Adjustment For C-reactive Protein Research Articles

Relationship of neutrophil-to-lymphocyte ratio, in addition to C-reactive protein, with cardiovascular events in patients with type 2 diabetes

AimTo quantify the relationship of neutrophil-to-lymphocyte ratio (NLR) with cardiovascular events and all-cause mortality in patients with type 2 diabetes (T2D), independent of C-reactive protein (CRP). MethodsPatients with T2D from the UCC-SMART-cohort were studied using multivariable-adjusted Cox regression. The relationship of NLR and CRP with vascular events (cerebrovascular events, myocardial infarction and vascular death) and all-cause mortality was quantified. ResultsDuring 10,833 person-years, 232 vascular events and 302 deaths occurred in 1,239 patients with T2D. Risk of vascular events and all-cause mortality increased per standard deviation (SD) in NLR (hazard ratio (HR) 1.27; 95 % confidence interval (CI):1.11–1.46) and 1.15; 95 % CI:1.02–1.30) after adjustment for CRP. CRP was not associated with vascular events after adjustment for NLR, (HR per SD 1.03; 95 % CI: 0.90–1.19), but was associated with all-cause mortality (HR per SD 1.18; 95 % CI: 1.04–1.33). Notably, NLR was related to vascular events in patients with CRP < 2 mg/L (HR per unit 1.45; 95 % CI: 1.19–1.77). ConclusionIn patients with T2D, NLR is related to higher risk of CVD and all-cause mortality, independently from CRP. NLR is related to CVD even when CRP is low, indicating that NLR is a marker of CVD-risk in addition to CRP. Both NLR and CRP are independently related to all-cause mortality in T2D patients.

Exploring complement biomarkers in suspected axial spondyloarthritis

ObjectivesTo investigate lectin pathway proteins (LPPs) as biomarkers for axial spondyloarthritis (axSpA) in a cross-sectional cohort with a suspicion of axSpA, comprising newly diagnosed axSpA and chronic low back pain...

Association between bleeding periodontal pockets and eczemas: Results of the Northern Finland Birth Cohort 1966.

To investigate whether the periodontal condition as measured by bleeding periodontal pockets is associated with atopic dermatitis, seborrheic dermatitis, and eczema nummulare. The study population (n=1871) was obtained from the 46-year follow-up study of the Northern Finland Birth Cohort 1966 study (NFBC1966). The periodontal condition was measured by the number of sites with bleeding periodontal pockets that were ≥4 mm deep. The whole skin of the participants was clinically examined, and diagnoses of skin diseases were made according to the International Classification of Diseases. Prevalence rate ratios (PRR) and 95% confidence intervals (95% CIs) were estimated using Poisson regression models with robust error variance. In this cohort, comprising 46-year-old participants of NFBC1966, the presence of 1-3 and ≥4 bleeding-deepened periodontal pockets (≥4 mm deep) were associated with seborrheic dermatitis (PRR 1.9, 95% CI: 1.3-2.8 and PRR 2.2, 95% CI: 1.4-3.3, respectively) and with eczema nummulare (PRR 1.7, 95% CI: 0.9-3.1 and PRR 1.7, 95% CI: 0.9-3.3, respectively). For non-smokers, the corresponding estimates were 1.7 for seborrheic dermatitis (95% CI: 1.1-2.6) and 1.8 (95% CI: 1.1-3.1) and 1.4 for eczema nummulare (95% CI: 0.7-2.9) and 1.2 (95% CI: 0.5-2.9), respectively. No association was found between bleeding-deepened periodontal pockets and atopic dermatitis. Further adjustments for C-reactive protein, diabetes, and inflammatory diseases did not essentially change the risk estimates among either the total population or the non-smokers. Bleeding periodontal pockets appeared to be associated with the presence of seborrheic dermatitis and eczema nummulare.

Association of vitamin A with anemia and serum hepcidin levels in children aged 6 to 59 mo

ObjectiveThis study evaluates the association of serum retinol, hepcidin levels, and anemia in children. MethodsThis cross-sectional study included 312 children, ages 6 to 59 mo, from Rio de Janeiro, Brazil. The association between hepcidin and retinol levels, hematologic parameters, and body mass index (BMI) was analyzed using a generalized linear model with and without adjustment for C-reactive protein (CRP) level. Logistic regression analysis was used to test anemia as an outcome and serum retinol level as a predictive variable using the odds ratio (OR) function. ResultsAnemia was present in 14.6% of the children, 5.8% presented iron deficiency anemia, and 9.6% had vitamin A deficiency. The increase in serum retinol levels reduced the chances of anemia (OR = 0.13; confidence interval = 0.29–0.59). When CRP level was not adjusted for in the multiple regression analyses, retinol, ferritin levels, and BMI/age were predictors of serum hepcidin levels (β = –3.36, 0.14, 1.02, respectively; P = 0.032). Accordingly, serum retinol levels were inversely associated with CRP levels (β = –0.025 and P < 0.001). ConclusionsThe association between serum retinol and hepcidin levels in children ages 6 to 59 mo seems to be dependent on inflammation. Taken together, the results reinforce the need for the development of further studies to better understand the relationship between vitamin A and anemia of inflammation.

Elevated plasma concentration of complement factor C5 is associated with risk of future venous thromboembolism

AbstractThe role of complement in the pathogenesis of venous thromboembolism (VTE) is unclear. We wanted to investigate (1) whether plasma complement component C5 (C5) levels are influenced by genetic variants or chronic inflammation and (2) the association between plasma C5 and risk of future VTE in a nested case-control study of 415 patients with VTE and 848 age- and sex-matched controls derived from the Tromsø Study. Plasma C5 levels were measured at inclusion. Odds ratios (ORs) with 95% confidence intervals (95% CIs) for provoked and unprovoked VTE across tertiles of C5 concentrations were estimated by logistic regression. Adjustment for C-reactive protein (CRP) served as a proxy for general inflammation. Whole-exome sequencing and protein quantitative trait loci analyses were performed to assess genetic influence on C5 concentrations. There was no association between genome-wide or C5-related gene variants and C5 levels. The association between plasma C5 levels and VTE risk displayed a threshold effect, where subjects with C5 levels above the lowest tertile had increased risk of VTE. Subjects in tertile 3 (highest C5 levels) had an age- and sex-adjusted OR of 1.45 (95% CI, 1.07-1.96) compared with tertile 1 (lowest). These statistics were more pronounced for unprovoked VTE (OR, 1.70; 95% CI, 1.11-2.60). Adjustments for body mass index and CRP had minor impact on risk estimates. The OR increased substantially with shorter time between blood sampling and VTE event. In conclusion, plasma C5 was associated with risk of future VTE. C5 levels were not genetically regulated and were only slightly influenced by chronic inflammation.

Infliximab treatment reduces depressive symptoms in patients with ankylosing spondylitis: an ancillary study to a randomized controlled trial (ASSERT)

BackgroundPatients with ankylosing spondylitis (AS) are at increased risk of depression. This increased risk has been hypothesized to be solely secondary due to AS-related symptoms, or additionally due to a common inflammatory pathway. From a clinical perspective, it is important to know whether treatment with tumor necrosis factor alpha inhibitors reduces depressive symptoms, while from a pathophysiological point of view, it would be insightful to understand whether such an effect would be a direct result of reduced inflammation, the result of reduced AS-related symptoms, or both. The objective of this study was to evaluate the effect of infliximab on depressive symptoms in patients with AS in a randomized-controlled trial setting.MethodsData were retrieved from a subgroup of patients from the AS Study for the Evaluation of Recombinant Infliximab Therapy (ASSERT). Patients were randomly allocated to infliximab (n = 16) or placebo (n = 7) until week 24, after which all received infliximab until week 54. Associations between treatment group and depressive symptoms, measured with the Center for Epidemiological Studies Depression scale (CES-D, range 0–60 (best-worst)) at baseline and over time, were explored with generalized estimating equations (GEE).ResultsMean CES-D score at baseline was 15.5 (SD 9.3) in the infliximab group and 17.3 (SD 5.7) in the placebo group. Twelve patients (52%) had a CES-D score > 16, suggestive for clinical depression. After 24 weeks, mean CES-D had decreased to 9.5 (SD 11.4) in the infliximab group, but was 18.0 (SD 6.9) in the placebo group. GEE revealed larger improvements in depressive symptoms (B = − 6.63, 95%CI − 13.35 to 0.09) and odds of possible depression (OR = 0.02, 95%CI 0.00 to 0.72) in the infliximab group, compared to the placebo group. Both associations largely disappeared when adjusted for self-reported disease activity and/or physical function. Additional adjustment for C-reactive protein (CRP) did not change results.ConclusionsDepressive symptoms are common in patients with AS and active disease. Infliximab improves these depressive symptoms in AS when compared to placebo by improving disease symptoms. We did not find an indication for a direct link between CRP-mediated inflammation and depressive symptoms.Trial registrationTrial registration (ASSERT): NCT00207701. Registered on September 21, 2005 (retrospectively registered).

Oxidative Stress and Inflammation as Predictors of Mortality and Cardiovascular Events in Hemodialysis Patients: The DREAM Cohort.

Aim: Both oxidative stress and inflammation are involved in the pathogenesis of cardiovascular disease (CVD). The serum level of derivatives of reactive oxygen metabolites (d-ROMs) is a measure of the total amount of hydroperoxides serving as a marker of oxidative stress. We investigated whether d-ROMs could predict the clinical outcomes in hemodialysis patients and whether the associations of d-ROMs with the outcomes are independent of a marker of inflammation, C-reactive protein (CRP).Methods: This was a prospective cohort study in hemodialysis patients. The key exposures were the serum levels of d-ROMs and CRP. The outcome measures were all-cause mortality and new CVD events.Results: A total of 517 patients were analyzed. d-ROMs correlated positively with CRP. During follow-up for 5 years, 107 patients died, and 190 patients experienced new CVD events. In the Kaplan–Meier analyses, both higher d-ROMs and higher CRP levels predicted higher risks for mortality and CVD events. By Cox proportional-hazard regression analysis adjusted for potential confounders excluding CRP, d-ROMs exhibited a significant association with all-cause mortality, but this association was no longer significant after further adjustment for CRP. Using the same model, CRP exhibited a significant association with all-cause mortality, but this association was no longer significant after further adjustment for d-ROMs. When we analyzed new CVD events as the outcome, CRP was a significant predictor, whereas the level of d-ROMs was not.Conclusions: Although d-ROMs predicted mortality and CVD events in unadjusted models, the associations of d-ROMs with these outcomes were not independent of CRP. Oxidative stress and inflammation appear to share common causal pathways.

Abstract P300: C-reactive Protein and Racial Differences in Type 2 Diabetes Incidence: Reasons for Geographic and Racial Differences in Stroke (REGARDS)

Introduction: Black Americans have a higher incidence of diabetes and have elevated inflammatory biomarkers compared to white Americans. Elevated inflammation is a risk factor for diabetes but the impact of inflammation on the racial disparity in diabetes is unknown. Hypothesis: Elevated C-reactive protein (CRP) attenuates the observed black-white difference in incident diabetes. Methods: REGARDS enrolled 30,239 black and white adults aged ≥45 years from the contiguous US in 2003-07. This analysis included REGARDS participants without baseline diabetes who were assessed for diabetes 9 years later. RRs for incident diabetes by race were calculated using modified Poisson regression adjusting for risk factors known to contribute to the racial difference in diabetes incidence. The attenuation by CRP of the black-white RR of incident diabetes was calculated as the percent difference in the race RR in models with and without CRP adjustment; 95% CI for the difference was estimated using bootstrapping. Results: Of 11,073 participants without baseline diabetes (33% black, 67% white), black participants had higher CRP than white participants, and 12.5% developed incident diabetes. The black-white RR for incident diabetes in the base model was 1.74 (95% CI: 1.52, 1.99) for women and 1.44 (1.25, 1.66) for men. Baseline CRP mediated 21% (14, 29%) of this association in women and 20% (12, 34%) in men. These percent attenuations were similar in models adjusting for other diabetes risk factors but were diminished in a fully adjusted model; 5% (-4, 25%) in women and 7% (-43, 50%) in men (Figure). Conclusion: Adjustment for CRP in base models accounted for 20% and 21% of the excess risk of incident diabetes observed in black men and women, respectively, in this study. This substantial mediation persisted after adjusting for other risk factors but was diminished in the fully adjusted model. This suggests a role of inflammation in the diabetogenic effects of risk factors contributing to the observed racial difference in diabetes incidence.

The high risk for type 2 diabetes among ethnic minority populations is not explained by low-grade inflammation

Our aim was to identify whether low-grade inflammation, reflected by C-reactive protein (CRP), explains the higher risk for incident type 2 diabetes (T2D) among ethnic minorities. We included 837 Dutch, 712 South-Asian Surinamese, 797 African Surinamese, 804 Ghanaian, 817 Turkish and 778 Moroccan origin participants of the HELIUS study (Amsterdam, the Netherlands). We used multiple linear regression to assess ethnic differences in CRP levels. We determined the association of CRP with T2D and the modifying effect of ethnicity by cox regression, and compared hazard ratios for the association between ethnicity and T2D before and after adjustment for CRP. CRP levels were higher in ethnic minority groups than in Dutch origin participants. CRP was associated with a higher T2D incidence, similarly across ethnic groups (overall HR per SD 1.38 [95% CI 1.14; 1.68]). However, the association was attenuated and no longer statistically significant after adjustment for adiposity measures (HR 1.11 [95% CI 0.90; 1.37]). CRP accounted for a very small part of the ethnic differences in T2D, but only in models unadjusted for adiposity. Low-grade inflammation does not substantially contribute to the higher risk of T2D among ethnic minority populations compared to the Dutch.

Associations between sarcopenia and nonalcoholic fatty liver disease and advanced fibrosis in the USA.

Nonalcoholic fatty liver disease (NAFLD) may be associated with sarcopenia. This study aims to determine whether sarcopenia is independently associated with NAFLD and advanced fibrosis. Cross-sectional data from 11 325 participants in the third National Health and Nutrition Examination Survey were analyzed. NAFLD was defined as the presence of hepatic steatosis from the ultrasound. Sarcopenia was defined as the skeletal muscle index. NAFLD was more common in participants with sarcopenia than in those without (46.7 vs. 27.5%). Univariate analysis showed that sarcopenia was associated with NAFLD [odds ratio (OR): 2.31; 95% confidence interval (CI): 2.01-2.64], which remained significant after adjustment for age, sex, ethnicity, metabolic risk factors (OR: 1.24; 95% CI: 1.03-1.48). This finding persisted after adjustment for C-reactive protein as a marker of chronic inflammation. NAFLD-associated advanced fibrosis was more common in participants with sarcopenia than in those without (7.8 vs. 1.6%). Sarcopenia was associated with NAFLD-associated advanced fibrosis independent of metabolic risk factors (OR: 1.79; 95% CI: 1.18-2.72). Sarcopenia was independently associated with increased odds of NAFLD and NAFLD-associated advanced fibrosis independent of well-defined risk factors. Interventions to strengthen muscle mass may reduce the burden of NAFLD and advanced fibrosis.

Interplay Between Systemic Inflammation, Visceral Fat, and Cognitive Control in People with Excess Fat Mass (OR32-06-19)

ObjectivesExcess fat mass has been associated with poorer cognitive function. Elevated visceral adiposity (VAT) has also been associated with cardiometabolic risk factors including chronic systemic low-grade inflammation. Whereas the cognitive implications of inflammation have been extensively studied in preclinical models, the influence of inflammatory cytokines on human cognition is unclear. Thus, this study aimed to investigate the relations among VAT, inflammatory cytokines and cognitive control. We hypothesized that elevated VAT and inflammation would be related to poorer performance during a cognitive control task. MethodsParticipants between 25–45 years (N = 77 48 females) with overweight/obesity (BMI ≥ 25 kg/m2) underwent a DXA scan to quantify VAT. A Flanker Task was used to assess cognitive control while Event-Related Potentials were recorded. Following an overnight fast, blood was collected to quantify plasma C-reactive protein (CRP) and Interleukin-6 (IL-6) concentrations using ELISAs. Spearman’s correlations were used to analyze relations using a 1-tailed approach. ResultsGreater VAT was related to lower congruent (r = −.19, P = .05) and incongruent trial accuracy (r = −.26, P = .01), as well as lower congruent P3 peak amplitude (r = −.23, P = .02) and slower latency (r = .37, P < .001). Similarly, elevated CRP and IL-6 were associated with poorer congruent (rCRP = −.22 pCRP = .03; rIL6 = −.20 pIL6 = .03), and incongruent (rCRP = −.33 pCRP = .002; rIL6 = −.32 pIL6 = .002) accuracy. Additionally, CRP was related to slower incongruent P3 peak latency (r = .22, P = .02). Partial correlations controlling for CRP and IL-6 showed that VAT was no longer associated with cognitive performance (all p’s > 0.07); however, the association between VAT and P3 peak amplitude (r = −.26, P = .01) and latency (r = .35, P = .001) persisted even following adjustment for CRP and IL-6. ConclusionsThis work replicates previous research indicating that VAT is related to poorer attentional abilities; however, we extend the literature by elucidating the role of low-grade inflammation as a contributing factor in this relationship in adults with excess fat mass. Funding SourcesThis work was supported by funds provided by the Dept of Kinesiology & Community Health at UIUC & the USDA National Institute of Food and Agriculture, Hatch Project 1009249. Partial support provided by the Hass Avocado Board.

The association between circulating endostatin levels and incident myocardial infarction

Objective. Increased levels of circulating endostatin have been observed in patients with prevalent ischemic heart disease. However, the association between circulating endostatin, and incident myocardial infarction (MI) is less studied. Our main aim was to study the association between circulating endostatin and incident MI in the community adjusted for established cardiovascular risk factors in men and women. Design. Circulating endostatin was measured in a nested case control study based on three large community-based Swedish cohorts, including 533 MI cases, and 1003 age-, sex- and cohort-matched controls. Odds ratios (OR) with 95% confidence intervals (CI) were calculated with adjustments for established cardiovascular risk factors. Results. Higher endostatin was associated with a higher incidence of MI independently of established cardiovascular risk factors (OR 1.19, 95% CI 1.03–1.37, p = .02), but this association was abolished after additional adjustment for C-reactive protein. Sex-stratified analyses suggest that the association was substantially stronger in women as compared to men. Conclusions. In our community based sample, higher endostatin predicted incident myocardial infarction predominantly in women but not independently of CRP. Thus, our findings do not support a broad utility of endostatin measurements for the prediction of incident myocardial infarction in clinical practice.

Dietary intake of magnesium and the risk of epilepsy in middle-aged and older Finnish men: A 22-year follow-up study in a general population.

Magnesium may play an important role in the prevention or treatment of epilepsy. We aimed to examine the association between dietary intake of magnesium and the incidence of epilepsy in middle-aged Finnish men in a prospective setting. As a secondary analysis, we also considered a possible association between dietary intake of magnesium and inflammation in subjects with epilepsy. The study included 2442 men, ages 42 to 60 y, from the prospective Kuopio Ischaemic Heart Disease Risk Factor Study who were free of epilepsy at baseline between 1984 and 1989. Dietary intake of magnesium was assessed with a 4-d food record. The hospital discharge diagnosis of epilepsy was used as an outcome variable. During the average follow-up period of 22.4 y, 74 men (3%) developed epilepsy. Those who followed the recommended dietary intake (>350 mg/d) of magnesium had a lower risk of epilepsy (hazard ratio [HR]: 0.52; confidence interval [CI], 0.28-0.99; P = 0.045) after multivariate adjustments. However, the risk was not significant after adjustment for C-reactive protein (CRP). We also found that CRP concentration was directly associated with the risk of epilepsy (HR: 1.24; CI, 1.00-1.54; P = 0.048). This association was attenuated after adjustment for dietary intake of magnesium and no longer significantly associated with the risk of epilepsy (HR: 1.22; CI, 0.99-1.52; P = 0.07). A higher dietary intake of magnesium was associated with lower incident epilepsy, and this association was slightly mediated by CRP. Further studies are required to identify the potential mechanisms.

Long-chain omega-3 fatty acids and headache in the U.S. population

The objective of this study was to assess whether dietary intake of long-chain omega-3 polyunsaturated fatty acids (PUFAs) is associated with lower prevalence of headache in the U.S. population. This cross-sectional study used data for a nationally representative sample of 12,317 men and women aged ≥ 20 years participating in the National Health and Nutrition Examination Surveys of 1999–2004. Interviewers recorded self-report of severe headache or migraine in the past three months. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were quantified from 24-hour dietary recall using the U.S. Department of Agriculture National Nutrient Database. Serum concentration of C-reactive protein, a marker of inflammation and potential mediator of PUFA's analgesic properties, was quantified by latex-enhanced nephelometry. Multivariable generalized linear models estimated prevalence ratios (PR) with 95% confidence limits (CL) for severe headache or migraine adjusting for NHANES cycle, sociodemographic characteristics, body mass index and total energy intake. The unadjusted prevalence of severe headache or migraine was 22.0% (females 28.2%, males 15.5%). In multivariable analysis, greater intake of omega-3 PUFAs was associated with lower prevalence of severe headache or migraine: PR 0.94 (95% CL: 0.88, 0.99, p = 0.035) per log unit increase in EPA, and PR 0.94 (95% CL: 0.90, 0.99, p = 0.023) per log unit increase in DHA. The strength of association was greater for non-Mexican Hispanics than for other racial/ethnic groups but was not attenuated after adjustment for C-reactive protein. In conclusion, higher dietary intakes of EPA and DHA were associated with lower prevalence of headache supporting the hypothesis that omega-3 PUFAs may prevent or reduce headache.

Plasma hepcidin is associated with future risk of venous thromboembolism

AbstractRed cell distribution width (RDW) is associated with venous thromboembolism (VTE), but the underlying mechanism(s) is unclear. Iron deficiency is associated with high RDW, and studies suggest an association between iron deficiency and VTE. To assess whether iron deficiency is a risk factor for VTE that explains the association between RDW and VTE, we conducted a nested case-control study of 390 patients with VTE and 802 age- and sex-matched controls selected from the population-based cohort of the Tromsø Study. Physical measurements and blood samples were collected from 1994 to 1995. Logistic regression models were used to calculate odds ratios (ORs) with 95% confidence intervals (CIs) for VTE by RDW, hepcidin, and ferritin light chain (FtL). RDW was inversely associated with hepcidin, FtL, and hemoglobin. The risk of VTE increased linearly across categories of higher plasma hepcidin levels. Participants with hepcidin in the highest quartile had an OR for VTE of 1.32 (95% CI, 1.00-2.42), and those in the >90% percentile had an OR for VTE of 1.66 (95% CI, 1.14-2.42) compared with the reference group (quartiles 2 and 3). The risk estimates remained similar after adjustment for C-reactive protein. The risk of VTE increased by categories of higher RDW and was strengthened after inclusion of hepcidin and FtL in the multivariable model. Our findings reject the hypothesis that iron deficiency explains the association between RDW and VTE and suggest, in contrast, that high body iron levels might increase the risk of VTE.

Relative peak exercise oxygen pulse is related to sudden cardiac death, cardiovascular and all-cause mortality in middle-aged men.

Background Preliminary evidence suggests that peak exercise oxygen pulse - peak oxygen uptake/heart rate-, a variable obtained during maximal cardiopulmonary exercise testing and a surrogate of stroke volume, is a predictor of mortality. We aimed to assess the associations of peak exercise oxygen pulse with sudden cardiac death, fatal coronary heart disease and cardiovascular disease and all-cause mortality. Design A prospective study. Methods Peak exercise oxygen pulse was assessed in a maximal cycling test at baseline in 2227 middle-aged men of the Kuopio Ischaemic Heart Disease cohort study using expired gas variables and electrocardiograms. Relative peak exercise oxygen pulse was obtained by dividing the absolute value by body weight. Results During a median follow-up of 26.1 years 1097 subjects died; there were 220 sudden cardiac deaths, 336 fatal coronary heart diseases and 505 fatal cardiovascular diseases. Relative peak exercise oxygen pulse (mean 19.5 (4.1) mL per beat/kg/102) was approximately linearly associated with each outcome. Comparing extreme quartiles of relative peak exercise oxygen pulse, hazard ratios (95% confidence intervals) for sudden cardiac death, fatal coronary heart disease and cardiovascular disease, and all-cause mortality on adjustment for cardiovascular risk factors were 0.55 (0.36-0.83), 0.58 (0.42-0.81), 0.60 (0.46-0.79) and 0.59 (0.49-0.70), respectively ( P < 0.001 for all). The hazard ratios were unchanged on further adjustment for C-reactive protein and the use of beta-blockers. The addition of relative peak exercise oxygen pulse to a cardiovascular disease mortality risk prediction model significantly improved risk discrimination (C-index change 0.0112; P = 0.030). Conclusion Relative peak exercise oxygen pulse measured during maximal exercise was linearly and inversely associated with fatal cardiovascular and all-cause mortality events in middle-aged men. In addition, relative peak exercise oxygen pulse provided significant improvement in cardiovascular disease mortality risk assessment beyond conventional risk factors.

HDL functionality and cardiovascular outcome among nondialysis chronic kidney disease patients [S

CVD remains the leading cause of morbidity and mortality in patients with chronic kidney disease (CKD). CKD profoundly affects HDL composition and functionality, but whether abnormal HDL independently contributes to cardiovascular events in CKD patients remains elusive. In the present study, we assessed whether compositional and functional properties of HDL predict cardiovascular outcome among 526 nondialysis CKD patients who participate in the CARE FOR HOMe study. We measured HDL cholesterol, the content of HDL-associated proinflammatory serum amyloid A (SAA), and activities of the HDL enzymes paraoxonase and lipoprotein-associated phospholipase A2 (Lp-PLA2). In addition, we assessed the antioxidative activity of apoB-depleted serum. During a mean follow-up of 5.1 ± 2.1 years, 153 patients reached the predefined primary endpoint, a composite of atherosclerotic cardiovascular events including cardiovascular mortality and death of any cause. In univariate Cox regression analyses, lower HDL-cholesterol levels, higher HDL-associated SAA content, and lower paraoxonase activity predicted cardiovascular outcome, while Lp-PLA2 activity and antioxidative capacity did not. HDL-cholesterol and HDL-paraoxonase activity lost their association with cardiovascular outcome after adjustment for traditional cardiovascular and renal risk factors, while SAA lost its association after further adjustment for C-reactive protein. In conclusion, our data suggest that neither HDL quantity nor HDL composition or function independently predict cardiovascular outcome among nondialysis CKD patients.

The relationship of plasma Trans fatty acids with dietary inflammatory index among US adults

BackgroundIt has been suggested that trans fatty acids (TFAs) play an important role in cardiovascular diseases. We investigated the association between plasma TFAs and the dietary inflammatory index (DII) ™ in US adults.MethodsNational Health and Nutrition Examination Survey (NHANES) participants with data on plasma TFAs measured from 1999 to 2010 were included. Energy-adjusted-DII ™ (E-DII ™) expressed per 1000 kcal was calculated from 24-h dietary recalls. All statistical analyses accounted for the survey design and sample weights.ResultsOf the 5446 eligible participants, 46.8% (n = 2550) were men. The mean age of the population was 47.1 years overall, 47.8 years for men and 46.5 years for women (p = 0.09). After adjustment for C-reactive protein, body-mass-index, smoking, race, age, education, and marital status in linear regressions, trans 9-hexadecenoic acid [β coefficient 0.068 (95% CI: 0.032 to 0.188)], trans 11-octadecenoic acid [β coefficient 0.143 (95% CI: 0.155 to 0.310)], trans 9-octadecenoic acid [β coefficient 0.122 (95% CI: 0.120 to 0.277)], trans 9, and trans 12-octadienoic acid [β coefficient 0.103 (95% CI: 0.090 to 0.247)] were positively associated with the DII (all p < 0.001).ConclusionThe association of plasma TFAs with a marker of dietary inflammation suggests an underlying mechanism in the initiation and progression of cardiovascular diseases.

Vegetarian diet reduces the risk of hypertension independent of abdominal obesity and inflammation: a prospective study.

A vegetarian diet may prevent elevation of blood pressures and lower the risk for hypertension through lower degrees of obesity, inflammation, and insulin resistance. This study investigated the association between a vegetarian diet and hypertension incidence in a cohort of Taiwanese adult nonsmokers and examined whether this association was mediated through inflammation, abdominal obesity, or insulin resistance (using fasting glucose as a proxy). This matched cohort study was from the 1994-2008 MJ Health Screening Database. Each vegetarian was matched with five nonvegetarians by age, sex, and study site. The analysis included 4109 nonsmokers (3423 nonvegetarians and 686 vegetarians), followed for a median of 1.61 years. The outcome includes hypertension incidence, as well as SBP and DBP levels. Regression analysis was performed to assess the association between vegetarian diet and hypertension incidence or future blood pressure levels in the presence/absence of potential mediators. Vegetarians had a 34% lower risk for hypertension, adjusting for age and sex (odds ratio: 0.66, 95% confidence interval: 0.50-0.87; SBP: -3.3 mmHg, P < 0.001; DBP: -1.5 mmHg, P < 0.001). The results stay statistically significant after further adjustment for C-reactive protein, waist circumference, and fasting glucose (odds ratio: 0.72, 95% confidence interval: 0.55-0.86; SBP: -2.4 mmHg, P < 0.05; DBP: -1.1 mmHg, P < 0.05). The protective association between vegetarian diet and hypertension appeared to be consistent across age groups. Taiwanese vegetarians had lower incidence of hypertension than nonvegetarians. Vegetarian diets may protect against hypertension beyond lower abdominal obesity, inflammation, and insulin resistance.

Soluble CD163, adiponectin, C-reactive protein and progression of dysglycaemia in individuals at high risk of type 2 diabetes mellitus: the ADDITION-PRO cohort.

Our aim was to investigate the association between the macrophage-activation marker soluble CD163 (sCD163), adiponectin, C-reactive protein (CRP) and changes in glycaemia, insulin resistance and insulin secretion in individuals at high risk of type 2 diabetes mellitus. This prospective study included 1014 individuals at high risk of type 2 diabetes mellitus participating in the Danish arm of the Anglo-Danish-Dutch study of Intensive Treatment In PeOple with ScreeN-detected Diabetes in Primary Care (ADDITION-Europe trial) baseline examination in 2001-2006 and follow-up examination (ADDITION-Progression [ADDITION-PRO]) in 2009-2011. Baseline serum samples were analysed for sCD163, adiponectin and CRP. The associations between sCD163, adiponectin and CRP per doubling of concentration, and changes per year in HbA1c, fasting plasma glucose, 2h glucose, fasting insulin, HOMA-IR and HOMA-β were assessed using a mixed-effects model. A doubling of sCD163 concentration was positively associated with changes in fasting insulin (β = 1.078 per year, 95% CI 0.454, 1.702) and HOMA-β (β = 1.313 per year, 95% CI 0.537, 2.089), and a doubling of CRP concentration was positively associated with HbA 1c (β = 0.004 per year, 95% CI 0.001, 0.007) and fasting insulin (β = 0.267 per year, 95% CI 0.029, 0.504) after adjustment for age and sex. A doubling of adiponectin was inversely associated with changes in fasting glucose (β = −0.017 per year, 95% CI −0.028, −0.005), 2 h glucose (β = −0.063 per year, 95% CI −0.107, −0.019), fasting insulin (β = −1.558 per year, 95% CI −2.020, −1.096), HOMA-IR (β = −0.040 per year, 95% CI −0.062, −0.019) and HOMA-β (β = −1.009 per year, 95% CI −1.589, −0.429) after adjustment for age and sex. The associations were robust to adjustment for baseline waist circumference and smoking. Adjustment for CRP did not change the associations for sCD163 or adiponectin. Our findings indicate that mechanisms related to inflammation, including macrophage activation and adipocyte metabolism, may play a role in changes in glucose homeostasis in individuals at high risk of type 2 diabetes mellitus.