Obesity in Teen Years Associated with SLE in Black Women

Black women who are obese as teenagers have a higher risk of systemic lupus erythematous (SLE) in adulthood, according to a recent analysis. 

Researchers used data from the Black Women’s Health Study to assess the relationship between body mass index (BMI kg/m2) and incident SLE. American College of Rheumatology criteria confirmed incident SLE cases. Women (median age 38 at entry in 1995) self-reported height and weight at age 18 and again during follow-up. Normal BMI was considered 20.0-24.9.

 

Researchers did not find an association between adult obesity and SLE risk (hazard ratio [HR] for BMI ≥ 30.0 [obese] relative to normal BMI at ≥ four years prior to SLE diagnosis, 0.90 [95% CI 0.53-1.54]). But obesity at 18 years old was correlated with increased SLE risk (HR for BMI ≥ 30.0 relative to normal BMI, 2.38 [95% CI 1.26-4.51]). 

Previous research found that obese women with SLE have worse patient-reported outcomes, including disease activity, depressive symptoms, and symptoms of pain and fatigue. But most studies primarily assessed white women, even though black women are at an increased risk for obesity and SLE, the researchers noted. 

One study found that SLE affects 1 in 537 black women. Black SLE patients are younger when they receive their diagnosis, have a more than twofold increase in SLE incidence, and have greater incidence of renal disease and end-stage renal disease when compared with white patients. According to a study published in Arthritis & Rheumatology, “Compared with non‐Hispanic white women (64.3), [SLE] prevalence was higher among non‐Hispanic black (210.9), Hispanic (138.3), and non‐Hispanic Asian (91.2) women. Incidence rates were higher among non‐Hispanic black women (15.7) compared with non‐Hispanic Asian (6.6), Hispanic (6.5), and non‐Hispanic white (6.5) women.” 

Researchers for the present study called for further studies “to understand the biologic mechanisms and windows of exposure for the relationship of obesity to SLE pathogenesis.” 

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Source: Seminars in Arthritis and Rheumatism