The role of adiposity,diet and inflammation on the discordance between LDL-C and apolipoprotein B |
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| Affiliation: | 1. School of Health Sciences, Faculty of Science, Liverpool Hope University, Hope Park Campus, Taggart Avenue, Liverpool, L16 9JD, United Kingdom;2. Nuffield Department of Population Health, Richard Doll Building, Old Road Campus, University of Oxford, Oxford, OX3 7LF, United Kingdom;3. Department of Twin Research & Genetic Epidemiology, King''s College London, 4th Floor, South Wing, St Thomas'', London, SE1 7EH, United Kingdom;4. Liverpool Centre for Cardiovascular Science, University of Liverpool and Liverpool Heart & Chest Hospital, Liverpool L14 3PE, United Kingdom;5. Aalborg Thrombosis Research Unit, Department of Clinical Medicine, Aalborg University, DK-9100 Aalborg, Denmark;6. Non-Communicable Diseases Research Unit, South African Medical Research Council, 7505, Cape Town, South Africa;7. Cardiovascular Research Centre, University of Zielona Gora, 65-046, Zielona Gora, Poland;8. Department of Preventive Cardiology and Lipidology, Medical University of Lodz (MUL), 93-338, Lodz, Poland;9. Research Institute of Sport and Exercise Science, Liverpool John Moores University, Liverpool, L3 3AF, United Kingdom;1. Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Medical College of Soochow University, Suzhou, China;2. Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, USA;3. Department of Neurology, Affiliated Hospital of Nantong University, Nantong, China;4. Department of Medicine, Tulane University School of Medicine, New Orleans, LA, USA;1. Department of Biostatistics and Epidemiology, School of Public Health, Shenzhen University Health Science Center, No.1066 Xueyuan Avenue, Nanshan District, Shenzhen, Guangdong 518060, People''s Republic of China;2. Department of Health Management, Beijing Xiaotangshan Hospital, Xiaotangshan Town, Changping, Beijing 102200, People''s Republic of China;3. Department of Non-Communicable Disease Prevention and Control, Shenzhen Nanshan Center for Chronic Disease, No.7 Huaming Road, Shenzhen, Guangdong 518054, People''s Republic of China;4. Department of Endocrine, Shenzhen University General Hospital, Shenzhen, Guangdong 518055, People''s Republic of China;1. Department of Pathology and Immunology, Baylor College of Medicine, Houston, TX, USA;2. Department of Pathology, Texas Children''s Hospital, Houston, TX, USA;3. Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA;4. Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, MN, USA;5. Lipoprotein Metabolism Section, National Heart Lung and Blood Institute, Bethesda, MD, USA;6. Salveo Diagnostics, Inc, Richmond, VA, USA;7. School of Medicine, Case Western Reserve University, Cleveland, OH, USA;8. Department of Pathology, MetroHealth Medical Center, Cleveland, OH, USA;1. Department of Emergency and Critical Care Medicine, Guangdong Provincial People''s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China;2. Division of Vascular Surgery, National-Local Joint Engineering Laboratory of Vascular Disease Treatment, Engineering and Technology Center for Diagnosis and Treatment of Vascular Diseases, Guangdong Engineering Laboratory of Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China;3. Department of Radiation Oncology, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou, 510060, China;4. State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University, Guangzhou, 510060, China;5. General Division, Guangdong Geriatric Institute, Guangdong Provincial People''s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China;6. Department of Cardiology, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Provincial People''s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China;1. Department of Family Medicine, Yonsei University College of Medicine, Gangnam Severance Hospital Seoul, Republic of Korea;2. Department of Medicine, Yonsei University Graduate School, Seoul, Republic of Korea;3. Biostatistics Collaboration Unit, Department of Research Affairs, Yonsei University College of Medicine, Seoul, Republic of Korea;4. Department of Family Medicine, Nowon Eulji Medical Center, Eulji University School of Medicine, Seoul, Republic of Korea |
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| Abstract: | Background and aimsWhile low-density lipoprotein cholesterol (LDL-C) is a good predictor of atherosclerotic cardiovascular disease, apolipoprotein B (ApoB) is superior when the two markers are discordant. We aimed to determine the impact of adiposity, diet and inflammation upon ApoB and LDL-C discordance.Methods and resultsMachine learning (ML) and structural equation models (SEMs) were applied to the National Health and Nutrition Examination Survey to investigate cardiometabolic and dietary factors when LDL-C and ApoB are concordant/discordant. Mendelian randomisation (MR) determined whether adiposity and inflammation exposures were causal of elevated/decreased LDL-C and/or ApoB. ML showed body mass index (BMI), dietary saturated fatty acids (SFA), dietary fibre, serum C-reactive protein (CRP) and uric acid were the most strongly associated variables (R2 = 0.70) in those with low LDL-C and high ApoB. SEMs revealed that fibre (b = ?0.42, p = 0.001) and SFA (b = 0.28, p = 0.014) had a significant association with our outcome (joined effect of ApoB and LDL-C). BMI (b = 0.65, p = 0.001), fibre (b = ?0.24, p = 0.014) and SFA (b = 0.26, p = 0.032) had significant associations with CRP. MR analysis showed genetically higher body fat percentage had a significant causal effect on ApoB (Inverse variance weighted (IVW) = Beta: 0.172, p = 0.0001) but not LDL-C (IVW = Beta: 0.006, p = 0.845).ConclusionOur data show increased discordance between ApoB and LDL-C is associated with cardiometabolic, clinical and dietary abnormalities and that body fat percentage is causal of elevated ApoB. |
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