Individuals with obesity, particularly abdominal obesity, are at an increased risk of hypertension, dyslipidemia, diabetes, coronary heart disease, stroke, cancer, and all-cause mortality. Several studies have observed an association between obesity and increased risk of rheumatoid arthritis (RA). Abdominal obesity is associated with visceral fat and has been a stronger predictor of obesity-related health risk, such as cardiovascular disease, than overall obesity as measured by BMI. We sought to investigate whether abdominal obesity per se predicts RA risk in two large prospective cohorts, the Nurses’ Health Study (NHS) and Nurses’ Health Study II (NHSII).
Over 90,000 women without RA at baseline in the combined NHS cohorts were followed to identify incident RA. Abdominal obesity was defined as waist circumference ≥88cm, based on WHO recommendations for women. Incident RA cases and RA serologic status were identified by the medical record.
During up to 28 years of follow-up, we identified 803 incident RA cases. Women with waist circumference >88cm had a 27 percent increased RA risk compared with women with <88cm. Among young and middle-aged women (age ≤ 55 years), abdominal obesity increased the risk of RA by 65 percent, and increased the risk of seropositive RA by 94 percent. After further adjusting for BMI, abdominal obesity remained associated with 51 percent increased risk for seropositive RA (Figure).
The biologic pathway by which adiposity may increase the risk of RA is unknown. Adipose tissue, particularly visceral fat, is thought to be responsible for the generation of pro-inflammatory adipokines (e.g. leptin, resistin, visfatin, TNFα and IL6) which are significantly elevated in pre-clinical RA. Future studies will examine the potential role of adipokines in RA development and pathogenesis.