Racial and ethnic disparities in utilization of total knee arthroplasty among older women.

OBJECTIVE: To evaluate racial and ethnic disparities in utilization of total knee arthroplasty (TKA) in relation to demographic, health, and socioeconomic status variables. DESIGN: Prospective study of 102,767 Women's Health Initiative postmenopausal women initially aged 50-79, examining utilization rates of primary TKA between non-Hispanic Black/African American, non-Hispanic White, and Hispanic/Latina women (hereafter referred to as Black, White, and Hispanic). A total of 8,942 Black, 3,405 Hispanic, and 90,420 White women with linked Medicare claims data were followed until time of TKA, death, or transition from fee-for-service coverage. Absolute disparities were determined using utilization rates by racial/ethnic group and relative disparities quantified using multivariable hazards models in adjusting for age, arthritis, joint pain, mobility disability, body mass index, number of comorbidities, income, education, neighborhood socioeconomic status (SES), and geographic region. RESULTS: TKA utilization was higher among White women (10.7/1,000 person-years) compared to Black (8.5/1,000 person-years) and Hispanic women (7.6/1,000 person-years). Among women with health indicators for TKA including diagnosis of arthritis, moderate to severe joint pain, and mobility disability, Black and Hispanic women were significantly less likely to undergo TKA after adjusting for age [Black: HR (95% confidence interval) = 0.70 (0.63-0.79); Hispanic: HR = 0.58 (0.44-0.77)]. Adjustment for SES modestly attenuated the measured disparity, but significant differences remained [Black: HR = 0.75 (0.67-0.89); Hispanic: HR = 0.65 (0.47-0.89)]. CONCLUSIONS: Compared to White women, Black and Hispanic women were significantly less likely to undergo TKA after considering need and appropriateness for TKA and SES. Further investigation into personal-level and provider-level factors that may explain these disparities is warranted.

Neighborhood socioeconomic status and coronary heart disease risk prediction in a nationally representative sample.

OBJECTIVES: Test the association between coronary heart disease (CHD) risk scores and neighborhood socioeconomic status (NSES) in a US nationally-representative sample and describe whether the association varies by gender and race/ethnicity. STUDY DESIGN: Cross-sectional study. METHODS: We use Health and Nutrition Examination Survey (NHANES) data from 1999 to 2004 linked with Census tract data. Multivariable regression models and propensity score adjusted models are employed to test the association between NSES and 10-year risk of CHD based on the Framingham Risk Score (FRS), adjusting for individual-level characteristics. RESULTS: An individual living in a neighborhood at the 75th percentile of NSES (high NSES) has, on average, a 10-year CHD risk that is 0.16 percentage points lower (95% Confidence Interval 0.16, 0.17) than a similar person residing in a neighborhood at the 25th percentile of NSES (low NSES). Race/ethnicity and gender were found to significantly modify the association between NSES and CHD risk: the association is larger in men than women and in whites than minorities. Propensity score models showed that findings on the main effects of NSES were robust to self-selection into neighborhoods. Similar results were observed between NSES and risk of cardiovascular disease events. CONCLUSIONS: NSES is significantly associated with CHD risk, and the relationship varies by gender and race/ethnicity.

Effects of aminoglutethimide on delta 5-androstenediol metabolism in postmenopausal women with breast cancer.

delta-5-Androstene-3 beta, 17 beta-diol has potential estrogenic activity because it is known to bind to receptors and translocate to the nucleus of certain estrogen target tissues. Its role in the biology of breast cancer is unclear. Aminoglutethimide plus hydrocortisone ("medical adrenalectomy") has been used to treat postmenopausal women with metastatic breast cancer. We studied delta 5-androstene-3 beta, 17 beta-diol metabolism in postmenopausal women with breast cancer before and during aminoglutethimide-plus-hydrocortisone therapy, utilizing the constant infusion technique. The metabolic clearance rate for five subjects was 799 +/- 89 liters/24 hr (470 +/- 47 liters/24 hr/sq m) before and 751 +/- 93 liters/24 hr (444 +/- 57 liters/24 hr/sq m) during therapy. Plasma delta 5-androstene-3 beta, 17 beta-diol and delta 5-androstene-3 beta, 17 beta-diol free index decreased despite absence of change in the metabolic clearance rate. Increased dehydroepiandrosterone/delta 5-androstene-3 beta, 17 beta-diol conversion ratios in individual patients suggested an increase in 17 beta-hydroxysteroid dehydrogenase activity during therapy. There were no alterations in the formation of the estrogen precursors testosterone and delta 4-androstene-3,17-dione.

Functional correlates of reduced central conduction velocity in diabetic subjects.

In a previous publication, we presented evidence of slowed conduction speed in the central nervous systems of insulin-dependent diabetic subjects, manifest in a delay in the latency of the brainstem auditory-evoked response (BAER). In this article, we present the results of a multivariate study conducted on a larger sample of 50 insulin-dependent, adult diabetic subjects. The purpose of the study was to determine some of the functional correlates of the BAER delay; each patient received an assessment of the BAER, the late auditory-evoked potential (EP), the conduction velocities of the sural, median, and common peroneal nerves, and intellectual and emotional function, in addition to neurologic and audiologic examinations. A nondiabetic control group was matched with the diabetic group as to age and sex. The results indicated a delay in the latency of wave V, and in interpeak latencies I-III and I-V, of the BAER. The most reliable effect was on interpeak latency I-V; this suggested that the locus of the delay was in the central auditory projections, rather than in the acoustic nerve. In addition, BAER waves I, II, III, IV, and V were reduced in amplitude, as was the N1 component of the late auditory EP; the most reliable reduction in amplitude was in wave V. The effect was similar in magnitude for males and females, relative to their counterparts in the control group. The slowed BAER response appeared early in the disease and was not related to the duration of insulin treatment. It was correlated with a chronic loss of energy and the presence of sexual dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Dehydroepiandrosterone: kinetics of metabolism in normal men and women.

The single injection and constant infusion techniques were utilized to study the kinetics of dehydroepiandrosterone (DHEA) metabolism and its peripheral conversion to several other C19-steroids including C19-steroid sulfates. The MCRs (mean +/- SEM) for normal men and normal women were 1866 +/- 144 and 1901 +/- 87 liters/24 h, respectively. The single injection technique yielded values for rate constants (units) and volumes of distribution (1) as follows: K1, 42.6 +/- 7.7 for men and 37.1 +/- 5.0 for women; K2, 64.3 +/- 11.2 for men and 55.5 +/- 5.0 for women; K2, 64.3 +/- 11.2 for men and 55.5 +/- 5.0 for women; V1, 38.5 +/- 6.0 for men and 33.7 +/- 2.5 for women; V2, 30.4 +/- 7.3 for men and 27.5 +/- 9.9 for women. The constant infusion technique yielded values for the conversion ratios for the transformation of DHEA to several products: delta 5-androstene-3 beta, 17 beta-diol to DHEA of 0.10 +/- 0.01 for men and 0.16 +/- 0.03 for women, delta 4-androstenedione to DHEA of 0.04 +/- 0.01 for men and 0.07 +/- 0.02 for women, DHEA sulfate (DHEAS) to DHEA of 6.36 +/- 0.81 for men and 10.09 +/- 0.87 for women, delta 5-androstene-3 beta, 17 beta-diol sulfate to DHEA of 0.42 +/- 0.06 for men and 0.50 +/- 0.04 for women, and androsterone sulfate to DHEA of 1.11 +/- 0.13 for men and 2.06 +/- 0.18 for women. The ratios for the conversion to DHEA sulfate and androsterone sulfate were significantly higher for women than men. The plasma concentrations of DHEA were 8.50 +/- 0.95 and 8.75 +/- 1.01 ng/ml for men and women, respectively. The calculated production rates for DHEA were 16.34 +/- 2.66 and 16.19 +/- 1.78 mg/24 h for men and women, respectively. There was no sex difference in the binding of DHEA to plasma proteins and this is reflected in the lack of sex difference in the MCRs. Calculations indicate that DHEA is a major precursor of circulating delta 5-diol.

Delta5-androstenediol: kinetics of metabolism and binding to plasma proteins in normal men and women.

Using the constant fusion and single injection technique the metabolic clearance rates (mean +/- SEM) for delta5-androstene-3beta, 17beta-diol (delta5-idol) were measured for 19 normal men (1311 +/- 67 1/24 h) and 10 normal women (858 +/- 63 1/24 h). The constant infusion technique yielded values for the conversation ratios for the transformation of delta5-diol to several products: dehydroepiandrosterone (DHEA)/delta5-diol of 0.06+/-0.01 for men and 0.05 +/- 0.01 for women, of delta5-diol sulfate/delta5-diol of 0.45 +/- 0.04 for men and 0.52 +/- 0.03 for women and of DHEA sulfate/delta5-diol of 5.53 +/- 0.26 for men and 5.02 +/- 0.42 for women. The single injection technique yielded rate constants (units) and volumes of distribution (liters) for delta5-diol; Ki = 34.3 +/- 4.3 for men and 35.0 +/- 3.9 for women, K2 = 63.7 +/- 4.1 for men and 75.1 +/- 4.2 for women, V1 = 23.1 +/- 3.2 for men and 11.9 +/- 2.3 for women, V2 = 14.8 +/- 3.7 for men and 9.2 +/- 3.2 for women. The mean delta5-diol plasma concentration was 1.08 +/- 0.10 ng/ml for 12 men and 1.17 +/- 0.16 ng/ml for 9 women. (he calculated blood production rates for delta5-diol were 1357 +/- 117 mug/24 h for 12 men and 969 +/- 131 mug/24 h for 9 women. The per cent binding (equilibrium dialysis) was higher for women (94.9 +/- 0.3) than for men (93.0 +/- 0.2). Paper electrophoresis showed that significant fractions of 3H-delta5-diol migrated with both the beta-globulin and albumin fractions. Estrogen administration to two normal men increased the per cent binding of delta5-diol to plasma proteins and decreased the metabolic clearance rate towards the values found for normal women.

PIP: Studies on the kinetics of delta 5-androstene-3beta,17beta-diol (delta 5-diol) metabolism and on the binding of delta 5-diol to plasma proteins in normal men and women are reported. Using the constant infusion and single injection technique the mean metabolic clearance rate for delta 5-diol was found to be 1311 1/24 hours in 19 normal men and 858 1/24 hours in 10 normal women (p less than .01). The constant infusion technique yielded values for the conversion ratios for the transformation of delta 5-diol to dehydroepiandrosteroe (DHEA)/delta 5-diol of .06 for men and .05 for women, of delta 5-diol sulfate/delta 5-diol .45 for men and .52 for women. The single injection technique yeilded rate constants (units=K) and volumes of distribution (liters) for delta 5-diol as K1=34.3 for men and 35 for women, K2-63.7 for men and 75.1 for women, V1=23.2 for men and 11.9 for women, V2-14.8 for men and 9.2 for women. mean delta 5-diol concentration was 1.08 and 1.17 ng/ml for 12 men and 9 women, respectively, while blood production rates were 1357 and 969 mcg/24 hours, respectively. Using equilibrium dialysis, the binding was 93 for men and 94.9 for women (p less than .01). Paper electrophoresis revealed significantly (p less than .01) more tritiated delta 5-diol associated with the beta-globulin area for women than for men. Estrogen administration to 2 normal men increased the percent binding of delta 5-diol to plasma proteins and decreased the metabolic clearance rate.

Androgen metabolism and regulation of rat ventral prostate growth and acid phosphatase during sexual maturation.

Androgen metabolism and the regulation of rat ventral prostate cell proliferation and secretory function were examined during sexual maturation. Changes in acid phosphatase (AP) characteristics were measured as a marker of androgen-dependent prostatic secretory function. In immature (21-day-old) rats, total AP activity per cell was low (14.2 +/- 1.3 mol p-nitrophenol phosphate hydrolysed/h per mg DNA); it increased threefold as the weight, protein and DNA contents of the prostate increased to adult (65-day) levels. This corresponded with significant (P less than 0.001) increases in the staining intensities of three of the four bands of secretory AP on isoelectric focusing gels. The extent of inhibition of AP by tartrate decreased at the same time. Secretory AP is known to be relatively tartrate-resistant. The changes in AP activity occurred after prostatic 5 alpha-dihydrotestosterone (5 alpha-DHT) levels increased from 4.6 +/- 0.7 pmol/mg DNA (21 days) to reach a peak of 17.6 +/- 2.3 pmol/mg DNA at 58 days. Prostatic 5 alpha-DHT concentrations were always higher than testosterone levels. Prostatic 5 alpha-androstane-3 alpha,17 beta-diol (3 alpha-Adiol) levels were lower than 5 alpha-DHT levels except on day 58 when levels peaked dramatically at 26.2 +/- 5.5 pmol/mg DNA. Changes in prostatic 5 alpha-DHT and 3 alpha-Adiol levels corresponded with changes in 5 alpha-reductase and 3 alpha-hydroxysteroid oxidoreductase (3 alpha-HSOR) activities. The oxidative reaction of 3 alpha-HSOR was approximately fourfold higher than the reductive reaction, indicating a preference for the formation of 5 alpha-DHT. The plasma levels of testosterone, 5 alpha-DHT and 3 alpha-Adiol cannot account for their respective prostatic levels, indicating the importance of the steroid-metabolizing enzymes in regulating intracellular androgen levels. Changes in the AP characteristics could be correlated with the androgen status of the prostate.

Androgen 5 alpha-reductase and 3 alpha-hydroxysteroid dehydrogenase activities in ventral prostate epithelial and stromal cells from immature and mature rats.

To study androgen-mediated differentiation in the rat ventral prostate, we separated the two principal cell types (epithelial and stromal) derived from prostates of immature and mature rats on two continuous Percoll gradients. Cells were immediately placed in culture medium. Testosterone metabolism by the two prostatic cell types was evaluated using [3H]testosterone and quantifying the formation of 5 alpha-[3H]dihydrotestosterone (5 alpha-DHT) and 5 alpha-[3H]androstane-(3 alpha or 3 beta), 17 beta-diols. In epithelial cells from both immature and mature rat prostates the major testosterone metabolites were 5 alpha-DHT and 5 alpha-androstane-3 alpha, 17 beta-diol. Stromal cells metabolized less testosterone than did the epithelial cells. Differences in the relative levels of the various metabolites were observed for the two age groups. To examine in more detail the changes in testosterone metabolism observed in vitro both types of cells and unfractionated cells from immature and mature rat prostates were assayed for testosterone 5 alpha-reductase (using testosterone as substrate) and 3 alpha-hydroxysteroid dehydrogenase (using 5 alpha-DHT as substrate) activities (expressed as pmol substrate reduced/min per 10(6) cells). In immature rats both 5 alpha-reductase and 3 alpha-hydroxysteroid dehydrogenase activities were localized in the epithelial cell fraction (17 and 52 respectively); stromal cells showed lower 5 alpha-reductase and 3 alpha-hydroxysteroid dehydrogenase activity (4 and 4). Relative to epithelial cells from immature rats epithelial cells from mature rats showed a decrease in 5 alpha-reductase (7) and an increase in 3 alpha-hydroxysteroid dehydrogenase (160) activity while stromal 5 alpha-reductase showed little change (3) and 3 alpha-hydroxysteroid dehydrogenase increased to 22.(ABSTRACT TRUNCATED AT 250 WORDS)

The role of androgen metabolism in the control of androgen action in the rat prostate.

Recent results from a number of laboratories have led us to re-examine the role of 3 beta-androstanediol in the rat ventral prostate. Whereas previously 5 alpha-dihydrotestosterone and 3-beta androstanediol were thought to have distinctly separate effects on the prostate, we suggest that 3 beta-androstanediol serves only as an intermediate in the metabolism and removal of 5 alpha-dihydrotestosterone from the organ. In our view the action of androgens on the prostate are exerted exclusively through the binding of 5 alpha-dihydrotestosterone to the androgen receptor and its subsequent translocation to the nucleus. Differences in effects are related to the amount of 5 alpha-dihydrotestosterone available to the gland. 3 alpha-Hydroxysteroid dehydrogenase may play a critical role in modulating the level of 5 alpha-dihydrotestosterone available to the translocatable receptor.

Small doses of 5 alpha-dihydrotestosterone mimic the effects of 5 alpha-androstane-3 beta, 17 beta-diol on acid phosphatase activity in the adult rat prostate gland.

These studies were designed to further investigate whether 5 alpha-androstane-3 beta, 17 beta-diol was exerting unique effects on rat prostate acid phosphatase activity or could possibly be exerting its actions by a small peripheral conversion to 5 alpha-dihydrotestosterone. Intraperitoneal administration of 5 alpha-dihydrotestosterone in doses of 1 mg, 100 microgram or 50 microgram per day starting 7 days after castration led to the restoration of normal characteristics of acid phosphatase activity. However, when 5 alpha-dihydrotestosterone was given in a dose of only 25 microgram per day starting 7 days after castration, the changes in acid phosphatase activity were indistinguishable from those found when 5 alpha-androstane-3 beta, 17 beta-diol was administered in a dose of 2 mg per day. This suggests that the effects of 5 alpha-androstane-3 beta, 17 beta-diol can be explained by its conversion to small amounts of 5 alpha-dihydrotestosterone.

Plasma C19-delta 5-steroid levels during normal human pregnancy.

Plasma levels of dehydroepiandrosterone sulfate, dehydroepiandrosterone and delta 5-androstenediol were measured in several women throughout pregnancy. The levels of both dehydroepiandrosterone and its sulfate decreased while those of delta 5-androstenediol did not. The levels of binding of the latter steroid to plasma proteins increased.

Plasma testosterone free index: a better indicator of plasma androgen activity?

Testosterone, quantitatively the most important androgen in the circulation, must enter cells to exert an androgenic effect. It is accepted that it is that fraction of the hormone not bound to the specific, binding, beta-globulin which is available for entry into the cells. By equilibrium dialysis we obtained an in vitro measurement of the unbound fraction. The product of this fraction and the total testosterone level gave us a testosterone free index (TFI). In normal men and women, our ranges were 24.6 to 93.6 and 0.8 to 3.8 ng/100 ml, respectively. Of 54 hirsute women, 24 had an elevated TFI; 4 of these had normal plasma testosterone levels. Thirteen men with hypogonadism had a decreased TFI. Nine of ten women and two men with hyperthyroidism had a normal TFI, although there was an elevated plasma testosterone level in most instances. The calculated TFI, which reflects both the extent of binding and the total testosterone level, may therefore be a better indicator of circulating androgen activity.

In vivo metabolism of 3H-testosterone in adult male rats: effects of estrogen administration.

The metabolism of testosterone (T) was studied in normal adult male rats using a constant infusion of trace amounts of the 3H-steroid into a tail vein for 3 h in order to attain a state of equilibrium. Samples of plasma, liver, kidney, prostate, seminal vesicles and muscle were analysed for 3H-testosterone, 3H-5alpha-dihydrotestosterone (5alphaDHT) and 3H-5alpha-androstanediol (Adiol). When compared to the 3H-T level in plasma there were high levels of 3H-T in kidney and of 3H-5alphaDHT in prostate and seminal vesicles. Intraperitoneal estradiol valerate administration (100 mug/day) for 4 days decreased and 3H-5alphaDHT levels in the prostate and seminal vesicles. The estrogen administration increased the T metabolic clearance rate from 17.5 1/24 h/100 g body wt to 22.6 1/24 h/100 g body wt.

Kinetics of testosterone metabolism in normal postmenopausal women and women with breast cancer.

The constant infusion and single injection techniques were utilized to study the kinetics of 3H-testosterone (T) metabolism in posmenopausal women with and without breast cancer. The metabolic clearance rates (mean +/- SEM) for normal postmenopausal women were 578 +/- 82 and 644 +/- 128 1/24 has obtained by the constant infusion and single injection techniques, respectively. The corresponding results for the women with breast cancer (patients) are 644 +/- 25 and 617 +/- 106 1/24 h. The single injection technique yielded values for rate constants (units) and volumes of distribution (1); K1 = 37.5 +/- 1.6 for the normals and 34.5 +/- 1.9 for the patients, K = 76.6 +/- 5.1 for the normals and 71.1 +/- 1.6 for the patients, V1 = 7.9 +/- 2.2 for the normals and 8.7 +/- 1.4 for the patients and V2 = 7.0 +/- 1.5 for the normals and 6.4 +/- 1.2 for the patients. The constant infusion technique yielded values for the conversion ratios for the transformation of T to several products; 4-androstene-3,17-dione/T of 0.02 +/- 0.003 for normals and 0.03 +/- 0.002 for patients, 5alpha-dihydrotestosterone/T of 0.02 +/- 0.002 for normals and 0.03 +/- 0.002 for patients, estrone/T of 0.04 +/- 0.01 for normals and 0.04 +/- 0.01 for patients, estradiol-17beta/T of 0.02 +/- 0.005 for normals and 0.03 +/- 0.005 for patients and estrone sulfate/T of 0.16 +/- 0.02 for normals and 0.24 +/- 0.06 for patients. The T plasma concentrations and production rates were similar for the two groups of subjects. Hence there were no significant differences between the normals and the patients for all the kinetic parameters. It was determined that all the estradiol being produced in postmenopausal women could be coming from circulating T.

Gender matters: an integrated model for understanding men's and women's health.

Health research has failed to adequately explore the combination of social and biological sources of differences in men's and women's health. Consequently, scientific explanations often proceed from reductionist assumptions that differences are either purely biological or purely social. Such assumptions and the models that are built on them have consequences for research, health care and policy. Although biological factors such as genetics, prenatal hormone exposure and natural hormonal exposure as adults may contribute to differences in men's and women's health, a wide range of social processes can create, maintain or exacerbate underlying biological health differences. Researchers, clinicians and policy makers would understand and address both sex-specific and non-sex-specific health problems differently if the social as well as biological sources of differences in men's and women's health were better understood.

Mammography-related anxiety: effect of preprocedural patient education.

OBJECTIVES: To determine the effect of preprocedural education on mammography-related anxiety. MATERIALS AND METHODS: A total of 613 women undergoing mammography were surveyed regarding anxiety about the procedure and expected results. Half the study population watched an educational videotape and half watched an entertaining movie in the waiting room. RESULTS: Anxiety levels about results were significantly higher than anxiety levels about the procedure (P <.001). There was no difference in procedural or cancer anxiety levels among women shown the educational tape and those shown the entertaining movie. CONCLUSION: The fear of discovering breast cancer generates most of mammography-related anxiety. Preprocedural education did not affect procedural or cancer-related anxiety.

Gender, household labor, and psychological distress: the impact of the amount and division of housework.

Using a national longitudinal survey of a representative sample of 1,256 adults, I assess the impact of the amount of household labor performed and its division within the household on men's and women's depression levels, adjusting for prior mental health status. I test two alternative explanations of the contributions of household labor and the division of household labor to gender differences in depression: differential exposure and differential vulnerability. The results indicate that men's lower contributions to household labor explain part of the gender difference in depression. Inequity in the division of household labor has a greater impact on distress than does the amount of household labor. Employment status moderates the effect of the division of labor on depression. Among those who describe themselves as keeping house, depression was lowest for those who performed 79.8 percent of housework. In contrast, for those employed full-time the minimum level of depression occurs at 45.8 percent of the household labor. Men report performing 42.3 percent of the housework in their homes compared to 68.1 percent reported by women. Thus, on average women are performing household labor beyond the point of maximum psychological benefit, whereas men are not. Social support mediates the effects of the division of household labor. The only gender difference in effects occurred among those who are married, for whom social support was associated with lower levels of depression for women than men.

Sex stratification and health lifestyle: consequences for men's and women's perceived health.

A representative national sample of 2,031 adults aged 18 to 90 was interviewed by telephone in 1990. Results showed that men report better health than women, but that the gap closes with age. We argue that a gender difference in labor and lifestyles explains sex differences in perceived health across the life course: gender inequality in paid and unpaid work and the subjective experience of inequality disadvantage women, whereas lifestyle disadvantages men. Women are less likely to be employed, and are more likely to work part-time, have lower incomes and more economic hardship, and to do more unpaid domestic labor than men, all of which except domestic labor are associated with poor health. Domestic labor improves health, up to doing 60 percent of the housework. Women also have more distress and fewer subjective work rewards, both of which are associated with poor health. If women had the same levels of paid work, household income, economic hardship, work rewards, and distress as men, their health would equal that of men's and surpass it by age 59. Although we expected to find an overwhelming male disadvantage in lifestyle, we did not. Men are more likely than women to walk and to exercise strenuously, both of which are associated with good health. If women's labor and leisure-time physical activity equalled men's, women over the age of 54 would experience better health than men. Men's lifestyle disadvantage comes from their greater tendency to smoke and to be overweight, both of which are associated with poor health.

Gender, time use, and health.

One of the continuing paradoxes facing social epidemiologists concerns sex differences in morbidity and mortality. Although women live longer than men, they apparently get sick more. We hypothesize that women's higher morbidity levels result from less paid work and lower wages combined with more hours spent in household labor, child care, and helping others, and fewer hours of leisure and sleep. Men and women hold different social roles; men hold most of the highly rewarding roles. We operationalize social roles as time commitments to various role-related activities. This approach provides interval-level measures such as time spent in caring for children instead of simple dichotomies such as parent/nonparent. We find that when gender differences in social roles are controlled, being male is associated with poorer health than being female. We conclude that if gender roles were more equal, women would experience better health than men, more consistent with their greater longevity.