Browsing by Author "Collins, Kelsey H"

Now showing 1 - 2 of 2
  • Thumbnail Image
    ItemOpen Access
    Association of Metabolic Markers with self-reported osteoarthritis among middle-aged BMI-defined non-obese individuals: a cross-sectional study
    (2018-09-03) Collins, Kelsey H; Sharif, Behnam; Reimer, Raylene A; Sanmartin, Claudia; Herzog, Walter; Chin, Rick; Marshall, Deborah A
    Abstract Background Osteoarthritis (OA) is a chronic degenerative joint disease. While it is well-established that obesity affects OA through increased axial loading on the joint cartilage, the indirect effect of obesity through metabolic processes among the body mass index (BMI)-defined non-obese population, i.e., BMI < 30 kg/m2, is less known. Our goal was to evaluate the association of metabolic markers including body fat percentage (BF%), waist circumference, maximum weight gain during adulthood and serum creatinine with self-reported OA to establish if such measures offer additional information over BMI among the non-obese population between 40 and 65 years of age. Methods Cross-sectional data from two cycles of the Canadian Health Measures Survey (CHMS) in 2007–2009 and 2009–2011 were analyzed. Sex-specific logistic regression models were developed to evaluate the association of self-reported OA with metabolic markers. Models were separately adjusted for age, BMI categories and serum creatinine, and a stratified analysis across BM categories was performed. In a secondary analysis, we evaluated the association of self-reported OA, cardiovascular diseases and hypertension across BF% categories. Results Of 2462 individuals, 217 (8.8%) self-reported OA. After adjusting for age and BMI, those within BF%-defined overweight/obese category had 2.67 (95% CI: 1.32–3.51) and 2.11(95% CI: 1.38–3.21) times higher odds of reporting self-reported OA compared to those within BF%-defined athletic/acceptable category for females and males, respectively. BF% was also significantly associated with self-reported OA after adjusting for age and serum creatinine only among females (OR: 1.47, 95%CI: 1.12–1.84). Furthermore, among the BMI-defined overweight group, the age-adjusted odds of self-reported OA was significantly higher for overweight/obese BF% compared to athletic/acceptable BF% in both females and males. In a secondary analysis, we showed that the association of self-reported OA and hypertension/cardiovascular diseases is significantly higher among BF% overweight/obese (OR: 1.37, 95%CI: 1.19–3.09) compared to BF% athletic/acceptable (OR: 1.13, 95%CI: 0.87–2.82). Conclusion Our results provide corroborating evidence for a relationship between body fat and OA in a population-based study, while no significant independent correlates were found between other metabolic markers and OA prevalence. Future investigation on the longitudinal relationship between BF and OA among this sub-population may inform targeted prevention opportunities.
  • Thumbnail Image
    ItemOpen Access
    Relationship between inflammation, the gut microbiota, and metabolic osteoarthritis development: studies in a rat model
    (2016) Herzog, Walter; Collins, Kelsey H; Paul, Heather A; Reimer, Raylene A; Seerattan, Ruth A; Hart, David A
    Western-type diets, high in fat and sugars, lead to obesity. Obesity in turn is associated with chronic inflammation, and thought to be a risk factor for the onset and increased rate of progression of metabolic osteoarthritis (OA) in joints. Emerging evidence suggests that intrinsic inflammatory mediators secreted by body fat, or adipose tissue, including cytokines, adipokines, and advanced glycation end products, may be sufficient to lead to onset and progression of OA. It appears that these obesity-associated, intrinsic inflammatory factors define a metabolic subtype of osteoarthritis. Characterizing the factors that comprise this unhealthy metabolic phenotype is critical to understanding the influence of obesity on OA. Furthermore, establishing the “indirect” role of the microbiota and the gut is required to fully understand the initiators and drivers of metabolic OA.