Inflammation acids, dietary

Tate G, Mandell BF, Laposata M, Ohliger D, Baker DG, et al. 1989. Suppression of acute and chronic inflammation by dietary y-linolenic acid. J. Rheumatol. 16 1729-36... 

Hyperuricemia may be produced by overproduction of uric acid or under-excretion of uric add by the kidneys. Kyperuricemia may progress to acute and chronic gouty arthritis if uric acid (monosodium urate) is deposited in joints and surrounding soft tissue, where it causes inflammation, Uric add is produced from excess endogenous purines as shown in Figure 1-18-5, and is also produced from dietary purines (digestion of nucleic acid in the intestine) by intestinal epithe-lia. Both sources of uric acid are transported in the blood to the kidneys for excretion in urine. 

CN202 Kozak, W., D. Soszynski, K. Rudolph, C. A. Conn, and M. J. Kluger. Dietary n-3 fatty acids differentially affect sickness behavior in mice during local and systemic inflammation. Am J Physiol 1997 272(4 Pt. 2) 1298-1307. 

The toxicity of aluminum has been recognized most clearly by the development of bone disease caused by deposition of A1 in bones of patients on hemodialysis and in infants on intravenous therapy/ 6 Excessive A1 in the water used for dialysis may also cause brain damage. Dietary aluminum may be one cause of Alzheimer s disease/ h but this is controversial as is a possible role of aluminum in vaccines in causing inflammation in muscle.1) Solubilization of soil aluminum by acid rain has been blamed for the decline of forests in Europe and North America,) for the death of fish in acid waters,k and for very large reductions in yield for many crops/ An aluminum-resistant strain of buckwheat makes and secretes from its roots large amounts of oxalate which binds and detoxifies the Al3+ ions. ... 

Inflammation is now recognized as a key process in atherogenesis [Libby, 2002]. The potential for dietary flavonoids to inhibit inflammatory activities is of particular interest. A potential anti-inflammatory feature of the flavonoids is the ability to inhibit the biosynthesis of eicosanoids. Selected phenolic acids and some flavonoids have been shown to inhibit both cyclooxygenase (COX) and 5-lipoxygenase (5-LO) pathways [Nijveldt et al., 2001 Takano-Ishikawa et al., 2006], Epicatechin and related flavonoids have been shown to inhibit the synthesis of pro-inflammatory cytokines in vitro [Sanbongi et al., 1997], and plasma metabolites of catechin and quercetin inhibit the adhesion of monocytes to cultured endothelial cells [Koga and Meydani, 2001]. Silymarin has been shown to inhibit the production of inflammatory cytokines, such as interleukin-1, interferon-, and tumor necrosis factor-a (TNFa), from macrophages and T-cells [Matsuda et al., 2005], Some flavonoids can inhibit neutrophil... 

In addition to dietary sources, a significant amount of nitrate is formed endogenously by the metabolism of nitric oxide - 1 mg per kg of body weight per day (about the same as the average dietary intake), increasing 20-fold in response to inflammation and immune stimulation. There is considerable secretion of nitrate in saliva, and up to 20% of this may be reduced to nitrite by oral bacteria. Under the acidic conditions of the stomach, nitrite can react with amines in foods to form carcinogenic N-nitrosamines, although it is not known to what extent this occurs in vivo. 

Mozaffarian D, Kschon T, Hankinson SE, Rifai N, Joshipura K, Willett WC, Rimm EB. Dietary intake of trans fatty acids and systemic inflammation in women. Am. J. Clin. Nutr. 2004 79 606-612. 

Numerous animal and human studies suggest that dietary cholesterol and certain saturated fatty acids increase serum as well as LDL-cholesterol concentrations. Even though humans with elevated serum cholesterol levels may be at risk, evidence also is mounting to suggest that the complicated processes that occur during atherosclerosis involve not only the participation of modified lipoproteins, but also low level and chronic inflammation and related disorders of the immune... 

Crohn s disease involves inflammation of the gut. Us cause is not known, but evidence suggests that infection with Mifcobactefium paraluberculosis may be a contributing factor (Herm on-Taylor, 1993). The inflammation results in steatorrhea, diarrhea, abdominal pain, and weight loss. Crohn s disease is usually treated with drugs (corticosteroids), but it may also be treated by the elimination of a normal diet and its replacement with an elemental diet. The elemental diet consists of oligosaccharides, amino acids, and short-chain faltj acids. This diet is not very palatable, but it can result in relief of symptoms and a reduction in inflammation of the intestines. Two weeks of dietary treatment may be sufficient to allow inflammation to subside (Lochs et iJt., 1991). 

Chapkin, R., McMurray, D., and Jolly, C. 2000. Dietary n-3 polyunsaturated fatty acids modulate T-lymphocyte activation Clinical relevance in treating diseases of chronic inflammation. InNutrition and immunology, ed. C. Keen, 121-34. Totowa, NJ Humana Press. 

Dietary intake of n-6 fatty acids such as linoleic acid, and n-3 fatty acids, such as the fish oils eicosapentanoic acid and docosahexaenoic acid, lowers plasma cholesterol and antagonizes platelet activation, but the fish oils are much more potent in this regard [26]. In particular, n-3 fatty acids competitively inhibit thromboxane synthesis in platelets but not prostacyclin synthesis in endothelial cells. These fatty acids have also been shown to have other potentially anti-atherogenic effects, such as inhibition of monocyte cytokine synthesis, smooth muscle cell proliferation, and monocyte adhesion to endothelial cells. While dietary intake of n-3 fatty acid-rich fish oils appears to be atheroprotective, human and animal dietary studies with the n-6 fatty acid linoleic acid have yielded conflicting results in terms of effects on both plasma lipoproteins and atherosclerosis. Indeed, excess amounts of both n-3 and n-6 fatty acids may actually promote oxidation, inflammation, and possibly atherogenesis (M. Toberek, 1998). In this context, enzymatic and non-enzymatic oxidation of linoleic acid in the sn-2 position of LDL phospholipids to 9- and 13-hydroxy derivatives is a key event in LDL oxidation (Section 6.2). 

Ln recent years, interest increased in the ratio of omega-6 (n-6) to omega-3 (n-3) PUFA, or LA ALA, in part due to the link between inflammation and several lifestyle diseases, such as cardiovascular disease (CVD) and Type LL diabetes. However, whether this ratio is directly associated with an increased risk of inflammatory diseases is unclear. Furthermore, the low conversion of dietary ALA to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (Goyens et al., 2005 Hussein et al., 2005 Pawlosky et al., 2001) means that a lower n-6 n-3 PUFA ratio does not necessarily reflect physiologically important increases in EPA and DLiA (Harris, 2006). Consequently, evaluating absolute dietary intakes of specific n-6 and n-3 PUFAs may be most appropriate, particularly when few human experimental and clinical trial data exist to support the use of an n-6 n-3 PUFA ratio. Nevertheless, when considering the composition of SBO, notably, SBO has a lower n-6 n-3 PUFA ratio than other commonly used vegetable oils, such as corn oil. 

Baer, D.J. J.T. Judd B.A. Clevidence R.P. Tracy. Dietary fatty acids affect plasma markers of inflammation in healthy men fed controlled diets A randomized crossover study. Am. J. Clin. Nutr. 2004, 79, 969-973. 

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