Martin Adam1, Medea Imboden2, Emmanuel Schaffner3, Eva Boes4, Florian Kronenberg5, Marco Pons6, Robert Bettschart7, Jean-Claude Barthelemy8, Christian Schindler9, Nicole Probst-Hensch10. 1. Swiss Tropical and Public Health Institute, Basel, Switzerland; University of Basel, Basel, Switzerland. Electronic address: martin.adam@unibas.ch. 2. Swiss Tropical and Public Health Institute, Basel, Switzerland; University of Basel, Basel, Switzerland. Electronic address: medea.imboden@unibas.ch. 3. Swiss Tropical and Public Health Institute, Basel, Switzerland; University of Basel, Basel, Switzerland. Electronic address: emmanuel.schaffner@unibas.ch. 4. Swiss Tropical and Public Health Institute, Basel, Switzerland; University of Basel, Basel, Switzerland. 5. Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, Innsbruck, Austria. Electronic address: florian.kronenberg@i-med.ac.at. 6. Division of Pulmonary Medicine, Regional Hospital of Lugano, Lugano, Switzerland. Electronic address: marco.pons@eoc.ch. 7. Lungenzentrum, Hirslanden Klinik Aarau, Aarau, Switzerland. Electronic address: robert.bettschart@hin.ch. 8. Laboratory SNA-EPIS EA4607, Department of Physiology, University Hospital of Saint-Etienne, PRES Lyon, France. Electronic address: jc.barthelemy@univ-st-etienne.fr. 9. Swiss Tropical and Public Health Institute, Basel, Switzerland; University of Basel, Basel, Switzerland. Electronic address: christian.schindler@unibas.ch. 10. Swiss Tropical and Public Health Institute, Basel, Switzerland; University of Basel, Basel, Switzerland. Electronic address: nicole.probst@unibas.ch.
Abstract
BACKGROUND: Overweight has been associated with an increase in inflammatory markers and with an imbalance in the autonomic nervous system, such as a decrease in heart rate variability (HRV). In this study we aimed to investigate the modifying effect of a genetic variation in a major anti-inflammatory marker gene, NFE2L2, on the relationship between overweight and HRV. METHODS: We analyzed participants of the SAPALDIA cohort aged 50years and older, twice in 2002/2003 (N=1472) and 2010/2011 (N=1235). We included persons with valid genotype data, who underwent ambulatory 24-h electrocardiogram monitoring, and reported on medical history and lifestyle. The association between HRV and BMI, measured as standard deviation of normal-to-normal intervals (SDNN) by BMI and the modifying effect of the cardiovascular health-related NFE2L2 gene variant rs2364723 were tested, applying multivariable mixed linear regression models. RESULTS: We found study participants with overweight (BMI>25) over two follow-up surveys 10years apart to have a negative association between SDNN, calculated as geometric means, with BMI. The examined NFE2L2 variant sustainably modified (pinteraction=0.014) the found inverse association between a BMI increment and SDNN, causing a stronger decrement in SDNN for participants with the CC genotype (-20.7%; 95%-confidence interval: -12.33 to -28.28) compared with participants carrying the GC (-7.43; 95%CI: -3.56 to -11.15) or GG (-11.26%; 95%CI: -7.68 to -14.7) genotype, estimated for the difference from the 90th to the 10th percentile of BMI by the NFE2L2 variant. CONCLUSIONS: Our results are consistent with the hypothesis that overweight decreases heart rate variability through inflammatory processes.
BACKGROUND: Overweight has been associated with an increase in inflammatory markers and with an imbalance in the autonomic nervous system, such as a decrease in heart rate variability (HRV). In this study we aimed to investigate the modifying effect of a genetic variation in a major anti-inflammatory marker gene, NFE2L2, on the relationship between overweight and HRV. METHODS: We analyzed participants of the SAPALDIA cohort aged 50years and older, twice in 2002/2003 (N=1472) and 2010/2011 (N=1235). We included persons with valid genotype data, who underwent ambulatory 24-h electrocardiogram monitoring, and reported on medical history and lifestyle. The association between HRV and BMI, measured as standard deviation of normal-to-normal intervals (SDNN) by BMI and the modifying effect of the cardiovascular health-related NFE2L2 gene variant rs2364723 were tested, applying multivariable mixed linear regression models. RESULTS: We found study participants with overweight (BMI>25) over two follow-up surveys 10years apart to have a negative association between SDNN, calculated as geometric means, with BMI. The examined NFE2L2 variant sustainably modified (pinteraction=0.014) the found inverse association between a BMI increment and SDNN, causing a stronger decrement in SDNN for participants with the CC genotype (-20.7%; 95%-confidence interval: -12.33 to -28.28) compared with participants carrying the GC (-7.43; 95%CI: -3.56 to -11.15) or GG (-11.26%; 95%CI: -7.68 to -14.7) genotype, estimated for the difference from the 90th to the 10th percentile of BMI by the NFE2L2 variant. CONCLUSIONS: Our results are consistent with the hypothesis that overweight decreases heart rate variability through inflammatory processes.
Authors: Mukesh Kumar Sinha; G Arun Maiya; Ana Maria Moga; Shivashankar K N; Ravi Shankar N; Vaishali K Journal: BMJ Open Date: 2022-04-25 Impact factor: 3.006
Authors: Farrukh Majeed; Talay Yar; Ahmed Alsunni; Ali Fouad Alhawaj; Ahmed AlRahim; Muneer Alzaki Journal: Ann Saudi Med Date: 2017 May-Jun Impact factor: 1.526