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Heart Inflammation Reduce 2.

core10
06.06.2018

Content:

  • Heart Inflammation Reduce 2.
  • 6 Ways To Reduce Heart Inflammation Without A Statin
  • Why People With Arthritis Are at Greater Risk for Heart Disease
  • Many major diseases that plague us—including cancer, heart disease, risk for chronic diseases such as type 2 diabetes and heart disease are also On the flip side are beverages and foods that reduce inflammation, and. 6 Ways to Reduce Heart Inflammation Without a Statin . 2. Consume a Mediterranean diet. Research published in the New England Journal. Targeting inflammation to reduce cardiovascular disease risk: a realistic clinical . any possibility of clinically meaningful benefits (Myung et al., ) (Figure 2).

    Heart Inflammation Reduce 2.

    The production of these cytokines leads to joint swelling, pain, and eventual joint destruction. In addition, T lymphocytes promote the activity of macrophages and B lymphocytes, which intensify the inflammatory response and hasten joint damage. Nutrition and Inflammation Nutrients play a key role in both promoting and combating inflammatory processes. Evidence linking nutrients with inflammatory processes comes from laboratory, clinical, and epidemiologic studies. Excessive energy intake stimulates adipose cell growth and proliferation, and promotes abdominal obesity, thereby increasing the risk of diabetes, metabolic syndrome, and other chronic diseases.

    Carbohydrate intake has been linked to chronic diseases such as obesity, metabolic syndrome, and type 2 diabetes. Of particular interest are foods low in fiber and rich in sugars and starches, and those that produce a high glycemic value based on the glycemic index GI scale.

    A prospective study conducted in Australia among postmenopausal women demonstrated that the risk of death from inflammatory disease, including digestive, respiratory, nervous system, and endocrine disorders, was nearly three times greater among women consuming a high-GI diet compared with women eating a low-GI diet.

    Consuming trans fatty acids is a known risk factor for sudden cardiac death. A possible mechanism suggests that trans fatty acids induce an inflammatory response in cardiac tissue through their effect on cell membranes.

    Data from an in vitro study published in the British Journal of Nutrition showed that trans In addition, studies of patients with chronic heart failure have demonstrated significant associations between the trans fatty acid level of red blood cell membranes and plasma biomarkers of inflammation, including IL-1, IL-6, and TNF-alpha.

    In vitro studies have shown that saturated fatty acids play a role in the inflammatory process by stimulating macrophage production and the secretion of the proinflammatory cytokines TNF-alpha, IL-6, and IL During the last several decades, the consumption of oils rich in the omega-6 fatty acid linoleic acid eg, soybean, corn, safflower, sunflower steadily has risen in the United States, resulting in an increased ratio of omega-6 to omega-3 fatty acids in the American diet.

    Ideal dietary levels of omega-6 to omega-3 fatty acids are believed to be 1 to 4: This change has been associated with an increased risk of chronic inflammatory diseases, including atherosclerosis and cardiovascular disease, rheumatoid arthritis, and IBD. Omega-6 fatty acids are precursors to proinflammatory eicosanoids, signaling molecules that help regulate immune function and are active in the inflammatory process.

    These molecules have potent negative effects on platelet aggregation, blood pressure, and immune system function and trigger proinflammatory cytokine production. The omega-3 fatty acids EPA and DHA, found in fatty fish and fish oil supplements, suppress the production of proinflammatory eicosanoids and stimulate the synthesis of anti-inflammatory eicosanoids lipoxins from arachadonic acid.

    Although most studies have focused on the effects of fish oil, consuming approximately 3 oz of fatty fish eg, salmon, herring five times per week for eight weeks resulted in significant lowering of plasma levels of proinflammatory cytokines TNF-alpha and IL-6 among elderly Chinese women with dyslipidemia. Chia seed, walnuts, canola oil, and flaxseed oil are sources of the omega-3 fatty acid alpha-linolenic acid ALA. A powerful antioxidant, ascorbic acid vitamin C defends cells against lipid peroxidation and scavenges reactive oxygen and nitrogen species such as hydroxyl, peroxyl, superoxide, nitroxide radical, and peroxynitrite.

    Ascorbic acid supports phagocytosis by macrophages and stimulates the activity of natural killer lymphocytes generated during the innate immune response. Through its function as a cofactor in enzymes controlling collagen synthesis, vitamin C also reduces tissue damage at inflammation sites.

    Vitamin E exists in nature as different chemical structures; the most common forms in the diet are alpha- and gamma-tocopherol. Foods such as seeds, nuts, and vegetable oils are sources of gamma-tocopherol, while supplements commonly contain alpha-tocopherol. Alpha- and gamma-tocopherol have different biological activities. Alpha-tocopherol has long been recognized for its capacity to scavenge free radicals and prevent lipid oxidation.

    In addition, it inhibits the release of proinflammatory cytokines and reduces CRP levels. Most clinical trials assessing the anti-inflammatory effects of vitamin E primarily have looked at alpha-tocopherol supplementation and not tocopherols from foods.

    Alpha-tocopherol significantly decreases circulating levels of gamma-tocopherol, decreasing its anti-inflammatory properties. In addition, alpha- and gamma-tocopherol may have a synergistic effect on inflammation. Vitamin E shows some promise in the treatment of rheumatoid arthritis symptoms. These aromatic compounds are found in fruits, vegetables, grains, chocolate, coffee, olive oil, and tea.

    To date, thousands of polyphenols have been identified and classified into different subgroups. Flavonoids include the flavanones naringenin and hesperidin found in citrus fruit ; flavonols such as myricetin, kaempferol, and quercetin found in apples, cocoa, and onions ; and the flavones luteolin and apigenin found in celery , catechins found in tea , and anthocyanins found in berries.

    Phenolic acids caffeic acid, gallic acid, and ferulic acid are found in coffee, olive oil, tea, grains, peanuts, and berries. Lignans secoisolariciresinol and matairesinol are found primarily in flaxseeds. The polyphenol resveratrol, classified as a stilbenoid, is found in red wine and berries. Many polyphenols show powerful anti-inflammatory effects.

    Laboratory investigations, clinical trials, and prospective studies suggest that polyphenols inhibit enzymes involved in prostaglandin and leukotriene synthesis, prevent free radical formation, decrease proinflammatory cytokine production, and block the activity of proinflammatory signaling systems.

    Prebiotics are defined as nondigestible, nonabsorbable substances that can be fermented by bacteria in the gut, promote the growth of desirable microflora, and impart improvements to health. Prebiotics include oligofructose, a short-chain fructose polymer, and inulin, a type of dietary fiber. Food sources of prebiotics include chicory, Jerusalem artichokes, and onions. Inulin is an additive in many commercially prepared foods and sold as a dietary supplement. Animal studies have shown that both prebiotics and probiotics can decrease the activity of proinflammatory cytokines and NF-kB, and increase levels of anti-inflammatory TGF-beta within the gut mucosa.

    Both prebiotics and probiotics appear to interact directly with gut epithelium cells to block pathogens from entering. Clinical trials have helped corroborate the anti-inflammatory effects of prebiotics seen in laboratory studies.

    Infants and children with diarrheal illness showed marked improvement in symptoms eg, decreased diarrhea, vomiting, fever when given supplemental inulin. Administered to patients with ulcerative colitis or precancerous colon polyps, inulin improved measures of disease activity and reduced levels of intestinal proinflammatory proteins.

    The results have been mixed but generally support a role for probiotics in decreasing disease activity and improving clinical symptoms. In addition, consuming cultured dairy foods has been found to alleviate symptoms of IBD, ulcerative colitis, and pouchitis. Anti-Inflammatory Foods and Dietary Patterns Various foods and dietary patterns are effective in reducing the underlying inflammatory processes associated with chronic disease.

    A diet high in fruits and vegetables may be one of the best defenses against chronic inflammation. Fruits and vegetables are a highly bioavailable source of vitamins, minerals, fiber, and polyphenols with anti-inflammatory activity. A cross-sectional study investigating self-reported fruit and vegetable intake among adults found that individuals reporting the highest consumption more than two servings of fruit and three servings of vegetables daily had significantly lower plasma levels of proinflammatory CRP, IL-6, and TNF-alpha as well as decreased biomarkers of oxidative stress.

    Four to five servings daily each of fruits and vegetables are recommended to combat inflammation and chronic disease. The Mediterranean diet is characterized by the generous consumption of vegetables, fruits, grains, legumes, and nuts; a minimal intake of red meat and whole-fat dairy products; increased fish consumption; moderate red wine intake; and liberal use of olive oil in cooking and food preparation.

    Compared with Western diets, the Mediterranean diet is rich in fiber, polyphenols, antioxidants, and omega-3 fatty acids and low in saturated fat and refined carbohydrate. Data from epidemiologic and clinical studies have demonstrated that consuming a Mediterranean-type diet reduces plasma levels of proinflammatory biomarkers, including endothelial adhesion molecules, CRP, TNF-alpha, and NF-kB.

    High-fiber, low-GI foods appear to have a beneficial effect on inflammatory biomarkers. Adhering to a low-GI diet for one year resulted in significantly lower plasma levels of CRP in a clinical randomized trial of subjects with type 2 diabetes compared with adhering to high-GI and low-carbohydrate diets.

    Whole grain foods consist of the unaltered grain with intact bran and germ components, which are valuable sources of fiber, phytochemicals, vitamins, and minerals. Prospective and clinical studies have suggested that consuming whole grain foods such as oats, barley, and brown rice may help decrease inflammation associated with metabolic syndrome, diabetes, and cardiovascular disease.

    Weight loss is known to have beneficial effects on metabolic syndrome, type 2 diabetes, and other chronic conditions. Additional research is needed to identify the independent and interactive effects of foods and nutrients and to evaluate the protective role of supplements in fighting inflammation. Clinical Recommendations There are many simple dietary strategies that may effectively reduce levels of chronic inflammation and decrease disease risk.

    In addition, they may be unaware of the role diet plays in affecting the inflammatory processes underlying many chronic illnesses. Dietitians can support their clients and patients by emphasizing dietary changes that will help reduce inflammation levels in the body and begin to restore normal immune function. Encouraging clients to increase their intake of fruits, vegetables, whole grains, nuts, olive oil, and fatty fish is a positive message that can accompany advice to reduce their consumption of refined starches and sweets, and foods laden with trans and saturated fat.

    Focusing on personalized goals and setting achievable objectives eg, eat an extra serving of fruit at lunch is key to helping clients make lasting dietary changes that will combat inflammation and enhance overall health.

    The right foods can help reduce the amount of inflammation in the body and improve health. Here are 10 suggestions for clients and patients for eating to decrease inflammation:. Boost consumption of fruits and vegetables. Aim to eat four to five servings each of fruits and vegetables daily. Choose fruits and vegetables that are deep green, orange, yellow, and purple, since these have the greatest nutritional value.

    Ten servings per day may sound like too much, but serving sizes are small: Cook with olive oil as much as possible and use it to make salad dressings. Virgin olive oil is best since it has more inflammation-fighting antioxidants than refined olive oil. Snack on walnuts instead of chips. Walnuts provide fiber, minerals, antioxidants, and the kinds of fatty acids that are good for your heart.

    Eat a whole grain cereal such as oatmeal for breakfast, and replace refined grains with whole grains, such as substituting brown rice for white rice. Eat fatty fish such as salmon two to three times per week to get more omega-3 fatty acids. Wild salmon has more omega-3s than farmed salmon. Eat fewer fast foods. Many tend to be cooked in oils that contain trans fatty acids, which increase inflammation.

    If you eat at fast-food restaurants, order a grilled chicken sandwich or salad with vinaigrette dressing. Replace white potatoes with sweet potatoes. Cut down on sugary drinks such as juice, soda, and punch. Add small amounts of cider, fruit juice, or wedges of lemon or orange to plain water to enhance the flavor.

    Eat more lentils and beans. Munch on dark chocolate and fresh raspberries for dessert. Both are loaded with antioxidants. Learning Objectives After completing this continuing education course, nutrition professionals should be better able to:. Assess the potential benefits of anti-inflammatory foods and nutrients to clients and patients. Abdominal obesity has which of the following effects? It increases circulating levels of C-reactive protein CRP. It decreases circulating levels of proinflammatory cytokines.

    It decreases fat cell necrosis. It normalizes adipose cell adipokine activity. Foods rich in polyphenols help fight inflammation by which of the following mechanisms? They decrease anti-inflammatory cytokine production. They inhibit enzymes involved in prostaglandin and leukotriene synthesis.

    They reduce omega-6 to omega-3 fatty acid ratios. What are the two types of adaptive immunity? Innate and receptive b. Humoral and cell mediated c. Antigenic and phagocytic d. Based on this article, which of the following statements about metabolic syndrome is true? Which of the following is true of prebiotics and probiotics, based on this article?

    Both are strains of lactobacillus bacteria. Both are found in foods and are available as dietary supplements. Neither is effective in reducing gastrointestinal disease activity. Both can be obtained by eating cultured dairy foods. Which of the following are two examples of proinflammatory cytokines?

    CRP and serum amyloid A b. Interleukin 6 and tumor necrosis factor alpha c. Transforming growth factor beta and nuclear factor kappa B NF-kB d. Fibrinogen and clotting factor VII. Suppression of proinflammatory eicosanoids b.

    Conversion of linoleic acid to arachidonic acid c. Strengthening of the gut mucosa d. Stimulation of collagen synthesis. Acute phase reactants are biomarkers of chronic inflammation. A positive acute phase reactant has which of the following effects? This benefit appears in considerable measure independent of the well-known effect of statin therapy on cholesterol concentration.

    Thus, the clinical benefit of statins appears related to their antiinflammatory effect. However, lipid lowering is an antiinflammatory therapy in and of itself, and this activity is central to the clinical benefit of statin therapy. The best approach to treating coronary artery disease is controversial and sometimes pits angioplasty and stenting against coronary bypass surgery. However, comparing these end-stage interventions as alternative choices for routine therapy is a colossal admission of failure.

    Indeed, although revascularization can effectively relieve angina, it poorly prevents MI or prolongs life We must find new approaches to combat this disease.

    For many years, cardiologists focused on the stenosis. Stenotic lesions are easy targets because patients have symptoms, and measuring blood flow or imaging a blocked artery is easy as well. However, the more common nonstenotic lesion masks MI. As we have seen, nonstenotic lesions, which are hidden in the artery wall without causing discrete stenosis, more often cause acute complications. Clinically, we certainly often need to used revascularization strategies to relieve compromised tissue blood flow.

    We must, however, couple such therapies with systemic interventions including lifestyle modification and appropriate drug therapy. Perhaps most importantly, we need to prevent cardiovascular complications in individuals without signs and symptoms of compromised blood flow. Health professionals must identify overtly healthy individuals who are at increased risk of first cardiovascular events and introduce effective approaches to prevention.

    Reducing inflammation is one effective way to prevent cardiovascular complications. Inflammation is central to cardiovascular disease. It often begins with inflammatory changes in the endothelium, which begins to express the adhesion molecule VCAM VCAM-1 attracts monocytes, which then migrate through the endothelial layer under the influence of various proinflammatory chemoattractants.

    Once within the arterial intima, the monocytes continue to undergo inflammatory changes, transform into macrophages, engulf lipids, and become foam cells. T lymphocytes also migrate into the intima, where they release proinflammatory cytokines that amplify the inflammatory activity. Through these inflammatory processes, the initial lesion of atherosclerosis, the fatty streak, is formed.

    Furthermore, inflammation is central to the progression from fatty streak to complex plaque. As the plaque evolves, T cells activate macrophages by either cyto-signaling or contact through CD40 ligation to secrete a panoply of molecules, including cytokines and MMPs, that make up the collagen that forms the fibrous cap, which ordinarily protects the plaque.

    As a result, the fibrous cap becomes thin and friable and can rupture, thus creating a thrombus that can lead to an MI or other complications.

    This sequence of events differs greatly from the former perspective of cardiovascular disease as a lipid storage problem. We now know that critical stenoses do not cause most MIs. Our assessment and management of cardiovascular disease risk must evolve in step with a deepened understanding of pathophysiologic mechanisms. Inflammatory markers such as CRP merit careful consideration for inclusion in our risk assessment algorithms.

    Lifestyle modification and proven medical therapies must join stenting and coronary bypass surgery. If we are to embrace fully our new appreciation of inflammation in the initiation and development of atherosclerosis, we must reduce new biological insights to practice to aid in the identification of individuals at risk of cardiovascular events, with the goal of lessening our dependence on late-stage and invasive treatments.

    Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Close mobile search navigation Article navigation.

    Inflammation and cardiovascular disease mechanisms Peter Libby. ABSTRACT The traditional view of atherosclerosis as a lipid storage disease crumbles in the face of extensive and growing evidence that inflammation participates centrally in all stages of this disease, from the initial lesion to the end-stage thrombotic complications. View large Download slide. Changes in the endothelium of the aorta and the behaviour of macrophages in experimental atheroma of rabbits.

    Endothelial expression of a mononuclear leukocyte adhesion molecule during atherogenesis. An atherogenic diet rapidly induces VCAM-1, a cytokine-regulatable mononuclear leukocyte adhesion molecule, in rabbit aortic endothelium. Nitric oxide decreases cytokine-induced endothelial activation.

    Nitric oxide selectively reduces endothelial expression of adhesion molecules and proinflammatory cytokines. MCP-1 and IL-8 trigger firm adhesion of monocytes to vascular endothelium under flow conditions. Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. Macrophage colony-stimulating factor gene expression in vascular cells and in experimental and human atherosclerosis.

    Macrophage colony-stimulating factor mRNA and protein in atherosclerotic lesions of rabbits and humans. Decreased atherosclerosis in mice deficient in both macrophage colony-stimulating factor op and apolipoprotein. Heterozygous osteopetrotic op mutation reduces atherosclerosis in LDL receptor-deficient mice. Differential expression of three T lymphocyte-activating CXC chemokines by human atheroma-associated cells. Overexpression of eotaxin and the CCR3 receptor in human atherosclerosis: High prevalence of coronary atherosclerosis in asymptomatic teenagers and young adults: Coronary artery atherosclerosis revisited in Korean war combat casualties.

    Endotoxin and tumor necrosis factor induce interleukin-1 gene expression in adult human vascular endothelial cells. Inhibition of CD40 signaling limits evolution of established atherosclerosis in mice. Pre-existing coronary stenoses in patients with first myocardial infarction are not necessarily severe. Influence of plaque configuration and stress distribution on fissuring of coronary atherosclerotic plaques.

    Effects of fibrous cap thickness on peak circumferential stress in model atherosclerotic vessels. Cytokines and growth factors positively and negatively regulate interstitial collagen gene expression in human vascular smooth muscle cells. Evidence for increased collagenolysis by interstitial collagenases-1 and -3 in vulnerable human atheromatous plaques. Ligation of CD40 on vascular smooth muscle cells mediates loss of interstitial collagen via matrix metalloproteinase activity. Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction.

    Effect of statins on risk of coronary disease: Dietary lipid lowering reduces tissue factor expression in rabbit atheroma. Lipid lowering by diet reduces matrix metalloproteinase activity and increases collagen content of rabbit atheroma: C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women.

    Elevation of tumor necrosis factor-alpha and increased risk of recurrent coronary events after myocardial infarction.

    Plasma concentration of interleukin-6 and the risk of future myocardial infarction among apparently healthy men. Associations of elevated interleukin-6 and C-reactive protein levels with mortality in the elderly.

    Strong decrease of high sensitivity C-reactive protein with high-dose atorvastatin in patients with type 2 diabetes mellitus. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Measurement of C-reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events. Effect of statin therapy on C-reactive protein levels: Inflammatory predictors of mortality in the Scandinavian Simvastatin Survival Study.

    Comparison of effect of intensive lipid lowering with atorvastatin to less intensive lowering with lovastatin on C-reactive protein in patients with stable angina pectoris and inducible myocardial ischemia.

    Differential hs-CRP reduction in patients with familial hypercholesterolemia treated with aggressive or conventional statin therapy. Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: Coronary artery bypass surgery: Email alerts New issue alert.

    Receive exclusive offers and updates from Oxford Academic. More on this topic Differential effects of polyphenols and alcohol of red wine on the expression of adhesion molecules and inflammatory cytokines related to atherosclerosis: Arterial endothelial dysfunction in baboons fed a high-cholesterol, high-fat diet.

    Lipid and macrophage accumulations in arteries of children and the development of atherosclerosis. Related articles in Google Scholar. Association between neutrophil to lymphocyte ratio and depressive symptoms among Chinese adults: Citing articles via Google Scholar. Latest Most Read Most Cited Randomized double-blind, placebo-controlled trial evaluating oral glutamine on radiation-induced oral mucositis and dermatitis in head and neck cancer patients.

    Consumption of cashew nuts does not influence blood lipids or other markers of cardiovascular disease in humans: Serum metabolites associated with dietary protein intake: Grape or grain but never the twain?

    6 Ways To Reduce Heart Inflammation Without A Statin

    Statins are not as helpful for reducing inflammation of the heart can help in reducing heart inflammation. Photo Credit: iStock. 2. Stop smoking. Although it is not proven that inflammation causes cardiovascular disease, might lower inflammation in arteries and reduce the risk of heart attack and stroke . This type of inflammation can drive illnesses like diabetes, heart disease, fatty liver disease, and cancer (1, 2, 3, 4). Chronic inflammation can.

    Why People With Arthritis Are at Greater Risk for Heart Disease



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    Statins are not as helpful for reducing inflammation of the heart can help in reducing heart inflammation. Photo Credit: iStock. 2. Stop smoking.

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