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Background: Prior research has indicated an association between insulin resistance and stroke; we sought to determine if this association persists after adjusting for stroke risk factors, including glycemic control., Methods: We used data from the Third National Health and Nutrition Survey (1988-1994), including participants aged > or =40 years. We assessed insulin sensitivity using the homeostasis model assessment (HOMA): HOMA = (FPGSI x FPI)/22.5, where FPGSI refers to fasting plasma glucose (mmol/l) and FPI refers to fasting plasma insulin (microU/l). Increasing HOMA indicates decreasing insulin sensitivity. We used glycosylated hemoglobin (HbA1c) to measure glycemic control. Multivariable logistic regression analysis was used to identify factors that were independently associated with stroke., Results: Among 3,844 participants, 168 (4%) reported a stroke history. Participants with stroke had lower insulin sensitivity than participants without stroke: HOMA mean +/- standard deviation, 4.0 +/- 4.0 vs. 3.3 +/- 3.0; p = 0.022. HOMA was independently associated with stroke (odds ratio 1.06, 95% CI: 1.01-1.12; adjusted for age, hypertension, myocardial infarction, claudication, activity, and HbA1c). The strength of the association between HOMA and stroke was similar to the association between claudication and stroke (index R(2): 0.0032 vs. 0.0036)., Conclusions: Impaired insulin sensitivity is independently associated with stroke, even after adjustment for glycemic control., (Copyright (c) 2005 S. Karger AG, Basel.)

Background and Objective: Two methods for measuring insulin sensitivity, fasting plasma insulin (FPI) and homeostasis model assessment (HOMA) have been proposed for use in large epidemiological research and clinical practice. This project describes the range of observed values of the HOMA and FPI in a large sample of the U.S. population., Methods: We used fasting plasma glucose and insulin values from the Third National Health and Nutrition Survey (NHANES III) to identify the FPI and HOMA values. For both FPI and HOMA, higher values indicate lower insulin sensitivity., Results: Among 6,511 participants without treated diabetes mellitus, FPI ranged from 1.8 to 175.8 microU/mL, with 25th percentile=6.7, median=9.3, 75th percentile=13.3, and mean+/-1 SD=11.2+/-7.5; HOMA ranged from 0.3 to 52.6 (mmol)(microU)/L(2), with 25th percentile=1.5, median=2.2, 75th percentile=3.3, and mean+/-SD=2.8+/-2.4., Conclusion: These findings describe the spectrum of insulin sensitivity and may be useful in helping physicians develop a clinical understanding of the dynamic range of both FPI and HOMA measures.

Most studies of sex hormones and insulin resistance (IR) have focused on androgens; few have examined the association of endogenous estrogens and IR. We determined the cross-sectional association of endogenous levels of total and bioavailable testosterone and estradiol and SHBG with IR among 845 healthy, postmenopausal women aged 45-65 yr. Women were within 10 yr of menopause and not using hormone replacement therapy. Total adiposity was estimated by body mass index, visceral adiposity by waist to hip ratio (WHR), and IR by the homeostasis model assessment. We defined homeostasis model assessment-IR as the highest quartile (cutpoint, 2.1) of the distribution in this cohort. In logistic regression analyses, the odds for IR were significant and increased in a dose-response fashion across each quartile of total estradiol, bioavailable estradiol, and bioavailable testosterone (all P < 0.001 for linear trend). These associations remained significant after adjusting for WHR; adjusted odds ratios were 4.0, 6.1, and 2.7 for total estradiol, bioavailable estradiol, and bioavailable testosterone, respectively, comparing the highest to the lowest quartile (all P < 0.001). Adjusting for body mass index and WHR together eliminated the linear association of IR with total estradiol and bioavailable testosterone, but the association with bioavailable estradiol remained (adjusted odds ratio, 2.7; P < 0.001, comparing the highest to the lowest quartile). IR was not associated with total testosterone before or after adjusting for adiposity. Lower SHBG levels were associated with higher odds of IR, independent of adiposity. These results suggest that estrogen may be equally or more important than testosterone in the pathway to IR in healthy, young postmenopausal women, with differences not entirely explained by body size.