This study suggests that curcuminoids inhibit lipoxygenase and cyclo-oxygenase enzymes, and also act as an antioxidant. In a paw edema model, it was found that among natural curcuminoids, curcumin III was the most effective anti- inflammatory agent, inhibiting 86.8% of the mice paw edema at a concentration of 50 mg/kg body weight. Curcumin I and curcumin II produced an inhibition of 72.4% and 65.1%, respectively, at the same concentration. Among synthetic curcuminoids, salicyl, veratryl and piperonal inhibited inflammation by 63.0%, 62.6% and 61.1%, respectively.
Anto, Ruby John, et al: Anti-Inflammatory Activity of Natural and Synthetic Curcuminoids, Pharm. Pharmacol. Commun., 1998;4:103-106.
Arachidonic Acid (Inflammation)
Data on the effect of dietary arachidonic acid (AA) (20:4n-6) on the synthesis of thromboxane and prostacyclin (PGI2) in humans are lacking.
Both the metabolites of thromboxane and PGI2 increase on the high-AA diet. Furthermore, both indicated changes in metabolite excretion may be associated with measurable effects on several physiologically significant cellular functions, such as platelet aggregation in vivo and inflammation in response to immune challenges.
Ferretti A et al., Increased dietary arachidonic acid enhances the synthesis of vasoactive eicosanoids in humans. Lipids, 1997 Apr, 32:4, 435-9.
Evaluated the rationale behind the most commonly used treatments of osteoarthritis, including nonsteroidal anti-inflammatory drugs (NSAIDs), and to assess more effective conservative treatment options.
The rationales for using NSAIDs in the treatment of osteoarthritis is controversial and openly contested. Given the detrimental effects of NSAIDs on joints and other organs, their use should be discouraged and their classification as a first choice conservative treatment should be abolished.
An effective and conservative approach to the treatment of osteoarthritis should include chiropractic manipulation, essential nutrient supplementation, exogenous administration of glucosamine sulfate and rehabilitative stretches and exercises to maintain joint function.
NSAIDs should be limited to the treatment of gross inflammation and analgesics should only be used in the short-term when absolutely necessary for pain palliation.
Gottlieb MS: Conservative management of spinal osteoarthritis with glucosamine sulfate and chiropractic treatment. J Manipulative Physiol Ther, 1997 Jul-Aug, 20:6, 400-14.
During "stress" or inflammation there is a reduction in "zinc" concentrations of certain tissues and a redistribution of zinc internally(mainly to the "liver", which may be due to the need for acute phase "proteins"). "Serum" "copper" is increased during acute phase response where zinc is reduced.
The increased serum copper is due to the increased production of ceruloplasmin, the major copper binding "protein". Thermal injury patients do not follow this characteristic pattern of elevated copper and in fact have a reduction in serum copper concentrations. This is probably due to the cutaneous absorption of topically applied silver sulfadiazine, which alters copper "metabolism" through inhibition of ceruloplasmin production.
"Minerals and Inflammatory Response", McClain, C.J., et al, Journal of the American College of Nutrition, October 1992;11(5):598/Abstract 4.
Inflammatory Bowel Disease (IBD) (1)
Inflammatory Bowel Disease (IBD) (1)
The effect of environmental factors has been demonstrated in the pathogenesis of inflammatory bowel disease (IBD). Nutrition may be one of them.
Investigated the pre-illness diet in patients with recent IBD in comparison with matched population and clinic controls.
A high sucrose consumption was associated with an increased risk for IBD. Lactose consumption showed no effect while fructose intake was negatively associated with risk for IBD (NS). Similar trends were noted in Ulcerative Colitis and Crohn's Disease.
A high fat intake was associated with an increased risk for Ulcerative Colitis; this was particularly marked for animal fat and cholesterol.
A high intake of fluids, magnesium, vitamin C, and fruits (NS) was negatively associated with the risk for IBD, while a positive association was found for retinol.
Reif S et all., Pre-illness dietary factors in inflammatory bowel disease. Gut, 1997 Jun, 40:6, 754-60.
Inflammatory Bowel Disease (2)
Inflammatory Bowel Disease (2)
It has never been convincingly documented that food sensitivity is of pathogenetic importance in chronic inflammatory bowel disease. However, many patients may relate their gastrointestinal symptoms to specific food items ingested and may restrict their diet accordingly.
Of patients in the study: (# 53) (41%) had Crohn's disease (CD), 69 (53%) ulcerative colitis (UC), and 8 (6%) unclassified colitis.
65% of the patients and 14% of the controls reported being intolerant to one or more food items. The intolerance covered a wide range of food products. The commonest symptoms among patients were diarrhoea, abdominal pain, and meteorism and among controls, regurgitation.
Food intolerance was equally common in CD (66%) and UC (64%) and was not related to previous operation, disease activity or disease location.
Most patients with chronic inflammatory bowel intolerance disease feel intolerant to different food items and may restrict their diet accordingly. The frequency and pattern of food intolerance did not differ between patients with CD and UC. The food intolerance was probably unspecific rather than of pathogenetic importance.
Ballegaard M et al., Self-reported food intolerance in chronic inflammatory bowel disease. Scand J Gastroenterol, 1997 Jun, 32:6, 569-71.
Intestinal Nutrient Transport
Intestinal Nutrient Transport
The physiology of glucose transport with specific emphasis on transporters of the brush border membrane (BBM) and the basolateral membrane (BLM). On the BBM, the sodium (Na)/glucose transporters (SGLT1 and SGLT2), the Na-independent transporter (GLUT5) and on the BLM the hexose transporter (GLUT2) are discussed. The molecular biology of these transporters is also reviewed.
Also discuss the manner in which intestinal adaptation may be modified by alterations in the diet, especially the lipid constituents, and two important examples of intestinal adaptation will be given: diabetes mellitus and inflammatory bowel disease.
Thomson AB & Wild G: Adaptation of intestinal nutrient transport in health and disease. Part II. Dig Dis Sci, 1997 Mar, 42:3, 470-88.
"Niacin" or "vitamin B3" deficiency can result in glossitis, stomatitis, "insomnia", "anorexia", weakness, "irritability", abdominal "pain", forgetfulness
"Skin Signs of Nutritional Disorders", Prendiville, Julie S. and Manfredi, Liliana N.., Seminars in Dermatology, March 1992; 11 (1):88-97.
It is generally thought that nonsteroidal anti-inflammatory medications (NSAIDs) are inhibitors of "prostaglandin" synthesis. The NSAIDs[ sulfasalazine, sulindac, "indomethacin", "naproxen", "salicylic acid", "ibuprofen", piroxicam and mefenamic acid] are competitive inhibitors of "folate" dependent "enzymes". In contrast, "aspirin" and the "antipyretic" "analgesic" drugs acetaminophen and antipyrine are weak inhibitors of these enzymes. (Aspirin exerts its anti-inflammatory effect after it is converted into salicylic acid, which has greater antifolate activity than its parent compound.)
"Inhibition of Folate-Dependent Enzymes by Nonsteroidal Anti-Inflammatory Drugs", Baggott, Joseph E., et al, Biochemistry Journal, 1992;282:197-202.
The rationale for nutritional therapy is that inflammation during these clinical situations is from activated macrophages. It is hypothesized that N-3 "unsaturated fatty acids" would decrease prostaglandin E2 and cytokine release, and stimulate the T "cell" proliferative response. "Arginine" and "RNA" directly stimulate T cell proliferative responses. These "nutrients" are being tried in human models with encouraging results.
"Nutrient Modulation of Inflammatory and Immune Response", Cerra, Frank B., MD, et al, The American Journal of Surgery, February 1991;161:230-234.
Systemic Inflammatory Response Syndrome
Systemic Inflammatory Response Syndrome (SIRS)
Reviews the "metabolic" alterations that occur in SIRS and "sepsis" and the management of these patients nutritionally.
Practical clinical assessment parameters are presented. Issues related to enteral and "parenteral" routes of "delivery" and disease-specific nutritional formulas are discussed. An understanding of the determination of metabolic and nutrition needs and the provision of adequate support to meet those needs are vital to the care of the "hypermetabolic" "septic" patient.
Systemic inflammatory response syndrome, sepsis, and nutritional support. Ackerman-MH; Evans-NJ; Ecklund-MM. Crit-Care-Nurs-Clin-North-Am. 1994 Jun; 6(2): 321-40.
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