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Comparative Study
. 2003 Sep 1;92(5):533-7.
doi: 10.1016/s0002-9149(03)00720-3.

Association of lipoprotein(a), insulin resistance, and reproductive hormones in a multiethnic cohort of pre- and perimenopausal women (The SWAN Study)

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Comparative Study

Association of lipoprotein(a), insulin resistance, and reproductive hormones in a multiethnic cohort of pre- and perimenopausal women (The SWAN Study)

MaryFran Sowers et al. Am J Cardiol. .

Abstract

Because evidence suggests lipoprotein (Lp(a)) may be an important cardiovascular risk factor in women, we evaluated whether reproductive hormones may influence Lp(a) concentrations and insulin resistance in a large multicenter study of women transitioning to postmenopause. Data were taken from the Study of Women's Health Across the Nation (SWAN), a prospective multiethnic study of menopausal transition (1,368 Caucasians, 808 African-Americans, 220 Chinese, 216 Hispanic, and 251 Japanese). Blood was assayed for Lp(a), follicle stimulating hormone, estradiol (E2), testosterone, and sex hormone binding globulin (free estradiol index and free androgen index), thyroid stimulating hormone, and glucose and insulin (to calculate insulin resistance). African-American women had twofold higher mean Lp(a) values than women of the other 4 race/ethnic groups, adjusted for body mass index (BMI). Lp(a) was modestly correlated with E2 (r = 0.10) in women without self-reported diagnosed heart disease but not in women with self-reported heart disease. Lp(a) was positively associated with log insulin resistance in women without self-reported heart disease but not in women with self-reported heart disease, an association that was not significant after adjusting for ethnicity, BMI, smoking, age, and site. Race/ethnicity, particularly being African-American, accounted for most of the explained Lp(a) variations. Lp(a) was very modestly associated (r = -0.04) with insulin resistance after adjusting for ethnicity and BMI, and this association was not modified by reproductive hormones, including androgens.

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