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Abstract
Objective: To evaluate how obesity mediates effects of caffeine (measured by caffeine metabolite 1, 7-dimethylxantine) on glycohemoglobin and on low density lipoprotein (LDL), while adjusting for age, gender, race/ethnicity, smoking, and alcohol intake.
Design: A secondary data analysis was done using data from the 2009-2010 National Health and Examination Surveys.
Subjects: Respondents were included if they participated in caffeine data collection and were ≥ 20 years of age. Respondents were excluded if they had pregnancy confirmation or required a proxy for data collection. The final sample used was 1,976.
Results: Using structural equation modeling, the paths between 1, 7-dimethlxanthine and waist circumference (WC) [β = .029, p =.02, 95% CI: (.005, .053)] and between WC and glycohemoglobin level [β = .013, p < 0.001, 95% CI: (.010, .016)], were significant, adjusting for covariates, but not the path between 1, 7-dimethlxanthine and glycohemoglobin level [β = -.001, p = .260, 95% CI: (-.002, .000), indicating the full mediator role of obesity in the relationship between 1,7-dimethylxanthine level and glycohemoglobin level. However, the total effect of 1, 7-dimethlxanthine on glycohemoglobin, adjusting covariates, was minimal (β = -.001).
The direct path between 1, 7-dimethlxanthine and WC, adjusting for covariates, was significant [β = .029, p =.021, 95% CI: (.005, .054)]. However, the direct path between 1, 7-dimethylxanthine and LDL [β = .012, p = .717, 95% CI: (-.056, .080)] and the direct path between WC and LDL, adjusting for covariates, were not significant [β = .111, p = .264, 95% CI: (-.092, .315)]. Thus, obesity did not mediate the relationship between 1, 7-dimethylxanthine level and LDL, adjusting for covariates.
Conclusions: Obesity fully mediated the relationship between 1, 7-dimethylxanthine level and glycohemoglobin level, but not LDL, indicating that increased levels of 1, 7-dimethylxanthine was associated with reduced glycohemyoglobin through the effects on obesity, but the total effect was minimal. Further longitudinal studies are needed to determine if caffeine consumption caused the suggested effects on obesity, and, in turn, the reduction in glycohemoglobin levels. If confirmed, caffeine consumption could be considered as one modality in the management of obesity and diabetes in the future.
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