Mild and Moderate Obesity Remains the Sole Cause for Rise in Hs-Crp, TNF Α and Leptin in Obese Individuals in Spite of Performing Moderate Activity and Consuming Antioxidant and Prebiotic Rich Foods Frequently – A Cross Sectional Study in Urban Vadodara.

Abstract

Background:-Obesity has reached pandemic proportions globally leading to various co-morbidities and the risk factors contributing to these morbidities need to be researched more intensively.Objectives:-To determine the various factors contributing to levels of inflammatory markers in obese individuals and compare with non obese subjects.Method:-Using a cross sectional study design, from a total of 252 subjects, 167 obese and 87 non obese subjects living in urban Vadodara, aged 20-50 years, were studied for their BMI (kg/ m2) and physical activity level, serum hs-CRP levels (measured by nephelometry) TNFα and leptin levels (analyzed using Milliplex Map, Human Metabolic Hormone Magnetic Bead Panel (HMHAG). Frequency of intake of antioxidant and prebiotic rich foods was measured using a food frequency questionnaire and fecal Bifidobacteria was determined using standard methods.Results:-The mean BMI of the subjects was 28.6 and 21.39 kg/m 2 respectively whereas the mean physical activity levels were 694 and 717 MET mins/week for obese and non obese respectively. ANOVA test revealed a significant linear rise in the hs-CRP, TNF α and leptin levels with increase in obesity. Hs-crp was positively and significantly correlated with physical activity and negatively correlated with Bifidobacteria colonization in the gut. No significant correlation was found between the frequency of intake of antioxidant and prebiotic rich foods and all inflammatory markers.Conclusion:-Moderate obesity stands as a major cause for rise in the inflammatory markers followed by poor colonization of Bifidobacteria in the Gut. Moderate activity and increased intake of antioxidant rich foods does not lower the hs-CRP, TNFα and leptin significantly.Copy Right, IJAR, 2016,. All rights reserved.