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The effect of omega-3 fatty acids on biomarkers of inflammation: a rapid evidence assessment of the literature.
Khorsan, R, Crawford, C, Ives, JA, Walter, AR, Jonas, WB
Military medicine. 2014;(11 Suppl):2-60
Abstract
INTRODUCTION Previous studies of omega-3 fatty acids report improved outcomes where inflammation is a key factor. The objective of this systematic review is to evaluate effects of omega-3s on inflammatory biomarkers. METHODS Randomized clinical studies that measured the influence of omega-3 fatty acids on inflammatory biomarkers were identified using a comprehensive search. Eligible studies were rated with the American Dietetic Association Evidence Analysis Manual and Grading of Recommendations, Assessment, Development and Evaluation (GRADE) process to examine study quality and risk/benefit. RESULTS 112 studies were included. Over 65% reported statistically significant effects. The majority were scored as low risk of bias (high quality) and scored strong (cardiac populations and critically ill) to weak (Alzheimer's Disease, hypertriglyceridemia/diabetes, and obesity) on the risk/benefit ratio evidence for modulation of inflammatory biomarkers. There was inadequate data to determine a GRADE for inflammatory biomarker studies for some conditions (healthy individuals, rheumatoid arthritis, metabolic syndrome, renal disease, pregnancy, or children). CONCLUSION Clinical literature on the effects of omega-3 fatty acids on inflammatory biomarkers contains mostly small sample sizes, is neutral to high quality, and report mixed effects. Larger studies examining dose and delivery are needed.
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Association between carbohydrate quality and inflammatory markers: systematic review of observational and interventional studies.
Buyken, AE, Goletzke, J, Joslowski, G, Felbick, A, Cheng, G, Herder, C, Brand-Miller, JC
The American journal of clinical nutrition. 2014;(4):813-33
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Abstract
BACKGROUND Chronic low-grade inflammation is a likely intermediary between quality of carbohydrate and chronic disease risk. OBJECTIVE We conducted a systematic literature search to evaluate the relevance of carbohydrate quality on inflammatory markers in observational and intervention studies. DESIGN MEDLINE, EMBASE, and the Cochrane Library were searched for studies on associations between glycemic index (GI), glycemic load (GL), dietary fiber or fiber supplements or whole grain intake, and high-sensitivity C-reactive protein (hsCRP) or interleukin 6 (IL-6). Included studies had to be conducted on adults (healthy, overweight, with type 2 diabetes or metabolic syndrome features, but without inflammatory disease) with ≥20 participants and a 3-wk duration. RESULTS In total, 22 of the 60 studies that met our inclusion criteria examined GI/GL: 5 of 9 observational studies reported lower concentrations of hsCRP or IL-6 among persons with a lower dietary GI/GL; 3 of 13 intervention studies showed significant antiinflammatory effects of a low-GI/GL diet, and 4 further studies suggested beneficial effects (trends or effects in a subgroup). For fiber intake, 13 of 16 observational studies reported an inverse relation with hsCRP or IL-6, but only 1 of 11 intervention studies showed a significant antiinflammatory effect of fiber intake, and a further trial reported a beneficial trend. For whole-grain intake, 6 of 7 observational studies observed an inverse association with inflammatory markers, but only 1 of 7 intervention studies reported significant antiinflammatory effects, 1 further study was suggestive (in a subgroup) of such, and another study found an adverse effect (trend only). CONCLUSIONS Evidence from intervention studies for antiinflammatory benefits is less consistent for higher-fiber or whole-grain diets than for low-GI/GL diets. Benefits of higher fiber and whole-grain intakes suggested by observational studies may reflect confounding.
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Diet/genetic interactions and their effects on inflammatory markers.
Ordovas, J
Nutrition reviews. 2007;(12 Pt 2):S203-7
Abstract
The importance of a healthy diet to living well is well recognized. A growing array of experimental, epidemiological, and clinical studies have revealed an association between pro-inflammatory responses and the progression of numerous serious disease states, including the metabolic syndrome, type 2 diabetes, and cardiovascular diseases. Further studies have established a "diet/genetic interaction" that further modulates markers of inflammation, producing both positive and negative effects, depending on the net changes in gene expression. Yet, there are few studies that reveal the mechanisms underlying this modulation of the inflammatory response. Highlighted here are several such recent and ongoing studies that investigate the mechanisms underlying the effects of diet/genetic interactions on inflammatory biomarkers, followed by a discussion of to what extent these interactions may translate into healthier aging and increased longevity. Whether these interactions translate into healthier aging and increased longevity remains to be determined; however, the prospects are enticing.
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Inflammatory biomarkers and risks of myocardial infarction, stroke, diabetes, and total mortality: implications for longevity.
Ridker, PM
Nutrition reviews. 2007;(12 Pt 2):S253-9
Abstract
Inflammation is recognized as a major etiologic determinant of multiple disease states including myocardial infarction, stroke, diabetes, and metabolic syndrome, and individuals with elevated levels of the inflammatory biomarker high-sensitivity C-reactive protein (hsCRP) are at increased risk of mortality and morbidity from these conditions. Novel screening algorithms, such as the Reynolds Risk Score, that incorporate inflammation can greatly improve risk detection in primary prevention. In high-risk secondary prevention settings such as acute coronary syndrome patients being treated with statin therapy, achieving low levels of plasma hsCRP concentration appears to be of similar importance as achieving low levels of LDL cholesterol. Whether inflammation in general or CRP in particular are appropriate targets for therapy remains controversial and is under investigation. Several novel methods to reduce CRP have been proposed, including direct inhibitors as well as antisense technologies.
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[Inflammatory biomarkers: the link between obesity and associated pathologies].
Zulet, MA, Puchau, B, Navarro, C, Martí, A, Martínez, JA
Nutricion hospitalaria. 2007;(5):511-27
Abstract
[corrected] of this article is to review biomarkers that have been suggested in recent years as the link between inflammation, obesity and associated co-morbidities, as well as some questions that yet remain unclear. Increasing evidence indicates the important role of inflammation in the etiology of major public health problems. In the last years, several studies have proposed that obesity might be a inflammatory disorder. In addition, oxidative stress has been suggested as a potential inductor of inflammatory status and susceptibility to obesity and related disorders. Several biomarkers are being suggested as the link between obesity, insulin resistance, cardiovascular disease and metabolic syndrome, such as tumor necrosis factor alfa, interleukin-6 and -18, angiotensinogen, transforming grow factor beta, plasminogen activator inhibitor-1, leptin, resistin, C-reactive protein, serum amyloid A, sialic acid, fibrinogen, markers of endothelial dysfunction (von Willebrand factor, ICAMs, VCAMs), complement factor 3, haptoglobin, Zinc-alpha2-glycoprotein, eotaxin, visfatin, apelin, alpha1-antitrypsin, vaspin, omentin, retinol binding protein 4, ceruloplasmin, adiponectin and desnutrin. Some of this biomarkers are good predictors of cardiovascular risk (plasminogen activator inhibitor-1, sialic acid, fribrinogen, complement factor 3, C-reactive protein), adiposity (leptin, visfatin, resistin, haptoglobin) and/or insulin resistance (sialic acid, C-reactive protein, plasminogen activator inhibitor-1, von Willebrand factor). However, it is currently unclear the role of many of them concerning inflammatory processes in humans, as well as the factors involved in their regulation.
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Etiology and pathogenesis of necrolytic migratory erythema: review of the literature.
Tierney, EP, Badger, J
MedGenMed : Medscape general medicine. 2004;(3):4
Abstract
CONTEXT Necrolytic migratory erythema (NME) is a characteristic skin condition seen in the presence of a pancreatic glucagonoma. The presence of NME in the absence of a pancreatic tumor has been termed the pseudoglucagonoma syndrome. In such cases, NME is commonly associated with conditions, such as liver disease, inflammatory bowel disease, pancreatitis, malabsorption disorders (ie, celiac sprue), and other malignancies. There are many theories on the pathogenesis of NME, which include the direct action of glucagon in inducing skin necrolysis, hypoaminoacidemia-inducing epidermal protein deficiency and necrolysis, a nutritional or metabolic deficiency of zinc or essential fatty acids, liver disease, glucagon induction of inflammatory mediators, a substance secreted from pancreatic and other visceral tumors associated with NME, and generalized malabsorption. OBJECTIVE To present a review of the literature on the clinical presentation, etiology, pathogenesis, and treatment of NME. DESIGN Review of the literature on NME occurring in patients both with and without a pancreatic glucagonoma. METHODS We performed a PubMed review of the literature on the etiology and pathogenesis of NME to identify case reports and reviews published in both the internal medicine and dermatology literature. RESULTS Our literature review encompassed 17 primary case reports and literature reviews published in the dermatologic and internal medicine literature on NME in patients both with and without a pancreatic glucagonoma. Although we found no clear consensus among the investigators of a universally accepted pathogenesis for NME, we did identify 4 main categories of etiologic/pathogenetic mechanisms for NME (glucagon excess, nutritional deficiencies, inflammatory mediators, and liver disease) that were discussed by many of the investigators and validated by both clinical and scientific evidence. CONCLUSION The exact pathogenesis and treatment of NME remain ill-defined despite many case reports and studies on NME in the literature. The many systemic diseases and nutritional deficiencies that have been found to be associated with NME suggest a multifactorial model for the pathogenesis of the disease. The most comprehensive, postulated mechanism for NME involves a combination of zinc, amino acid, and fatty acid deficiencies (arising from a wide variety of causes, such as dietary insufficiency, malabsorption syndromes, liver disease, elevated glucagon levels, and disorders of metabolism) that contributes to increased inflammation in the epidermis in response to trauma and to the necrolysis observed in NME. The importance of gaining an understanding of the etiology and pathogenesis of NME lies in the fact that there is no universally accepted mechanism of pathogenesis for NME, and that the only treatment reported to resolve the rash in these patients is to adequately identify and treat the underlying associated systemic condition or nutritional deficiency.
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[Predictors of mortality in dialysis patients--association between malnutrition, inflammation and atherosclerosis (MIA syndrome)].
Perunicić-Peković, G, Rasić-Milutinović, Z, Pljesa, S
Medicinski pregled. 2004;(3-4):149-52
Abstract
INTRODUCTION Numerous recent studies have shown increased comorbidity and mortality in dialysis patients with malnutrition. Protein-energy malnutrition with muscle wasting occurs in a large proportion of patients with chronic renal failure and is, in addition to atherosclerosis, a strong risk factor for mortality in patients undergoing dialysis. Malnutrition is also associated with increased cardiovascular mortality in dialysis patients. PATHOGENIC FACTORS OF MALNUTRITION IN DIALYSIS PATIENTS Malnutrition is associated with a number of metabolic and vascular abnormalities. These factors include hypoalbuminemia, dyslipidemia with raised triglyceride concentrations, low-density lipoprotein and very low-density lipoprotein concentrations, insulin resistance and high concentrations of acute-phase proteins. Low serum albumin concentration, usually used as an index of malnutrition, is highly associated with increased mortality risk in dialysis patients. However, serum albumin is affected by factors other than malnutrition and high concentrations of acute-phase proteins, such as C-reactive protein (CRP), which correlate with low serum albumin in malnourished patients on dialysis. Oxidative stress has emerged as an important cofactor for development of endothelial dysfunction as premature atherosclerosis. In this context, malnutrition, inflammation and markers of oxidative stress are associated with vascular diseases. ETIOLOGY OF MALNUTRITION IN DIALYSIS PATIENTS In recent studies several reports have suggested that inflammation, alone or in combination with low protein intake, plays a significant role in etiology of malnutrition in uremic patients. Lipid abnormalities may not only be a consequence of renal disease, but also contribute to its progression. Lipoprotein (a) is also associated with various atherosclerotic diseases. THERAPY OPTIONS New treatment strategies, such as high protein/energy vs. standard protein/energy nutritional regimens, are necessary as well as food intake and dietary supplements. Intensive supplementation of (1.5 g protein/kg/d and 45 kcal/kg/d) is necessary to improve nutritional status of dialysis patients. CONCLUSION Cellular basis of pathogenetic factors in malnutrition is unclear. It is, however, now recognized that oxidative stress and inflammatory cytokine aggravates the nutritional status of these patients.
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Lipid mediators in the pathophysiology of critical illness.
Bulger, EM, Maier, RV
Critical care medicine. 2000;(4 Suppl):N27-36
Abstract
Inflammatory lipid mediators are produced by the metabolism of membrane phospholipids following a number of different stimuli. These mediators lead to a variety of cellular and systemic responses which contribute to the manifestations of the systemic inflammatory response syndrome in the critically ill patient. These mediators include platelet-activating factor and the eicosanoids, including prostaglandins, thromboxanes, leukotrienes, and HETEs. This review seeks to evaluate the current role of these mediators in the pathophysiology of critical illness. We will focus on recent studies concerning the modulation of these pathways as a potential therapeutic strategy for management of these critically ill patients. This includes the gamut from nutritional strategies to alter the cellular membrane lipid composition, thereby effecting the substrate available to produce these lipid byproducts, to intracellular inhibitors to alter production of these mediators, to receptor blockage and enhanced clearance to inhibit their effects.