Yvette C Cozier1, Medha Barbhaiya2, Nelsy Castro-Webb3, Carolyn Conte3, Sara Tedeschi4, Cianna Leatherwood4, Karen H Costenbader4, Lynn Rosenberg3. 1. Slone Epidemiology Center at Boston University, 72 East Concord St, Boston, MA 02118, United States. Electronic address: yvettec@bu.edu. 2. Division of Rheumatology, Department of Medicine, Hospital for Special Surgery, New York, NY, United States. 3. Slone Epidemiology Center at Boston University, 72 East Concord St, Boston, MA 02118, United States. 4. Division of Rheumatology, Immunology, and Allergy, Department of Medicine, Brigham and Women's Hospital, Boston, MA, United States.
Abstract
BACKGROUND: Obesity may influence systemic lupus erythematous (SLE) pathogenesis via stimulation of systemic inflammation, but the relationship between obesity and SLE risk is unclear. Past studies have predominantly assessed White women, while Black women have higher prevalence of both obesity and SLE. METHODS: We prospectively assessed the relationship between Body Mass Index (BMI, kg/m2) and incident SLE within the Black Women's Health Study (median age 38 at entry in 1995). Height and weight at age 18 and during follow-up were self-reported. We confirmed incident SLE cases by updated American College of Rheumatology criteria and collected covariates prospectively. Cox proportional hazards regression models, adjusted for potential confounders, estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for categories of updated BMI and risk of SLE, relative to BMI 20-24.9 ("normal" BMI). Secondary analyses investigated BMI at age 18, BMI in 1995 at cohort entry, cumulative updated BMI and "lagged" BMI (≥4 years prior to outcome window to address possible reverse causation). RESULTS: Adult obesity was not related to SLE risk: HR for BMI ≥30 ("obesity") relative to normal BMI at ≥4 years prior to SLE diagnosis was 0.90 (95% CI 0.53-1.54). However, obesity at age 18 was associated with increased risk: HR 2.38 (95% CI 1.26-4.51) for ≥30 vs. normal BMI. CONCLUSIONS: Among these Black women, obesity as a teenager was associated with increased SLE risk in adulthood. Further studies are necessary to understand the biologic mechanisms and windows of exposure for the relationship of obesity to SLE pathogenesis.
BACKGROUND:Obesity may influence systemic lupus erythematous (SLE) pathogenesis via stimulation of systemic inflammation, but the relationship between obesity and SLE risk is unclear. Past studies have predominantly assessed White women, while Black women have higher prevalence of both obesity and SLE. METHODS: We prospectively assessed the relationship between Body Mass Index (BMI, kg/m2) and incident SLE within the Black Women's Health Study (median age 38 at entry in 1995). Height and weight at age 18 and during follow-up were self-reported. We confirmed incident SLE cases by updated American College of Rheumatology criteria and collected covariates prospectively. Cox proportional hazards regression models, adjusted for potential confounders, estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for categories of updated BMI and risk of SLE, relative to BMI 20-24.9 ("normal" BMI). Secondary analyses investigated BMI at age 18, BMI in 1995 at cohort entry, cumulative updated BMI and "lagged" BMI (≥4 years prior to outcome window to address possible reverse causation). RESULTS: Adult obesity was not related to SLE risk: HR for BMI ≥30 ("obesity") relative to normal BMI at ≥4 years prior to SLE diagnosis was 0.90 (95% CI 0.53-1.54). However, obesity at age 18 was associated with increased risk: HR 2.38 (95% CI 1.26-4.51) for ≥30 vs. normal BMI. CONCLUSIONS: Among these Black women, obesity as a teenager was associated with increased SLE risk in adulthood. Further studies are necessary to understand the biologic mechanisms and windows of exposure for the relationship of obesity to SLE pathogenesis.
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