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Social isolation and loneliness have been associated with poor health and increased risk for mortality, and inflammation might explain this link. We used data from the Danish TRIAGE Study of acutely admitted medical patients (N = 6,144, mean age 60 years), and from two population-representative birth cohorts: the New Zealand Dunedin Longitudinal Study (N = 881, age 45) and the UK Environmental Risk (E-Risk) Longitudinal Twin Study (N = 1448, age 18), to investigate associations of social isolation with three markers of systemic inflammation: C-reactive protein (CRP), interleukin-6 (IL-6), and a newer inflammation marker, soluble urokinase plasminogen activator receptor (suPAR), which is thought to index systemic chronic inflammation. In the TRIAGE Study, socially isolated patients (those living alone) had significantly higher median levels of suPAR (but not CRP or IL-6) compared with patients not living by themselves. Social isolation prospectively measured in childhood was longitudinally associated with higher CRP, IL-6, and suPAR levels in adulthood (at age 45 in the Dunedin Study and age 18 in the E-Risk Study), but only suPAR remained associated after controlling for covariates. Dunedin Study participants who reported loneliness at age 38 or age 45 had elevated suPAR at age 45. In contrast, E-Risk Study participants reporting loneliness at age 18 did not show any elevated markers of inflammation. In conclusion, social isolation was robustly associated with increased inflammation in adulthood, both in medical patients and in the general population. It was associated in particular with systemic chronic inflammation, evident from the consistently stronger associations with suPAR than other inflammation biomarkers., Social isolation and loneliness have been associated with poor health and increased risk for mortality, and inflammation might explain this link. We used data from the Danish TRIAGE Study of acutely admitted medical patients (N = 6,144, mean age 60 years), and from two population-representative birth cohorts: the New Zealand Dunedin Longitudinal Study (N = 881, age 45) and the UK Environmental Risk (E-Risk) Longitudinal Twin Study (N = 1448, age 18), to investigate associations of social isolation with three markers of systemic inflammation: C-reactive protein (CRP), interleukin-6 (IL-6), and a newer inflammation marker, soluble urokinase plasminogen activator receptor (suPAR), which is thought to index systemic chronic inflammation. In the TRIAGE Study, socially isolated patients (those living alone) had significantly higher median levels of suPAR (but not CRP or IL-6) compared with patients not living by themselves. Social isolation prospectively measured in childhood was longitudinally associated with higher CRP, IL-6, and suPAR levels in adulthood (at age 45 in the Dunedin Study and age 18 in the E-Risk Study), but only suPAR remained associated after controlling for covariates. Dunedin Study participants who reported loneliness at age 38 or age 45 had elevated suPAR at age 45. In contrast, E-Risk Study participants reporting loneliness at age 18 did not show any elevated markers of inflammation. In conclusion, social isolation was robustly associated with increased inflammation in adulthood, both in medical patients and in the general population. It was associated in particular with systemic chronic inflammation, evident from the consistently stronger associations with suPAR than other inflammation biomarkers.

Social isolation and loneliness have been associated with poor health and increased risk for mortality, and inflammation might explain this link. We used data from the Danish TRIAGE Study of acutely admitted medical patients (N = 6,144, mean age 60 years), and from two population-representative birth cohorts: the New Zealand Dunedin Longitudinal Study (N = 881, age 45) and the UK Environmental Risk (E-Risk) Longitudinal Twin Study (N = 1448, age 18), to investigate associations of social isolation with three markers of systemic inflammation: C-reactive protein (CRP), interleukin-6 (IL-6), and a newer inflammation marker, soluble urokinase plasminogen activator receptor (suPAR), which is thought to index systemic chronic inflammation. In the TRIAGE Study, socially isolated patients (those living alone) had significantly higher median levels of suPAR (but not CRP or IL-6) compared with patients not living by themselves. Social isolation prospectively measured in childhood was longitudinally associated with higher CRP, IL-6, and suPAR levels in adulthood (at age 45 in the Dunedin Study and age 18 in the E-Risk Study), but only suPAR remained associated after controlling for covariates. Dunedin Study participants who reported loneliness at age 38 or age 45 had elevated suPAR at age 45. In contrast, E-Risk Study participants reporting loneliness at age 18 did not show any elevated markers of inflammation. In conclusion, social isolation was robustly associated with increased inflammation in adulthood, both in medical patients and in the general population. It was associated in particular with systemic chronic inflammation, evident from the consistently stronger associations with suPAR than other inflammation biomarkers., Social isolation and loneliness have been associated with poor health and increased risk for mortality, and inflammation might explain this link. We used data from the Danish TRIAGE Study of acutely admitted medical patients (N = 6,144, mean age 60 years), and from two population-representative birth cohorts: the New Zealand Dunedin Longitudinal Study (N = 881, age 45) and the UK Environmental Risk (E-Risk) Longitudinal Twin Study (N = 1448, age 18), to investigate associations of social isolation with three markers of systemic inflammation: C-reactive protein (CRP), interleukin-6 (IL-6), and a newer inflammation marker, soluble urokinase plasminogen activator receptor (suPAR), which is thought to index systemic chronic inflammation. In the TRIAGE Study, socially isolated patients (those living alone) had significantly higher median levels of suPAR (but not CRP or IL-6) compared with patients not living by themselves. Social isolation prospectively measured in childhood was longitudinally associated with higher CRP, IL-6, and suPAR levels in adulthood (at age 45 in the Dunedin Study and age 18 in the E-Risk Study), but only suPAR remained associated after controlling for covariates. Dunedin Study participants who reported loneliness at age 38 or age 45 had elevated suPAR at age 45. In contrast, E-Risk Study participants reporting loneliness at age 18 did not show any elevated markers of inflammation. In conclusion, social isolation was robustly associated with increased inflammation in adulthood, both in medical patients and in the general population. It was associated in particular with systemic chronic inflammation, evident from the consistently stronger associations with suPAR than other inflammation biomarkers.

Background and aims: The homeostatic chemokines CCL21 and CCL19 have been explored as biomarkers in cardiovascular disease prediction in patients with established cardiovascular disease, but associations between these chemokines and first-time coronary event incidence have not been investigated before. Here, we explored associations between CCL21 or CCL19 and first-time incident coronary events in the general population-based Malmo spacing diaeresis Diet and Cancer cohort with two decades of follow-up.Methods: CCL21 and CCL19 levels in plasma were analysed with ELISA and proximity extension assay and as-sociations with disease incidence were explored with conditional logistic regression in a nested case-control cohort (CCL21; n = 676) and with Cox regression in a population-based cohort (CCL19; n = 4636).Results: High CCL21 levels in plasma were associated with incident first-time coronary events independently of traditional risk factors (odds ratio of 2.64 with 95% confidence interval 1.62-4.31, p < 0.001, comparing the highest versus the lowest tertile of CCL21), whereas CCL19 was not. CCL19 was, however, associated with incident heart failure, as well as increased all-cause, cardiovascular and cancer mortality independently of age and sex.Conclusions: Even though CCL21 and CCL19 both signal through CCR7, these chemokines may not be inter-changeable as disease predictors and CCL21 could be used for prediction of future coronary events in individuals without any previous coronary heart disease history.

Background and aims: The homeostatic chemokines CCL21 and CCL19 have been explored as biomarkers in cardiovascular disease prediction in patients with established cardiovascular disease, but associations between these chemokines and first-time coronary event incidence have not been investigated before. Here, we explored associations between CCL21 or CCL19 and first-time incident coronary events in the general population-based Malmo spacing diaeresis Diet and Cancer cohort with two decades of follow-up.Methods: CCL21 and CCL19 levels in plasma were analysed with ELISA and proximity extension assay and as-sociations with disease incidence were explored with conditional logistic regression in a nested case-control cohort (CCL21; n = 676) and with Cox regression in a population-based cohort (CCL19; n = 4636).Results: High CCL21 levels in plasma were associated with incident first-time coronary events independently of traditional risk factors (odds ratio of 2.64 with 95% confidence interval 1.62-4.31, p < 0.001, comparing the highest versus the lowest tertile of CCL21), whereas CCL19 was not. CCL19 was, however, associated with incident heart failure, as well as increased all-cause, cardiovascular and cancer mortality independently of age and sex.Conclusions: Even though CCL21 and CCL19 both signal through CCR7, these chemokines may not be inter-changeable as disease predictors and CCL21 could be used for prediction of future coronary events in individuals without any previous coronary heart disease history.

Crohn’s Disease (CD) is a chronic Inflammatory Bowel Disease (IBD), common in the UAE. Microbiota is necessary to maintain a balanced gut environment which is essential for good health. Dysbiosis can predispose to many diseases including CD. The oral cavity has the second largest and most diverse microbiota after the gut harboring over 700 species of bacteria. This study aims to investigate the alterations in the salivary microbiome in patients with CD compared to Healthy controls (HC). It also aims to compare CD patients for salivary microbiome complexity and diversity according to different factors that can contribute to dysbiosis, including oral health, IBD drug use, disease duration, activity of the disease and relapse of symptoms. Finally, it aims to find any correlation between the inflammatory biomarkers in CD with their levels in saliva, and any possible link to oral dysbiosis. A total of 80 saliva samples were collected from CD patients and HC (n=40 in each group) seeking healthcare from two hospitals in Abu Dhabi, UAE. Information related to the participants’ oral and general health was recorded. DNA was extracted from saliva and sequenced using Oxford nanopore technology for salivary microbiome profiling. Salivary supernatant was used to measure inflammatory biomarkers including C-reactive protein (CRP) and Calprotectin (CAL) by Enzyme-linked immunosorbent assay (ELISA). Data was analyzed using appropriate bioinformatics and biostatistics tools. Obvious differences in the salivary microbiome of CD were found when compared to HC. Five dominant species were enriched in CD and depleted in HC, namely Veillonella dispar, Megasphaera stantonii, Prevotella jejuni, Dolosigranulum pigrum and Lactobacillus backii. Oral health is confirmed to have paramount significance in the dysbiosis of the oral microbiota since most significant features are cariogenic such as Streptococcus mutans or periopathogenic such as Fusobacterium periodonticum. Loss of op

Ageing is associated with a gradual physical decline accompanied by changes in body composition. The occurrence of a low-grade yet chronic state of systemic inflammation has gained interest for its potential consequences in the ageing process. Importantly, a physically active lifestyle may promote the maintenance of muscle mass, reduction in adipose tissue, and alleviate progression of a chronic pro-inflammatory state. The overall aim of this thesis was to explore relationships between biomarkers of systemic inflammation, body composition, and physical activity behaviours in community-dwelling older adults aged 65 to 70 years. A main finding of the thesis is the existence of associations between body composition and systemic inflammation in older adults, where excess adipose tissue is adversely associated with levels of inflammatory biomarkers in older women. Inverse associations were also observed between muscle mass and levels of pro-inflammatory biomarkers in older women. This thesis also highlights sex-specific associations between systemic inflammation and physical activity behaviours. Longer time spent sedentary was also associated with higher levels of proinflammatory biomarkers in older women and lower level of antiinflammatory biomarkers in older men. Reallocating time spent in activities of lower intensities with higher intensities was associated with lower levels of pro-inflammatory biomarkers in older women. Overall, the findings of this thesis support efforts promoting physical activity at the expense of sedentary time in order to combat age-related systemic inflammation and metabolic risk in older adults.

Inflammation is an enabling characteristic of the hallmarks of cancer. There has therefore been increasing interest in the clinical value of circulating inflammatory biomarkers in cancer. In this review, we summarize results on C-reactive protein (CRP), alone or as part of the Glasgow Prognostic Score (GPS, composed of CRP and serum albumin), as a biomarker of prognosis or prediction and monitoring of therapeutic response in patients with breast cancer. A systematic literature search was performed in Medline and Embase from 1990 to August 2021. The association of serum CRP and overall survival and disease/progression-free survival was summarized in meta-analyses using a random effects model. The results from a total of 35 included studies (20,936 patients) were divided according to three identified patient settings (metastatic, non-metastatic, and general setting). Most of the studies examined prognostic utility. Several larger studies observed associations between high serum CRP and poor survival, but the meta-analyses suggested a limited value in a non-metastatic and general breast cancer setting (populations with unknown or varied disease stage). In metastatic patients, however, more consistent findings supported an association between serum CRP and prognosis (hazard ratio for overall survival: 1.87 (95% CI 1.31-2.67). Only five studies examined a role in prediction or monitoring of therapeutic response. One study reported a significant association between serum CRP levels and response to chemotherapy. Findings regarding serum CRP as a biomarker in breast cancer appear inconsistent, particularly in non-metastatic and general breast cancer, where the prognostic value could not be confirmed. In patients with metastatic breast cancer we suggest that high serum CRP is an indicator of poor prognosis. Too few studies assessed the role of serum CRP in prediction or monitoring of treatment response to allow conclusions.

The association between pre-and perioperative inflammatory biomarkers, major compli-cations, and survival rates after resection of colorectal cancer (CRC) in older patients is largely unknown. The aim was to investigate age-dependent differences in these associations. Serum CRP, IL-6, and YKL-40 were measured preoperatively and on the first and second day after resection of CRC (stages I–III) in 210 older (≥70 years) and 191 younger patients (<70 years). The results from the complications was presented as an odds ratio (OR, with a 95% confidence interval (CI)) with logistic regression. Results from the mortality rates were presented as a hazard ratio (HR, with a 95% CI) using Cox proportional hazards regression. The preoperative inflammatory biomarkers were higher in the older vs. the younger patients. The risk of complications was increased in older patients with a high preoperative CRP (OR = 1.25, 95% CI 1.03–1.53), IL-6 (OR = 1.57, 95% CI 1.18–2.08), and YKL-40 (OR = 1.66, 95% CI 1.20–2.28), but not in younger patients. Mortality was higher in younger patients with high preoperative YKL-40 (HR = 1.66, 95% CI 1.06–2.60). This was not found in older patients. Elevated preoperative inflammatory biomarkers among older patients were associated with an increased risk of complications, but not mortality. Preoperative inflammatory biomarkers may be useful in assessing the risk of a complicated surgical course in older patients with CRC.

Ageing is associated with a gradual physical decline accompanied by changes in body composition. The occurrence of a low-grade yet chronic state of systemic inflammation has gained interest for its potential consequences in the ageing process. Importantly, a physically active lifestyle may promote the maintenance of muscle mass, reduction in adipose tissue, and alleviate progression of a chronic pro-inflammatory state. The overall aim of this thesis was to explore relationships between biomarkers of systemic inflammation, body composition, and physical activity behaviours in community-dwelling older adults aged 65 to 70 years. A main finding of the thesis is the existence of associations between body composition and systemic inflammation in older adults, where excess adipose tissue is adversely associated with levels of inflammatory biomarkers in older women. Inverse associations were also observed between muscle mass and levels of pro-inflammatory biomarkers in older women. This thesis also highlights sex-specific associations between systemic inflammation and physical activity behaviours. Longer time spent sedentary was also associated with higher levels of proinflammatory biomarkers in older women and lower level of antiinflammatory biomarkers in older men. Reallocating time spent in activities of lower intensities with higher intensities was associated with lower levels of pro-inflammatory biomarkers in older women. Overall, the findings of this thesis support efforts promoting physical activity at the expense of sedentary time in order to combat age-related systemic inflammation and metabolic risk in older adults.

The association between pre-and perioperative inflammatory biomarkers, major compli-cations, and survival rates after resection of colorectal cancer (CRC) in older patients is largely unknown. The aim was to investigate age-dependent differences in these associations. Serum CRP, IL-6, and YKL-40 were measured preoperatively and on the first and second day after resection of CRC (stages I–III) in 210 older (≥70 years) and 191 younger patients (<70 years). The results from the complications was presented as an odds ratio (OR, with a 95% confidence interval (CI)) with logistic regression. Results from the mortality rates were presented as a hazard ratio (HR, with a 95% CI) using Cox proportional hazards regression. The preoperative inflammatory biomarkers were higher in the older vs. the younger patients. The risk of complications was increased in older patients with a high preoperative CRP (OR = 1.25, 95% CI 1.03–1.53), IL-6 (OR = 1.57, 95% CI 1.18–2.08), and YKL-40 (OR = 1.66, 95% CI 1.20–2.28), but not in younger patients. Mortality was higher in younger patients with high preoperative YKL-40 (HR = 1.66, 95% CI 1.06–2.60). This was not found in older patients. Elevated preoperative inflammatory biomarkers among older patients were associated with an increased risk of complications, but not mortality. Preoperative inflammatory biomarkers may be useful in assessing the risk of a complicated surgical course in older patients with CRC.

Ageing is associated with a gradual physical decline accompanied by changes in body composition. The occurrence of a low-grade yet chronic state of systemic inflammation has gained interest for its potential consequences in the ageing process. Importantly, a physically active lifestyle may promote the maintenance of muscle mass, reduction in adipose tissue, and alleviate progression of a chronic pro-inflammatory state. The overall aim of this thesis was to explore relationships between biomarkers of systemic inflammation, body composition, and physical activity behaviours in community-dwelling older adults aged 65 to 70 years. A main finding of the thesis is the existence of associations between body composition and systemic inflammation in older adults, where excess adipose tissue is adversely associated with levels of inflammatory biomarkers in older women. Inverse associations were also observed between muscle mass and levels of pro-inflammatory biomarkers in older women. This thesis also highlights sex-specific associations between systemic inflammation and physical activity behaviours. Longer time spent sedentary was also associated with higher levels of proinflammatory biomarkers in older women and lower level of antiinflammatory biomarkers in older men. Reallocating time spent in activities of lower intensities with higher intensities was associated with lower levels of pro-inflammatory biomarkers in older women. Overall, the findings of this thesis support efforts promoting physical activity at the expense of sedentary time in order to combat age-related systemic inflammation and metabolic risk in older adults.

Ageing is associated with a gradual physical decline accompanied by changes in body composition. The occurrence of a low-grade yet chronic state of systemic inflammation has gained interest for its potential consequences in the ageing process. Importantly, a physically active lifestyle may promote the maintenance of muscle mass, reduction in adipose tissue, and alleviate progression of a chronic pro-inflammatory state. The overall aim of this thesis was to explore relationships between biomarkers of systemic inflammation, body composition, and physical activity behaviours in community-dwelling older adults aged 65 to 70 years. A main finding of the thesis is the existence of associations between body composition and systemic inflammation in older adults, where excess adipose tissue is adversely associated with levels of inflammatory biomarkers in older women. Inverse associations were also observed between muscle mass and levels of pro-inflammatory biomarkers in older women. This thesis also highlights sex-specific associations between systemic inflammation and physical activity behaviours. Longer time spent sedentary was also associated with higher levels of proinflammatory biomarkers in older women and lower level of antiinflammatory biomarkers in older men. Reallocating time spent in activities of lower intensities with higher intensities was associated with lower levels of pro-inflammatory biomarkers in older women. Overall, the findings of this thesis support efforts promoting physical activity at the expense of sedentary time in order to combat age-related systemic inflammation and metabolic risk in older adults.

Ageing is associated with a gradual physical decline accompanied by changes in body composition. The occurrence of a low-grade yet chronic state of systemic inflammation has gained interest for its potential consequences in the ageing process. Importantly, a physically active lifestyle may promote the maintenance of muscle mass, reduction in adipose tissue, and alleviate progression of a chronic pro-inflammatory state. The overall aim of this thesis was to explore relationships between biomarkers of systemic inflammation, body composition, and physical activity behaviours in community-dwelling older adults aged 65 to 70 years. A main finding of the thesis is the existence of associations between body composition and systemic inflammation in older adults, where excess adipose tissue is adversely associated with levels of inflammatory biomarkers in older women. Inverse associations were also observed between muscle mass and levels of pro-inflammatory biomarkers in older women. This thesis also highlights sex-specific associations between systemic inflammation and physical activity behaviours. Longer time spent sedentary was also associated with higher levels of proinflammatory biomarkers in older women and lower level of antiinflammatory biomarkers in older men. Reallocating time spent in activities of lower intensities with higher intensities was associated with lower levels of pro-inflammatory biomarkers in older women. Overall, the findings of this thesis support efforts promoting physical activity at the expense of sedentary time in order to combat age-related systemic inflammation and metabolic risk in older adults.

Inflammation is an enabling characteristic of the hallmarks of cancer. There has therefore been increasing interest in the clinical value of circulating inflammatory biomarkers in cancer. In this review, we summarize results on C-reactive protein (CRP), alone or as part of the Glasgow Prognostic Score (GPS, composed of CRP and serum albumin), as a biomarker of prognosis or prediction and monitoring of therapeutic response in patients with breast cancer. A systematic literature search was performed in Medline and Embase from 1990 to August 2021. The association of serum CRP and overall survival and disease/progression-free survival was summarized in meta-analyses using a random effects model. The results from a total of 35 included studies (20,936 patients) were divided according to three identified patient settings (metastatic, non-metastatic, and general setting). Most of the studies examined prognostic utility. Several larger studies observed associations between high serum CRP and poor survival, but the meta-analyses suggested a limited value in a non-metastatic and general breast cancer setting (populations with unknown or varied disease stage). In metastatic patients, however, more consistent findings supported an association between serum CRP and prognosis (hazard ratio for overall survival: 1.87 (95% CI 1.31-2.67). Only five studies examined a role in prediction or monitoring of therapeutic response. One study reported a significant association between serum CRP levels and response to chemotherapy. Findings regarding serum CRP as a biomarker in breast cancer appear inconsistent, particularly in non-metastatic and general breast cancer, where the prognostic value could not be confirmed. In patients with metastatic breast cancer we suggest that high serum CRP is an indicator of poor prognosis. Too few studies assessed the role of serum CRP in prediction or monitoring of treatment response to allow conclusions.

Introduction Recent guidelines suggest treating acute uncomplicated diverticulitis (AUD) without antibiotics. We tested the efficacy of Limosilactobacillus reuteri ATCC PTA 4659 in AUD. Primary outcome was the reduction of abdominal pain and inflammatory markers [C-reactive protein (C-RP) and calprotectin]. Secondary outcome was the reduction of hours of hospitalization. Patients and methods A double-blind, randomized controlled trial was conducted in 119 patients with AUD. The probiotic group (61 patients) was treated with fluids, bowel rest and L. reuteri/b.i.d. for 10 days. The placebo group (58 patients) was treated with the same therapy and placebo/b.i.d. for 10 days. All patients completed a daily visual analogue scale (VAS) for abdominal pain. Results Both groups showed a mean VAS score of 7 at enrolment and a reduction of 4 points after 3 days. C-RP value, after 72 h, decreased by 58.8% in the probiotic group and by only 40% in the placebo group (P < 0.05). Calprotectin levels, after 72 h, decreased by 17% in the probiotic group and by only 10.6% in the control group (P < 0.05). In the probiotic group, the hospitalization was done for 75.5 h compared to 83.5 in the placebo group. Conclusions The supplementation with L. reuteri 4659 together with bowel rest and fluids significantly reduced both blood and faecal inflammatory markers compared to the placebo group.

The study aimed to examine sex-specific associations between objectively measured sedentary patterns and pro- and anti-inflammatory biomarkers in older adults when considering the moderating impact of physical activity (PA). Accelerometer-based monitoring of sedentary patterns and PA was conducted in a population of older men (n = 83; age: 67.4 ± 1.5; height: 178.7 ± 6.6 cm; weight: 80.9 ± 10.6 kg) and women (n = 146; age: 67.4 ± 1.6; height: 164.2 ± 6.1 cm; weight: 64.6 ± 10.1 kg) aged 65-70. Blood samples were collected for the assessment of the inflammatory biomarkers C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6), IL-10, IL-18, and monocyte chemoattractant protein-1 (MCP-1). Data were analyzed using multiple linear regression models. Total and bouts of ≥10 min of sedentary time were inversely associated with the anti-inflammatory marker IL-10 in older men (accumulated sedentary time: β = -0.116; bouts: β = -0.099; all p < 0.05). Associations were independent of moderate-to-vigorous physical activity (MVPA) and total PA volume. In women, total and bouts of ≥10 min of sedentary time were detrimentally associated with the pro-inflammatory marker fibrinogen (accumulated sedentary time: β = -0.130; bouts: β = -0.085; all p < 0.05). Associations remained between accumulated sedentary time and fibrinogen when adjusting for MVPA and total PA volume. This study highlights sex-specific routes by which sedentary patterns impact on pro- and anti-inflammatory biomarkers in older adults. The findings support efforts to promote accumulation of time spent in PA at the expense of time in sedentary pursuits on low-grade inflammation in older men and women., Funding Agency:European Commission through the Marie Skodowska-Curie Actions, Cofunding of Regional, National and International Programs (MSCA COFUND)

Social relationships may be a protective factor for cognitive decline. Elevated levels of inflammatory biomarkers are associated with cognitive decline. We aim to estimate the effect of social relationships (family support and local ties in particular) on cognitive function (measured by Modified Mini Mental State Exam and the Spanish and English Verbal Learning Test) and investigate whether the elevated level of inflammatory biomarkers mediates this effect among 1,374 Hispanic participants from the Sacramento Area Latino Study on Aging (1998–2007). The total effects of social relationship measures on follow-up cognitive functions were assessed. A mediation analysis (potential outcome framework) was applied to decompose direct and indirect effects. The results were compatible with a protective effect of family support on cognitive function with a larger effect estimated in earlier follow-up time. The null 95% CI of indirect effect estimates suggest there is limited mediation through inflammatory biomarkers within this study sample.

Background: Due to the prevalence and incidence worldwide of type 2 diabetes, and the significant role physical activity plays in these patients, a systematic review has been conducted to find out the effects that high-intensity interval training has on inflammatory biomarkers in subjects with type 2 diabetes. This project aims to determine the effect this training modality has on inflammatory biomarkers, in addition to observing its effects on the values of body composition and determining if this is a more effective, less effective or equally effective alternative to standard aerobic or resistance training. Methods: A search was conducted in the months of November and December 2020 on different databases: Pubmed, WoS and PEDro. A protocol for this systematic review was registered in PROSPERO (Registration number: CRD42021281186). The studies selected met the previously defined inclusion criteria, and the methodological quality of the papers used was evaluated according to the Downs and Black Checklist. Results: Out of 46 studies found, seven were included. The most relevant data concerning the characteristics of the clinical trials and HIIT characteristics, the values of body composition and the biomarkers under study were extracted from each study. Moreover, the results obtained from the different studies were described. Conclusions: HIIT could have an effect on inflammatory biomarkers. There is likely to be a relationship between changes in inflammatory profile and fat loss. A controlled diet may be a good complement to reduce the inflammatory profile. Further studies are required to determine whether HIIT is a better, worse or an equivalent alternative to medium-intensity aerobic exercise to improve the inflammatory profile

Atrial fibrillation (AF) is common and associated with increased risk of stroke, heart failure (HF) and mortality. Inflammation is linked to AF. The overall aim of this thesis was to investigate inflammatory activity and cardiovascular outcomes and mortality in patients with AF on effective oral anticoagulation. Levels of the inflammatory biomarkers interleukin 6 (IL-6), C-reactive protein (CRP) and fibrinogen at study entry and serial changes of IL-6 over time were investigated and related to stroke or systemic embolism, mortality and other cardiovascular events, including major bleeding. Associations between IL-6, CRP and biomarkers of cardiorenal dysfunction (NT-proBNP, troponin, GDF-15 and cystatin C) and HF hospitalisation, recurrent HF hospitalisations and mortality, were also investigated in patients with AF stratified for HF symptoms and reduced or preserved ejection fraction. The study populations consisted of patients with AF included in the biomarker substudies of the large multicentre randomised controlled trials RE-LY (n=6,187) and ARISTOTLE (n=14,954) with a median follow-up of 2.0 and 1.9 years, respectively. Repeated IL-6 measurements were available at study entry and at any postbaseline time point at 3, 6 and 12 months in RE-LY (n=2,559), and at study entry and at 2 months in ARISTOTLE (n=4,830). For HF stratification, patients in ARISTOTLE with information on HF symptoms and left ventricular function at study entry and with IL-6, CRP, NT-proBNP, troponin T, GDF-15 and cystatin C available at randomisation (n=11,818) were included. Higher level of IL-6, but not of CRP, was significantly associated with higher risk of mortality in Cox models adjusted for established clinical risk factors and other cardiovascular biomarkers. The level of any of the studied inflammatory biomarkers was not independently associated with any other cardiovascular outcome, including stroke or systemic embolism or major bleeding, in presence of other strong cardiovascular bi

Social relationships may be a protective factor for cognitive decline. Elevated levels of inflammatory biomarkers are associated with cognitive decline. We aim to estimate the effect of social relationships (family support and local ties in particular) on cognitive function (measured by Modified Mini Mental State Exam and the Spanish and English Verbal Learning Test) and investigate whether the elevated level of inflammatory biomarkers mediates this effect among 1,374 Hispanic participants from the Sacramento Area Latino Study on Aging (1998–2007). The total effects of social relationship measures on follow-up cognitive functions were assessed. A mediation analysis (potential outcome framework) was applied to decompose direct and indirect effects. The results were compatible with a protective effect of family support on cognitive function with a larger effect estimated in earlier follow-up time. The null 95% CI of indirect effect estimates suggest there is limited mediation through inflammatory biomarkers within this study sample.

Atrial fibrillation (AF) is common and associated with increased risk of stroke, heart failure (HF) and mortality. Inflammation is linked to AF. The overall aim of this thesis was to investigate inflammatory activity and cardiovascular outcomes and mortality in patients with AF on effective oral anticoagulation. Levels of the inflammatory biomarkers interleukin 6 (IL-6), C-reactive protein (CRP) and fibrinogen at study entry and serial changes of IL-6 over time were investigated and related to stroke or systemic embolism, mortality and other cardiovascular events, including major bleeding. Associations between IL-6, CRP and biomarkers of cardiorenal dysfunction (NT-proBNP, troponin, GDF-15 and cystatin C) and HF hospitalisation, recurrent HF hospitalisations and mortality, were also investigated in patients with AF stratified for HF symptoms and reduced or preserved ejection fraction. The study populations consisted of patients with AF included in the biomarker substudies of the large multicentre randomised controlled trials RE-LY (n=6,187) and ARISTOTLE (n=14,954) with a median follow-up of 2.0 and 1.9 years, respectively. Repeated IL-6 measurements were available at study entry and at any postbaseline time point at 3, 6 and 12 months in RE-LY (n=2,559), and at study entry and at 2 months in ARISTOTLE (n=4,830). For HF stratification, patients in ARISTOTLE with information on HF symptoms and left ventricular function at study entry and with IL-6, CRP, NT-proBNP, troponin T, GDF-15 and cystatin C available at randomisation (n=11,818) were included. Higher level of IL-6, but not of CRP, was significantly associated with higher risk of mortality in Cox models adjusted for established clinical risk factors and other cardiovascular biomarkers. The level of any of the studied inflammatory biomarkers was not independently associated with any other cardiovascular outcome, including stroke or systemic embolism or major bleeding, in presence of other strong cardiovascular bi

Atrial fibrillation (AF) is common and associated with increased risk of stroke, heart failure (HF) and mortality. Inflammation is linked to AF. The overall aim of this thesis was to investigate inflammatory activity and cardiovascular outcomes and mortality in patients with AF on effective oral anticoagulation. Levels of the inflammatory biomarkers interleukin 6 (IL-6), C-reactive protein (CRP) and fibrinogen at study entry and serial changes of IL-6 over time were investigated and related to stroke or systemic embolism, mortality and other cardiovascular events, including major bleeding. Associations between IL-6, CRP and biomarkers of cardiorenal dysfunction (NT-proBNP, troponin, GDF-15 and cystatin C) and HF hospitalisation, recurrent HF hospitalisations and mortality, were also investigated in patients with AF stratified for HF symptoms and reduced or preserved ejection fraction. The study populations consisted of patients with AF included in the biomarker substudies of the large multicentre randomised controlled trials RE-LY (n=6,187) and ARISTOTLE (n=14,954) with a median follow-up of 2.0 and 1.9 years, respectively. Repeated IL-6 measurements were available at study entry and at any postbaseline time point at 3, 6 and 12 months in RE-LY (n=2,559), and at study entry and at 2 months in ARISTOTLE (n=4,830). For HF stratification, patients in ARISTOTLE with information on HF symptoms and left ventricular function at study entry and with IL-6, CRP, NT-proBNP, troponin T, GDF-15 and cystatin C available at randomisation (n=11,818) were included. Higher level of IL-6, but not of CRP, was significantly associated with higher risk of mortality in Cox models adjusted for established clinical risk factors and other cardiovascular biomarkers. The level of any of the studied inflammatory biomarkers was not independently associated with any other cardiovascular outcome, including stroke or systemic embolism or major bleeding, in presence of other strong cardiovascular bi

Background: Asthma and COPD diagnoses are used to classify chronic airway diseases; however, both diseases are related to phenotypic traits like allergy, obesity, cough, sputum production, low-grade inflammation, smoking, elevated blood eosinophil count, comorbidities, and occupational exposures. Whether such traits can replace asthma and COPD diagnoses when assessing risk of exacerbation is unclear. We tested the hypothesis that individuals with either asthma or COPD diagnoses have similar risk of moderate and severe exacerbations when adjusted for differences in phenotypic traits.Methods: From the Copenhagen General Population Study, a cohort study of the general population, we included 7190 individuals with chronic airway disease. Phenotypic traits were recorded at baseline and risk of exacerbations was assessed during follow-up from 2003 to 2013.Results: The incidence rate ratio (IRR) of moderate exacerbations in individuals with clinical COPD was 1.61 (95% Confidence Interval, 1.27-2.02) compared to individuals with asthma in a model only adjusted for age, sex, and education, but after the inclusion of phenotypic traits IRR was 1.05 (0.82-1.35). Corresponding IRRs of severe exacerbations in individuals with clinical COPD versus asthma were 3.82 (2.73-5.35) and 2.28 (1.63-3.20), respectively.Conclusions: When taking phenotypic traits into account, individuals with asthma and COPD had comparable risk of moderate exacerbations; however, corresponding risk of severe exacerbations was higher in individuals with COPD than in those with asthma.

Background: Asthma and COPD diagnoses are used to classify chronic airway diseases; however, both diseases are related to phenotypic traits like allergy, obesity, cough, sputum production, low-grade inflammation, smoking, elevated blood eosinophil count, comorbidities, and occupational exposures. Whether such traits can replace asthma and COPD diagnoses when assessing risk of exacerbation is unclear. We tested the hypothesis that individuals with either asthma or COPD diagnoses have similar risk of moderate and severe exacerbations when adjusted for differences in phenotypic traits.Methods: From the Copenhagen General Population Study, a cohort study of the general population, we included 7190 individuals with chronic airway disease. Phenotypic traits were recorded at baseline and risk of exacerbations was assessed during follow-up from 2003 to 2013.Results: The incidence rate ratio (IRR) of moderate exacerbations in individuals with clinical COPD was 1.61 (95% Confidence Interval, 1.27-2.02) compared to individuals with asthma in a model only adjusted for age, sex, and education, but after the inclusion of phenotypic traits IRR was 1.05 (0.82-1.35). Corresponding IRRs of severe exacerbations in individuals with clinical COPD versus asthma were 3.82 (2.73-5.35) and 2.28 (1.63-3.20), respectively.Conclusions: When taking phenotypic traits into account, individuals with asthma and COPD had comparable risk of moderate exacerbations; however, corresponding risk of severe exacerbations was higher in individuals with COPD than in those with asthma.

Atrial fibrillation (AF) is common and associated with increased risk of stroke, heart failure (HF) and mortality. Inflammation is linked to AF. The overall aim of this thesis was to investigate inflammatory activity and cardiovascular outcomes and mortality in patients with AF on effective oral anticoagulation. Levels of the inflammatory biomarkers interleukin 6 (IL-6), C-reactive protein (CRP) and fibrinogen at study entry and serial changes of IL-6 over time were investigated and related to stroke or systemic embolism, mortality and other cardiovascular events, including major bleeding. Associations between IL-6, CRP and biomarkers of cardiorenal dysfunction (NT-proBNP, troponin, GDF-15 and cystatin C) and HF hospitalisation, recurrent HF hospitalisations and mortality, were also investigated in patients with AF stratified for HF symptoms and reduced or preserved ejection fraction. The study populations consisted of patients with AF included in the biomarker substudies of the large multicentre randomised controlled trials RE-LY (n=6,187) and ARISTOTLE (n=14,954) with a median follow-up of 2.0 and 1.9 years, respectively. Repeated IL-6 measurements were available at study entry and at any postbaseline time point at 3, 6 and 12 months in RE-LY (n=2,559), and at study entry and at 2 months in ARISTOTLE (n=4,830). For HF stratification, patients in ARISTOTLE with information on HF symptoms and left ventricular function at study entry and with IL-6, CRP, NT-proBNP, troponin T, GDF-15 and cystatin C available at randomisation (n=11,818) were included. Higher level of IL-6, but not of CRP, was significantly associated with higher risk of mortality in Cox models adjusted for established clinical risk factors and other cardiovascular biomarkers. The level of any of the studied inflammatory biomarkers was not independently associated with any other cardiovascular outcome, including stroke or systemic embolism or major bleeding, in presence of other strong cardiovascular bi

Atrial fibrillation (AF) is common and associated with increased risk of stroke, heart failure (HF) and mortality. Inflammation is linked to AF. The overall aim of this thesis was to investigate inflammatory activity and cardiovascular outcomes and mortality in patients with AF on effective oral anticoagulation. Levels of the inflammatory biomarkers interleukin 6 (IL-6), C-reactive protein (CRP) and fibrinogen at study entry and serial changes of IL-6 over time were investigated and related to stroke or systemic embolism, mortality and other cardiovascular events, including major bleeding. Associations between IL-6, CRP and biomarkers of cardiorenal dysfunction (NT-proBNP, troponin, GDF-15 and cystatin C) and HF hospitalisation, recurrent HF hospitalisations and mortality, were also investigated in patients with AF stratified for HF symptoms and reduced or preserved ejection fraction. The study populations consisted of patients with AF included in the biomarker substudies of the large multicentre randomised controlled trials RE-LY (n=6,187) and ARISTOTLE (n=14,954) with a median follow-up of 2.0 and 1.9 years, respectively. Repeated IL-6 measurements were available at study entry and at any postbaseline time point at 3, 6 and 12 months in RE-LY (n=2,559), and at study entry and at 2 months in ARISTOTLE (n=4,830). For HF stratification, patients in ARISTOTLE with information on HF symptoms and left ventricular function at study entry and with IL-6, CRP, NT-proBNP, troponin T, GDF-15 and cystatin C available at randomisation (n=11,818) were included. Higher level of IL-6, but not of CRP, was significantly associated with higher risk of mortality in Cox models adjusted for established clinical risk factors and other cardiovascular biomarkers. The level of any of the studied inflammatory biomarkers was not independently associated with any other cardiovascular outcome, including stroke or systemic embolism or major bleeding, in presence of other strong cardiovascular bi

Objectives: Shift work is associated with several negative health effects. The underlying pathophysiological mechanisms are unclear, but low-grade inflammation has been suggested to play a role. This project aimed to determine whether levels of immunological biomarkers differ depending on work schedule, self-reported sleep duration, self-reported sleep quality, and presence of shift work disorder (study 1). Furthermore, we aimed to determine whether these biomarkers differ after a night of sleep vs. at the end of a night or a day shift (study 2). Methods: In study 1, 390 nurses provided blood samples after a night of sleep with the dried blood spot method. In study 2, a subset of 55 nurses also provided blood samples after a day shift and after a night shift. The following biomarkers were measured: interleukin-1alpha, interleukin-1beta, interleukin-4, interleukin-6, interleukin-8, interleukin-10, interleukin-13, monocyte chemoattractant protein-1, interferon-gamma, and tumor necrosis factor-alpha. Multiple linear regressions with adjustment for age, sex and body mass index (study 1) and ANOVAs with repeated measures (study 2) were conducted. Results: In study 1, neither work schedule, number of night shifts, number of quick returns (<11 h between consecutive shifts), sleep duration, poor sleep quality, nor shift work disorder were systematically associated with most of these biomarkers. Compared with day only work, day-evening work was associated with higher levels of IL-1alpha and IL-13, quick returns were associated with higher levels of IL-1beta and MCP-1, short sleep duration (<6 h) was associated with lower levels of IL-1beta and higher levels of TNF-alpha, and long sleep duration (8+ h) was associated with higher levels of IL-13. In study 2, IL-1beta levels were higher (large effect size) both after a day shift (14% increase) and a night shift (75% increase) compared with levels after a night of sleep. Similarly, TNF-alpha levels were higher (moderate-la

BACKGROUND: The key characteristics (KCs) of human carcinogens provide a uniform approach to evaluating mechanistic evidence in cancer hazard identification. Refinements to the approach were requested by organizations and individuals applying the KCs.METHODS: We assembled an expert committee with knowledge of carcinogenesis and experience in applying the KCs in cancer hazard identification. We leveraged this expertise and an examination of the literature to more clearly describe each KC; identify current and emerging assays and in vivo biomarkers that can be used to measure them; and, make recommendations for future assay development.RESULTS: We found that the KCs are clearly distinct from the Hallmarks of Cancer, that interrelationships among the KCs can be leveraged to strengthen the KC approach (and an understanding of environmental carcinogenesis), and that the KC approach is applicable to the systematic evaluation of a broad range of potential cancer hazards in vivo and in vitro. We identified gaps in coverage of the KCs by current assays.CONCLUSION: Future efforts should expand the breadth, specificity and sensitivity of validated assays and biomarkers that can measure the 10 KCs.IMPACT: Refinement of the KC approach will enhance and accelerate carcinogen identification, a first step in cancer prevention.

Background: The relations between diet, chronic inflammation, and musculoskeletal health are unclear, especially among older men. Objective: This study aimed to determine associations of the Dietary Inflammatory Index (DII) with inflammatory biomarkers, musculoskeletal health, and falls risk in community-dwelling older men. Methods: The cross-sectional analysis included 794 community-dwelling men, mean age 81.1 ± 4.5 y, who participated in the 5-y follow-up of the Concord Health and Aging in Men Project. Of these, 616 were seen again 3 y later for the longitudinal analysis. Energy-adjusted DII (E-DII) was calculated from a validated diet history questionnaire. Bone mineral density (BMD) was measured using DXA. Twenty-four inflammatory biomarkers were analyzed. Incident falls over 3 y were determined through telephone interviews every 4 mo. Multiple regression, linear mixed effects models, negative binomial regression, and mediation analysis were utilized in this study. Results: A higher E-DII score (indicating a more proinflammatory diet) was associated with higher concentrations of IL-6 (β: 0.028 pg/mL; 95% CI: 0.003, 0.053), IL-7 (β: 0.020 pg/mL; 95% CI: 0.002, 0.037), and TNF-α (β: 0.027 pg/mL; 95% CI: 0.003, 0.051). A higher E-DII score was also associated with lower appendicular lean mass adjusted for BMI (ALMBMI) (β: −0.006 kg/m2; 95% CI: −0.010, −0.001). For every unit increase in E-DII (range: −4.91 to +3.66 units), incident falls rates increased by 13% (incidence rate ratio: 1.13; 95% CI: 1.05, 1.21) over 3 y. Mediation analysis showed that the association between E-DII and 3-y incident falls was influenced by the concentrations of IL-7 by 24%. There was no association between E-DII and BMD. Conclusions: Consumption of a proinflammatory diet was associated with increased concentrations of IL-6, IL-7, and TNF-α; increased falls risk; and lower ALMBMI in community-dwelling older men. The associati

Oxidative stress could help explain the relationship between childhood obesity and a metabolically unhealthy (MU) status. Moreover, puberty could also influence this relationship, since it entails physiological cardiometabolic changes. We aimed to evaluate plasma antioxidants and oxidative stress biomarkers in MU and metabolically healthy (MH) prepubertal and pubertal children and their associations with pro-inflammatory and endothelial damage biomarkers, taking puberty into account. A total of 1444 Spanish children aged 3–17 years (48.9% males, 66% prepubertal, 47.1% with obesity) were recruited. Blood pressure, anthropometric and biochemical parameters were measured, and children were categorized as having a MU or MH status according to risk factors. Retinol, carotenes, tocopherols, total antioxidant capacity (TAC), oxidized low-density lipoprotein and selected pro-inflammatory and endothelial damage biomarkers were analyzed. General linear models adjusted for age, sex, recruitment center and body mass index, partial correlations and stepwise linear regressions were performed. Lower carotenes and tocopherols levels were found in MU than in MH children. Plasma TAC was lower in prepubertal and higher in pubertal children with obesity compared to normal-weight children. Antioxidants and oxidative stress biomarkers showed novel associations with several pro-inflammatory and endothelial damage biomarkers, with pubertal differences, supporting the importance of considering both the antioxidant and oxidative stress status and puberty in the prevention of metabolic diseases in childhood

BACKGROUND: The key characteristics (KCs) of human carcinogens provide a uniform approach to evaluating mechanistic evidence in cancer hazard identification. Refinements to the approach were requested by organizations and individuals applying the KCs.METHODS: We assembled an expert committee with knowledge of carcinogenesis and experience in applying the KCs in cancer hazard identification. We leveraged this expertise and an examination of the literature to more clearly describe each KC; identify current and emerging assays and in vivo biomarkers that can be used to measure them; and, make recommendations for future assay development.RESULTS: We found that the KCs are clearly distinct from the Hallmarks of Cancer, that interrelationships among the KCs can be leveraged to strengthen the KC approach (and an understanding of environmental carcinogenesis), and that the KC approach is applicable to the systematic evaluation of a broad range of potential cancer hazards in vivo and in vitro. We identified gaps in coverage of the KCs by current assays.CONCLUSION: Future efforts should expand the breadth, specificity and sensitivity of validated assays and biomarkers that can measure the 10 KCs.IMPACT: Refinement of the KC approach will enhance and accelerate carcinogen identification, a first step in cancer prevention.

[Background] The involvement of SARS-CoV-2 antibodies in mediating immunopathogenetic events in COVID-19 patients has been suggested. By using several experimental approaches, we investigated the potential association between SARS-CoV-2 IgGs recognizing the spike (S) protein receptor-binding domain (RBD), neutralizing antibodies (NtAb) targeting S, and COVID-19 severity., [Patients and methods] This unicenter, retrospective, observational study included 51 hospitalized patients (24 at the intensive care unit; ICU). A total of 93 sera from these patients collected at different time points from the onset of symptoms were analyzed. SARS-CoV-2 RBD IgGs were quantitated by ELISA and NtAb50 titers were measured in a GFP reporterbased pseudotyped virus platform. Demographic and clinical data, complete blood counts, as well as serum levels of ferritin, Dimer-D, C reactive protein (CRP), lactose dehydrogenase (LDH), and interleukin-6 (IL-6) were retrieved from clinical charts., [Results] The overall correlation between levels of both antibody measurements was good (Rho = 0.82; P = 0 < 0.001). SARS-CoV-2 RBD IgG and NtAb50 levels in sera collected up to day 30 after the onset of symptoms were comparable between ICU and non-ICU patients (P=>0.1). Four ICU patients died; two of these achieved NtAb50 titers ≥1/160 while the other two exhibited a 1/80 titer. Very weak (Rho=>0.0–<0.2) or weak (Rho=>0.2–<0.4) correlations were observed between anti-RBD IgGs, NtAb50, and serum levels pro-inflammatory biomarkers., [Conclusions] The data presented herein do not support an association between SARS-CoV-2 RBD IgG or NtAb50 levels and COVID-19 severity.

Background: The involvement of SARS-CoV-2 antibodies in mediating immunopathogenetic events in COVID-19 patients has been suggested. By using several experimental approaches, we investigated the potential association between SARS-CoV-2 IgGs recognizing the spike (S) protein receptor-binding domain (RBD), neutralizing antibodies (NtAb) targeting S, and COVID-19 severity. Patients and Methods: This unicenter, retrospective, observational study included 51 hospitalized patients (24 at the intensive care unit; ICU). A total of 93 sera from these patients collected at different time points from the onset of symptoms were analyzed. SARS-CoV-2 RBD IgGs were quantitated by ELISA and NtAb50 titers were measured in a GFP reporter-based pseudotyped virus platform. Demographic and clinical data, complete blood counts, as well as serum levels of ferritin, Dimer-D, C reactive protein (CRP), lactose dehydrogenase (LDH), and interleukin-6 (IL-6) were retrieved from clinical charts. Results: The overall correlation between levels of both antibody measurements was good (Rho=0.79; P=0<0.001). SARS-CoV-2 RBD IgG and NtAb50 levels in sera collected up to day 30 after the onset of symptoms were comparable between ICU and non-ICU patients (P=>0.1). The percentage of patients who exhibited high NtAb50 titers (≥160) was similar (P=0.20) in ICU (79%) and non-ICU (60%) patients. Four ICU patients died; two of these achieved NtAb50 titers ≥1/160 while the other two exhibited a 1/80 titer. Very weak (Rho=>0.0-<0.2) or weak (Rho=>0.2-<0.4) correlations were observed between anti-RBD IgGs, NtAb50, and serum levels pro-inflammatory biomarkers. Conclusions: The data presented herein do not support an association between SARS-CoV-2 RBD IgG or NtAb50 levels and COVID-19 severity

Background and aims: Recent research indicates a previously unknown low-grade systemic or neurogenic inflammation in groups of chronic pain (CP) patients. Low-grade inflammation may have an important role in symptoms that have previously not been well depicted: widespread pain, tiredness and cognitive dysfunctions frequently seen in severely impaired CP patients. This study aimed to investigate the plasma inflammatory profile in a group of very complex CP patients at baseline and at a 1-year follow-up after participation in a cognitive behavior therapy (CBT)-based multimodal pain rehabilitation program (PRP). Methods: Blood samples were collected from 52 well-characterized CP patients. Age- and sex-matched healthy blood donors served as controls. The samples were analyzed with a multiple Proximal Extension Analysis allowing a simultaneous analysis of 92 inflammation-related proteins consisting mainly of cytokines, chemokines and growth-factors. At follow-up, 1-year after participation in the RPR samples from 28 patients were analyzed. The results were confirmed by a multi-array technology that allows quantitative estimation. Results: Clear signs of increased inflammatory activity were detected in the CP patients. Accepting a false discovery rate (FDR) of 5%, there were significant differences in 43/92 inflammatory biomarkers compared with the controls. In three biomarkers (CXCL5, SIRT2, AXIN1) the expression levels were elevated more than eight times. One year after the PRP, with the patients serving as their own controls, a significant decrease in overall inflammatory activity was found. Conclusions: Our results indicate that the most impaired CP patients suffer from low-grade chronic systemic inflammation not described earlier with this level of detail. The results may have implications for a better understanding of the cluster of co-morbid symptoms described as the "sickness-syndrome" and the wide-spread pain seen in this group of patients. The decrease in inflam

The purpose of this thesis was to describe the true prevalence of widespread arterial disease in a cohort with patients with a recent myocardial infarction (MI) to find valuable clinical methods to detect these patients. Our aim was also to investigate biomarker relationships with peripheral artery disease (PAD) and the importance of PAD in patients’ long-term outcomes. We studied patients with a recent MI in a prospective observational study, the REBUS ((Relevance of Biomarkers for Future Risk of Thromboembolic Events in Unselected Post-myocardial Infarction Patients) trial. A total of 421 patients were included in the study, 390 of whom had their ankle-brachial index (ABI) measured and a mean-time follow up of 5.5 years. Atherosclerotic changes were assessed in three arterial beds by coronary angiography, measuring the ABI and carotid ultrasound. Ninety-two biochemical biomarkers were assessed at baseline by a proximity extension assay (PEA) chip. 263 out of 421 filled in a self-administered Walking Impairment Questionnaire (WIQ). Polyvascular (PvD) disease was defined as pathological findings in all three arterial beds. We found that PAD and PvD are underdiagnosed in patients who suffered a recent MI. We also found the ABI to be a strong and useful method to identify patients with PAD as well as patients with more widespread arterial disease, such as PvD (paper I). The results of the scoring system, the WIQ, showed it is useful for finding patients with PAD and PvD, even when completed soon after an acute MI event (paper II). We also found that biochemical biomarkers associated with the inflammatory pathway – tumour necrosis factor receptor 1 (TNFR-1), tumor necrosis factor receptor 2 (TNFR-2) and growth differentiation factor 15 (GDF-15) – were able to predict pathological ABI, i.e. PAD, in these MI patients. These results could also be validated in another observational study and cohort of MI patients, the VaMIS cohort (paper III). Pathological ABI was also fou

Neuroinflammation is a major contributor to the progressive brain injury process induced by traumatic brain injury (TBI), and may play an important role in the pathophysiology of axonal injury. The immediate neuroinflammatory cascade cannot be characterized in the human setting. Therefore, we used the midline fluid percussion injury model of diffuse TBI in rats and a novel microdialysis (MD) method providing stable diffusion-driven biomarker sampling. Immediately post-injury, bilateral amphiphilic tri-block polymer coated MD probes (100 kDa cut off membrane) were inserted and perfused with Dextran 500 kDa-supplemented artificial cerebrospinal fluid (CSF) to optimize protein capture. Six hourly samples were analyzed for 27 inflammatory biomarkers (9 chemokines, 13 cytokines, and 5 growth factors) using a commercial multiplex biomarker kit. TBI (n = 6) resulted in a significant increase compared with sham-injured controls (n = 6) for five chemokines (eotaxin/CCL11, fractalkine/CX3CL1, LIX/CXCL5, monocyte chemoattractant protein [MCP]1α/CCL2, macrophage inflammatory protein [MIP]1α /CCL3), 10 cytokines (interleukin [IL]-1α, IL-1β, IL-4, IL-6, IL-10, IL-13, IL-17α, IL-18, interferon [IFN]-γ, tumor necrosis factor [TNF]-α), and four growth factors (epidermal growth factor [EGF], granulocyte-macrophage colony-stimulating factor [GM-CSF], leptin, vascular endothelial growth factor [VEGF]). Therefore, diffuse TBI was associated with an increased level of 18 of the 27 inflammatory biomarkers at one through six time points, during the observation period whereas the remaining 9 biomarkers were unaltered. The study shows that diffuse TBI induces an acute increase in a number of inflammatory biomarkers. The novel MD technique provides stable MD sampling suitable for further studies on the early neuroinflammatory cascade in TBI.

The purpose of this thesis was to describe the true prevalence of widespread arterial disease in a cohort with patients with a recent myocardial infarction (MI) to find valuable clinical methods to detect these patients. Our aim was also to investigate biomarker relationships with peripheral artery disease (PAD) and the importance of PAD in patients’ long-term outcomes. We studied patients with a recent MI in a prospective observational study, the REBUS ((Relevance of Biomarkers for Future Risk of Thromboembolic Events in Unselected Post-myocardial Infarction Patients) trial. A total of 421 patients were included in the study, 390 of whom had their ankle-brachial index (ABI) measured and a mean-time follow up of 5.5 years. Atherosclerotic changes were assessed in three arterial beds by coronary angiography, measuring the ABI and carotid ultrasound. Ninety-two biochemical biomarkers were assessed at baseline by a proximity extension assay (PEA) chip. 263 out of 421 filled in a self-administered Walking Impairment Questionnaire (WIQ). Polyvascular (PvD) disease was defined as pathological findings in all three arterial beds. We found that PAD and PvD are underdiagnosed in patients who suffered a recent MI. We also found the ABI to be a strong and useful method to identify patients with PAD as well as patients with more widespread arterial disease, such as PvD (paper I). The results of the scoring system, the WIQ, showed it is useful for finding patients with PAD and PvD, even when completed soon after an acute MI event (paper II). We also found that biochemical biomarkers associated with the inflammatory pathway – tumour necrosis factor receptor 1 (TNFR-1), tumor necrosis factor receptor 2 (TNFR-2) and growth differentiation factor 15 (GDF-15) – were able to predict pathological ABI, i.e. PAD, in these MI patients. These results could also be validated in another observational study and cohort of MI patients, the VaMIS cohort (paper III). Pathological ABI was also fou

The purpose of this thesis was to describe the true prevalence of widespread arterial disease in a cohort with patients with a recent myocardial infarction (MI) to find valuable clinical methods to detect these patients. Our aim was also to investigate biomarker relationships with peripheral artery disease (PAD) and the importance of PAD in patients’ long-term outcomes. We studied patients with a recent MI in a prospective observational study, the REBUS ((Relevance of Biomarkers for Future Risk of Thromboembolic Events in Unselected Post-myocardial Infarction Patients) trial. A total of 421 patients were included in the study, 390 of whom had their ankle-brachial index (ABI) measured and a mean-time follow up of 5.5 years. Atherosclerotic changes were assessed in three arterial beds by coronary angiography, measuring the ABI and carotid ultrasound. Ninety-two biochemical biomarkers were assessed at baseline by a proximity extension assay (PEA) chip. 263 out of 421 filled in a self-administered Walking Impairment Questionnaire (WIQ). Polyvascular (PvD) disease was defined as pathological findings in all three arterial beds. We found that PAD and PvD are underdiagnosed in patients who suffered a recent MI. We also found the ABI to be a strong and useful method to identify patients with PAD as well as patients with more widespread arterial disease, such as PvD (paper I). The results of the scoring system, the WIQ, showed it is useful for finding patients with PAD and PvD, even when completed soon after an acute MI event (paper II). We also found that biochemical biomarkers associated with the inflammatory pathway – tumour necrosis factor receptor 1 (TNFR-1), tumor necrosis factor receptor 2 (TNFR-2) and growth differentiation factor 15 (GDF-15) – were able to predict pathological ABI, i.e. PAD, in these MI patients. These results could also be validated in another observational study and cohort of MI patients, the VaMIS cohort (paper III). Pathological ABI was also fou

The purpose of this thesis was to describe the true prevalence of widespread arterial disease in a cohort with patients with a recent myocardial infarction (MI) to find valuable clinical methods to detect these patients. Our aim was also to investigate biomarker relationships with peripheral artery disease (PAD) and the importance of PAD in patients’ long-term outcomes. We studied patients with a recent MI in a prospective observational study, the REBUS ((Relevance of Biomarkers for Future Risk of Thromboembolic Events in Unselected Post-myocardial Infarction Patients) trial. A total of 421 patients were included in the study, 390 of whom had their ankle-brachial index (ABI) measured and a mean-time follow up of 5.5 years. Atherosclerotic changes were assessed in three arterial beds by coronary angiography, measuring the ABI and carotid ultrasound. Ninety-two biochemical biomarkers were assessed at baseline by a proximity extension assay (PEA) chip. 263 out of 421 filled in a self-administered Walking Impairment Questionnaire (WIQ). Polyvascular (PvD) disease was defined as pathological findings in all three arterial beds. We found that PAD and PvD are underdiagnosed in patients who suffered a recent MI. We also found the ABI to be a strong and useful method to identify patients with PAD as well as patients with more widespread arterial disease, such as PvD (paper I). The results of the scoring system, the WIQ, showed it is useful for finding patients with PAD and PvD, even when completed soon after an acute MI event (paper II). We also found that biochemical biomarkers associated with the inflammatory pathway – tumour necrosis factor receptor 1 (TNFR-1), tumor necrosis factor receptor 2 (TNFR-2) and growth differentiation factor 15 (GDF-15) – were able to predict pathological ABI, i.e. PAD, in these MI patients. These results could also be validated in another observational study and cohort of MI patients, the VaMIS cohort (paper III). Pathological ABI was also fou

The purpose of this thesis was to describe the true prevalence of widespread arterial disease in a cohort with patients with a recent myocardial infarction (MI) to find valuable clinical methods to detect these patients. Our aim was also to investigate biomarker relationships with peripheral artery disease (PAD) and the importance of PAD in patients’ long-term outcomes. We studied patients with a recent MI in a prospective observational study, the REBUS ((Relevance of Biomarkers for Future Risk of Thromboembolic Events in Unselected Post-myocardial Infarction Patients) trial. A total of 421 patients were included in the study, 390 of whom had their ankle-brachial index (ABI) measured and a mean-time follow up of 5.5 years. Atherosclerotic changes were assessed in three arterial beds by coronary angiography, measuring the ABI and carotid ultrasound. Ninety-two biochemical biomarkers were assessed at baseline by a proximity extension assay (PEA) chip. 263 out of 421 filled in a self-administered Walking Impairment Questionnaire (WIQ). Polyvascular (PvD) disease was defined as pathological findings in all three arterial beds. We found that PAD and PvD are underdiagnosed in patients who suffered a recent MI. We also found the ABI to be a strong and useful method to identify patients with PAD as well as patients with more widespread arterial disease, such as PvD (paper I). The results of the scoring system, the WIQ, showed it is useful for finding patients with PAD and PvD, even when completed soon after an acute MI event (paper II). We also found that biochemical biomarkers associated with the inflammatory pathway – tumour necrosis factor receptor 1 (TNFR-1), tumor necrosis factor receptor 2 (TNFR-2) and growth differentiation factor 15 (GDF-15) – were able to predict pathological ABI, i.e. PAD, in these MI patients. These results could also be validated in another observational study and cohort of MI patients, the VaMIS cohort (paper III). Pathological ABI was also fou

AIDS-related Kaposi's sarcoma (AIDS-KS) risk remains substantially elevated compared with the general population, even among patients who receive effective combination antiretroviral therapy. This study investigated the role of inflammatory and immune activating biomarkers in AIDS-KS in men who have sex with men in the Multicenter AIDS Cohort study between 1984 and 2010. Concentrations of 24 serum biomarkers; IL-1β, IL-2, IL-6, IL-8, IL-10, IL-12p70, sGP130, sIL-2Rα, sIL-6R, eotaxin, MCP-1, MCP4, MIP 1β, TARC, BLC-BCA1, IP-10, GM-CSF, IFN-γ, BAFF, sCD14, CD27, sTNFR-2, sCRP, and TNF-α were tested longitudinally in 1,501 men. The concentrations of each biomarker were compared between AIDS-KS cases and controls at multiple time points, 0-1 years, 1-2 years, 2-3 year, 3-5 years and over 5 years, prior to KS diagnosis or study termination, using univariate non-parametric Kruskal-Wallis tests and logistic regression, adjusted for HBV and HCV co-infection, race/ethnicity, age at last visit, education, smoking and CD4+ cell count. In univariate analyses, concentrations of four markers were consistently higher in cases; sIL-2Rα, IP-10, sTNFR-2, MCP-1, and five were higher in controls; GM-CSF, IL-6, MIP-1β, sCRP, sGP130. In the adjusted models concentrations of four markers were significantly inversely associated with AIDS-KS risk including sGP130 (OR=0.14, 95% CI = 0.03-0.73, BAFF (OR=0.60, 95% CI =0.16-0.90), sCRP (OR=0.61, 95% CI = 0.43-0.87) and IL-6 (OR=0.51, 95% CI = 0.35-0.76). These results support a role for markers of immune activation and inflammation in AIDS-KS and may highlight pathways to be targeted for risk stratification or therapeutics.

BackgroundWe investigated whether epicardial adipose tissue (EAT) volume and density are related to early atherosclerosis, plaque inflammation and major adverse cardiac events (MACE, cardiac death and myocardial infarction) in asymptomatic subjects.MethodsEAT volume and density were quantified from non-contrast cardiac CT in 456 asymptomatic individuals (age 60.3 ± 8.3; 68% with CCS>0) from the prospective EISNER trial. EAT volume and density were examined in relation to coronary calcium score (CCS), inflammatory biomarkers and MACE.ResultsEAT volume was higher and EAT density lower in subjects with coronary calcium compared to subjects without [89 vs 74 cm3, p < 0.001] [-76.9 vs -75.7 HU,p = 0.024]. EAT volume was lowest in individuals with no coronary calcium and was significant higher in subjects with early atherosclerosis (CCS 1-99) [74 vs 87 cm3,p = 0.016] and in subjects with more advanced atherosclerosis (CCS≥100) [89 cm3,p = 0.002]). EAT volume was independently related to serum levels of PAI-1, and MCP-1 and inversely related to adiponectin and HDL-cholesterol (p < 0.05). EAT density was inversely related to PAI-1 and LDL-cholesterol and positively associated to adiponectin, sICAM-1 and HDL-cholesterol (p < 0.05). EAT density was more significantly associated with MACE [(HR 0.8, 95%CI:0.7-0.98), p = 0.029] than EAT volume or CCS.ConclusionEAT volume was higher and density lower in subjects with coronary calcium compared to subjects with CCS = 0, with similar EAT volume in CCS<100 and CCS≥100. Lower EAT density and increased EAT volume were associated with coronary calcification, serum levels of plaque inflammatory markers and MACE, suggesting that dysfunctional EAT may be linked to early plaque formation and inflammation.

Background: Copper is an abundant trace element in humans where alterations in the circulating concentration could inform on chronic disease aetiology. To date, data are lacking to study how copper may associate with cardiovascular disease (CVD) risk factors in young and healthy population. Molecular evidence suggests an important role of copper in liver metabolism, an essential organ in maintaining cardiovascular health and inflammation, therefore supporting copper as an associated biomarker of the risk. Objective: We performed a cross-sectional analysis to examine the possible associations between blood copper levels and risk factors for CVD and pre-inflammatory process. Design: The data has been collected from a sub-sample set of the Northern Finland Birth Cohort 1966 (NFBC1966) at 31 years. Participants: The study included 206 individuals, 116 men and 90 women. To reduce environmental individual variations affecting both copper and the metabolic profile in the study sample, the participants were selected as: i) being born in Finnish Lapland and ii) living in their birth place for the last five years preceding blood sampling. Main outcome measures: Fasting blood copper concentration was measured by inductively coupled plasma mass spectrometer. The CVD risk factors included 6 metabolic clusters (30 cardiovascular and pro-inflammatory factors) assessed by nuclear magnetic resonance. Multivariate linear regression analysis was performed to test the linear association between blood copper and 6 metabolic clusters for CVD risk. Associations were assessed under correction for multiple testing. Results: Copper (Cu) levels were comparable in men and women, with no difference between sexes (p-value <0.60). In multiple regression models, sex adjusted, copper was associated with 9 metabolites from 4 metabolic clusters. After adjustment with BMI, copper was associated with 4 metabolites from 3 metabolic clusters: glutamine, beta-hydroxybutyrate, alpha-1-acid gly

High dietary polyphenol intake is associated with reduced all-cause mortality and a lower incidence of cardiovascular events. However, the mechanisms involved are not fully understood. The aim of the present substudy of the PREvención con DIetaMEDiterránea (Prevention with Mediterranean diet; PREDIMED) trial was to analyse the relationship between polyphenol intake measured by total urinary polyphenol excretion (TPE), and circulating inflammatory biomarkers and cardiovascular risk factors in elderly individuals. A substudy of 1139 high-risk participants was carried out within the PREDIMED trial. The subjects were randomly assigned to a low-fat control diet or to two Mediterranean diets, supplemented with either extra-virgin olive oil or nuts. Dietary intake, anthropometric data, clinical and laboratory assessments, including inflammatory biomarkers, and urinary TPE were measured at baseline and after the one-year intervention. Participants in the highest tertile of changes in urinary TPE (T3) showed significantly lower plasma levels of inflammatory biomarkers [vascular cell adhesion molecule 1 (VCAM-1) (-9.47 ng ml-1 ), intercellular adhesion molecule 1 (-14.71 ng ml-1 ), interleukin 6 (-1.21 pg ml-1 ), tumour necrosis factor alpha (-7.05 pg ml-1 ) and monocyte chemotactic protein 1 (-3.36 pg ml-1 )] than those inthe lowest tertile (T1, P < 0.02; all). A significant inverse correlation existed between urinary TPE and the plasma concentration of\VCAM-1 (r = -0.301; P < 0.001). In addition, systolic and diastolic blood pressure (BP) decreased and plasma high-density lipoprotein cholesterol increased in parallel with increasing urinary TPE (T3 vs. T1) (P < 0.005 and P = 0.004, respectively). Increases in polyphenol intake measured as urinary TPE are associated with decreas

The study was initiated to examine magnesium intake, supplementation and their relation to inflammation. Magnesium is the second most abundant extracellular ion following potassium. Outside the cell, magnesium can be found in bone tissue, cardiac muscle tissue, other tissues and in the blood. Magnesium form compounds which operate in several essential metabolic processes in the body. Magnesium deficiency may have an impact on insulin resistance and endothelial dysfunction, which may result in an increased level of inflammation. Increased inflammation over a longer period has been seen to increase the risk of common lifestyle induced diseases such as diabetes type II and coronary heart diseases. The study of magnesium and its influence on inflammation is thereby becoming important and interesting for all societies and in their effort to find solutions to maintain and increase the well-being of its individuals. The study is a literature study based on searches made in One Search and Pub Med databases. A total of ten studies were included, five for magnesium intake and five for supplementation. The majority of the studies showed a significant correlation between increased magnesium intake, dietary and supplementary, with decreased levels of inflammatory biomarkers and hints that magnesium might have a role in the inflammation process. What needs to be taken into account is that fiber intake in two studies attenuated magnesium’s inverse relation to inflammation. In addition of a decrease in inflammatory biomarker levels the risk for developing diabetes type II seemed to decrease as well with an increased intake of magnesium in one of the studies. Further studies need to be executed in order to establish the role of magnesium in inflammation and optimal dosage for prevention of metabolic and cardiovascular diseases., Studien undersöker magnesiumintag och supplementering med magnesium samt dess inverkan på inflammation. Magnesium är den vanligast förekommande jonen intracellulärt efter kalium. Extracellulärt magnesium förekommer i benvävnad, hjärtmuskelvävnad och i blodet. Magnesium bildar ämnen som medverkar i flera viktiga metabola processer i kroppen. Magnesiumbrist kan ha en inverkan på insulin resistans och endotel dysfunktion som följaktligen skulle kunna resultera i en ökad nivå av inflammation. Ökad inflammation under en längre tid har visat sig öka risken för vanliga livsstilssjukdomar som diabetes typ II och hjärt- och kärlsjukdomar. Forskning om magnesium och dess effekt på inflammation blir därmed viktig och intressant för samhällen i deras strävan att hitta lösningar till att bibehålla och öka välmåendet hos populationen. Studien är en litteraturstudie och är grundad på sökningar via databaserna One Search och Pub Med. Totalt tio studier inkluderades i arbetet, fem som undersökte magnesiumintag och inflammation samt fem som undersökte supplementering av magnesium och inflammation. Majoriteten av studierna visade på en signifikant korrelation mellan ett ökat magnesiumintag, via kosten och kosttillskott, och minskade nivåer av biomarkörer för inflammation. Det antyder att magnesium kan ha en roll i inflammationsprocessen. I de två studier som mätte fiberintaget var relationen mellan magnesiumintag och inflammation försvagad. Utöver en minskning av biomarkörer för inflammation sågs en minskad risk för att utveckla diabetes typ II vid ett ökat magnesiumintag i en av studierna. Fler studier krävs för att fastställa magnesiums betydelse vid inflammation samt den optimala doseringen för prevention av metabola och kardiovaskulära sjukdomar.

The study was initiated to examine magnesium intake, supplementation and their relation to inflammation. Magnesium is the second most abundant extracellular ion following potassium. Outside the cell, magnesium can be found in bone tissue, cardiac muscle tissue, other tissues and in the blood. Magnesium form compounds which operate in several essential metabolic processes in the body. Magnesium deficiency may have an impact on insulin resistance and endothelial dysfunction, which may result in an increased level of inflammation. Increased inflammation over a longer period has been seen to increase the risk of common lifestyle induced diseases such as diabetes type II and coronary heart diseases. The study of magnesium and its influence on inflammation is thereby becoming important and interesting for all societies and in their effort to find solutions to maintain and increase the well-being of its individuals. The study is a literature study based on searches made in One Search and Pub Med databases. A total of ten studies were included, five for magnesium intake and five for supplementation. The majority of the studies showed a significant correlation between increased magnesium intake, dietary and supplementary, with decreased levels of inflammatory biomarkers and hints that magnesium might have a role in the inflammation process. What needs to be taken into account is that fiber intake in two studies attenuated magnesium’s inverse relation to inflammation. In addition of a decrease in inflammatory biomarker levels the risk for developing diabetes type II seemed to decrease as well with an increased intake of magnesium in one of the studies. Further studies need to be executed in order to establish the role of magnesium in inflammation and optimal dosage for prevention of metabolic and cardiovascular diseases., Studien undersöker magnesiumintag och supplementering med magnesium samt dess inverkan på inflammation. Magnesium är den vanligast förekommande jonen intracellulärt efter kalium. Extracellulärt magnesium förekommer i benvävnad, hjärtmuskelvävnad och i blodet. Magnesium bildar ämnen som medverkar i flera viktiga metabola processer i kroppen. Magnesiumbrist kan ha en inverkan på insulin resistans och endotel dysfunktion som följaktligen skulle kunna resultera i en ökad nivå av inflammation. Ökad inflammation under en längre tid har visat sig öka risken för vanliga livsstilssjukdomar som diabetes typ II och hjärt- och kärlsjukdomar. Forskning om magnesium och dess effekt på inflammation blir därmed viktig och intressant för samhällen i deras strävan att hitta lösningar till att bibehålla och öka välmåendet hos populationen. Studien är en litteraturstudie och är grundad på sökningar via databaserna One Search och Pub Med. Totalt tio studier inkluderades i arbetet, fem som undersökte magnesiumintag och inflammation samt fem som undersökte supplementering av magnesium och inflammation. Majoriteten av studierna visade på en signifikant korrelation mellan ett ökat magnesiumintag, via kosten och kosttillskott, och minskade nivåer av biomarkörer för inflammation. Det antyder att magnesium kan ha en roll i inflammationsprocessen. I de två studier som mätte fiberintaget var relationen mellan magnesiumintag och inflammation försvagad. Utöver en minskning av biomarkörer för inflammation sågs en minskad risk för att utveckla diabetes typ II vid ett ökat magnesiumintag i en av studierna. Fler studier krävs för att fastställa magnesiums betydelse vid inflammation samt den optimala doseringen för prevention av metabola och kardiovaskulära sjukdomar.

Introduction: Persistent hypertension is a key risk factor for coronary heart disease, stroke and other cardiovascular diseases, such as heart failure. For primary care physicians, hypertension is the number one diagnosis for office visits and for our communities, the treatment of high blood pressure (BP) and its consequences constitutes a substantial economic burden. Aim: To evaluate yoga as a treatment for hypertension in primary care. Methods: The thesis is based on two quantitative studies and one qualitative study: •A prospective three-arm single-centre study of two types of yoga (83 adult primary care patients diagnosed with hypertension). BP measurement, blood sampling and a questionnaire on self-rated quality of life (QOL) were carried out at baseline and after 12 weeks of intervention. There were two intervention groups and one control group. The groups were matched based on baseline systolic BP (SBP). (Papers I and II) •A three-centre parallel group randomized controlled trial (RCT) with follow-up after 12-week intervention completion (191 adult primary care patients diagnosed with hypertension). At baseline and follow-up, the participants underwent standardized BP measurements and completed questionnaires on QOL, stress, anxiety and depression. (Paper III) •A qualitative study based on individual semi-structured interviews with 13 participants from the intervention group of the RCT. We used a semi-structured interview guide according to Kvale. Qualitative analysis was conducted by systematic text condensation inspired by Malterud. (Paper IV) Results: Paper I: The patients who performed a short home-based yoga programme 15 minutes daily had a decline in diastolic BP (DBP) of 4.4 mmHg (p <0.05) and a significant improvement in self-rated QOL compared to the control group (p <0.05). Paper II: We recorded no evidence that yoga altered inflammatory biomarkers or metabolic risk factors in our study population. Paper III: There was a significant reduction in SBP

PurposeMany dietary factors have either proinflammatory or anti-inflammatory properties. We previously developed a dietary inflammatory index (DII) to assess the inflammatory potential of diet. In this study, we conducted a construct validation of the DII based on data from a food frequency questionnaire and three inflammatory biomarkers in a subsample of 2567 postmenopausal women in the Women's Health Initiative Observational Study.MethodsWe used multiple linear and logistic regression models, controlling for potential confounders, to test whether baseline DII predicted concentrations of interleukin-6, high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor alpha receptor 2, or an overall biomarker score combining all three inflammatory biomarkers.ResultsThe DII was associated with the four biomarkers with beta estimates (95% confidence interval) comparing the highest with lowest DII quintiles as follows: interleukin-6: 1.26 (1.15-1.38), Ptrend < .0001; tumor necrosis factor alpha receptor 2: 81.43 (19.15-143.71), Ptrend = .004; dichotomized hs-CRP (odds ratio for higher vs. lower hs-CRP): 1.30 (0.97-1.67), Ptrend = .34; and the combined inflammatory biomarker score: 0.26 (0.12-0.40), Ptrend = .0001.ConclusionsThe DII was significantly associated with inflammatory biomarkers. Construct validity of the DII indicates its utility for assessing the inflammatory potential of diet and for expanding its use to include associations with common chronic diseases in future studies.