Association between cardiometabolic index and all-cause and cause-specific mortality among the general population: NHANES 1999-2018

被引:4
作者
Liu, Mingjie [1 ]
Wang, Chendong [2 ]
Liu, Rundong [3 ]
Wang, Yan [1 ]
Wei, Bai [1 ]
机构
[1] Huazhong Univ Sci & Technol, Liyuan Hosp, Tongji Med Coll, Dept Oncol, Wuhan, Hubei, Peoples R China
[2] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Hepat Surg Ctr, Wuhan, Hubei, Peoples R China
[3] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Oncol, Wuhan, Hubei, Peoples R China
关键词
LIPID-METABOLISM; RISK-FACTOR; ADIPOSE-TISSUE; BREAST-CANCER; OBESITY; DISEASE; INFLAMMATION; STEATOHEPATITIS; EXPLANATION; SURVIVAL;
D O I
10.1186/s12944-024-02408-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background Cardiometabolic index (CMI) is a comprehensive clinical parameter which integrates overweight and abnormal lipid metabolism. However, its relationship with all-cause, cardiovascular disease (CVD), and cancer mortality is still obscure. Thus, a large-scale cohort study was conducted to illustrate the causal relation between CMI and CVD, cancer, and all-cause mortality among the common American population. Methods Our research was performed on the basis of National Health and Nutrition Examination Survey (NHANES) database, involving 40,275 participants ranging from 1999 to 2018. The formula of CMI is [waist circumference (cm) / height (cm)] x [triglyceride (mg/dL) / high-density lipoprotein cholesterol (mg/dL)]. Outcome variables consisted of CVD, cancer, and all-cause mortality, which were identified by the International Classification of Diseases (ICD)-10. The correlation between CMI and mortality outcomes was analyzed utilizing the Kaplan-Meier survival modeling, univariate/multivariate Cox regression analysis, smooth curve fitting analysis, threshold effect analysis, and subgroup analysis. Stratification factors for subgroups included age, race/ethnicity, sex, smoking behavior, drinking behavior, BMI, hypertension, and diabetes. Results The baseline characteristics table includes 4,569 all-cause-induced death cases, 1,113 CVD-induced death cases, and 1,066 cancer-induced death cases. Without adjustment for potential covariates, significantly positive causal correlation existed between CMI and all-cause mortality (HR = 1.03, 95% CI 1.02,1.04, P-value<0.05), CVD mortality (HR = 1.04, 95% CI 1.03, 1.05, P-value<0.05) and cancer mortality(HR = 1.03, 95% CI 1.02, 1.05, P-value<0.05); whereas, after confounding factors were completely adjusted, the relationship lost statistical significance in CMI subgroups (P for trend>0.05). Subgroup analysis found no specific subgroups. Under a fully adjusted model, a threshold effect analysis was performed combined with smooth curve fitting, and the findings suggested an L-shaped nonlinear association within CMI and all-cause mortality (the Inflection point was 0.98); in particular, when the baseline CMI was below 0.98, there existed a negative correlation with all-cause mortality with significance (HR 0.59, 95% CI 0.43, 0.82, P-value<0.05). A nonlinear relation was observed between CMI and CVD mortality. Whereas, the correlation between CMI and cancer mortality was linear. Conclusions Among the general American population, baseline CMI levels exhibited an L-shaped nonlinear relationship with all-cause mortality, and the threshold value was 0.98. What's more, CMI may become an effective indicator for CVD, cancer, and all-cause mortality prediction. Further investigation is essential to confirm our findings.
引用
收藏
页数:15
相关论文
共 92 条
[31]   Dual Specificity Phosphatase 12 Regulates Hepatic Lipid Metabolism Through Inhibition of the Lipogenesis and Apoptosis Signal-Regulating Kinase 1 Pathways [J].
Huang, Zhen ;
Wu, Lei-Ming ;
Zhang, Jie-Lei ;
Sabri, Abdelkarim ;
Wang, Shou-Jun ;
Qin, Gui-Jun ;
Guo, Chang-Qing ;
Wen, Hong-Tao ;
Du, Bin-Bin ;
Zhang, Dian-Hong ;
Kong, Ling-Yao ;
Tian, Xin-Yu ;
Yao, Rui ;
Li, Ya-Peng ;
Liang, Cui ;
Li, Peng-Cheng ;
Wang, Zheng ;
Guo, Jin-Yan ;
Li, Ling ;
Dong, Jian-Zeng ;
Zhang, Yan-Zhou .
HEPATOLOGY, 2019, 70 (04) :1099-1118
[32]  
Hwang I, 2019, DIABETES METAB J, V43, P752
[33]   Subcutaneous and visceral adipose tissue: structural and functional differences [J].
Ibrahim, M. Mohsen .
OBESITY REVIEWS, 2010, 11 (01) :11-18
[34]   Integrated Quantitative Targeted Lipidomics and Proteomics Reveal Unique Fingerprints of Multiple Metabolic Conditions [J].
Ivanova, Anna A. ;
Rees, Jon C. ;
Parks, Bryan A. ;
Andrews, Michael ;
Gardner, Michael ;
Grigorutsa, Eunice ;
Kuklenyik, Zsuzsanna ;
Pirkle, James L. ;
Barr, John R. .
BIOMOLECULES, 2022, 12 (10)
[35]  
Jain Minal, 2013, Neurosci J, V2013, P870608, DOI 10.1155/2013/870608
[36]  
Johnson Clifford L, 2014, Vital Health Stat 2, P1
[37]   Obesity and Its Metabolic Complications: The Role of Adipokines and the Relationship between Obesity, Inflammation, Insulin Resistance, Dyslipidemia and Nonalcoholic Fatty Liver Disease [J].
Jung, Un Ju ;
Choi, Myung-Sook .
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2014, 15 (04) :6184-6223
[38]   Exploring Visceral and Subcutaneous Adipose Tissue Secretomes in Human Obesity: Implications for Metabolic Disease [J].
Kahn, Darcy ;
Macias, Emily ;
Zarini, Simona ;
Garfield, Amanda ;
Berry, Karin Zemski ;
MacLean, Paul ;
Gerszten, Robert E. ;
Libby, Andrew ;
Solt, Claudia ;
Schoen, Jonathan ;
Bergman, Bryan C. .
ENDOCRINOLOGY, 2022, 163 (11)
[39]   Cardiovascular Risk Factors in Childhood and Adulthood and Cardiovascular Disease in Middle Age [J].
Kartiosuo, Noora ;
Raitakari, Olli T. ;
Juonala, Markus ;
Viikari, Jorma S. A. ;
Sinaiko, Alan R. ;
Venn, Alison J. ;
Jacobs, David R. ;
Urbina, Elaine M. ;
Woo, Jessica G. ;
Steinberger, Julia ;
Bazzano, Lydia A. ;
Daniels, Stephen R. ;
Magnussen, Costan G. ;
Rahimi, Kazem ;
Dwyer, Terence .
JAMA NETWORK OPEN, 2024, 7 (06)
[40]  
King Brian, 2011, Morbidity and Mortality Weekly Report, V60, P1207