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Introduction: Obesity is characterized by chronic low-grade inflammation. This study presents an updated systematic review and meta-analysis on the effect of caloric restriction (CR) and intermittent fasting (IF) on plasma inflammatory biomarkers (C-reactive protein [CRP], tumor necrosis factor [TNF]-alpha, and interleukin [IL]-6) in individuals with obesity/overweight compared with unrestricted or ad libitum feeding., Methods: PubMed, Web of Science, and SCOPUS databases were searched for randomized controlled trials (RCTs) reporting inflammatory biomarkers after at least 8 weeks of intervention. Standardized mean differences (SMDs) were calculated using a fixed effect model. Heterogeneity was determined using I 2 statistics. Sensitivity analysis was conducted using the "leave-one-out" approach., Results: Relatively few RCTs have investigated the effect of IF on inflammatory biomarkers than with CR (6 vs. 15). Analysis of pooled data showed that CR was associated with a significant reduction in CRP with low heterogeneity (SMD -0.15 mg/L [95% CI -0.30 to -0.00], p = 0.04; I 2  = 0%, p = 0.69) and IL-6 with high heterogeneity (SMD -0.31 pg/mL [95% CI -0.51 to -0.10], p = 0.004; I 2  = 73%, p = 0.001). IF was associated with a significant decrease in TNF-alpha with moderate heterogeneity (SMD -0.32 pg/mL [95% CI -0.63 to -0.02], p = 0.04; I 2  = 44%, p = 0.13). No associations were detected between IF and CRP or IL-6 and CR and TNF-alpha., Conclusion: CR may be more effective in reducing chronic low-grade inflammation than IF. However, there were some concerns regarding the included studies' randomization and allocation sequence concealment process., (© 2024 World Obesity Federation.)

The results suggested that obesity may aggravate the inflammatory status in the body of children on the basis of OSA, which was undoubtedly a further impact on systematic inflammation, namely, obesity could amplify the short-term and long-term damage of OSA. Keywords: obstructive sleep apnea, obesity, propensity score matching, hematological parameter, inflammation, hypercoagulation Introduction Obstructive sleep apnea (OSA) is a condition secondary to partial or complete obstruction of upper airway during sleep. 8 Notwithstanding previous mentioned studies have described the relationship between OSA and inflammation, obesity and inflammation, respectively, 2,9 few studies focus on the inflammatory status in children affected with both OSA and obesity. 24,28,39 In our study, obvious results were observed that the levels of WBC, NEUT, NLR, FIB in the obese children with OSA were significantly higher than those in the normal weight children with OSA, while the level of APTT in the obese children with OSA was lower than that in the normal weight children with OSA. [Extracted from the article]

HIV associated neurocognitive disorders (HAND) are the spectrum of cognitive impairments present in patients infected with human immunodeficiency virus type 1 (HIV-1). The number of patients affected with HAND ranges from 30 to 50% of HIV infected individuals and although the development of combinational antiretroviral therapy (cART) has improved longevity, HAND continues to pose a significant clinical problem as the current standard of care does not alleviate or prevent HAND symptoms. At present, the pathological mechanisms contributing to HAND remain unclear, but evidence suggests that it stems from neuronal injury due to chronic release of neurotoxins, chemokines, viral proteins, and proinflammatory cytokines secreted by HIV-1 activated microglia, macrophages and astrocytes in the central nervous system (CNS). Furthermore, the blood–brain barrier (BBB) not only serves as a route for HIV-1 entry into the brain but also prevents cART therapy from reaching HIV-1 brain reservoirs, and therefore could play an important role in HAND. The goal of this review is to discuss the current data on the epidemiology, pathology and research models of HAND as well as address the potential pharmacological treatment approaches that are being investigated. [ABSTRACT FROM AUTHOR]

Background: Inflammation is defined as body tissues response to harmful stimuli. Obesity-related inflammation leads to increased risk chronic diseases including diabetic polyneuropathy (DPN). The present study was performed to determine association between body mass index (BMI) and inflammatory markers including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) in DPN patients. Methods: In this cross-sectional study, 200 DPN patients with a mean (SD) of age 58.76 (9.53) years were selected. All patients completed the questionnaire including demographic data and chronic disease history. In addition, anthropometric measures and clinical laboratory tests were taken. Multivariate linear regression was used to detect the association between BMI, CRP, and ESR levels. Results: BMI was associated with increase in ESR and CRP levels (ß-ESR = 4.67, P < 0.001 and ß-CRP = 0.71, P < 0.001). Also, this association remained after adjustment for other different variables. Conclusions: These findings indicate that higher BMI is related to increase inflammatory markers including CRP and ESR in DPN patients. Therapies for DPN and reducing inflammation should target the weight loss among obese patients. [ABSTRACT FROM AUTHOR]

In the current pilot study, we examined whether insecure or disorganized attachment was associated with elevated inflammation (i.e. C-reactive protein [CRP]) in children with histories of child protective services (CPS) involvement, and whether early childhood CRP predicted body mass index (BMI) in middle childhood. Participants included 45 CPS-referred children and 39 low-risk comparison children, for whom we assessed levels of CRP in early childhood (Mean age = 4.9 years). For the CPS-referred children, who were drawn from an ongoing longitudinal study, we had attachment classifications (assessed during infancy with the Strange Situation) and BMI data (assessed during early and middle childhood); these data were not available for the low-risk comparison group. CPS-referred children who had insecure or disorganized attachments during infancy had higher levels of CRP in early childhood than CPS-referred children who had secure attachments, who had similar levels of CRP to low-risk comparison children. Among CPS-referred children, early childhood CRP predicted age 8 BMI, controlling for BMI at age 4. Findings offer preliminary support for the association between attachment quality and inflammation in early childhood, which may have implications for later physical health. [ABSTRACT FROM AUTHOR]

Clinical trials with sodium–glucose cotransporter 2 (SGLT2) inhibitors (empagliflozin, dapagliflozin, and canagliflozin) have shown a decrease in the progression of chronic kidney disease (CKD). SGLT2 inhibitors represent a new category of oral antidiabetic agents that can also reduce systolic and diastolic blood pressure, as well as serum uric acid, and improve the glomerular filtration rate. Apart from affecting renal hemodynamics and glycotoxicity, evidence suggests that SGLT2 inhibitors may be renoprotective due to their effects on inflammation in renal tissues. Inflammatory responses play a prominent role in the pathophysiology of CKD as several structural and functional disorders of renal failure are strongly related to the overproduction of proinflammatory mediators. The present review discusses the anti‐inflammatory properties of SGLT2 inhibitors. The different molecular pathways through which SGLT2 inhibitors may affect inflammation in the kidneys are also commented upon. Clinical trials with sodium–glucose cotransporter 2 (SGLT2) inhibitors (empagliflozin, dapagliflozin, and canagliflozin) have shown a decrease in the progression of chronic kidney disease (CKD). SGLT2 inhibitors represent a new category of oral antidiabetic agents that can also reduce systolic and diastolic blood pressure, as well as serum uric acid, and improve the glomerular filtration rate; apart from affecting renal hemodynamics and glycotoxicity, evidence suggests that SGLT2 inhibitors may be renoprotective due to their effects on inflammation in renal tissues. Inflammatory responses play a prominent role in the pathophysiology of CKD as several structural and functional disorders of renal failure are strongly related to the overproduction of proinflammatory mediators; the present review discusses the anti‐inflammatory properties of SGLT2 inhibitors and the different molecular pathways through which SGLT2 inhibitors may affect inflammation in the kidneys are also commented upon. [ABSTRACT FROM AUTHOR]

Diet quality has been postulated as a relevant factor in disorders like obesity and osteoporosis as it modulates inflammatory biomarkers. The aim of this study was to investigate whether the dietary inflammatory index (DII) is associated with bone health status and body composition parameters in a population of young adults. The study population consisted of 599 young adults (aged 20.41 ± 2.72). Linear regression analysis revealed that weight and fat-free mass (FFM) were significantly associated with the DII after adjustments for age, sex and total energy (β = -0.91, 95% CI -1.782, -0.213, p = .013 and β = -0.059, 95% CI -0.842, -0.107, p = .011, respectively). Our results suggest that the inflammatory potential of diet, measured using the DII, is associated with obesity-related parameters such as FFM and weight, although it may not contribute to osteoporosis in early adulthood. [ABSTRACT FROM AUTHOR]

Biological aging is characterized by a chronic low-grade inflammation level. This chronic phenomenon has been named "inflamm-aging" and is a highly significant risk factor for morbidity and mortality in the older persons. The most common theories of inflamm-aging include redox stress, mitochondrial dysfunction, glycation, deregulation of the immune system, hormonal changes, epigenetic modifications, and dysfunction telomere attrition. Inflamm-aging plays a role in the initiation and progression of age-related diseases such as type II diabetes, Alzheimer's disease, cardiovascular disease, frailty, sarcopenia, osteoporosis, and cancer. This review will cover the identification of pathways that control age-related inflammation across multiple systems and its potential causal role in contributing to adverse health outcomes. [ABSTRACT FROM AUTHOR]

Aim The role of inflammation in the bronchopulmonary dysplasia ( BPD) survivors is indistinct. We evaluated lung function in relation to inflammatory markers in plasma, exhaled breath condensate and exhaled air in school-aged very low birthweight ( VLBW) survivors with and without radiographic BPD. Methods Pre- and postbronchodilator impulse oscillometry were performed by 21 six to 14-year-old VLBW children with radiographic BPD, 19 VLBW children without radiographic BPD and 19 age-matched nonasthmatic term controls. Eosinophilic cationic protein, interleukins 6 and 8, adiponectin, adipsin, leptin and resistin in plasma, leukotriene B4 and 8-isoprostane in exhaled breath condensate, and bronchial and alveolar nitric oxide output were measured. Results Abnormal lung function was found in 12.5% of the former VLBW children. Airway resistance at 5 Hz was highest in the radiographic BPD, but bronchodilator responses were most prominent in the non- BPD group. Plasma adiponectin had a modest positive correlation with obstruction and with bronchodilator responses, and alveolar nitric oxide and plasma interleukin 6 with bronchodilator responses. Conclusion Very low birthweight children with radiographic BPD had poorest lung function. The most pronounced bronchodilator responses were found in VLBW children without radiographic BPD. Current detected inflammatory markers had only a minor association with lung function in school-aged BPD survivors. [ABSTRACT FROM AUTHOR]

Chronic inflammation may contribute to neuropsychological impairments in individuals with HIV, and modulation of this inflammatory response by opiate receptor ligands is important in light of the prevalence of drug use in HIV populations. Exogenous MOR and KOR agonists have differential effects on central nervous system (CNS) immunity and, while some data suggest KOR agonists are immunosuppressive, the KOR agonist dynorphin has been shown to stimulate human monocyte chemotaxis. In this study, we examined mRNA levels of endogenous opioid receptors OPRK1 and OPRM1, prodynorphin (PDYN), macrophage scavenger receptor CD163, and microglia/macrophage marker CD68 in the caudate and anterior cingulate of postmortem brains from HIV-positive and HIV-negative subjects. Brain tissues of HIV-infected (n = 24) and control subjects (n = 15) were obtained from the Manhattan HIV Brain Bank. Quantification of the gene mRNA was performed using SYBR Green RT-PCR. CD68 and CD163 were increased in HIV-positive (HIV+) compared to HIVnegative (HIV-) individuals in both brain regions. There were higher OPRK1 (P <0.005), and lower PDYN mRNA (P <0.005) levels in the anterior cingulate of HIV+ compared to HIVsubjects. This difference between the clinical groups was not found in the caudate. There was no difference in the levels of OPRM1 mRNA between HIV+ and HIV- subjects. Using linear regression analysis, we examined the relationship of OPRK1 and PDYN mRNA levels in the HIV+ subjects with seven cognitive domain T scores of a neuropsychological test battery. Within the HIV+ subjects, there was a positive correlation between anterior cingulate PDYN mRNA levels and better T-scores in the motor domain. Within the HIV+ subjects there were also positive correlations of both OPRK1 and PDYN mRNA levels with the antiinflammatory marker CD163, but not with proinflammatory CD68 levels. In this setting, decreased PDYN mRNA may reflect a homeostatic mechanism to reduce monocyte migration, accompanied by compensatory increases in the cognate receptor (KOR) to dampen pro-inflammatory responses. It is possible that enhanced neuroprotection and better motor performance are associated with higher levels of dynorphin and the recruitment of neuroprotective CD163-positive macrophages. Further studies are needed to test this hypothesis. [ABSTRACT FROM AUTHOR]

Obesity has been associated with elevated levels of C-reactive protein ( CRP), a marker of inflammation and predictor of cardiovascular risk. The objective of this systematic review and meta-analysis was to estimate the associations between obesity and CRP according to sex, ethnicity and age. MEDLINE and EMBASE databases were searched through October 2011. Data from 51 cross-sectional studies that used body mass index ( BMI), waist circumference ( WC) or waist-to-hip ratio ( WHR) as measure of obesity were independently extracted by two reviewers and aggregated using random-effects models. The Pearson correlation ( r) for BMI and ln( CRP) was 0.36 (95% confidence interval [ CI], 0.30-0.42) in adults and 0.37 ( CI, 0.31-0.43) in children. In adults, r for BMI and ln( CRP) was greater in women than men by 0.24 ( CI, 0.09-0.37), and greater in North Americans/ Europeans than Asians by 0.15 ( CI, 0-0.28), on average. In North American/ European children, the sex difference in r for BMI and ln( CRP) was 0.01 ( CI, −0.08 to 0.06). Although limited to anthropometric measures, we found similar results when WC and WHR were used in the analyses. Obesity is associated with elevated levels of CRP and the association is stronger in women and North Americans/ Europeans. The sex difference only emerges in adulthood. [ABSTRACT FROM AUTHOR]

Despite the effectiveness of combined antiretroviral therapy (cART) in suppressing virus replication, chronic inflammation remains one of the cardinal features intersecting HIV-1, cART, drug abuse, and likely contributes to the accelerated neurocognitive decline and aging in people living with HIV-1 (PLWH) that abuse drugs. It is also estimated that ~30–60% of PLWH on cART develop cognitive deficits associated with HIV-1-associated neurocognitive disorders (HAND), with symptomatology ranging from asymptomatic to mild, neurocognitive impairments. Adding further complexity to HAND is the comorbidity of drug abuse in PLWH involving activated immune responses and the release of neurotoxins, which, in turn, mediate neuroinflammation. Premature or accelerated aging is another feature of drug abusing PLWH on cART regimes. Emerging studies implicate the role of HIV-1/HIV-1 proteins, cART, and abused drugs in altering the inflammasome signaling in the central nervous system (CNS) cells. It is thus likely that exposure of these cells to HIV-1/HIV-1 proteins, cART, and/or abused drugs could have synergistic/additive effects on the activation of inflammasomes, in turn, leading to exacerbated neuroinflammation, ultimately resulting in premature aging referred to as "inflammaging" In this review, we summarize the current knowledge of inflammasome activation, neuroinflammation, and aging in central nervous system (CNS) cells such as microglia, astrocytes, and neurons in the context of HIV-1 and drug abuse. [ABSTRACT FROM AUTHOR]