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Oméga-3
Le petit abécédaire des oméga-3
Les quantités d'oméga-3 qu'il vous faut
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Posologie dans la thérapeutique et la guérison
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Essai capsules d'huile de poisson

Etudes sur les oméga-3 en version originale anglaise:
Alzheimer
Artériosclérose
Arthrite
Vue
Lipides sanguins, cholestérol, hypertonie
Rectocolite hémorragique, maladies intestinales
Dépression
Diabète sucré
Maladies de peau, névrodermite, psoriasis
Pontage coronarien
Infarctus du myocarde
Hyperactivité chez l'enfant
Capacités neurologiques et visuelles chez le jeune enfant
Sommeil chez le jeune enfant
Douleurs menstruelles
Migraines
Maladie de Crohn
Sclérose en plaques
Resténose sur ACTP
Rhumatismes
Formation de tumeurs: cancer de l'œsophage, cancer du sein, cancer du gros intestin

Kompendium Omega-3: 6/2001
Omega-3
Omega-6
Arachidonsäure = Omega-6
Versorgung mit Omega-3
Empfehlung für Omega-3
Therapeutische Menge
Wirkung von Omega-3
Häufig gestellte Fragen
Toxizität
Fleischesser
Vegetarier
Kinder
Lebertran
Test: 9 Produkte im Vergleich
Info zum Thema Übersäuerung:
Säuren-Basen Haushalt
Übersäuerung
Test: 14 Basendrinks im Vergleich
Aufbau des Tests
Mineralgehalt
Bioverfügbarkeit
Geschmack
Gebrauchsanweisung
Deklaration
Testresultate
E-Nummer
Nebenwirkungen der
Lebensmittel-Zusatzstoffe
Aminosäuren
5HTP-Tryptophan
Melatonin
DACH-Referenzwerte
empfohlene Werte für Omega-3
empfohlene Werte für Vitamine
geschätzte Werte für Vitamine
Proteine
Glykämischer Index
Die blutzuckersteigernde Wirkung verschiedener Kohlenhydrate
Blutgruppendiät
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Übersäuerung

E-Nummer

Aminosäuren

DACH-Referenzwerte

Oméga-3: faits - thérapeutique et posologie

Rectocolite hémorragique (maladies du gros intestin): env. 5,6g/jour EPA et DHA
Les journaux spécialisés ont consacré aux oméga-3 les articles suivants. La liste de ces publications a été établie en avril 2003 et n'aspire nullement à l'exhaustivité. Source: MEDLINE.
Ces données servent de référence pour les médecins et les thérapeutes, de sorte à déterminer la dose thérapeutique dans le cadre de la rectocolite hémorragique.

Distal proctocolitis and n-3 polyunsaturated fatty acids (n-3 PUFAs): the mucosal effect in situ.
Almallah YZ: Department of Surgery, University of Aberdeen, United Kingdom; Ewen SW, El-Tahir A, Mowat NA, Brunt PW, Sinclair TS, Heys SD, Eremin O
J Clin Immunol 2000 Jan 20:68-76

Abstract
It has been postulated that patients with ulcerative colitis (UC) have altered reactivity of gut-associated lymphoid tissue. In such cases there is intense infiltration of the mucosa with immune competent cells and associated tissue damage. We have shown previously that the dietary supplementation with the n-3 polyunsaturated fatty acids (n-3 PUFAs), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) results in significant systemic immune suppression. The aim of this study, therefore, was to evaluate the in situ effect of n-3 PUFAs on distal proctocolitis. Each patient received either fish oil extract (EPA 3.2 g, DHA 2.4 g) (n = 9) or sunflower oil (n = 9) daily in a double blind manner for six months. Monthly assessment included: (1) disease activity using clinical, sigmoidoscopic, and histological scores and (2) immunohistochemical analysis (immunoglobulins, CD profiles) of rectal biopsy specimens (before and after six months supplementation) using monoclonal antibodies and quantitative computer-assisted video image analysis. Prior to receiving supplementation, patients with proctocolitis (n = 18) showed significantly higher numbers of cells expressing CD3 (pan T cells) and HLA-DR and IgM containing cells compared with non-colitic controls (n = 8). Six months supplementation with n-3 PUFAs resulted in significant reduction in the number of cells expressing CD3 and HLA and the percentage of cells containing IgM. There was no significant change in the CD20 nor the percentage of IgG or IgA containing cells in either group of patients with procto-colitis. In patients receiving n-3 PUFA supplementation, there was improvement in the disease activity and histological scores, compared with pretreatment evaluation. This study has demonstrated both evidence of suppression of in situ immune reactivity and concurrent reduction in disease activity in patients with proctocolitis receiving n-3 PUFA supplementation. This may have important implication for therapy in patients with ulcerative colitis.

Polyunsaturated fatty acids and inflammatory diseases.
Gil A: Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de Granada, Spain
Biomed Pharmacother 2002 Oct 56:388-96
Abstract
Inflammation is overall a protective response, whose main goal is to liberate the human being of cellular lesions caused by micro-organisms, toxins, allergens, etc., as well as its consequences, and of death cells and necrotic tissues. Chronic inflammation, which is detrimental to tissues, is the basic pathogenic mechanism of hypersensitivity reactions against xenobiotics. Other frequent pathologies, for instance atherosclerosis, chronic hepatitis, inflammatory bowel disease (IBD), liver cirrhosis, lung fibrosis, psoriasis, and rheumatoid arthritis are also chronic inflammatory diseases. Chemical mediators of inflammation are derived from blood plasma or different cell-type activity. Biogenic amines, eicosanoids and cytokines are within the most important mediators of inflammatory processes. The different activities of eicosanoids derived from arachidonic acid (20:4 n-6) versus those derived from eicosapentaenoic acid (20:5 n-3) are one of the most important mechanisms to explain why n-3, or omega-3, polyunsaturated fatty acids (PUFA) exhibit anti-inflammatory properties in many inflammatory diseases. Dietary supplements ranging 1-8 g per day of n-3 PUFA have been reportedly beneficial in the treatment of IBD, eczema, psoriasis and rheumatoid arthritis. In addition, recent experimental studies in rats with experimental ulcerative colitis, induced by intrarectal injection of trinitrobenzene sulphonic acid, have documented that treatment with n-3 long-chain PUFA reduces mucosal damage as assessed by biochemical and histological markers of inflammation. Moreover, the defence antioxidant system in this model is enhanced in treated animals, provided that the n-3 PUFA supply is adequately preserved from oxidation..

Distal procto-colitis and n-3 polyunsaturated fatty acids: the mechanism(s) of natural cytotoxicity inhibition.
Almallah YZ: Department of Surgery, University of Aberdeen, UK; El-Tahir A, Heys SD, Richardson S, Eremin O
Eur J Clin Invest 2000 Jan 30:58-65
Abstract
BACKGROUND: Altered natural killer (NK) and lymphokine-activated killer (LAK) cell activities have been reported with ulcerative colitis (UC). Previously, we have shown that in patients with UC, the n-3 polyunsaturated fatty acids (PUFAs), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), specifically inhibit natural cytotoxicity with clinical improvement in disease activity. The aim of this study therefore was to evaluate the possible mechanism(s) involved in this inhibition, and in particular the alteration of production of interleukin 2 (IL2) and the arachidonic acid metabolite leukotriene B4 (LTB4), both known to modulate NK cell activity. MATERIALS AND METHODS: Each patient with procto-colitis received either fish oil extract (EPA 3.2 g, DHA 2.4 g; n = 9) or placebo (n = 9) daily for 6 months. Monthly assessment included disease activity using clinical and sigmoidoscopic scores. Peripheral blood mononuclear (PBMN) cells were isolated and NK cell cytotoxic activity in vitro was measured. Monthly serum samples were analysed for LTB4, IL2 and soluble IL2 receptors (sIL2R). RESULTS: The n-3 PUFAs group had significantly reduced NK cell activity, compared with the placebo group (P < 0.05, Mann-Whitney U-test). In the n-3 PUFA group, incubation of PBMN cells for 72 h with recombinant interleukin 2 (rIL2) reversed the NK inhibition. In patients with active proctocolitis, serum levels of LTB4 correlated positively with NK cell cytotoxicity (r = 0.873, P < 0.05, Kendall's correlation coefficient). After six months of n-3 PUFAs supplementation, serum levels of LTB4 were undetectable with concurrent significant reduction in NK cell cytotoxic activity. The latter was associated with significant reduction of serum IL2 and sIL2R levels (P < 0.05). CONCLUSION: This study has demonstrated both evidence of suppression of immune reactivity and concurrent reduction in disease activity in patients with proctocolitis receiving n-3 PUFAs supplementation. This may have important implications for therapy in patients with UC.

Plasma and mucosal fatty acid pattern in colectomized ulcerative colitis patients.
Esteve M: Department of Gastroenterology, Hospital Universitari Germans Trias i Pujol, Badalona, Catalonia, Spain; Navarro E, Klaassen J, Abad-Lacruz A, Gonzalez-Huix F, Cabre E, Ramos E, Condom E, Fernandez-Bajares F, Pastor C, Humbert P, Marte-Rague J, Gassull MA
Dig Dis Sci 1998 May 43:1071-8
Abstract
Patients with inflammatory bowel disease (IBD) have increased plasma n3 polyunsaturated fatty acids (PUFAs), which in ulcerative colitis (UC) patients persists six months after colectomy, suggesting a primary abnormality in fatty acid (FA) metabolism in IBD. This finding needed to be confirmed in a larger series of UC long-term colectomized patients. We aimed to assess the plasma FA pattern in UC colectomized patients with either Brooke's ileostomy (UC-BI) or ileal pouch anal anastomosis (UC-IPAA) and the mucosal FA pattern in the ileal reservoir of the UC-IPAA patients. Plasma FAs were assessed in 63 UC colectomized patients (31 with BI and 32 with IPAA) and 30 controls. In 26 UC-IPAA (8 with pouchitis and 18 without pouchitis) and in 13 healthy controls gut mucosal FAs were also investigated. FAs were detected by capillary column gas-liquid chromatography. Increased levels of saturated fatty acids (SFAs) and decreased percentages of monounsaturated fatty acids (MUFAs) were observed in both groups of patients. There were no changes in plasma n3 and n6 PUFAs. The mucosal FA pattern of the ileal reservoir consisted of increased long-chain PUFAs, specially n6 PUFA, and a decrease of their essential precursors. High percentages of SFAs and low percentages of MUFAs were also seen. The plasma FA profile previously described in IBD is not observed long-term after colectomy in UC, suggesting that it is related with the presence of inflamed intestine. High concentrations of SFAs and decreased percentages of MUFAs might represent early events in disturbed FA metabolism in IBD. The changes in FAs of the ileal reservoir, which closely resemble those found in human and experimental IBD, probably represent a common pattern of intestinal inflammation.

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