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Dr maldiney pierre: cardiologue, gérontologue, médecin morphologue et anti âge Micronutrition et longévité: lintestin et le foie au quotidien.

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Présentation au sujet: "Dr maldiney pierre: cardiologue, gérontologue, médecin morphologue et anti âge Micronutrition et longévité: lintestin et le foie au quotidien."— Transcription de la présentation:

1 Dr maldiney pierre: cardiologue, gérontologue, médecin morphologue et anti âge Micronutrition et longévité: lintestin et le foie au quotidien

2 AU COURS DU 20 E SIECLE, LES MALADIES ONT BEAUCOUP EVOLUEES Les troubles de santé rencontrés actuellement : Ne sont pas liés a une cause spécifique, mais sont multifactoriels comme origine : innadéquation entre GENES et ENVIRONNEMENT Ce qui provoquent une altération des réserves fonctionnelles (fatigue psychique,physique;troubles digestifs......) Et créent le terrain propice a léclosion des maladies de civilisation(maladies chroniques) et au vieillissement prématuré Environnement alimentaire inadapté… Réponses cellulaires perturbées

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4 INFLAMMATION NFKb Cancer Maladies Cardiovasculaires Alzheimer Diabète de Type II Maladies Auto-Immunes Allergies Parkinson Maladies Pulmonaires

5 Deux Mécanismes Majeurs du Vieillissement Oxydation Rouillage Glycation Caramélisation

6 Le tube Digestif et en particulier lintestin est le système le plus vulnérable de notre organisme Cest par lui que naissent la plupart des maladies chroniques

7 Barrière Intestinale 6197 publications /2012

8 INFLAMMATIONPATHOLOGIQUEINFLAMMATIONPATHOLOGIQUE Pourquoi ? Pourquoi ?

9 Défense NIVEAU I Les Barriéres NIVEAU II Immunité Innée NIVEAU III Immunité Spécifique

10 Prise en Charge Micronutritionnelle des Maladies CHRONIQUES donc des infections chroniques a bas bruit!! lApproche Pratique

11 1.Anamnése fouillée Contrôle Nutritionnel des Maladie Dysimmunitaires 2.Bilan Nutritionnel 3.Contrôle Nutritionnel

12 1.Anamnése fouillée Contrôle Nutritionnel

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15 Stress

16 2.Bilan Nutritionnel Vitamine D Evaluation du Tube Digestif: IGG /MOU Nutribilan (acides gras, Zn, CU,SE…) Contrôle Nutritionnel

17 Chiara G. 15/02/1971 Statut IgG Alimentaires

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20 Statut Acides Organiques Urinaires

21 Le Tube digestif Travail à la Chaîne

22 Dégrader les aliments en molécules assimilables Absorber les molécules nutritives Détruire lidentité antigénique des polymères et empêcher la pénétration de micro-organismes, macromolécules et composés toxiques. Buts de la digestion

23 Rôle clé de la Mastication!

24 Relationship of number of remaining teeth to health-related quality of life in community-dwelling elderly. Akifusa S, Soh I, Ansai T, Hamasaki T, Takata Y, Yohida A, Fukuhara M, Sonoki K,Takehara T. Department of Preventive Dentistry, Kyushu Dental College, Fukuoka, Japan. Gerodontology Jun;22(2):91-7. OBJECTIVE: The aim of this study was to evaluate the relationship between number of remaining teeth and health-related quality of life in community- dwelling elderly. SUBJECTS: A total of 207 participants who were community-dwelling, 85 years of age. Data were from a population-based study of age- related general and oral health in Fukuoka Prefecture, Japan. MEASUREMENTS: The Japanese version of the Short Form 36 Health Survey (SF-36). RESULTS: The mental component score for the participants, from the SF-36, was higher than the Japanese national norm for those aged > or = 70 years. There were no significant differences in the mean of any scores on the SF-36 by having spouse, living with family, or education level. The mean of the SF-36 scores of physical functioning (PF) and of the physical component scores were significantly higher in the 85-year-old participants with > or = 20 teeth than in those with or = 20 teeth and those with or = 20 teeth had better subjective physical health than those with < or = 19 teeth. CONCLUSIONS: Cette étude indique que les participants âgés de 85 ans avec 20 dents ou + ont une meilleure santé physique subjective que ceux avec 19 dents ou +. Relation entre nombre de dents restantes et qualité de vie liée à la santé dans une maison de retraite pour personnes âgées. Akifusa S, Soh I, Ansai T, Hamasaki T, Takata Y, Yohida A, Fukuhara M, Sonoki K,Takehara T. Department of Preventive Dentistry, Kyushu Dental College, Fukuoka, Japan. Gerodontology 2005 Jun;22(2):91-7.

25 Rôle clé de la Digestion! Effets néfastes des IPP, AI, AB….

26 CONCLUSIONS:augmentation de la dysbiose pendant traitement par IPP

27 Proton pump inhibitors exacerbate NSAID-induced small intestinal injury by inducing dysbiosis. Wallace JL, Syer S, Denou E, de Palma G, Vong L, McKnight W, Jury J, Bolla M, Bercik P, Collins SM, Verdu E, Ongini E. Gastroenterology Oct;141(4): , 1322.e1-5. BACKGROUND & AIMS: Proton pump inhibitors (PPIs) and nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most commonly used classes of drugs, with the former frequently coprescribed to reduce gastroduodenal injury caused by the latter. However, suppression of gastric acid secretion by PPIs is unlikely to provide any protection against the damage caused by NSAIDs in the more distal small intestine. METHODS: Rats were treated with antisecretory doses of omeprazole or lanzoprazole for 9 days, with concomitant treatment with anti-inflammatory doses of naproxen or celecoxib on the final 4 days. Small intestinal damage was blindly scored, and changes in hematocrit were measured. Changes in small intestinal microflora were evaluated by denaturing gradient gel electrophoresis and reverse-transcription polymerase chain reaction. RESULTS: Both PPIs significantly exacerbated naproxen- and celecoxib-induced intestinal ulceration and bleeding in the rat. Omeprazole treatment did not result in mucosal injury or inflammation; however, there were marked shifts in numbers and types of enteric bacteria, including a significant reduction ( 80%) of jejunal Actinobacteria and Bifidobacteria spp. Restoration of small intestinal Actinobacteria numbers through administration of selected (Bifidobacteria enriched) commensal bacteria during treatment with omeprazole and naproxen prevented intestinal ulceration/bleeding. Colonization of germ-free mice with jejunal bacteria from PPI-treated rats increased the severity of NSAID-induced intestinal injury, as compared with mice colonized with bacteria from vehicle-treated rats. CONCLUSIONS: PPIs exacerbate NSAID-induced intestinal damage at least in part because of significant shifts in enteric microbial populations. Prevention or reversal of this dysbiosis may be a viable option for reducing the incidence and severity of NSAID enteropathy.

28 DUALITE FONCTIONNELLE DE LA MUQUEUSE INTESTINALE Absorption des nutriments Barrière aux toxines, macromolécules et microorganismes

29 Molécules et Nutriments Nécessaires pour une Muqueuse Intestinale Fonctionnelle Prostaglandine PGI2 L-Glutamine n-Butyrate Zinc

30 Butyrate: implications for intestinal function. Leonel AJ, Alvarez-Leite JI. Curr Opin Clin Nutr Metab Care Jul 12. PURPOSE OF REVIEW: Butyrate is physiologically produced by the microbial fermentation of dietary fibers and plays a plurifunctional role in intestinal cells. This review examines the recent findings regarding the role and mechanisms by which butyrate regulates intestinal metabolism and discusses how these findings could improve the treatment of several gastrointestinal disorders. RECENT FINDINGS: Butyrate is more than a primary nutrient that provides energy to colonocytes and acts as a cellular mediator in those cells through several mechanisms. One remarkable property of butyrate is its ability to inhibit histone deacetylases, which is associated with the direct effects of butyrate and results in gene regulation, immune modulation, cancer suppression, cell differentiation, intestinal barrier regulation, oxidative stress reduction, diarrhea control, visceral sensitivity and intestinal motility modulation. All of these actions make butyrate an important factor for the maintenance of gut health. SUMMARY: From studies published over 30 years, there is no doubt of the important role that butyrate plays in maintaining intestinal homeostasis. However, despite these effects, clinical studies are still required to validate the routine use of butyrate in clinical practice and, specifically, in the treatment of intestinal diseases.!!!

31 Mechanisms of disease: the role of intestinal barrier function in the pathogenesis of gastrointestinal autoimmune diseases. Fasano A, Shea-Donohue T. Nat Clin Pract Gastroenterol Hepatol Sep;2(9): The primary functions of the gastrointestinal tract have traditionally been perceived to be limited to the digestion and absorption of nutrients and electrolytes, and to water homeostasis. A more attentive analysis of the anatomic and functional arrangement of the gastrointestinal tract, however, suggests that another extremely important function of this organ is its ability to regulate the trafficking of macromolecules between the environment and the host through a barrier mechanism. Together with the gut-associated lymphoid tissue and the neuroendocrine network, the intestinal epithelial barrier, with its intercellular tight junctions, controls the equilibrium between tolerance and immunity to nonself-antigens. When the finely tuned trafficking of macromolecules is dysregulated in genetically susceptible individuals, both intestinal and extraintestinal autoimmune disorders can occur. This new paradigm subverts traditional theories underlying the development of autoimmunity, which are based on molecular mimicry and/or the bystander effect, and suggests that the autoimmune process can be arrested if the interplay between genes and environmental triggers is prevented by re-establishing intestinal barrier function. Understanding the role of the intestinal barrier in the pathogenesis of gastrointestinal disease is an area of translational research that encompasses many fields and is currently receiving a great deal of attention. This review is timely given the increased interest in the role of a 'leaky gut' in the pathogenesis of gastrointestinal diseases and the advent of novel treatmen strategies, such as the use of probiotics. Together with the gut-associated lymphoid tissue and the neuroendocrine network, the intestinal epithelial barrier, with its intercellular tight junctions, controls the equilibrium between tolerance and immunity to nonself-antigens. When the finely tuned trafficking of macromolecules is dysregulated in genetically susceptible individuals, both intestinal and extra-intestinal autoimmune disorders can occur. strategies, such as the use of probiotics.

32 Leaky gut and autoimmune diseases. Fasano A. Clin Rev Allergy Immunol Feb ;42(1):71-8. Autoimmune diseases are characterized by tissue damage and loss of function due to an immune response that is directed against specific organs. This review is focused on the role of impaired intestinal barrier function on autoimmune pathogenesis. Together with the gut-associated lymphoid tissue and the neuroendocrine network, the intestinal epithelial barrier, with its intercellular tight junctions, controls the equilibrium between tolerance and immunity to non-self antigens. Zonulin is the only physiologic modulator of intercellular tight junctions described so far that is involved in trafficking of macromolecules and, therefore, in tolerance/immune response balance. When the zonulin pathway is deregulated in genetically susceptible individuals, autoimmune disorders can occur. This new paradigm subverts traditional theories underlying the development of these diseases and suggests that these processes can be arrested if the interplay between genes and environmental triggers is prevented by re-establishing the zonulin-dependent intestinal barrier function. Both animal models and recent clinical evidence support this new paradigm and provide the rationale for innovative approaches to prevent and treat autoimmune diseases.

33 Rôles de La Microflore colonique

34 Probiotiques 8392 publications /2012

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36 Le «Leaky Gut Syndrome» est probablement la cause méconnue principale de la majorité des maladies chroniques Vincent Castronovo

37 Hyperperméabilité intestinale = leaky gut Intestin en souffrance de labsorption passive de macromolécules, aliments mal digérés, molécules banales et inoffensives = antigènes déclenchement de la réponse immunitaire et inflammatoire. de labsorption des nutriments malnutrition qui va aggraver les perturbations structurelles et fonctionnelles.

38 CONSEQUENCES du Leaky Gut 1. Entrée massive dantigènes Phénomènes allergiques Phénomènes allergiques Maladies inflammatoires Maladies inflammatoires Maladies auto-immunes Maladies auto-immunes 2. Entrée de pathogènes Les Candidoses invasives Les Candidoses invasives Les Infections opportunistes Les Infections opportunistes 3. Entrée de toxines Mycotoxines altérant le fonctionnement cérébral générant des pulsions sucrées Surcharge des phases de la détoxication hépatique Surcharge des phases de la détoxication hépatique Fatigue consécutive à la dépense énergétique de leur prise en charge Fatigue consécutive à la dépense énergétique de leur prise en charge

39 Le Leaky gut Syndrome Dépression Obésité Colopathie Troubles hépatiques Troubles cardiaques Maladies auto- immunes Et bien plus encore….

40 Leaky gut and autoimmune diseases. Fasano A. Clin Rev Allergy Immunol Feb ;42(1):71-8. Autoimmune diseases are characterized by tissue damage and loss of function due to an immune response that is directed against specific organs. This review is focused on the role of impaired intestinal barrier function on autoimmune pathogenesis. Together with the gut-associated lymphoid tissue and the neuroendocrine network, the intestinal epithelial barrier, with its intercellular tight junctions, controls the equilibrium between tolerance and immunity to non-self antigens. Zonulin is the only physiologic modulator of intercellular tight junctions described so far that is involved in trafficking of macromolecules and, therefore, in tolerance/immune response balance. When the zonulin pathway is deregulated in genetically susceptible individuals, autoimmune disorders can occur. This new paradigm subverts traditional theories underlying the development of these diseases and suggests that these processes can be arrested if the interplay between genes and environmental triggers is prevented by re-establishing the zonulin-dependent intestinal barrier function. Both animal models and recent clinical evidence support this new paradigm and provide the rationale for innovative approaches to prevent and treat autoimmune diseases.

41 Leaky gut and diabetes mellitus: what is the link? de Kort S, Keszthelyi D, Masclee AA. Obes Rev Jun ;12(6): doi: /j X Diabetes mellitus is a chronic disease requiring lifelong medical attention. With hundreds of millions suffering worldwide, and a rapidly rising incidence, diabetes mellitus poses a great burden on healthcare systems. Recent studies investigating the underlying mechanisms involved in disease development in diabetes point to the role of the dys-regulation of the intestinal barrier. Via alterations in the intestinal permeability, intestinal barrier function becomes compromised whereby access of infectious agents and dietary antigens to mucosal immune elements is facilitated, which may eventually lead to immune reactions with damage to pancreatic beta cells and can lead to increased cytokine production with consequent insulin resistance. Understanding the factors regulating the intestinal barrier function will provide important insight into the interactions between luminal antigens and immune response elements. This review analyses recent advances in the mechanistic understanding of the role of the intestinal epithelial barrier function in the development of type 1 and type 2 diabetes. Given our current knowledge, we may assume that reinforcing the intestinal barrier can offer and open new therapeutic horizons in the treatment of type 1 and type 2 diabetes. Étant donné notre connaissance actuelle, nous pouvons supposer que le renforcement de la barrière intestinale peut offrir et ouvrir des nouveaux horizons thérapeutiques dans le traitement de type 1 et le diabète de type 2.

42 Intestinal barrier function in patients with acute myocardial infarction and the therapeutic effect of glutamine. Mao Y, Wang SQ, Mao XB, Zeng QT, Li YS. Int J Cardiol Feb 3;146(3):432-3.

43 3.Contrôle Nutritionnel Contrôle Nutritionnel

44 W6/W3 optimal MAK : EGCG Curcuma….. W6/W3 optimal MAK : EGCG Curcuma….. Lactobacillus NCFM® Bifidobacterium Bi-07 Lactobacillus NCFM® Bifidobacterium Bi-07 CALMER LINFLAMMATION LUTTER CONTRE LE STRESS OXYDANT RENFORCER LA MUQUEUSE INTESTINALE SOUTENIR LA FLORE EUBIOTIQUE INTESTINALE L-Glutamine Zinc Inuline, oligofructose Vit D genisteine L-Glutamine Zinc Inuline, oligofructose Vit D genisteine 3 Anti oxydants Anti oxydants

45 le foie est surchargé par les toxines de lintestin La détoxication est aux molécules toxiques ce que le systéme immunitaire est aux micro-organismes Soutenir détoxication hépatique 5

46 Merci pour Votre Ecoute!


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