40, age-adjustment using an age-truncated standard population that includes only those age groups at risk should be considered, particularly when the question to be addressed is one dealing with the impact of a characteristic, such as ethnicity or sex, on mortality risk.

BACKGROUNDNon-high-density lipoprotein cholesterol (non-HDL-C) contains all known and potential atherogenic lipid particles. Therefore, non-HDL-C level may be as good a potential predictor of risk for cardiovascular disease (CVD) as low-density lipoprotein cholesterol (LDL-C).OBJECTIVESTo determine whether non-HDL-C level could be useful in predicting CVD mortality and to compare the predictive value of non-HDL-C and LDL-C levels.METHODSData are from the Lipid Research Clinics Program Follow-up Study, a mortality study with baseline data gathered from 1972 through 1976, and mortality ascertained through 1995. A total of 2406 men and 2056 women aged 40 to 64 years at entry were observed for an average of 19 years, with CVD death as the main outcome measure.RESULTSA total of 234 CVD deaths in men and 113 CVD deaths in women occurred during follow-up. Levels of HDL-C and non-HDL-C at baseline were significant and strong predictors of CVD death in both sexes. In contrast, LDL-C level was a somewhat weaker predictor of CVD death in both. Differences of 0.78 mmol/L (30 mg/dL) in non-HDL-C and LDL-C levels corresponded to increases in CVD risk of 19% and 15%, respectively, in men. In women, differences of 0.78 mmol/L (30 mg/dL) in non-HDL-C and LDL-C levels corresponded to increases in CVD risk of 11% and 8%, respectively.CONCLUSIONSNon-HDL-C level is a somewhat better predictor of CVD mortality than LDL-C level. Screening for non-HDL-C level may be useful for CVD risk assessment.

Media coverage of scientific research plays a major role in shaping public opinion and influencing medical practice. When an association is controversial, such as with hormone replacement therapy (HRT) and breast cancer, it is important that a balanced picture of the scientific literature be reported. The objective of this study was to assess whether scientific publications that do and do not support an HRT/breast cancer association were cited in the media in proportions similar to those with which they appear in the scientific literature. Scientific publications reporting on the HRT/breast cancer association published from January 1, 1995, to June 30, 2000, were identified through a systematic Medline search. Media reports from newspapers, magazines, television, and radio that reported on HRT and breast cancer were retrieved from an online database. Investigators independently recorded characteristics of the scientific publications and media reports. A total of 32 scientific publications were identified: 20 (62.5%) concluded there was an increased risk of breast cancer associated with HRT (positive publications), and 12 (37.5%) concluded there was no evidence for an association (null publications). Nearly half (47%) of the scientific publications were not cited by the media. There were 203 media citations of scientific publications: 82% were of positive publications and 18% were of null publications, representing a significant excess of citations of positive publications (p < 0.01). Media coverage of this controversial issue is based on a limited sample of the scientific publications. Moreover, the excess of media citations for positive scientific publications suggests a bias against null scientific publications.

The beneficial effects of SERMs, specifically tamoxifen in the treatment and prevention of breast cancer and raloxifene in the prevention of osteoporosis, are well established. In addition, numerous groups of investigators have reported that these agents have a positive impact on cardiovascular health, possibly as a result of their cholesterol-lowering and anticoagulation actions. Although studies clearly showed that tamoxifen therapy improved the levels of some types of lipids, the changes did not appear to translate into a decreased risk of cardiovascular disease. However, the risk of thromboembolic events (as well as endometrial cancer) was increased with the use of tamoxifen, which is often prescribed for breast cancer prevention in healthy women. Similarly, raloxifene treatment had modest positive effects on cardiovascular risk factors but was associated with an increased risk of thromboembolism. When viewed as a whole, study results dictate that the benefits of SERM use for the prevention of cardiovascular disease be carefully weighed against the potential risks.

OBJECTIVE: To assess whether recent epidemiologic evidence supports an association between use of estrogen replacement therapy or hormone replacement therapy and risk of breast cancer.DATA SOURCES: The keywords "estrogen," "estrogen replacement therapy," or "hormone replacement therapy," and "breast cancer" or "breast neoplasm," were used to search for articles published from 1975-2000 in MEDLINE and Dialogweb. Only articles published in peer-reviewed journals and containing original data were included in this review.METHODS: Unadjusted or age-adjusted risk estimates for breast cancer among ever users of estrogen therapy compared with never users were abstracted from published articles or calculated using the data provided in the published reports.TABULATION, INTEGRATION, AND RESULTS: We found little consistency among studies that estimated the risk of breast cancer in hormone users compared with nonusers and in studies assessing the risk by duration of use. However, there was consistently a lower risk of death from breast cancer in hormone users compared with nonusers.CONCLUSION: The evidence did not support the hypotheses that estrogen use increases the risk of breast cancer and that combined hormone therapy increases the risk more than estrogen only. Additional observational studies are unlikely to alter this conclusion. Although a small increase in breast cancer risk with hormone therapy or an increased risk with long duration of use (15 years or more) cannot be ruled out, the likelihood of this must be small, given the large number of studies conducted to date. (C) 2001 by the American College of Obstetricians and Gynecologists.

In the premenopausal period, the risk of heart disease is considerably lower in women than in men; however, in the postmenopausal period, when estrogen levels are considerably lower, women's risk of heart disease increases dramatically and approaches that of men. Numerous animal studies, using a variety of models, also confirm estrogen's cardioprotective effect. Although the results of numerous population-based, observational studies have demonstrated a lower risk of heart disease in women who receive estrogen replacement therapy, evidence from prospective, randomized clinical trials is scant. The Postmenopausal Estrogen/Progestin Intervention (PEPI) trial evaluated cardiovascular risk factors, not events, in a large, prospective, randomized trial and found that estrogen improved lipid profiles and other known risk factors. In addition, the PEPI trial compared several estrogen/progestogen treatment regimens, including both medroxyprogesterone acetate (MPA) and micronized progesterone (MP), and found that combined hormone replacement therapy regimens including MP attenuated the beneficial effects of estrogen less than those containing MPA. In the Heart and Estrogen/Progestin Replacement Study (HERS), however, which prospectively evaluated whether estrogen and MPA use reduced the number of nonfatal myocardial infarctions and cardiovascular events, no effect was seen. Although HERS was a null trial, the vast literature base showing a cardioprotective effect should not be discounted. Further research will be required before blanket recommendations on the cardioprotective effects of hormone therapy can be made.

BACKGROUND:Tamoxifen-treated breast carcinoma survivors are at elevated risk of endometrial carcinoma. Whether to recommend annual surveillance for uterine abnormalities in this population is currently under debate. METHODS:This study was a cross-sectional, community-based investigation of tamoxifen use and the frequency of surveillance for endometrial carcinomas in 541 women with breast carcinoma. Study participants whose breast carcinoma was diagnosed in 1994 were interviewed in 1998. Data were collected from a telephone interview and from a cancer registry record. Tests for uterine abnormalities, based on participant reports of endometrial biopsy and transvaginal ultrasound, were categorized according to frequency. Testing for uterine abnormalities was defined as irregular if women reported tests once every 3 years, on average, and as regular, if they reported annual tests. RESULTS:Forty-nine percent of respondents were current tamoxifen users, 12% were former tamoxifen users, and 39% reported never taking tamoxifen. Of respondents with a uterus (n = 385), 19% reported irregular and 30% regular testing for uterine abnormalities after their breast carcinoma diagnosis. Respondents more frequently reported transvaginal ultrasound (37%) than endometrial biopsy (29%). Women 65 years of age and older were significantly less likely to report regular surveillance for uterine abnormalities (16%) than those younger than 65 years (35%). Current tamoxifen users more frequently reported regular surveillance (43%) than either former (35%) or never tamoxifen users (15%). Multivariable analyses showed tamoxifen users were more likely to have regular (odds ratio [OR], 9.8; 95% confidence interval [CI], 4.4-21.8) or to have irregular testing for uterine abnormalities (OR, 3.9; 95% CI, 1.9-8.1) compared with women who never used tamoxifen, after adjustment for age, number of recent gynecologic visits, and gynecologic symptoms. CONCLUSIONS:The results of the current study indicate that half of the breast carcinoma survivors in this population were tested for uterine abnormalities. Although at increased risk, 38% of tamoxifen users never had a test. Clear guidelines need to be established for the type and frequency of testing for uterine abnormalities among tamoxifen-treated breast carcinoma patients.

Several studies have reported an association between hormone replacement therapy (HRT) in postmenopausal women and increased risk of idiopathic venous thromboembolic events (VTEs). Given the widespread use of HRT, it is important to identify factors that may predispose women on HRT to VTEs. To address this concern, we examined potential risk factors for VTEs in women assigned to HRT in the Postmenopausal Estrogen/Progestin Interventions (PEPI) study, a three-year, double-blinded, placebo-controlled trial of 875 postmenopausal women designed to assess the effects of HRT on heart disease risk factors (HDL cholesterol, fibrinogen, blood pressure, and insulin). Women with a history of estrogen-associated VTEs were excluded from the trial. Ten women, all assigned to HRT, had a VTE during PEPI. Only baseline fibrinogen varied significantly between those who did (mean = 249.0 mg/dl) and did not (mean = 280.8 mg/dl) have a VTE while assigned to HRT (P < 0.03). Adjusting for covariates including age, smoking, body mass index, lipid levels, blood pressure, alcohol, exercise, and prior HRT or oral contraceptive use did not affect this finding. The significantly lower fibrinogen levels seen among women subsequently reporting VTEs may be a marker for a specific, but as yet undefined, coagulopathy that is magnified in the presence of exogenous hormones. However, larger studies are needed to confirm this finding.

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