Yong-Moon Park1,2, Jiajia Zhang2, Susan E Steck2, Teresa T Fung3,4, Linda J Hazlett2, Kyungdo Han5, Seung-Hyun Ko6, Anwar T Merchant7. 1. Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC. 2. Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC. 3. Department of Nutrition, Simmons College, Boston, MA. 4. Department of Nutrition, Harvard TH Chan School of Public Health, Boston, MA. 5. Department of Biostatistics and. 6. Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea. 7. Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC; merchant@mailbox.sc.edu.
Abstract
Background: The inverse association between Mediterranean diet (Med-diet) consumption and insulin resistance or inflammatory markers is well known. However, the extent to which obesity may act directly on or mediate this association is unclear.Objective: We aimed to investigate whether the associations between Med-diet consumption and markers of insulin resistance and inflammation are mediated by body mass index (BMI) or waist circumference (WC) in a representative US population. Methods: We used cross-sectional data from 4700 adults aged 20-90 y without any previous diagnosis of cancer, cardiovascular disease, diabetes, or hypertension based on the NHANES III, 1988-1994. A Med-diet score (MDS) was created to assess adherence to the Med-diet. Linear regression models were fitted in conventional and causal mediation analyses comparing extreme MDS tertiles. Results: Compared with the lowest MDS tertile, the highest tertile of MDS was associated with a 0.77 lower BMI (in kg/m2; P = 0.004) and a 2.7 cm lower WC (P < 0.001) after multivariable adjustment. WC mediated the association of MDS with insulin resistance and glucose intolerance markers (log insulin, log homoeostasis model assessment of insulin resistance, fasting glucose, and glycated hemoglobin) and inflammatory markers (white blood cell count and fibrinogen), whereas BMI mediated the association between MDS and insulin resistance and glucose intolerance markers only (all P < 0.05). The mediated effects of WC were consistently greater than those of BMI for all markers in both conventional and causal mediation analyses. Furthermore, the association between MDS and fasting glucose was fully mediated by adiposity, especially by WC in men aged <45 y and in premenopausal women. Conclusion: Our results suggest that reducing abdominal obesity may play an important role in the pathway through which Med-diet consumption reduces insulin resistance and inflammation.
Background: The inverse association between Mediterranean diet (Med-diet) consumption and insulin resistance or inflammatory markers is well known. However, the extent to which obesity may act directly on or mediate this association is unclear.Objective: We aimed to investigate whether the associations between Med-diet consumption and markers of insulin resistance and inflammation are mediated by body mass index (BMI) or waist circumference (WC) in a representative US population. Methods: We used cross-sectional data from 4700 adults aged 20-90 y without any previous diagnosis of cancer, cardiovascular disease, diabetes, or hypertension based on the NHANES III, 1988-1994. A Med-diet score (MDS) was created to assess adherence to the Med-diet. Linear regression models were fitted in conventional and causal mediation analyses comparing extreme MDS tertiles. Results: Compared with the lowest MDS tertile, the highest tertile of MDS was associated with a 0.77 lower BMI (in kg/m2; P = 0.004) and a 2.7 cm lower WC (P < 0.001) after multivariable adjustment. WC mediated the association of MDS with insulin resistance and glucose intolerance markers (log insulin, log homoeostasis model assessment of insulin resistance, fasting glucose, and glycated hemoglobin) and inflammatory markers (white blood cell count and fibrinogen), whereas BMI mediated the association between MDS and insulin resistance and glucose intolerance markers only (all P < 0.05). The mediated effects of WC were consistently greater than those of BMI for all markers in both conventional and causal mediation analyses. Furthermore, the association between MDS and fasting glucose was fully mediated by adiposity, especially by WC in men aged <45 y and in premenopausal women. Conclusion: Our results suggest that reducing abdominal obesity may play an important role in the pathway through which Med-diet consumption reduces insulin resistance and inflammation.
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