2006 Archives: Inflammation and Oxidative Stress
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Chronic inflammation and oxidative stress in the genesis and perpetuation of cancer: role of lipid peroxidation, DNA damage, and repair.
(Langenbecks Arch Surg. 2006) "CONCLUSION: Persistent oxidative/nitrosative stress and excess LPO are induced by inflammatory processes in a self-perpetuating process and cause progressive accumulation of DNA damage in target organs. Together with deregulation of cell homeostasis, the resulting genetic changes act as driving force in chronic inflammation-associated human disease pathogenesis."
C-Reactive Protein, Carotid Atherosclerosis, and Cerebral Small-Vessel Disease. Results of the Austrian Stroke Prevention Study.
(Stroke. 2006) "CONCLUSIONS: We found evidence for differential effects of CRP in different beds of the arterial brain supply. CRP was a marker for active carotid atherosclerosis but not for small vessel disease-related brain lesions."
Dual role of infections as risk factors for coronary heart disease. (Atherosclerosis. 2006) "CONCLUSIONS: Infections have a dual role in the genesis of CHD. EV, HSV and C. pneumoniae heat shock protein 60 IgG antibodies are associated with increased risk for CHD. Protection from infections usually suffered during the childhood before the era of MMR vaccination may predispose the individual to CHD."
Low-grade systemic inflammation and the risk of type 2 diabetes in obese children and adolescents.
(Neuro Endocrinol Lett. 2006) "CONCLUSIONS: Serum inflammatory markers were significantly correlated with most factors implicated in the development of type 2 diabetes. These data provide additional support for previously reported in adults relationship between subclinical inflammation and the risk of type 2 diabetes."
Parkinson's disease tied to allergic rhinitis "Adults with allergic rhinitis are nearly three times as likely to develop Parkinson's disease (PD) later in life, compared with those who do not have allergies…"
The Anti-Inflammation Diet "Most foods either fuel the fires of inflammation or tamp them down, Galland explains. And fat is the crux of the issue. The goal is to eat a good balance of inflammatory fats (mainly omega-6s, as found in safflower, sunflower, and corn oil) and anti-inflammatory fats (like omega-3s, found in fish, and omega-9s, which olive oil has). But most people chow down on up to 30 times more inflammatory fats than anti. … If you don’t want to mess with mercury, you’re not so fond of fish, or you just want to hedge your bets, try fish oil supplements. Look for a supplement with EPA and DHA and take 2,000 milligrams every day."
Type 2 diabetes mellitus as inflammatory disease.
(Diabetes Res Clin Pract. 2006) "Inflammation is defined as a cascade of phenomena induced in response to different pathological stimuli. This physiological occurrence that allows the restoration of homeostasis may also cause different diseases in various pathological conditions. Inflammatory process seems to play an important role in the development of diabetes and its late complications. Both genetic and environmental factors, such as diet, physical inactivity, smoking and stress are responsible for the activation and intensity of chronic inflammation."
The relationship of periodontal disease to cardiovascular diseases--review of literature. (J Pak Med Assoc. 2006) "A chronic oral infection such as periodontitis is a constant potential source of infection and has now been considered as a separate risk factor for cardiovascular diseases, cerebrovascular diseases, peripheral arterial disease and respiratory diseases as well as delivery of low-birth-weight infants. The possible pathways linking oral infections to systemic diseases are metastatic infections, bacterial endotoxins, and systemic vascular injury. People with a history of periodontal disease and/or tooth loss were found at higher risk for Peripheral arterial disease (PAD) as compared to those without periodontal disease and/or tooth loss."
Inflammation and cardiovascular disease mechanisms. (Am J Clin Nutr. 2006) "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. … we now understand that at least some of the cardiovascular benefits attributable to medical treatment and lifestyle modification (diet and physical activity) may result from reductions in inflammatory processes."
Inflammation, atherosclerosis, and stroke. (Neurologist. 2006) "BACKGROUND:: Inflammation has received increasing attention in recent years as a cause of atherosclerosis, coronary artery disease, and stroke. Basic and animal research has implicated inflammatory mechanisms in the pathogenesis and progression of atherosclerosis, as well as in clinical events related to plaque rupture and other atherothrombotic events. … CONCLUSION:: Inflammatory biomarkers, especially hsCRP, may allow improved prediction of the risk of stroke in primary and secondary stroke prevention. Modalities to reduce inflammation are becoming available that may help to modify this risk. Further studies, however, are needed before inflammatory markers become a routine part of the evaluation of stroke patients."
Inflammation and prostate cancer. (Can J Urol. 2006) "There is emerging evidence that prostate inflammation may contribute to prostatic carcinogenesis. Chronic inflammation has been associated with the development of malignancy in several other organs such as esophagus, stomach, colon, liver and urinary bladder. Inflammation is thought to incite carcinogenesis by causing cell and genome damage, promoting cellular turnover, and creating a tissue microenvironment that can enhance cell replication, angiogenesis and tissue repair. Epidemiological data have correlated prostatitis and sexually transmitted diseases with an increased risk of prostate cancer and intake of anti-inflammatory drugs and antioxidants with a decreased risk."
Inflammation in Atherosclerosis (Circulation. 2006) "Accumulating evidence supports a central role for inflammation in preclinical atherosclerosis, with acute coronary syndrome (ACS) as a principle clinical expression.4 Indeed, ACS, ischemic brain syndrome (stroke/transient ischemic attack), and peripheral arterial occlusion1–4 result from a chronic inflammatory process, as well as disorders of lipid metabolism, modified by genetic and environmental factors. Arterial wall function and structure are modulated by interactions between injurious agents, blood vessel wall elements and monocytes, T lymphocytes, and platelets. Invading mononuclear cells release enzymes (eg, matrix metalloproteinases [MMPs]) that degrade collagen and elastin, thereby allowing cells to invade by disrupting matrix layers that otherwise stabilize developing plaque … Clot forming and inflammatory pathways then work in tandem to accelerate local macrophage and T-cell activation, which contributes to plaque erosion or rupture, forming a surface on which activated platelets may initiate thrombosis and microembolism and perhaps lead to continuing inflammation."
Causes And Triggers Of Asthma: Understanding Inflammation
Association Between Circulating White Blood Cell Count and Cancer Mortality (Arch Intern Med. 2006) "Background Inflammatory processes are implicated in the development and progression of cancer. However, it is not clear whether systemic markers of inflammation predict cancer. We examined the prospective relationship between circulating white blood cell (WBC) count and cancer mortality. … Conclusion These data provide new epidemiological evidence of an association between circulating WBC count, a widely available marker of inflammation, and subsequent cancer mortality."
The Evolving Role of High-Sensitivity C-Reactive Protein in Cardiovascular Health: An Expert Interview With Paul M. Ridker, MD "The bottom line is that hs-CRP levels less than 1, 1 to 3, and greater than 3 mg/L generally correlate with low, moderate, and higher cardiovascular risk across the full spectrum of the Framingham Risk Score. If we can use this information to better inform our patients of risk and motivate them to live healthier lives -- in particular to increase exercise levels, reduce food intake, and stop smoking -- we will in turn be improving the health of many, many individuals."
Functional decline in patients with and without peripheral arterial disease: predictive value of annual changes in levels of C-reactive protein and D-dimer.
(J Gerontol A Biol Sci Med Sci. 2006) "BACKGROUND: Inflammation may be a potential mechanism of aging-related functional decline. We determined whether greater annual increases in levels of high sensitivity C-reactive protein (hsCRP) and D-dimer predicted greater decline in functioning among persons with and without lower extremity peripheral arterial disease (PAD). … CONCLUSION: These findings suggest that inflammation may play a role in functional decline in persons with and without PAD."
Combined Effects of Hemoglobin A1c and C-Reactive Protein on the Progression of Subclinical Carotid Atherosclerosis
(Stroke. 2006) "Conclusions— The combination of hyperglycemia and inflammation is associated with an advanced early carotid atherosclerosis progression and an increased risk of new vascular events in diabetic as well as nondiabetic subjects."
Association between dietary fiber and serum C-reactive protein (American Journal of Clinical Nutrition 2006) "Background: High sensitivity C-reactive protein (CRP) is a marker of acute inflammation recently recognized as an independent predictor of future cardiovascular disease and diabetes. The identification of modifiable factors, such as diet, that influence serum CRP concentrations may provide the means for reducing the risk of these diseases. … Conclusions: Our results suggest that dietary fiber is protective against high CRP, which supports current recommendations for a diet high in fiber."
Aerobic exercise, but not flexibility/resistance exercise, reduces serum IL-18, CRP, and IL-6 independent of beta-blockers, BMI, and psychosocial factors in older adults. (Brain Behav Immun. 2006) "Increased serum levels of inflammatory mediators have been associated with numerous disease states including atherosclerosis, Type II diabetes, hypertension, depression, and overall mortality. … In summary, we have observed that an aerobic exercise intervention can significantly reduce serum inflammatory mediators, but beta-adrenergic receptors and psychosocial factors do not appear to be involved."
Association among C-reactive protein, oxidative stress, and traditional risk factors in healthy Japanese subjects. (Int J Cardiol. 2006) "BACKGROUND: Inflammation and oxidative stress play a key role in the pathogenesis of atherosclerosis. This study was designed to examine the interrelationships among C-reactive protein (CRP), oxidative stress, and traditional cardiovascular risk factors. … CONCLUSIONS: CRP levels are associated not only with clinical cardiovascular risk factors but also with oxidative stress. There are significant interrelationships among inflammation, oxidative stress, and traditional cardiovascular risk factors."
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