Nourishment and the Gastrointestinal Ecosystem .


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Nourishment and the Gastrointestinal Environment. Leo Galland M.D. Establishment for Incorporated Solution www.mdheal.org. Past Assimilation. The gut is a tangible organ. Protozoa know their surroundings by ingestion.
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Sustenance and the Gastrointestinal Ecosystem Leo Galland M.D. Establishment for Integrated Medicine www.mdheal.org

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BEYOND DIGESTION The gut is a tangible organ. Protozoa know their surroundings by ingestion. The gut is a neuroendocrine organ. Each CNS neurotransmitter is available and dynamic here. The gut has its very own cerebrum, an in place and free sensory system. The gut is the biggest organ of safe capacity in the body; 70% of our lymphocytes live here.

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BEYOND DIGESTION The gut substance are an inward world that is "outside" the cell body. Its surface is a boondocks of 100 square meters and a thickness of one cell Gut vegetation are an organ that contains the same number of microbial cells as the cell body has mammalian cells (100 trillion) -Over 500 species -Over 90% are anaerobic

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BEYOND DIGESTION The ordinary intestinal microflora constitute an immense concoction industrial facility that adjusts our sustenance and our GI discharges The typical intestinal microflora give our invulnerable frameworks a mass of antigens that are somewhat assimilated

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Three Components of the GI Ecosystem Diet Microbial greenery Mucosa Epithelium Mucus layer Immune cells Blood vessels Nerve endings

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Gastric Ecosystem Low fasting pH Reduces bacterial populace Denatures protein, starts protein processing Enhances solvency of Ca, Mg, Fe, Zn… Thick layer of defensive bodily fluid Intermittent presentation to nourishment and oral or exogenous microorganisms Rapid purging (a hour)

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Gastric Acid Production Two liters of gastric juice every day Fasting HCl emission is 10% of most extreme, yielding pH 1.0-2.0 and bacteriostatic obstruction Food cushions gastric corrosive in spite of post-prandial HCl discharge. pH of the fed stomach is regularly 3.5 – 4.5 Aging moderates gastric reacidification however has little impact on fasting or sustained pH

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Gastric Ecosystem Disruptors H. pylori contamination Acid-bringing down medications NSAIDs Malnutrition (B12) Delayed exhausting (gastroparesis) Drugs (clonidine) Disease (diabetes)

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Helicobacter pylori Most basic unending bacterial pathogen of people Prevalence in grown-ups is around 1%/year of life Infection can be deep rooted Lives under the mucous layer, shielded from HCl Pathogenicity is related with incitement of TH1 cells and gastric mucosal IL-8 emission and bacterial union of CagA, a disruptor of mammalian cell flagging components Raises gastric pH by creating smelling salts and by harming gastric epithelial cells May bring about hyper causticity by crushing somatostatin-delivering antral mucosal cells

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H. Pylori Effects: GI Atrophic and immune system gastritis Erosive gastritis and NSAID gastropathy Hypertrophic gastritis Duodenal ulcer sickness Gastric carcinoma Gastric lymphoma Functional dyspepsia/gastroparesis

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H. Pylori Associations: Systemic coronary illness Stroke Rosacea Raynaud\'s disorder Sjogren\'s disorder Open edge glaucoma ( Kountouras et al. Curve Int Med 2002; 162: 1237-1244 .) Food sensitivities Vitamin B12 lack

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Atrophic Gastritis Atrophic gastritis is non-erosive aggravation related with loss of secretory capacity Usually asymptomatic yet may create Dyspepsia Abdominal torment Bloating Nausea/heaving May exist together with erosive peptic infection Allows gastric bacterial excess Increases helplessness to pathogens in sustenance

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Achlorhydria and Atrophic Gastritis Achlorhydria influences 15% of individuals > 25, 30% of individuals > 65 Achlorhydria is an indication of atrophic gastritis, not an ordinary impact of maturing Hurwitz et al, JAMA 1997;278: 659-62. Achlorhydria is generally brought about by H. pylori or by the utilization of corrosive bringing down medications

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H. Pylori: After Effects Residual gastritis and achlorhydria can take 2 years or more to determine. HCl supplementation: 2 grams of Betaine HCl is expected to take 400ml of gastric juice from impartial to pH 2.0 B12 repletion enhances gastroparesis Gumurdulu et al J Clin Gastroenterol 2003; 37:230-3 .

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Food Effects on H. Pylori Mastic gum (P lentiscus), utilized as a part of rice pudding and for treatment of dyspepsia, murders H. pylori Raw garlic and fluid garlic remove repress development (thiosulfinate, MIC of 40 mcg/ml) Garlic and onion utilization conversely connected with gastric tumor Sulforaphane (cabbage and broccoli) has MIC of <4 mcg/ml Cabbage juice and broccoli grows have been utilized to treat PUD

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Acid Lowering Drugs May build improvement of atrophic gastritis in H. pylori-contaminated people Allow gastric bacterial/yeast abundance and post-prandial intra-gastric generation of ethanol and nitrosamines May weaken retention of vitamin B12, folic corrosive, carotene, minerals and pharmaceutical

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Esophageal Reflux Results from reflex unwinding of the LES in light of gastric vagal mechanoreceptors (customized in brainstem, disconnected to gulping or gastric pH). Post-prandial gastric distension is a key trigger. PPI\'s and H-2 blockers change over indigestion into non-heartburn. Pepsin and bile display in gastric juice may in any case go about as esophageal aggravations. Intra-gastric calcium builds LES tone, free of acid neutralizer impacts, and might be a more physiologic treatment, alongside utilization of little suppers eaten gradually in a casual manner to diminish gastric extension. Red-pepper powder 800 mg t.i.d. diminishes side effects Bortolotti et al, NEJM 2002; 346: 947-8.

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Colonic Ecosystem Relatively moderate motility (around 48 hours) Immense bacterial number (100 trillion life forms, weight of around 3 lbs) pH of 6-8, controlled by SCFAs versus NH4 Water inclination brought about by re-retention of liquid Ileo-cecal reverse may harm the terminal ileum

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Colonic Ecosystem Disruptors Antibiotics Infection Unabsorbed bile acids Bacterial rottenness Altered motility Disease Drugs, supplements Stress, way of life

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GI MICROFLORA AND COLON CANCER Large gut growth is related with high fat, high protein, low fiber counts calories This impact is to some extent interceded by bacterial catalysts actuated by the way of the eating routine, the substrates provided for these compounds and the cancer-causing results of chemical enactment

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BILIARY STEROID METABOLISM BY GI MICROFLORA chenodeoxycholate lithocholate cholic corrosive deoxycholic(DCA) - DCA in dung corresponds with colon malignancy rate - DCA may 20-CH3-cholanthrene Deconjugation of bile salts

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GI MICROFLORA AND COLON CANCER Incidence relative to DCA discharge conversely corresponding to Lactobacillus focus Vegetarians have less tumor and lower bacterial chemicals in stool: Beta-glucuronidase, nitro-reductase, 7-alpha-dehydroxylase; Lactobacilli bring down these when sustained to omnivores and forestall colon malignancy in rats given dimethylhydrazine

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GI MICROFLORA AND COLON CANCER (proceeded with) High meat diets increment indole and skatole in stool: prompting bacterial tryptophanase Human fecal mutagen (FCM), a vinyl ether of propanediol, is related with a Western eating regimen. Requires bile and low oxygen. Delivered by 5 Bacteroides spp High protein abstains from food high GI smelling salts and high fecal pH. This increments fecal LCFA and bile corrosive solvency

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GI MICROFLORA AND COLON CANCER (proceeded with) High CHO/fiber slims down high SCFA and low fecal pH. This reductions fecal LCFA and bile corrosive solvency Dietary Ca additionally renders LCFA insoluble

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DIETARY PREVENTION OF COLONIC DYSBIOSIS Plant-based, high fiber slim down Fermented nourishments, Lactobacilli Crucifers, flavonoid-rich vegetables & natural products Vegetable cellulose, an insoluble fiber Colostrum, a wellspring of lactoferrins -Lactoferrins tie press, repressing the development of every single bacterial specie with the exception of lactic corrosive makers

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Probiotics Lactic corrosive makers: Lactobacilli (acidophilus, plantarum, casei, salivarius, sporogenes), Bifidobacteria, Streptococci Non-pathogenic E. coli Soil-determined living beings: Bacilli (laterosporus, subtilis) Saccharomyces boulardii (yeast against yeast)

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Prebiotics Foods that bolster the development of probiotics: wheat, psyllium, safe starch (high amylose), oligofructose (FOS), inulin, sprouted grain foodstuff (GBF) FOS is found in onions, garlic, rye, blueberries, bananas, chicory. Dietary admission midpoints 2-8 gm/day. Inulins are gotten from chicory and artichoke

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GBF and Ulcerative Colitis GBF 20-30 gm/day actuates and keep up reduction in patients with ulcerative colitis. System: Increased colonic butyrate creation diminishes NFkB enactment . Hanai et al. Int J Mol Med. 2004 May;13(5):643-7. Kanauchi et al. J Gastroenterol. 2003;38:134-41. Kanauchi et al, Int J Mol Med. 2003;12:701-4 Kanauchi et al. J Gastroenterol. 2002; 37 Suppl 14:67-72. .

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E.COLI AND ULCERATIVE COLITIS E. coli in colonic tombs of UC patients indicates strange adherence Burke, Axon J Clin Path 40: 782-786 (1987) After initiating reduction with gentamycin and prednisone, Nissle 917 strain E. coli were as powerful as mesalamine in keeping up reduction at 12 months Rembacken et al, Lancet 354: 635-640 (1999)

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BENEFITS OF BACILLUS LATEROSPORUS Laterosporamine: anti-infection Suppress auto-counter acting agent arrangement Suppress murine lupus nephritis Spergualin: hostile to tumor, anti-toxin

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BENEFITS OF SACCHAROMYCES BOULARDII Stimulates generation of sIgA Protects against anti-infection and explorer\'s looseness of the bowels Helps switch C difficile colitis Improves intense diarrheal ailment in kids

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LACTOBACILLI: BENEFICIAL EFFECTS Produce natural acids: bring down entrail pH Produce H202 Antagonize enteropathogenic E. Coli, Salmonella, Staphylococci, Candida albicans, and Clostridia spp Degrade N-nitrosamines Anti-tumor glycopeptides (L. bulgaricus) Stimulate adjusted safe reactions Decrease rate of post-operation disease (L plantarum) .:ts

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