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Shelley S Tworoger

Publications and source records attributed to Shelley S Tworoger.

At least 19 recordsLinked to original sources

Reproductive factors and family history of breast cancer in relation to plasma prolactin levels in premenopausal and postmenopausal women.

Many reproductive factors are associated with breast cancer risk, potentially through a hormonal pathway. The peptide hormone prolactin is essential in mammary development and lactation and may be a link between risk factors and breast cancer. While higher prolactin levels are associated with increased breast cancer risk, few determinants of prolactin levels are known. We conducted a cross-sectional analysis among 1,089 premenopausal and 1,311 postmenopausal women within the Nurses' Health Study (NHS) and the NHS II to examine the associations of reproductive factors, benign breast disease and family history of breast cancer with plasma prolactin levels. Parous women had significantly lower prolactin levels than nulliparous women (parous vs. nulliparous multivariate-adjusted geometric means = 14.1 ng/mL vs. 16.6 ng/mL, p<0.001 for premenopausal and 9.1 vs. 10.1, p=0.04 for postmenopausal women), although levels did not decrease with increasing number of children for either premenopausal (p-trend = 0.23) or postmenopausal (p-trend = 0.07) parous women. Age at first birth was not associated with prolactin levels. The reduction in prolactin levels among parous premenopausal women appeared to attenuate with increasing time since first birth, but the trend was not statistically significant (p-trend = 0.12). Age at menarche, duration of lactation and benign breast disease were not associated with prolactin levels. Family history of breast cancer was associated with significantly higher prolactin levels when compared with no family history among premenopausal (15.9 ng/mL vs. 14.3 ng/mL, p=0.04) but not postmenopausal (p=0.73) women. In conclusion, the associations of parity and family history with breast cancer risk may be mediated, at least in part, by prolactin levels.

Adult↗

Plasma adiponectin concentrations and risk of incident breast cancer.

INTRODUCTION: Previous retrospective case-control studies suggest that adiponectin, an obesity-related hormone, is inversely associated with breast cancer risk, particularly in postmenopausal women; however, no prospective studies exist. Therefore, we conducted a prospective case-control study nested within the Nurses' Health Study (NHS) and NHSII cohorts examining the association between plasma adiponectin concentrations and breast cancer risk. MATERIALS AND METHODS: Blood samples were collected from 1989 through 1990 (NHS) and 1996 through 1999 (NHSII); adiponectin was measured by RIA. The analysis included 1477 breast cancer cases diagnosed after blood collection and before June 2000 (NHS) or June 2003 (NHSII) who had one or two controls (n=2196) matched on age, menopausal status, postmenopausal hormone (PMH) use, fasting, and time of day and month of blood collection. We adjusted for body mass index at age 18, weight change from age 18 to blood draw, family history of breast cancer, history of benign breast disease, duration of PMH use, ages at menarche and first birth, and parity. RESULTS: Although we observed no association between adiponectin and breast cancer risk overall, there was a nearly significant interaction by menopausal status (P=0.08), with a relative risk, top vs. bottom quartile of 0.73 (95% confidence interval, 0.55-0.98; P trend=0.08) among postmenopausal women and 1.30 (95% confidence interval, 0.80-2.10; P trend=0.09) for premenopausal women. Among postmenopausal women, adiponectin appeared more strongly inversely associated in women who never used PMH (P heterogeneity=0.05) and women with low circulating estradiol levels (P heterogeneity=0.05). DISCUSSION: Our results suggest that adiponectin may be inversely associated with postmenopausal breast cancer risk, particularly in a low-estrogen environment.

Adiponectin↗

Circulating insulin and c-peptide levels and risk of breast cancer among predominately premenopausal women.

Insulin and insulin resistance have been hypothesized to increase the risk of breast cancer as insulin increases breast cell proliferation and inhibits sex hormone binding globulin. Although insulin is directly related to body weight, adiposity is inversely associated with breast cancer risk in premenopausal women but directly related to risk in postmenopausal women. To explore the association between insulin and c-peptide levels and breast cancer risk, we conducted a nested case-control study of predominantly premenopausal women within the Nurses' Health Study II cohort. From 1996 to 1999, blood samples were collected from 29,611 participants. A total of 317 cases were diagnosed after blood collection and before June 2003 and matched to 634 controls; 75% of these women were premenopausal at blood collection. Logistic regression models, controlling for breast cancer risk factors, were used to calculate relative risks (RR) and 95% confidence intervals (95% CI). Among women with fasting blood samples (n = 211 cases), insulin was suggestively inversely associated with breast cancer risk (highest versus lowest quartile: RR, 0.5; 95% CI, 0.3-1.0; P(trend) = 0.06). Among all women, c-peptide was not associated with breast cancer risk (highest versus lowest quartile: RR, 1.1; 95% CI, 0.7-1.7; P(trend) = 0.79); results were similar among fasting samples. These associations did not differ by age, body mass index, or waist-to-hip ratio. Overall, higher levels of insulin and c-peptide were not associated with a higher risk of breast cancer among predominantly premenopausal women.

Adult↗

Associations between the CYP17, CYPIB1, COMT and SHBG polymorphisms and serum sex hormones in post-menopausal breast cancer survivors.

Several polymorphisms have been identified in genes that code for enzymes involved with estrogen biosynthesis and metabolism. Little is known about the functional relevance of these polymorphisms on sex hormones in vivo. We examined the association between CYP17, CYP1B1, COMT or SHBG genotypes and serum concentrations of estrone, estradiol, free estradiol, sex hormone-binding globulin (SHBG), testosterone, free testosterone and dehyroepiandrosterone in 366 post-menopausal breast cancer survivors in New Mexico, California and Washington. Hormone levels were determined by high performance liquid chromatography and radioimmunoassay in blood drawn approximately 2 years post-diagnosis. We used generalized linear regression to calculate mean hormone levels by genotype, adjusting for age, race/ethnicity, stage, study site, tamoxifen use, number of remaining ovaries, hormone therapy use, marital status and BMI. No associations were observed between any of the genotypes and sex hormones when analyzing the main effects. In subgroup analyses, androgen levels of Hispanic women with the variant (A2) CYP17 genotype were 46-87% higher than those of women with the wild-type; androgen levels were 13-20% lower in non-Hispanic whites with the variant genotype; no difference by genotype was observed for African-American women. Current tamoxifen users with the variant asn(327) SHBG genotype had 81% higher serum SHBG and 39% lower free testosterone concentrations than women with the wild-type genotype. Non-tamoxifen users with the variant SHBG allele had elevated free estradiol levels. These results provide little evidence that the CYP17, CYP1B1, and COMT polymorphisms are associated with different sex hormone levels in post-menopausal breast cancer survivors.

Adolescent↗

Endogenous steroid hormone concentrations and risk of breast cancer among premenopausal women.

BACKGROUND: Higher levels of endogenous sex steroid hormones are associated with increased risks of breast cancer in postmenopausal women. Data for premenopausal women are sparse, in part because of the complexity of measuring hormone levels that vary cyclically. We prospectively evaluated associations between plasma sex hormone levels and breast cancer risk among premenopausal women in a case-control study nested within the Nurses' Health Study II. METHODS: From 1996 to 1999, blood samples were collected from 18,521 premenopausal women during the early follicular and midluteal phases of their menstrual cycles. A total of 197 cases of breast cancer were diagnosed among these women after blood collection and before June 1, 2003; these case subjects were matched to 394 control subjects. Logistic regression models, controlling for breast cancer risk factors, were used to calculate relative risks (RRs) and 95% confidence intervals (CIs). All statistical tests were two-sided. RESULTS: Women in the highest (versus the lowest) quartiles of follicular total and free estradiol levels had statistically significantly increased risks of breast cancer (RR = 2.1 [95% CI = 1.1 to 4.1], P(trend) = .08, and RR = 2.4 [95% CI = 1.3 to 4.5], P(trend) = .01, respectively); the associations were stronger for invasive breast cancer and for estrogen and progesterone receptor-positive (ER+/PR+) tumors. Luteal estradiol levels were not associated with breast cancer risk. Higher levels of total and free testosterone and androstenedione in both menstrual cycle phases were associated with modest, non-statistically significant increases in overall risk of breast cancer and with stronger, statistically significant increases in risks of invasive and ER+/PR+ cancers (e.g., RR of invasive cancers for the top [versus bottom] quartile of luteal total testosterone levels = 2.0 [95% CI = 1.1 to 3.6], P(trend) = .05, and RR of ER+/PR+ cancers = 2.9 [95% CI = 1.4 to 6.0], P(trend) = .02). Levels of estrone, estrone sulfate, progesterone, and sex hormone-binding globulin were not associated with breast cancer risk. The absolute number of cases observed over 3 years were 30 among women in the lowest 25% of follicular total estradiol levels and 50 among women in the highest 25%. CONCLUSIONS: Levels of circulating estrogens and androgens may be important in the etiology of premenopausal breast cancer.

Adult↗

A prospective study on habitual duration of sleep and incidence of breast cancer in a large cohort of women.

Mounting evidence suggests habitual sleep duration is associated with various health outcomes; both short and long sleep duration have been implicated in increased risk of cardiovascular disease, diabetes, and all-cause mortality. However, data on the relation between sleep duration and cancer risk are sparse and inconclusive. A link between low levels of melatonin, a hormone closely related to sleep, and increased risk of breast cancer has recently been suggested but it is unclear whether duration of sleep may affect breast cancer risk. We explored the association between habitual sleep duration reported in 1986 and subsequent risk of breast cancer in the Nurses' Health Study using Cox proportional hazards models. During 16 years of follow-up, 4,223 incident cases of breast cancer occurred among 77,418 women in this cohort. Compared with women sleeping 7 hours, covariate-adjusted hazard ratios and 95% confidence intervals for those sleeping < or =5, 6, 8, and > or =9 hours were 0.93 (0.79-1.09), 0.98 (0.91-1.06), 1.05 (0.97-1.13), and 0.95 (0.82-1.11), respectively. A moderate trend in risk increase towards longer sleep duration was observed when analyses were restricted to participants who reported same sleep duration in 1986 and 2000 (P(trend) = 0.05). In this prospective study, we found no convincing evidence for an association between sleep duration and the incidence of breast cancer.

Adult↗

Endogenous steroid hormone concentrations and risk of breast cancer: does the association vary by a woman's predicted breast cancer risk?

PURPOSE: To examine whether the associations of endogenous estrogens and testosterone with breast cancer risk differ between high- and low-risk women, as determined by the Gail model and the Rosner and Colditz model, and by family history of breast cancer. METHODS: We conducted a prospective nested case-control study within the Nurses' Health Study. From 1989 or 1990 until June 2000, blood samples were collected, 418 breast cancer patient cases were identified, and two controls (total n = 817) were matched to each case. We classified women as high or low risk based on their family history of breast cancer, their 5-year Gail risk score, and their 5-year Rosner and Colditz risk score. Multivariate relative risks (RR) and 95% CI were calculated by unconditional logistic regression, adjusting for matching and breast cancer risk factors. RESULTS: Estrone sulfate was statistically significantly associated with breast cancer risk among women with low (< 1.66%) and high (> or = 2.52%; 75th percentile) Gail predicted risk (fourth v first quartile RR = 3.6; 95% CI, 1.9 to 7.0; RR = 2.5; 95% CI, 1.2 to 5.1, respectively). Testosterone results were similar across strata of predicted risk, with two times the risk in the fourth (v first) quartile. Estradiol appeared more strongly associated with breast cancer in women with higher predicted risk (RR = 4.5; 95% CI, 2.1 to 9.5) compared with women with lower risk (RR = 2.1; 95% CI, 1.2 to 3.6), but differences were not statistically significant. Results were similar across predicted Rosner and Colditz risk scores. CONCLUSION: These data suggest that higher levels of endogenous estrogens and testosterone are associated with increased breast cancer risk, regardless of predicted risk or family history of breast cancer.

Adult↗

Intake of folate and related nutrients in relation to risk of epithelial ovarian cancer.

Assessments of the relation between folate intake and ovarian cancer risk have been limited and inconsistent. Therefore, the authors prospectively examined the association of dietary and supplemental intakes of folate, methionine, and vitamin B(6) with ovarian cancer risk among 80,254 Nurses' Health Study participants. Beginning in 1976, women completed biennial questionnaires assessing ovarian cancer risk factors; starting in 1980, food frequency questionnaires were administered every 2-4 years. During 22 years of follow-up (1980-2002), the authors confirmed 481 incident epithelial ovarian cancers. There were no associations between total folate (top quintile vs. bottom: relative risk (RR) = 1.21, 95% confidence interval (CI): 0.92, 1.60), methionine (RR = 1.00, 95% CI: 0.76, 1.33), dietary vitamin B(6) (RR = 1.09, 95% CI: 0.81, 1.47), or total vitamin B(6) (RR = 1.13, 95% CI: 0.85, 1.51) intake and ovarian cancer risk. Higher dietary folate was associated with a modestly decreased risk after exclusion of cases diagnosed during the 4 follow-up years after dietary assessment (RR = 0.66, 95% CI: 0.43, 1.03) and for the serous subtype (RR = 0.51, 95% CI: 0.31, 0.84). Results did not vary by alcohol intake, multivitamin use, menopausal status, or oral contraceptive use. There was little evidence that folate, methionine, and vitamin B(6) are important in ovarian cancer risk, although dietary folate was inversely associated with risk in some analyses.

Adult↗

Prolactin and breast cancer risk.

Prolactin, a hormone involved in normal breast development and lactation, has been hypothesized to be important in the etiology of breast cancer. This review summarizes in vitro, animal, and epidemiologic data supporting this hypothesis. Experimental evidence indicates that prolactin can promote cell proliferation and survival, increase cell motility, and support tumor vascularization. Animal data suggest that prolactin can increase tumor growth rates and the number of metastases, as well as induce both estrogen receptor +(ER) and ER--tumors in a transgenic mouse model in which ER+ tumors are very rare. Epidemiologic data for premenopausal women are sparse; however a recent study with 235 cases reported a significant positive association between plasma prolactin levels and breast cancer risk. Studies in postmenopausal women have reported a positive association as well, and in the largest study (n=851 cases) the association was strongest for ER+ tumors. Overall, the available data support the hypothesis that prolactin increases risk of breast cancer. Future research directions include better characterizing the potential interplay between prolactin and estrogen and determining whether genetic variability in prolactin-related genes is associated with breast cancer risk.

Animals↗

Association between plasma prolactin concentrations and risk of breast cancer among predominately premenopausal women.

Recent evidence suggests that prolactin may be positively associated with postmenopausal breast cancer risk; however, little data are available in younger women. Therefore, we conducted a prospective, nested case-control study to examine the relationship between plasma prolactin concentrations and breast cancer risk in predominately premenopausal women from the Nurses' Health Study II. Blood samples were collected from 1996 to 1999. The analysis includes 316 cases of breast cancer diagnosed after blood donation and before June 1, 2003, who had two controls matched on age, fasting status, time of day and month of blood collection, race/ethnicity, and timing of blood draw within the menstrual cycle. Sixty-three percent of participants provided a timed follicular and luteal menstrual phase blood sample; other women provided a single untimed sample. When including all women, we observed a positive association between prolactin and breast cancer risk [relative risk (RR), top quartile versus bottom quartile, 1.5; 95% confidence interval (95% CI), 1.0-2.3; P(trend) = 0.03] that was slightly stronger among estrogen receptor-positive/progesterone receptor-positive tumors (comparable RR, 1.9; 95% CI, 1.1-3.3; P(trend) = 0.04). Associations were similar among premenopausal women only. However, we did not find an association between prolactin and breast cancer risk among the subset of women who only provided timed samples (comparable RR, average of timed samples, 1.3; 95% CI, 0.8-2.3; P(trend) = 0.40). The association seemed stronger among women > or = 45 years old and for cases diagnosed within approximately 4 years of blood collection. Our data suggest a modest positive association between prolactin and breast cancer risk among predominately premenopausal women; however, further follow-up is needed to increase power for subgroup analyses.

Adult↗

Use of biomarkers in epidemiologic studies: minimizing the influence of measurement error in the study design and analysis.

The inclusion of biomarkers measured on the continuous scale, such as endogenous sex hormones or antioxidant levels, has become common in epidemiologic studies, and introduces additional sources of error that are specific to biomarkers. This includes error associated with specimen collection, processing, and storage; laboratory error (both within and between batch); and variability in the biomarker levels over time within an individual. In this review, we discuss and recommend study design and analytic strategies to deal with these sources of measurement error. In particular we describe methods to prevent or minimize some sources of error through appropriate sample collection and storage, communication with the laboratory, proper batching of samples, and participant matching. We also discuss how to quantify error related to biomarkers, focusing on issues of quality control, pilot studies, and how to measure within-person stability over time. Further, we discuss analytic issues for dealing with laboratory and within-person variability. Finally we recommend that journals standardize the reporting of biomarker assays in scientific manuscripts.

Biomarkers↗

The association of plasma DHEA and DHEA sulfate with breast cancer risk in predominantly premenopausal women.

Concentrations of adrenal androgens are positively associated with postmenopausal breast cancer risk; however, results in premenopausal women are conflicting. Therefore, we conducted a prospective nested case-control study within the Nurses' Health Study II cohort to examine the relationship of DHEA and DHEA sulfate (DHEAS) with breast cancer risk in predominantly premenopausal women. Blood samples were collected from 1996 to 1999. The analysis included 317 cases of breast cancer diagnosed after blood collection and before June 1, 2003; for each case, two controls were matched on age, fasting status, time of day and month of blood collection, race/ethnicity, and timing of blood draw within the menstrual cycle. No associations were observed between DHEA or DHEAS levels and breast cancer risk overall [in situ and invasive; DHEA relative risk (RR), top versus bottom quartile, 1.2; 95% confidence interval (95% CI), 0.8-1.8, P(trend) = 0.53; DHEAS RR, 1.3; 95% CI, 0.9-2.0; P(trend) = 0.07]. However, both DHEA and DHEAS were positively associated with estrogen receptor-positive/progesterone receptor-positive breast cancer (DHEA RR, 1.6; 95% CI, 0.9-2.8, P(trend) = 0.09; DHEAS RR, 1.9; 95% CI, 1.1-3.3, P(trend) = 0.02). We observed a significant interaction by age, with an RR for DHEAS of 0.8 (95% CI, 0.4-1.5, P(trend) = 0.62) for women <45 years old and 2.0 (95% CI, 1.2-3.5, P(trend) = 0.003) for women >/=45 years old; results were similar for DHEA. Our results suggest that adrenal androgens are positively associated with breast cancer among predominately premenopausal women, especially for estrogen receptor-positive/progesterone receptor-positive tumors and among women over age 45 years.

Adult↗

Collection, processing, and storage of biological samples in epidemiologic studies: sex hormones, carotenoids, inflammatory markers, and proteomics as examples.

The measurement of biomarkers in blood specimens has become an integral component of many epidemiologic studies and introduces several decision points about specimen collection, processing, and storage for the investigator. We briefly discuss the current state of knowledge for four commonly assessed biomarkers: estrogens and other sex hormones, ascorbic acid and carotenoids, cytokines involved in the inflammatory response, and proteomics. Sex hormones are relatively robust to type of sample collected, delayed processing (if chilled), and long-term storage at <-70 degrees C. Ascorbic acid and carotenoids also are relatively robust to sample type and delayed processing (if chilled); however, the blood sample should not be exposed to sunlight and must be stored at <-70 degrees C to prevent substantial degradation. If ascorbic acid is of primary interest, an acid stabilizer should be added during processing. Less is known for cytokines and proteomics, although initial research suggests that these assays are sensitive to varying collection, processing, and storage methods. Overall, we recommend conducting pilot studies if any nonstandard collection, processing, or storage procedure is used. Finally, decisions about these issues depend primarily on the scientific questions of most interest, cost, flexibility, and resources.

Ascorbic Acid↗

Birthweight and body size throughout life in relation to sex hormones and prolactin concentrations in premenopausal women.

The association of birthweight and body size throughout life with premenopausal breast cancer risk may be due, in part, to relationships with sex hormones. Therefore, we assessed whether birthweight, body shape at ages 5 and 10, body mass index (BMI) at age 18 and adulthood, adult waist circumference and waist-to-hip ratio (WHR), and attained height were associated with the plasma concentrations of estrogens, androgens, progesterone, prolactin, and sex hormone-binding globulin (SHBG) in 592 premenopausal women, ages 33 to 52 years old, from the Nurses' Health Study II. About 85% of women provided blood samples during follicular and luteal menstrual phases; other women had a single untimed sample. We observed few associations between sex hormone levels and birthweight or body shape in childhood. However, adult BMI was inversely associated with SHBG (P trend < 0.001) and positively associated with free testosterone (P trend < 0.001) concentrations. Adult BMI was not associated with follicular or luteal free estradiol levels (P trend >or= 0.15) because it was inversely associated with total estradiol levels (P trend < 0.001 for follicular and luteal estradiol levels). Testosterone, androstenedione, and progesterone were inversely associated with BMI. Comparing women with a BMI of >or=30 versus <20 kg/m2, levels were higher by 53% for free testosterone and lower by 51% for SHBG, 39% for follicular estradiol, 20% for luteal estradiol, 14% for androstenedione, 13% for testosterone, and 20% for progesterone. We observed no clear associations between BMI at age 18, waist circumference, WHR, or height, and sex hormone concentrations. Our results suggest that effects on premenopausal sex hormone levels may be one mechanism through which adult adiposity, but not birthweight or childhood body size, affects premenopausal breast cancer risk.

Adult↗

Serum lipoproteins in overweight/obese postmenopausal women: a one-year exercise trial.

INTRODUCTION: This analysis was conducted to study the effect of a 1-yr moderate-intensity aerobic exercise program on serum lipoproteins among overweight/obese postmenopausal women. METHODS: We randomized 173 sedentary (VO2max = 20.2 mL.kg(-1).min(-1)), overweight/obese women (body mass index (BMI) 25.0-42.0 kg.m(-2) or body fat > 33% if BMI 24.0-25.0) aged 50-75 yr, not using hormone therapy, living in the Seattle area, to an exercise intervention or stretching control group. The exercise intervention included facility and home-based exercise (45 min, 5 d.wk(-1) of moderate-intensity sports or recreational exercise). Total cholesterol (TC), triglycerides, and high-density lipoprotein (HDL) were determined by chemical assay; low-density lipoprotein (LDL) was then calculated. RESULTS: Of the 173 women, 170 (98.3%) completed the study with exercisers averaging 176 (SD 91) min.wk(-1) of moderate- to vigorous-intensity (60%-75% HRmax) exercise, expending approximately 3828 kJ.wk(-1) (SD 2053). Exercisers, compared with stretchers, significantly increased their VO2max (+11%, P<0.001) and lost more body weight (-1.4 kg, P < 0.05), DEXA-% total body fat (-1.0, P < 0.005), L4-5 computed tomography intraabdominal fat (-8.6 cm2, P < 0.05) and subcutaneous abdominal fat (-28.8 cm2, P < 0.005) after 12 months. Mean (SD) baseline lipoprotein levels for TC, LDL, HDL, and triglycerides were 231 (39), 152 (39), 52 (12), and 135 (65) mg.dL(-1), respectively. We observed no significant change in serum lipoprotein levels among exercisers compared with stretchers at either 3 or 12 months postrandomization. We did not observe a statistically significant effect of exercise on serum lipoproteins in subgroups that changed their intraabdominal and subcutaneous fat, percent total body fat, or VO2max the most, or that adhered to the exercise regimen the most over 1 yr. CONCLUSION: It appears that a year long moderate-intensity exercise program alone does not significantly alter serum lipoprotein levels among overweight/obese postmenopausal women.

Aged↗

Effect of exercise on bone mineral density and lean mass in postmenopausal women.

PURPOSE: To evaluate the effects of physical activity on bone mineral density, bone mineral content, and lean mass in postmenopausal, overweight/obese women. METHODS: We conducted a 12-month randomized controlled aerobic exercise intervention versus control in 173 sedentary, overweight/obese, postmenopausal women, aged 50-75 yr. The exercise prescription consisted of >or=45 min of moderate-intensity aerobic exercise (60-75% of maximal heart rate), 5 d.wk for 12 months. Control participants attended 45-min stretching sessions once a week. Ninety-eight percent (N=170) completed the trial. Exercisers averaged 172 min.wk (SD=89) of exercise and expended 3828 kJ.wk (SD=2053). We assessed body fat, total lean mass, and total body bone mineral density and content using dual-energy x-ray absortiometry (DXA). We compared baseline with 12-month changes in exercisers versus controls. RESULTS: Exercisers lost significantly more weight than stretchers (1.3-kg loss vs 0.1-kg gain, P=0.01). However, no differences between exercisers and controls in the change from baseline to 12 months were detected: exercisers' average bone mineral density increased by 0.005 g.cm and controls' by 0.003 g.cm (P=0.61). Similarly, no significant differences were detected for bone mineral content. Lean mass increased by 0.2 kg in both groups (P=0.84). CONCLUSION: Overall, the results from this randomized controlled study suggest that a yearlong moderate-intensity aerobic exercise intervention does not affect total body bone mineral density, bone mineral content, or lean mass in overweight/obese postmenopausal women.

Aged↗

Plasma sex hormone concentrations and subsequent risk of breast cancer among women using postmenopausal hormones.

BACKGROUND: Sex hormone concentrations are associated with breast cancer risk among women not using postmenopausal hormones (PMH); however, whether a relationship exists among PMH users is unknown. Therefore, we conducted a prospective, nested case-control study within the Nurses' Health Study (NHS) cohort to examine the association between plasma sex hormone concentrations and postmenopausal breast cancer among women using PMH at blood collection. METHODS: Blood samples were collected from 1989 to 1990. During follow-up through May 31, 2000, 446 women developed breast cancer and were matched by age, date and time of day of blood collection, and fasting status to 459 control subjects (PMH users) who did not develop cancer. We used conditional logistic regression to estimate relative risks (RRs) and 95% confidence intervals (CIs). We compared hormone concentrations of the 459 control subjects with those of 363 postmenopausal NHS participants not taking PMH. All statistical tests were two-sided. RESULTS: PMH users had statistically significantly higher estradiol, free estradiol, sex hormone-binding globulin, and testosterone, and lower free testosterone concentrations than non-PMH users. Among PMH users, we found modest associations with breast cancer risk when comparing the highest versus lowest quartiles of free estradiol (RR = 1.7, 95% CI = 1.1 to 2.7; P(trend) = .06), free testosterone (RR = 1.6, 95% CI = 1.1 to 2.4; P(trend) = .03), and sex hormone-binding globulin (RR = 0.7, 95% CI = 0.5 to 1.1; P(trend) = .04), but not of estradiol or of testosterone. However, estradiol and free estradiol were statistically significantly positively associated with breast cancer risk among women older than 60 years (RR = 2.8, 95% CI = 1.5 to 5.0; P(trend) = .002 and 2.6, 95% CI = 1.4 to 4.7; P(trend) = .001, respectively) and among women with a body mass index of less than 25 kg/m2 (RR = 1.8, 95% CI = 1.1 to 3.1, P(trend) = .01 and 2.4, 95% CI = 1.4 to 4.0, P(trend) = .003, respectively). CONCLUSION: Although women using PMH have a different hormonal profile than those not using PMH, plasma sex hormone concentrations appear to be associated with breast cancer risk among PMH users.

Aged↗

Factors associated with objective (actigraphic) and subjective sleep quality in young adult women.

OBJECTIVE: The aim of this study was to describe factors associated with actigraphic and subjective sleep quality in young women. METHODS: Participants were 73 regularly menstruating women, 20-40 years old, who were not taking oral contraceptives, pregnant, or shift workers. Women contributed an average of 7 nights of actigraphy data during the luteal menstrual cycle phase, resulting in a total of 595 nights of data. RESULTS: One night of actigraphy data was unreliable for measuring total sleep time, sleep onset, and time in bed (intraclass correlation < or =.15) but was acceptable for measuring sleep efficiency and total wake time (intraclass correlation [ICC]=.52). Going to bed late, medication use, employment, increased daylight hours, longer menstrual cycle length, and higher body mass index (BMI) were associated with poorer actigraphic sleep measures. Employment, age, and perceived stress were associated with subjective sleep quality. CONCLUSION: Multiple factors were associated with sleep quality in these young women who were sleeping at home. However, the associations differed for subjectively versus actigraphically assessed sleep quality. Actigraphy is feasible for measuring sleep, but multiple recording nights may be needed to obtain reliable estimates.

Adult↗