scholarly journals Body mass index moderates the relationship between C-reactive protein and depressive symptoms: evidence from the China Health and Retirement Longitudinal Study

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Tingting Qin ◽  
Wenhua Liu ◽  
Minghui Yin ◽  
Chang Shu ◽  
Mingming Yan ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Depressive Symptoms ◽  
Longitudinal Study ◽  
Body Mass ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
The Relationship

Serum C reactive protein levels and genetic variation in the CRP gene are not associated with the prevalence, incidence or progression of osteoarthritis independent of body mass index

2010 ◽  
Vol 69 (11) ◽  
pp. 1976-1982 ◽  
Author(s):  
Hanneke J M Kerkhof ◽  
Sita M A Bierma-Zeinstra ◽  
Martha C Castano-Betancourt ◽  
Moniek P de Maat ◽  
Albert Hofman ◽  
...  
Keyword(s):  
Systematic Review ◽  
Body Mass Index ◽  
Genetic Variation ◽  
Body Mass ◽  
Analysis Of Covariance ◽  
C Reactive Protein ◽  
Knee Oa ◽  
Reactive Protein ◽  
Serum Crp ◽  
The Relationship

ObjectiveTo study the relationship between serum C reactive protein (CRP) levels, genetic variation in the CRP gene and the prevalence, incidence and progression of radiographic osteoarthritis (ROA) in the Rotterdam Study-I (RS-I). A systematic review of studies assessing the relationship between osteoarthritis (OA) and CRP levels was also performed.MethodsThe association between CRP levels and genetic variation in the CRP gene and ROA was examined in 861 patients with hand OA, 718 with knee OA, 349 with hip OA and 2806 controls in the RS-I using one-way analysis of covariance and logistic regression, respectively. PubMed was searched for articles published between January 1992 and August 2009 assessing the relationship between CRP levels and OA.ResultsIn RS-I the prevalence of knee OA, but not hip OA or hand OA, was associated with 14% higher serum CRP levels compared with controls (p=0.001). This association disappeared after adjustment for age and especially body mass index (BMI) (p=0.33). Genetic variation of the CRP gene was not consistently associated with the prevalence, incidence or progression of OA within RS-I. The systematic review included 18 studies (including RS-I) on serum CRP levels and the prevalence, incidence or progression of OA. Consistently higher crude CRP levels were found in cases of prevalent knee OA compared with controls. No association was observed between serum CRP levels and the prevalence of knee OA following adjustment for BMI (n=3 studies, meta-analysis p value=0.61).ConclusionThere is no evidence of association between serum CRP levels or genetic variation in the CRP gene with the prevalence, incidence or progression of OA independent of BMI.

scholarly journals The Relationship Between C-Reactive Protein and Atherosclerosis Differs on the Basis of Body Mass Index

2012 ◽  
Vol 60 (13) ◽  
pp. 1148-1155 ◽  
Author(s):  
Nitin K. Gupta ◽  
James A. de Lemos ◽  
Colby R. Ayers ◽  
Shuaib M. Abdullah ◽  
Darren K. McGuire ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Body Mass ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
The Relationship

scholarly journals Associations Between Anti-Mullerian Hormone and Cardiometabolic Health in Reproductive Age Women Are Explained by Body Mass Index

2019 ◽  
Vol 105 (3) ◽  
pp. e555-e563 ◽  
Author(s):  
Julie S Rios ◽  
Eleni A Greenwood ◽  
Mary Ellen G Pavone ◽  
Marcelle I Cedars ◽  
Richard S Legro ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Body Mass ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Fasting Insulin ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
The Relationship ◽  
Total P

Abstract Context The relationship between reproductive and cardiometabolic aging is unclear. It is unknown if the relationship differs across different clinical populations. Objective To determine whether markers of ovarian reserve are associated with cardiometabolic risk in reproductive aged women with unexplained infertility (UI), polycystic ovary syndrome (PCOS), and regularly cycling women (OVA). Design and setting Cross-sectional data from 8 US-based academic centers. Participants Women aged 25–40 from 3 clinical populations: 870 with UI, 640 with PCOS, and 921 community-based OVA. Main Outcome Measures Multivariable linear regression models were used to relate anti-mullerian hormone (AMH) and antral follicle count with cardiometabolic parameters including body mass index (BMI), waist circumference (WC), fasting glucose and insulin, homeostasis model assessment-insulin resistance (HOMA-IR), lipids, and C-reactive protein. Results In age and study site-adjusted models, AMH inversely related to BMI in the UI and OVA groups (P = 0.02 and P < 0.001). Among women with PCOS, AMH inversely related to BMI (P < 0.001), and also to WC (P < 0.001), fasting insulin (P < 0.01), HOMA-IR (P < 0.01), triglycerides (P = 0.04), and C-reactive protein (P < 0.001) and directly related to higher total (P = 0.02), low-density lipoprotein (P < 0.01), and high-density lipoprotein cholesterol (P < 0.01). In OVA, AMH also varied inversely with WC (P < 0.001), fasting insulin (P = 0.02), and HOMA-IR (P = 0.02). Adjustment for BMI eliminated associations in the OVA group but in PCOS, the relationship of AMH to total (P = 0.03) and low-density lipoprotein cholesterol (P = 0.003) remained. Conclusion Associations observed between AMH and cardiometabolic indices are largely explained by BMI in women with and without PCOS. (J Clin Endocrinol Metab XX: 0-0, 2019)

scholarly journals Leveraging genetic data to elucidate the relationship between Covid-19 and ischemic stroke

2021 ◽  
Author(s):  
Verena Zuber ◽  
Alan Cameron ◽  
Evangelos P. Myserlis ◽  
Leonardo Bottolo ◽  
Israel Fernandez-Cadenas ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Ischemic Stroke ◽  
Body Mass ◽  
Mendelian Randomization ◽  
Genetic Data ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Increased Risk ◽  
The Relationship ◽  
Randomization Analysis

AbstractBackgroundThe relationship between coronavirus disease 2019 (Covid-19) and ischemic stroke is poorly defined. We aimed to leverage genetic data to investigate reported associations.MethodsGenetic association estimates for liability to Covid-19 and cardiovascular traits were obtained from large-scale consortia. Analyses primarily focused on critical Covid-19, defined as hospitalization with Covid-19 requiring respiratory support or resulting in death. Cross-trait linkage disequilibrium score regression was used to estimate genetic correlations of critical Covid-19 with ischemic stroke, other related cardiovascular outcomes, and risk factors common to both Covid-19 and cardiovascular disease (body mass index, smoking and chronic inflammation, estimated using C-reactive protein). Mendelian randomization analysis was performed to investigate whether liability to critical Covid-19 was associated with increased risk of any of the cardiovascular outcomes for which genetic correlation was identified.ResultsThere was evidence of genetic correlation between critical Covid-19 and ischemic stroke (rg=0.29, FDR p-value=4.65×10−3), body mass index (rg=0.21, FDR-p-value=6.26×10−6) and C-reactive protein (rg=0.20, FDR-p-value=1.35×10−4), but none of the other considered traits. In Mendelian randomization analysis, liability to critical Covid-19 was associated with increased risk of ischemic stroke (odds ratio [OR] per logOR increase in genetically predicted critical Covid-19 liability 1.03, 95% confidence interval 1.00-1.06, p-value=0.03). Similar estimates were obtained when considering ischemic stroke subtypes. Consistent estimates were also obtained when performing statistical sensitivity analyses more robust to the inclusion of pleiotropic variants, including multivariable Mendelian randomization analyses adjusting for potential genetic confounding through body mass index, smoking and chronic inflammation. There was no evidence to suggest that genetic liability to ischemic stroke increased the risk of critical Covid-19.ConclusionsThese data support that liability to critical Covid-19 is associated with an increased risk of ischemic stroke. The host response predisposing to severe Covid-19 is likely to increase the risk of ischemic stroke, independent of other potentially mitigating risk factors.

scholarly journals Leveraging Genetic Data to Elucidate the Relationship Between COVID‐19 and Ischemic Stroke

2021 ◽  
Author(s):  
Verena Zuber ◽  
Alan Cameron ◽  
Evangelos P. Myserlis ◽  
Leonardo Bottolo ◽  
Israel Fernandez‐Cadenas ◽  
...  
Keyword(s):  
Risk Factors ◽  
Body Mass Index ◽  
Ischemic Stroke ◽  
Body Mass ◽  
Mendelian Randomization ◽  
Genetic Data ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Increased Risk ◽  
The Relationship

Background The relationship between COVID‐19 and ischemic stroke is poorly understood due to potential unmeasured confounding and reverse causation. We aimed to leverage genetic data to triangulate reported associations. Methods and Results Analyses primarily focused on critical COVID‐19, defined as hospitalization with COVID‐19 requiring respiratory support or resulting in death. Cross‐trait linkage disequilibrium score regression was used to estimate genetic correlations of critical COVID‐19 with ischemic stroke, other related cardiovascular outcomes, and risk factors common to both COVID‐19 and cardiovascular disease (body mass index, smoking and chronic inflammation, estimated using C‐reactive protein). Mendelian randomization analysis was performed to investigate whether liability to critical COVID‐19 was associated with increased risk of any cardiovascular outcome for which genetic correlation was identified. There was evidence of genetic correlation between critical COVID‐19 and ischemic stroke (r g =0.29, false discovery rate [FDR]=0.012), body mass index (r g =0.21, FDR=0.00002), and C‐reactive protein (r g =0.20, FDR=0.00035), but no other trait investigated. In Mendelian randomization, liability to critical COVID‐19 was associated with increased risk of ischemic stroke (odds ratio [OR] per logOR increase in genetically predicted critical COVID‐19 liability 1.03, 95% CI 1.00–1.06, P ‐value=0.03). Similar estimates were obtained for ischemic stroke subtypes. Consistent estimates were also obtained when performing statistical sensitivity analyses more robust to the inclusion of pleiotropic variants, including multivariable Mendelian randomization analyses adjusting for potential genetic confounding through body mass index, smoking, and chronic inflammation. There was no evidence to suggest that genetic liability to ischemic stroke increased the risk of critical COVID‐19. Conclusions These data support that liability to critical COVID‐19 is associated with an increased risk of ischemic stroke. The host response predisposing to severe COVID‐19 is likely to increase the risk of ischemic stroke, independent of other potentially mitigating risk factors.

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