Supra-additive effect of chronic inflammation and atherogenic dyslipidemia on developing type 2 diabetes among young adults: a prospective cohort study
Both elevated inflammation and atherogenic dyslipidemia are prominent in young-onset diabetes and are increasingly identified as biologically intertwined processes that contribute to diabetogenesis. We aimed to investigate the age-specific risks of type 2 diabetes (T2D) upon concomitant chronic infl...
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Published in | Cardiovascular diabetology Vol. 22; no. 1; p. 181 |
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Main Authors | , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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England
BioMed Central
15.07.2023
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Abstract | Both elevated inflammation and atherogenic dyslipidemia are prominent in young-onset diabetes and are increasingly identified as biologically intertwined processes that contribute to diabetogenesis. We aimed to investigate the age-specific risks of type 2 diabetes (T2D) upon concomitant chronic inflammation and atherogenic dyslipidemia.
Age-stratified Cox regression analysis of the risk of incident diabetes upon co-exposure to time-averaged cumulative high-sensitivity C-reactive protein (CumCRP) and atherogenic index of plasma (CumAIP) among 42,925 nondiabetic participants from a real-world, prospective cohort (Kailuan Study).
During a median 6.41 years of follow-up, 3987 T2D developed. Isolated CumAIP and CumCRP were significantly associated with incident T2D in the entire cohort and across all age subgroups. Both CumAIP and CumCRP were jointly associated with an increased risk of diabetes (P-interaction = 0.0126). Compared to CumAIP < -0.0699 and CumCRP < 1 mg/L, co-exposure to CumAIP ≥ - 0.0699 and CumCRP ≥ 3 mg/L had a significant hazard ratio (HR) [2.55 (2.23-2.92)] after adjusting for socio-demographic, life-style factors, family history of diabetes, blood pressure, renal function and medication use. The co-exposure-associated risks varied greatly by age distribution (P-interaction = 0.0193): < 40 years, 6.26 (3.47-11.28); 40-49 years, 2.26 (1.77-2.89); 50-59 years, 2.51 (2.00-3.16); 60-69 years, 2.48 (1.86-3.30); ≥ 70 years, 2.10 (1.29-3.40). In young adults (< 45 years), both exposures had a significant supra-additive effect on diabetogenesis (relative excess risk due to interaction: 0.80, 95% CI 0.10-1.50).
These findings highlight the need for age-specific combined assessment and management of chronic inflammation and dyslipidemia in primary prevention against T2D, particularly for young adults. The clinical benefit derived from dual-target intervention against dyslipidemia and inflammation will exceed the sum of each part alone in young adults. |
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AbstractList | Abstract
Background
Both elevated inflammation and atherogenic dyslipidemia are prominent in young-onset diabetes and are increasingly identified as biologically intertwined processes that contribute to diabetogenesis. We aimed to investigate the age-specific risks of type 2 diabetes (T2D) upon concomitant chronic inflammation and atherogenic dyslipidemia.
Methods
Age-stratified Cox regression analysis of the risk of incident diabetes upon co-exposure to time-averaged cumulative high-sensitivity C-reactive protein (CumCRP) and atherogenic index of plasma (CumAIP) among 42,925 nondiabetic participants from a real-world, prospective cohort (Kailuan Study).
Results
During a median 6.41 years of follow-up, 3987 T2D developed. Isolated CumAIP and CumCRP were significantly associated with incident T2D in the entire cohort and across all age subgroups. Both CumAIP and CumCRP were jointly associated with an increased risk of diabetes (
P
-interaction = 0.0126). Compared to CumAIP < -0.0699 and CumCRP < 1 mg/L, co-exposure to CumAIP ≥ − 0.0699 and CumCRP ≥ 3 mg/L had a significant hazard ratio (HR) [2.55 (2.23–2.92)] after adjusting for socio-demographic, life-style factors, family history of diabetes, blood pressure, renal function and medication use. The co-exposure-associated risks varied greatly by age distribution (
P
-interaction = 0.0193): < 40 years, 6.26 (3.47–11.28); 40–49 years, 2.26 (1.77–2.89); 50–59 years, 2.51 (2.00–3.16); 60–69 years, 2.48 (1.86–3.30); ≥ 70 years, 2.10 (1.29–3.40). In young adults (< 45 years), both exposures had a significant supra-additive effect on diabetogenesis (relative excess risk due to interaction: 0.80, 95% CI 0.10–1.50).
Conclusions
These findings highlight the need for age-specific combined assessment and management of chronic inflammation and dyslipidemia in primary prevention against T2D, particularly for young adults. The clinical benefit derived from dual-target intervention against dyslipidemia and inflammation will exceed the sum of each part alone in young adults. BACKGROUNDBoth elevated inflammation and atherogenic dyslipidemia are prominent in young-onset diabetes and are increasingly identified as biologically intertwined processes that contribute to diabetogenesis. We aimed to investigate the age-specific risks of type 2 diabetes (T2D) upon concomitant chronic inflammation and atherogenic dyslipidemia.METHODSAge-stratified Cox regression analysis of the risk of incident diabetes upon co-exposure to time-averaged cumulative high-sensitivity C-reactive protein (CumCRP) and atherogenic index of plasma (CumAIP) among 42,925 nondiabetic participants from a real-world, prospective cohort (Kailuan Study).RESULTSDuring a median 6.41 years of follow-up, 3987 T2D developed. Isolated CumAIP and CumCRP were significantly associated with incident T2D in the entire cohort and across all age subgroups. Both CumAIP and CumCRP were jointly associated with an increased risk of diabetes (P-interaction = 0.0126). Compared to CumAIP < -0.0699 and CumCRP < 1 mg/L, co-exposure to CumAIP ≥ - 0.0699 and CumCRP ≥ 3 mg/L had a significant hazard ratio (HR) [2.55 (2.23-2.92)] after adjusting for socio-demographic, life-style factors, family history of diabetes, blood pressure, renal function and medication use. The co-exposure-associated risks varied greatly by age distribution (P-interaction = 0.0193): < 40 years, 6.26 (3.47-11.28); 40-49 years, 2.26 (1.77-2.89); 50-59 years, 2.51 (2.00-3.16); 60-69 years, 2.48 (1.86-3.30); ≥ 70 years, 2.10 (1.29-3.40). In young adults (< 45 years), both exposures had a significant supra-additive effect on diabetogenesis (relative excess risk due to interaction: 0.80, 95% CI 0.10-1.50).CONCLUSIONSThese findings highlight the need for age-specific combined assessment and management of chronic inflammation and dyslipidemia in primary prevention against T2D, particularly for young adults. The clinical benefit derived from dual-target intervention against dyslipidemia and inflammation will exceed the sum of each part alone in young adults. Abstract Background Both elevated inflammation and atherogenic dyslipidemia are prominent in young-onset diabetes and are increasingly identified as biologically intertwined processes that contribute to diabetogenesis. We aimed to investigate the age-specific risks of type 2 diabetes (T2D) upon concomitant chronic inflammation and atherogenic dyslipidemia. Methods Age-stratified Cox regression analysis of the risk of incident diabetes upon co-exposure to time-averaged cumulative high-sensitivity C-reactive protein (CumCRP) and atherogenic index of plasma (CumAIP) among 42,925 nondiabetic participants from a real-world, prospective cohort (Kailuan Study). Results During a median 6.41 years of follow-up, 3987 T2D developed. Isolated CumAIP and CumCRP were significantly associated with incident T2D in the entire cohort and across all age subgroups. Both CumAIP and CumCRP were jointly associated with an increased risk of diabetes (P-interaction = 0.0126). Compared to CumAIP < -0.0699 and CumCRP < 1 mg/L, co-exposure to CumAIP ≥ − 0.0699 and CumCRP ≥ 3 mg/L had a significant hazard ratio (HR) [2.55 (2.23–2.92)] after adjusting for socio-demographic, life-style factors, family history of diabetes, blood pressure, renal function and medication use. The co-exposure-associated risks varied greatly by age distribution (P-interaction = 0.0193): < 40 years, 6.26 (3.47–11.28); 40–49 years, 2.26 (1.77–2.89); 50–59 years, 2.51 (2.00–3.16); 60–69 years, 2.48 (1.86–3.30); ≥ 70 years, 2.10 (1.29–3.40). In young adults (< 45 years), both exposures had a significant supra-additive effect on diabetogenesis (relative excess risk due to interaction: 0.80, 95% CI 0.10–1.50). Conclusions These findings highlight the need for age-specific combined assessment and management of chronic inflammation and dyslipidemia in primary prevention against T2D, particularly for young adults. The clinical benefit derived from dual-target intervention against dyslipidemia and inflammation will exceed the sum of each part alone in young adults. BackgroundBoth elevated inflammation and atherogenic dyslipidemia are prominent in young-onset diabetes and are increasingly identified as biologically intertwined processes that contribute to diabetogenesis. We aimed to investigate the age-specific risks of type 2 diabetes (T2D) upon concomitant chronic inflammation and atherogenic dyslipidemia.MethodsAge-stratified Cox regression analysis of the risk of incident diabetes upon co-exposure to time-averaged cumulative high-sensitivity C-reactive protein (CumCRP) and atherogenic index of plasma (CumAIP) among 42,925 nondiabetic participants from a real-world, prospective cohort (Kailuan Study).ResultsDuring a median 6.41 years of follow-up, 3987 T2D developed. Isolated CumAIP and CumCRP were significantly associated with incident T2D in the entire cohort and across all age subgroups. Both CumAIP and CumCRP were jointly associated with an increased risk of diabetes (P-interaction = 0.0126). Compared to CumAIP < -0.0699 and CumCRP < 1 mg/L, co-exposure to CumAIP ≥ − 0.0699 and CumCRP ≥ 3 mg/L had a significant hazard ratio (HR) [2.55 (2.23–2.92)] after adjusting for socio-demographic, life-style factors, family history of diabetes, blood pressure, renal function and medication use. The co-exposure-associated risks varied greatly by age distribution (P-interaction = 0.0193): < 40 years, 6.26 (3.47–11.28); 40–49 years, 2.26 (1.77–2.89); 50–59 years, 2.51 (2.00–3.16); 60–69 years, 2.48 (1.86–3.30); ≥ 70 years, 2.10 (1.29–3.40). In young adults (< 45 years), both exposures had a significant supra-additive effect on diabetogenesis (relative excess risk due to interaction: 0.80, 95% CI 0.10–1.50).ConclusionsThese findings highlight the need for age-specific combined assessment and management of chronic inflammation and dyslipidemia in primary prevention against T2D, particularly for young adults. The clinical benefit derived from dual-target intervention against dyslipidemia and inflammation will exceed the sum of each part alone in young adults. Both elevated inflammation and atherogenic dyslipidemia are prominent in young-onset diabetes and are increasingly identified as biologically intertwined processes that contribute to diabetogenesis. We aimed to investigate the age-specific risks of type 2 diabetes (T2D) upon concomitant chronic inflammation and atherogenic dyslipidemia. Age-stratified Cox regression analysis of the risk of incident diabetes upon co-exposure to time-averaged cumulative high-sensitivity C-reactive protein (CumCRP) and atherogenic index of plasma (CumAIP) among 42,925 nondiabetic participants from a real-world, prospective cohort (Kailuan Study). During a median 6.41 years of follow-up, 3987 T2D developed. Isolated CumAIP and CumCRP were significantly associated with incident T2D in the entire cohort and across all age subgroups. Both CumAIP and CumCRP were jointly associated with an increased risk of diabetes (P-interaction = 0.0126). Compared to CumAIP < -0.0699 and CumCRP < 1 mg/L, co-exposure to CumAIP ≥ - 0.0699 and CumCRP ≥ 3 mg/L had a significant hazard ratio (HR) [2.55 (2.23-2.92)] after adjusting for socio-demographic, life-style factors, family history of diabetes, blood pressure, renal function and medication use. The co-exposure-associated risks varied greatly by age distribution (P-interaction = 0.0193): < 40 years, 6.26 (3.47-11.28); 40-49 years, 2.26 (1.77-2.89); 50-59 years, 2.51 (2.00-3.16); 60-69 years, 2.48 (1.86-3.30); ≥ 70 years, 2.10 (1.29-3.40). In young adults (< 45 years), both exposures had a significant supra-additive effect on diabetogenesis (relative excess risk due to interaction: 0.80, 95% CI 0.10-1.50). These findings highlight the need for age-specific combined assessment and management of chronic inflammation and dyslipidemia in primary prevention against T2D, particularly for young adults. The clinical benefit derived from dual-target intervention against dyslipidemia and inflammation will exceed the sum of each part alone in young adults. |
ArticleNumber | 181 |
Author | Guo, Zheng Balmer, Lois Li, Xingang Wang, Wei Cai, Zhiwei Wu, Shouling Song, Manshu Chen, Youren Ding, Xiong Gao, Jingli Lan, Shaocong Lan, Yulong Wu, Weiqiang Xu, Yuancheng Chen, Lan Wu, Dan |
Author_xml | – sequence: 1 givenname: Yulong surname: Lan fullname: Lan, Yulong organization: Department of Cardiology, Second Affiliated Hospital of Shantou University Medical College, 69 Dongxia North Road, Shantou, 515041, China – sequence: 2 givenname: Dan surname: Wu fullname: Wu, Dan organization: Department of Pediatrics, Second Affiliated Hospital of Shantou University Medical College, Shantou, 515041, China – sequence: 3 givenname: Zhiwei surname: Cai fullname: Cai, Zhiwei organization: Department of Cardiology, Second Affiliated Hospital of Shantou University Medical College, 69 Dongxia North Road, Shantou, 515041, China – sequence: 4 givenname: Yuancheng surname: Xu fullname: Xu, Yuancheng organization: Department of Urology, The University of Hong Kong-Shenzhen Hospital, Shenzhen, 518172, China – sequence: 5 givenname: Xiong surname: Ding fullname: Ding, Xiong organization: School of Public Health, Wuhan University, Wuhan, 430072, China – sequence: 6 givenname: Weiqiang surname: Wu fullname: Wu, Weiqiang organization: Department of Cardiology, Second Affiliated Hospital of Shantou University Medical College, 69 Dongxia North Road, Shantou, 515041, China – sequence: 7 givenname: Shaocong surname: Lan fullname: Lan, Shaocong organization: Guangdong Medical University, Zhanjiang, 524023, China – sequence: 8 givenname: Lan surname: Chen fullname: Chen, Lan organization: Department of Cardiology, The First Affiliated Hospital of Shantou University Medical College, Shantou, 515041, China – sequence: 9 givenname: Zheng surname: Guo fullname: Guo, Zheng organization: Centre for Precision Health, Edith Cowan University, Room 521, Building 21/270 Joondalup Drive, Perth, WA, 6027, Australia – sequence: 10 givenname: Lois surname: Balmer fullname: Balmer, Lois organization: Centre for Precision Health, Edith Cowan University, Room 521, Building 21/270 Joondalup Drive, Perth, WA, 6027, Australia – sequence: 11 givenname: Xingang surname: Li fullname: Li, Xingang organization: Centre for Precision Health, Edith Cowan University, Room 521, Building 21/270 Joondalup Drive, Perth, WA, 6027, Australia – sequence: 12 givenname: Manshu surname: Song fullname: Song, Manshu organization: Beijing Key Laboratory of Clinical Epidemiology, School of Public Health, Capital Medical University, Beijing, 100069, China – sequence: 13 givenname: Shouling surname: Wu fullname: Wu, Shouling email: drwusl@163.com organization: Department of Cardiology, Kailuan General Hospital, Xinghua East Road, Tangshan, 063000, China. drwusl@163.com – sequence: 14 givenname: Jingli surname: Gao fullname: Gao, Jingli email: tsgaojingli@163.com organization: Department of Intensive Care Unit, Kailuan General Hospital, Xinghua East Road, Tangshan, China. tsgaojingli@163.com – sequence: 15 givenname: Wei surname: Wang fullname: Wang, Wei email: wei.wang@ecu.edu.au, wei.wang@ecu.edu.au, wei.wang@ecu.edu.au organization: Beijing Key Laboratory of Clinical Epidemiology, School of Public Health, Capital Medical University, Beijing, 100069, China. wei.wang@ecu.edu.au – sequence: 16 givenname: Youren surname: Chen fullname: Chen, Youren email: yrchen3@stu.edu.cn organization: Department of Cardiology, Second Affiliated Hospital of Shantou University Medical College, 69 Dongxia North Road, Shantou, 515041, China. yrchen3@stu.edu.cn |
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Keywords | Type 2 diabetes Aging Inflammation Young adults Dyslipidemia |
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Snippet | Both elevated inflammation and atherogenic dyslipidemia are prominent in young-onset diabetes and are increasingly identified as biologically intertwined... Abstract Background Both elevated inflammation and atherogenic dyslipidemia are prominent in young-onset diabetes and are increasingly identified as... BackgroundBoth elevated inflammation and atherogenic dyslipidemia are prominent in young-onset diabetes and are increasingly identified as biologically... BACKGROUNDBoth elevated inflammation and atherogenic dyslipidemia are prominent in young-onset diabetes and are increasingly identified as biologically... Abstract Background Both elevated inflammation and atherogenic dyslipidemia are prominent in young-onset diabetes and are increasingly identified as... |
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SubjectTerms | Age composition Age groups Aging Antihypertensives Atherosclerosis - complications Atherosclerosis - diagnosis Atherosclerosis - epidemiology Blood pressure Body mass index C-reactive protein Cohort analysis Creatinine Diabetes Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - diagnosis Diabetes Mellitus, Type 2 - epidemiology Dyslipidemia Dyslipidemias - diagnosis Dyslipidemias - epidemiology Epidemiology Glucose Humans Hypertension Inflammation Inflammation - complications Inflammation - diagnosis Inflammation - epidemiology Insulin Kidney diseases Lipids Metabolic disorders Prospective Studies Renal function Risk Factors Trends Type 2 diabetes Variables Young Adult Young adults |
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Title | Supra-additive effect of chronic inflammation and atherogenic dyslipidemia on developing type 2 diabetes among young adults: a prospective cohort study |
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