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American Journal of Epidemiology Advance Access originally published online on September 19, 2007
American Journal of Epidemiology 2008 167(1):78-85; doi:10.1093/aje/kwm244
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American Journal of Epidemiology © The Author 2007. Published by the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

ORIGINAL CONTRIBUTIONS

Adiposity and Reporting of Vasomotor Symptoms among Midlife Women

The Study of Women's Health Across the Nation

Rebecca C. Thurston1,2, MaryFran R. Sowers3, Yuefang Chang4, Barbara Sternfeld5, Ellen B. Gold6, Janet M. Johnston2 and Karen A. Matthews1,2

1 Department of Psychiatry, School of Medicine, University of Pittsburgh, Pittsburgh, PA
2 Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA
3 Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI
4 Department of Neurosurgery, School of Medicine, University of Pittsburgh, Pittsburgh, PA
5 Division of Research, Kaiser Permanente Northern California, Oakland, CA
6 Department of Public Health Sciences, University of California, Davis, Davis, CA

Correspondence to Dr. Rebecca C. Thurston, Department of Psychiatry, University of Pittsburgh School of Medicine, 3811 O'Hara Street, Pittsburgh, PA 15213 (e-mail: thurstonrc{at}upmc.edu).

Received for publication May 9, 2007. Accepted for publication July 31, 2007.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
It has long been hypothesized that increased adiposity would be associated with decreased vasomotor symptoms during menopause because of conversion of androgens to estrogens in body fat. However, recent thermoregulatory models have postulated that increased adipose tissue would be associated with a greater likelihood of vasomotor symptoms. The authors evaluated these hypotheses in the Study of Women's Health Across the Nation, a multiethnic, community-based observational study of US women transitioning through menopause. The sample included 1,776 women aged 47–59 years with an intact uterus and at least one ovary who completed bioelectrical impedance analysis for assessment of body composition at the sixth annual study visit (2002–2004). Assessments also included reported vasomotor symptoms (hot flashes, night sweats) and serum levels of follicle-stimulating hormone, estradiol, and sex hormone-binding globulin-adjusted estradiol (free estradiol index). Results indicated that a higher percentage of body fat was associated with increased odds of reporting vasomotor symptoms (per standard deviation increase in percent body fat, odds ratio = 1.27, 95% confidence interval: 1.14, 1.42) in age- and site-adjusted models. Associations persisted in fully adjusted models and were not reduced when models included reproductive hormones. These findings support a thermoregulatory model of vasomotor symptoms.

adipose tissue; adiposity; body composition; body fat distribution; climacteric; hot flashes; menopause

Abbreviations: BIA, bioelectrical impedance analysis; CI, confidence interval; FEI, free estradiol index; FSH, follicle-stimulating hormone; OR, odds ratio; SD, standard deviation; SHBG, sex hormone-binding globulin; SWAN, Study of Women's Health Across the Nation


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Vasomotor symptoms are reported by 70–80 percent of women in the United States during the menopausal transition (1, 2) and up to one quarter of women in their 60s and 70s (3, 4). Vasomotor symptoms, or hot flashes and night sweats, are episodes of intense heat accompanied by flushing and sweating (2). They are associated with impaired quality of life (5), reported sleep disturbance (6), and depressed mood (7). For many years, hormone therapy was the primary treatment for vasomotor symptoms. However, in 2002, the hormone intervention arms of the Women's Health Initiative were terminated because of increased chronic disease among these postmenopausal women (8). Many women have discontinued hormone therapy (9), and the need for additional safe and effective methods for the management of vasomotor symptoms has become increasingly compelling and relevant (10). However, the limited understanding of risk factors for and the physiology of vasomotor symptoms has impeded development of alternate methods for managing them.

One factor that has been conceptualized both as a protective factor and as a risk factor is body fat. The pronounced alterations in reproductive hormone levels during menopause, including declining estrogen concentrations, have been implicated in the etiology of vasomotor symptoms (2, 11). Because androstenedione is aromatized into estrone in adipose tissue (12), body fat, as a supplemental source of estrogen, was long considered a protective factor for vasomotor symptoms (13). Thus, it was thought that women with higher adiposity should have higher estrogen concentrations than thinner women and a lower likelihood of vasomotor symptoms (14–17). This perspective was dubbed the "thin hypothesis."

Emerging findings showing increased vasomotor symptoms among women with higher body mass index (1, 18–20) have suggested that the thin hypothesis may be incomplete. These recent findings are consistent with thermoregulatory models of vasomotor symptoms that underscore the heat-dissipating function of vasomotor symptoms occurring in the context of a narrowed thermoneutral zone observed among symptomatic menopausal women (21, 22). Higher adiposity, a potent insulator (23), would thereby inhibit heat loss and increase levels of vasomotor symptoms, as more events would be required to achieve adequate heat loss (22).

Both of these models emphasize adipose tissue. However, previous investigations have been restricted to measures such as body mass index (1, 18–20), that do not clearly differentiate between lean and adipose tissue. One exception is our previous finding that abdominal adiposity is positively associated with hot flashes (24). However, whether these findings extend to total adiposity is not known. Moreover, our previous investigation was restricted to Caucasian and African-American women. Whether associations between adiposity and vasomotor symptoms vary across racial/ethnic groups is unclear.

Our primary aim in this investigation was to examine associations between adiposity and vasomotor symptoms among women transitioning through menopause. We hypothesized that women with a higher percentage of body fat would be more likely to report vasomotor symptoms. Moreover, we examined 1) whether these associations varied by race/ethnicity, 2) whether central adiposity as indexed by waist circumference was independently associated with vasomotor symptoms after accounting for total body fat, and 3) the role of reproductive hormones in these associations. Given their documented associations with vasomotor symptoms (11, 25, 26), we considered follicle-stimulating hormone (FSH), estradiol, and the free estradiol index (FEI), an estimate of biologically active estradiol.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 References
 
Study population
The Study of Women's Health Across the Nation (SWAN) is a multiethnic US cohort study designed to characterize biologic and psychosocial changes occurring during the menopausal transition. Details of the SWAN study design and recruitment procedures have been previously reported (27). Briefly, at each SWAN site, investigators recruited Caucasian women and a sample of a predetermined minority group (African-American women in Pittsburgh, Pennsylvania, Boston, Massachusetts, Detroit, Michigan, and Chicago, Illinois; Japanese women in Los Angeles, California; Hispanic women in Newark, New Jersey; and Chinese women in Oakland, California). To obtain large numbers of women of diverse backgrounds from the population, investigators at the Los Angeles, Newark, and Pittsburgh sites used random digit dialing sampling from banks of telephone numbers. At the Boston, Chicago, Detroit, and Oakland sites, investigators selected randomly from lists of names or household addresses. At most sites, the researchers supplemented primary sampling frames to obtain adequate numbers of racial/ethnic minority women. SWAN was approved by each site's institutional review board. Each participant provided written informed consent.

Baseline eligibility criteria for SWAN included being aged 42–52 years, having an intact uterus and at least one ovary, and in the previous 3 months, having had at least one menstrual cycle, without pregnancy, breastfeeding, or reproductive hormone use. Seventy-three percent of the women selected were contacted and provided sufficient information for determination of study eligibility. Of eligible women, 51 percent (n = 3,302) enrolled. SWAN baseline assessments were conducted in 1996–1997. At the sixth annual study visit (2002–2004), the investigators initiated measurement of adiposity via bioelectrical impedance analysis (BIA). Because a small, nonrepresentative sample of women from the New Jersey site (n = 23) underwent BIA, they were not included in this investigation. The present investigation was a cross-sectional analysis of associations between adiposity and vasomotor symptoms at SWAN visit 6.

This analysis was limited to the 1,985 women who underwent BIA. Of these women, 130 women who had had a surgical menopause and 79 women with missing data on a covariate or the dependent variable (hot flashes or night sweats (n = 57), smoking (n = 3), education (n = 11), waist circumference (n = 5), parity (n = 2), or anxiety symptoms (n = 5); four women had more than one missing value) were excluded from this analysis. Therefore, 1,776 women were included in the primary analyses. An additional 94 women were excluded from models incorporating hormone levels because of missing data. Women with missing data had higher percent body fat (p = 0.03) and were more likely than women without missing data to be African-American (p < 0.0001), to be a smoker (p = 0.01), and to have less than a college education (p = 0.05).

Design and procedures
Vasomotor symptoms.
SWAN included an interview, a physical examination, blood drawing, and questionnaires administered at baseline and annually thereafter. Vasomotor symptoms assessed via questionnaire at SWAN visit 6 were used in the present analyses. Vasomotor symptoms were based on two questions about the number of days in which hot flashes or night sweats had been experienced (not at all, 1–5 days, 6–8 days, 9–13 days, or every day) in the 2 weeks prior to the interview. Because findings for hot flashes and night sweats were similar, a combined vasomotor symptoms endpoint was used (1, 28). Women reporting either hot flashes or night sweats were categorized as having experienced vasomotor symptoms. While a three-level categorization was also considered (none, 1–5 days, or ≥6 days), results were similar, with some evidence of a threshold effect for any vasomotor symptoms versus none. Results utilizing the "any vs. none" categorization are presented here.

Body composition.
Adiposity was estimated from BIA (BIA-103 analyzer; RJL Systems, Inc., Mt. Clemens, Michigan). BIA is based on measurement of the transmission speed of an electrical pulse between electrodes attached at the feet and the knuckles of the hand. Electrical conductivity is greater in fat-free mass than in fat mass (29), and thereby resistance and reactance (impedance to this electrical current) can be used to estimate fat and lean mass (30). In the present investigation, we used the sex-specific validation equations of Chumlea et al. (31), with percent body fat estimated as total fat mass/weight.

Height and weight were assessed annually with a calibrated electronic or balance-beam scale and a stadiometer according to standardized protocols. Waist circumference was measured yearly at the level of the natural waist or the narrowest part of the torso from the anterior aspect. If waist narrowing was difficult to identify, the measure was taken at the smallest horizontal circumference between the ribs and the iliac crest.

Reproductive hormones.
Serum concentrations of FSH, estradiol, and sex hormone-binding globulin (SHBG) were obtained from a single morning fasting blood sample taken during SWAN visit 6. Samples were taken on days 2–5 of a spontaneous menstrual cycle; if a timed sample could not be obtained, a random fasting sample was taken. Estradiol assays were conducted in duplicate and FSH and SHBG assays in singulate. Assays were performed using an ACS-180 automated analyzer (Bayer Diagnostics, Tarrytown, New York). Estradiol was measured with a modified ACS-180 (estradiol-6) immunoassay, with inter- and intraassay coefficients of variation of 10.6 percent and 6.4 percent, respectively, and a lower limit of detection of 1.0 pg/ml. FSH assays were performed with a two-site chemiluminometric immunoassay, with inter- and intraassay coefficients of variation of 11.4 percent and 3.8 percent, respectively, and a lower limit of detection of 1.1 mIU/ml. The two-site chemiluminescent SHBG assay was developed on-site using rabbit anti-SHBG antibodies, with a lower limit of detection of 1.95 nM and inter- and intraassay coefficients of variation of 9.9 percent and 6.1 percent, respectively. FEI was calculated as 100 x estradiol (pg/ml)/272.11 x SHBG (nM) (32).

Covariates.
Race/ethnicity, parity (number of livebirths; any vs. none), and educational attainment (years of completed education; less than college degree vs. college degree or more) were derived from the baseline SWAN interview. Race/ethnicity was determined in response to the open-ended question "How would you describe your primary racial or ethnic group?" Data on age, smoking status (current smoker vs. past/never smoker), menopausal status, and anxiety symptoms were derived from SWAN visit 6. Menopausal status, determined from self-reported bleeding patterns over the year preceding the visit, was categorized as follows: Bleeding in the previous 3 months with no change in cycle predictability in the past year was considered premenopausal; bleeding in the previous 3 months with a decrease in cycle predictability in the past year was considered early perimenopausal; <12 and >3 months of amenorrhea was considered late perimenopausal; and ≥12 months of amenorrhea was considered postmenopausal. Women who reported having taken hormones (hormone therapy, oral contraceptives) within the previous month were classified as hormone users. Women previously classified as pre- or perimenopausal who reported having used hormones since the last study visit were considered to have an indeterminate status, because of the impact of hormone discontinuation on bleeding patterns. Information on use of hormone therapy (not oral contraceptives) in the past 3 months was available, and results were also examined after classifying as hormone users women who reported using hormones in the past 3 months; results were unchanged. The variable "anxiety symptoms" was a summary score of the reported number of days in the past 2 weeks (ranging from 0 (no days) to 4 (every day)) of irritability or grouchiness, heart pounding or racing, feeling tense or nervous, and feeling fearful for no reason.

Data analyses
Associations between demographic, psychosocial, and medical characteristics and vasomotor symptoms or percent body fat were estimated using t tests, chi-square tests, Pearson correlation coefficients, and linear regression. Standardized beta coefficients are presented for linear regression models. FSH, estradiol, and FEI were log-transformed to normalize their distributions. Associations between percent body fat and vasomotor symptoms were estimated in binary logistic regression models, first adjusted for age and site and subsequently adjusted for race/ethnicity, educational attainment, parity, past-month hormone use, menopausal status, smoking status, and anxiety symptoms. Covariates were selected on the basis of previously documented associations with vasomotor symptoms and obesity (1, 33, 34) and present associations with vasomotor symptoms at p < 0.10. Since waist circumference was highly correlated with total percent body fat (r = 0.83), a residualized waist circumference variable (waistresid) was defined from the linear regression model fitting waist to percent body fat (35). Use of waistresid allowed for examination of the portion of waist circumference associated with vasomotor symptoms apart from that associated with percent body fat. Linearity of the relation between percent body fat and log odds of the probability of vasomotor symptoms was verified by examining adiposity in quartiles, including a squared adiposity term in the model, and plotting the running mean average, all of which indicated that this linearity assumption was met.

FSH, estradiol, and FEI were separately included in multiple logistic regression models examining associations between percent body fat and vasomotor symptoms. Covariates for models including reproductive hormones were age, site, race/ethnicity, educational attainment, parity, cycle day of blood drawing, smoking status, hormone use in the past month, and anxiety symptoms. Cycle day of blood drawing and menopausal status were not included in the same model since they were collinear. Interactions between adiposity and both race/ethnicity and menopausal status in relation to vasomotor symptoms were examined. Since no significant interactions were observed, these interactions were not included in the primary models. Analyses were performed with SAS, version 9.1 (SAS Institute, Inc., Cary, North Carolina), and statistical tests were two-sided at {alpha} = 0.05.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 References
 
Approximately 59 percent of the sample reported experiencing vasomotor symptoms (see table 1). Factors associated with vasomotor symptoms included race/ethnicity, education, menopausal status, parity, smoking, waist circumference, anxiety symptoms, FSH, estradiol, and FEI. The mean percentage of body fat was 37.9 (standard deviation (SD), 7.8), with variation across ethnic groups. African-American women (mean = 42.5 (SD, 6.5), β = 0.58, p < 0.0001) and Caucasian women (mean = 38.1 (SD, 7.5), β = 0.38, p < 0.0001) had higher percentages of body fat than did Japanese women (mean = 32.1 (SD, 5.7)). Japanese and Chinese women (mean = 31.8 (SD, 6.0)) did not differ (β = –0.01, p = 0.72). Other factors associated with percent body fat included smoking (β = 0.06, p = 0.008), education (less than a college degree, relative to college degree or more: β = –0.17, p < 0.0001), anxiety symptoms (r = 0.13, p < 0.0001), log FSH (r = –0.09, p = 0.0002), log FEI (r = 0.20, p < 0.0001), and log estradiol (r = 0.07, p = 0.006).


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  		TABLE 1. Reporting of vasomotor symptoms according to sociodemographic and menopausal characteristics, Study of Women's Health Across the Nation, United States, 2002–2004

 
Results from multiple logistic regression models indicated that greater percentage of body fat was significantly associated with greater odds of reporting vasomotor symptoms after adjustment for age and site. This association persisted in models incorporating race/ethnicity, menopausal status, education, parity, smoking, hormone use, and anxiety symptoms (see table 2). When waistresid was included, percent body fat remained associated with vasomotor symptoms (per SD of adiposity, odds ratio (OR) = 1.14, 95 percent confidence interval (CI): 1.01, 1.28), although waistresid did not (OR = 1.00, 95 percent CI: 0.99, 1.28). Differences across racial/ethnic groups were evaluated by inclusion of an interaction term between race/ethnicity and percent body fat; the result was not statistically significant (p = 0.43).


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  		TABLE 2. Association between adiposity and odds of reporting vasomotor symptoms, Study of Women's Health Across the Nation, United States, 2002–2004

 
We next considered evidence for the thin hypothesis. In fully adjusted models, log FSH (OR = 1.41, 95 percent CI: 1.23, 1.60) was significantly and positively associated with vasomotor symptoms, and log estradiol (OR = 0.74, 95 percent CI: 0.66, 0.82) and log FEI (OR = 0.81, 95 percent CI: 0.73, 0.89) were significantly and negatively associated with vasomotor symptoms, consistent with previous SWAN findings (11). However, inclusion of FSH, estradiol, or FEI in models of percent body fat and vasomotor symptoms failed to diminish positive associations between adiposity and vasomotor symptoms (see table 3).


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  		TABLE 3. Association between adiposity and vasomotor symptoms in fully adjusted models{dagger} after controlling for serum levels of reproductive hormones, Study of Women's Health Across the Nation, United States, 2002–2004

 
Several additional analyses were conducted. Previous research has suggested that associations between body mass index and vasomotor symptoms may be most pronounced earlier in the menopausal transition (18, 20, 36, 37). The interaction between menopausal stage and adiposity in relation to vasomotor symptoms was examined and was not statistically significant (p = 0.70). However, stratified analyses suggested a somewhat more pronounced association between percent body fat among premenopausal/early perimenopausal women (OR = 1.31, 95 percent CI: 1.07, 1.60) relative to late perimenopausal/postmenopausal women (OR = 0.95, 95 percent CI: 0.79, 1.14) in models that adjusted for age, site, race/ethnicity, education, parity, smoking, hormone use, and anxiety symptoms.

Moreover, we compared the associations of lean and adipose tissue with vasomotor symptoms, although these measures were somewhat confounded by total body size. In age- and site-adjusted models, significant associations were observed for fat mass only (OR = 1.20, 95 percent CI: 1.07, 1.34). Findings for lean mass were not statistically significant (OR = 1.06, 95 percent CI: 0.96, 1.18). Neither lean mass nor fat mass was significant in fully adjusted models.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
References
 
The present findings indicated that increased body fat was associated with increased reporting of vasomotor symptoms in a large cohort of midlife women. Associations persisted after control for multiple covariates, including waist circumference, and did not vary by race/ethnicity. Although FSH and FEI were associated with both adiposity and vasomotor symptoms, positive associations between adiposity and vasomotor symptoms were not attenuated in models controlling for these hormones. One interpretation of these findings is that adipose tissue has both endocrine and thermoregulatory properties; however, its thermoregulatory function may play a more pronounced role in relation to vasomotor symptoms.

Higher adiposity was associated with increased odds of reporting vasomotor symptoms, providing support for a thermoregulatory model of vasomotor symptoms. According to this model, adiposity would inhibit heat dissipation. Thus, more vasomotor events may be required to dissipate a requisite amount of heat. Although the relative contributions of different body tissues to heat loss are complex (23), adipose tissue has been shown to have the strongest insulating capacity of any body tissue (23, 38), and the reduced ability of obese persons to efficiently dissipate heat is well-documented (23). The present findings are consistent with emerging findings showing body mass index to be positively associated with vasomotor symptoms (1, 18–20). However, with its delineation of lean versus adipose tissue, this investigation indicates that it is the adiposity component that places heavier women at risk for vasomotor symptoms.

The "thin hypothesis" postulates a decreased risk of vasomotor symptoms among women with greater body fat (13). The present findings do not support this hypothesis. Evidence in support of the thin hypothesis has been derived from studies that included very small clinical samples (16), did not adjust for key covariates (15), or used information on vasomotor symptoms (17) or weight (15) that was retrospectively recalled years prior to assessment. In the present study, although adiposity was associated with higher FSH and lower FEI, which in turn were associated with increased vasomotor symptoms, adjusting for these hormones did not reduce associations between adiposity and vasomotor symptoms. These findings should be interpreted with caution given the single blood sample taken and the lack of direct assessment of estrone. However, the overall positive association between adiposity and vasomotor symptoms is inconsistent with the thin hypothesis.

We previously found that abdominal adiposity was positively associated with hot flashes (24), and previous investigations have suggested that waist:hip ratio or waist circumference may have independent associations with vasomotor symptoms (20, 39). However, in this investigation, waist circumference did not show an independent association with vasomotor symptoms after we accounted for total body fat. These findings suggest that the distribution of fat around the abdomen may not place women at additional risk for vasomotor symptoms beyond total body fat. Notably, findings of variations in the thermoregulatory impact of adipose tissue depending on where it is distributed have been equivocal (23).

Previous investigations have suggested that positive associations between body mass index and vasomotor symptoms are primarily evident earlier in the menopausal transition. Indeed, null associations have been observed as women transition to the postmenopause and estrogen levels reflect shifts from the ovary to peripheral sources, including adipose tissue (18, 20, 36, 37). In the present investigation, exploratory analyses suggested that relations between adiposity and vasomotor symptoms may be more pronounced earlier in the transition. However, these differences were not statistically significant.

The present findings should be interpreted in light of several limitations. While the BIA equations used were validated relative to dual-energy x-ray absorptiometry in the Third National Health and Nutrition Examination Survey, that survey was not representative of US Asian populations (31), limiting our understanding of the validity of the measure in our two Asian subgroups. Moreover, vasomotor symptoms were assessed by means of two questions about the numbers of days of experiencing hot flashes and night sweats in the previous 2 weeks. Although they are frequently used in the epidemiologic literature, these measures yield relatively limited information. Future research should examine relations with more detailed assessments of vasomotor symptoms. Furthermore, the odds ratios reported here should not be interpreted as measures of relative risk. The odds ratio may overestimate relative risk, particularly when the outcome is frequent (40). Finally, given the observational and cross-sectional nature of this investigation, one cannot assume that the associations are causal. Since women with differential timing of the menopause may not be directly comparable (41), prospective investigations will be required to better understand how associations between adiposity and vasomotor symptoms may vary over the menopausal transition.

The present study had multiple strengths. To our knowledge, it was the first to examine associations between total adiposity and vasomotor symptoms, providing the strongest evidence to date that adiposity is the aspect of increased body size that is related to vasomotor symptoms. It was a large investigation that included a well-characterized sample of women across multiple racial/ethnic groups and menopausal stages, allowing examination of potential subgroup differences. The present findings documenting positive associations between adiposity and vasomotor symptoms are particularly relevant given the current interest in alternate methods of managing vasomotor symptoms, including behavioral approaches. One approach that may deserve greater attention is weight loss, with attention to loss of fat mass rather than lean mass. Weight loss may be particularly relevant during the menopausal transition, which is marked by both progressive increases in fat mass and adverse changes in certain cardiovascular risk factors (42, 43). Identification of the etiology of and risk factors for vasomotor symptoms has the potential to inform new, more effective approaches to the management of this often troublesome midlife symptom.


   ACKNOWLEDGMENTS
 
The Study of Women's Health Across the Nation has received grant support from the National Institutes of Health through the National Institute on Aging, the National Institute of Nursing Research, and the Office of Research on Women's Health (grants NR004061, AG012505, AG012535, AG012531, AG012539, AG012546, AG012553, AG012554, and AG012495).

Clinical Centers: University of Michigan, Ann Arbor, Michigan—Dr. MaryFran Sowers, Principal Investigator (PI); Massachusetts General Hospital, Boston, Massachusetts—Dr. Robert Neer, PI 1994–1999; Dr. Joel Finkelstein, PI 1999–present; Rush University Medical Center, Chicago, Illinois—Dr. Lynda Powell, PI; University of California, Davis, Davis, California/Kaiser Permanente Northern California, Oakland, California—Dr. Ellen Gold, PI; University of California, Los Angeles, Los Angeles, California—Dr. Gail Greendale, PI; University of Medicine and Dentistry–New Jersey Medical School, Newark, New Jersey—Dr. Gerson Weiss, PI 1994–2004; Dr. Nanette Santoro, PI 2004–present; University of Pittsburgh, Pittsburgh, Pennsylvania—Dr. Karen Matthews, PI. National Institutes of Health Program Office: National Institute on Aging, Bethesda, Maryland—Dr. Marcia Ory, 1994–2001; Dr. Sherry Sherman, 1994–present; National Institute of Nursing Research, Bethesda, Maryland—program officers. Central Laboratory: University of Michigan, Ann Arbor, Michigan—Dr. Daniel McConnell (Central Ligand Assay Satellite Services). Coordinating Center: New England Research Institutes, Watertown, Massachusetts—Dr. Sonja McKinlay, PI 1995–2001; University of Pittsburgh, Pittsburgh, Pennsylvania—Dr. Kim Sutton-Tyrrell, PI 2001–present. Steering Committee: Dr. Chris Gallagher, Chair; Dr. Susan Johnson, Chair.

Conflict of interest: none declared.


   References
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

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