Presentation on theme: "2.10.07nutrition.ppt1 DISORDERS OF NUTRITION, OBESITY AND ITS CONSEQUENCES LECTURES FROM GENERAL PATHOLOGICAL PHYSIOLOGY OLIVER RÁCZ, FRANTIŠEK NIŠTIAR,"— Presentation transcript:
2.10.07nutrition.ppt1 DISORDERS OF NUTRITION, OBESITY AND ITS CONSEQUENCES LECTURES FROM GENERAL PATHOLOGICAL PHYSIOLOGY OLIVER RÁCZ, FRANTIŠEK NIŠTIAR, IWAR KLIMEŠ, ANNA ŠOFRANKOVÁ DANIELA KUZMOVÁ, ANDREJ JANCO
2.10.07nutrition.ppt2 GLOBALISATION zUndernutrition, malnutrition - 1/3 of world zObesity - 1/3 of world (Globesity?) zObesity combined with malnutrition (micronutrient deficiency, McDonaldisation, Coca-colonisation) yARE WE LOSING THE BATTLE? yEconomical growth and cultural changes in developing regions (South Africa, Japanese in USA, etc.
2.10.07nutrition.ppt3 Undernutrition, malnutrition zAbsolute starvation - with water 2 months yglycogenolysis, gluconeogenesis, lipolysis, ketosis ycurtailed physiological processes, impaired immunity yweight loss 40-50 % threatens life (protein catabolism) yBlood glucose remains around the lower margin of the normal range! zKwashiorkor - protein malnutrition ymanifestation after lactation yweakness, growth retardation, hypalbuniemia, ascites, intercurrent infections, apatia... EATING DISODERS (ANOREXIA, BULIMIA) PSYCHIATRIC DISEASES?
2.10.07nutrition.ppt5 Undernutrition in rich countries??! Hospitals, hospices, chronic diseases zDecreased oral intake yanorexia, nausea, dysphagia, pain, dentition ypoverty, old age (tea & toast diet), social isolation, alcohol or drug abuse, depression zIncreased losses yDiarrhea, malabsorption, bleeding, nephrotic sy…. zIncreased requirements yfever, infection, burns, neoplasma, thyreotoxicosis...
2.10.07nutrition.ppt6 OBESITY Are we fighting a losing battle ? BMI = kg/(m) 2 norm19 - 25 (0) overweight 25 - 30 @ (I) obesity30 - 40 (II) extreme ob. > 40** (III) M W Fat 10-20% 20-30% WHR* < 1,0 < 0,8 Waist < 94 cm < 80 cm + weight %+ mortality % 58 1018 1528 2045 2556 3067 3581 45 116 But: in an obese type 2 diabetic 100 90 kg adds 7 years of life *Waist to hip ratio @ 27! or 22??!**120 kg for 1,72 m
2.10.07nutrition.ppt7 The obesity pandemic zCOUNTRYM/W > BMI 30 zSLOVAKIA19/14 zUSA20/25 zJAPAN8/3 zRUSSIA11/28 zSOUTH AFRICA8/44 zKUWAIT32/44 zGREECE27/18 zBUT! SIMPLE OVERWEIGHT IS 30/50 % zALARMING INCREASE IN THE PAST 20 YEARS zALARMING INCREASE IN CHILDREN
2.10.07nutrition.ppt10 OBESITY - external factors zPHYSICS yno obesity without excess calories (+ 1 % = 10kg in 10 years) yexcess calories - not always obesity (substrate cycles, UCP) zOnce a day, without breakfast zInfant formulas zFast food, quick eating zNibbling (TV) zStress zNight eating zBinge eating zAlcohol (beer) uEating disorders - anorexia mentalis & bulimia
2.10.07nutrition.ppt11 OBESITY - genes & forms z„Bodystat“ genes and regulators (glucostat, lipostat), appetite zBasal output of energy = 75 %; ion transport! zPostprandial output zSpontaneous physical activity – genetic? zLipid metabolism (lipases) zInsulin sensitivity uRare hereditary and/or endocrine diseases formy - hypothalamus, Prader-Willi sy, etc. (connected with hyperphagia) uGynoid (Renoir) and android [lower & upper body obesity; pear & apple] usugar & fat eaters ?
2.10.07nutrition.ppt12 Different types of obesity zGynoid and android y(female, male, lower and upper body, gluteal and abdominal, Renoir and Rubens) zMild gynoid – fertility zMild android – health risk zAnd visceral – very high risk zDiagnosis – waist circumference (or WHtR)
2.10.07nutrition.ppt15 OBESITY - which genes? zOb gene coding leptin (167 AA) wleptin is excreted from fat wbinds to its receptor in hypothalamus wthrough increased activity of SNS (?!) decreases food intake and increases energy output wob/ob mice are obese, leptin applications helps wobese men are not mice* (receptor mutation?) *John Steinbeck: About Mice and Men
2.10.07nutrition.ppt16 Many accelerators, few brakes, and a lot of other things zLeptin zResistin zAdiponectin zAdipsin zAgouti related p. zAcylation stimulating p. z... TNF FTO z Interleukin 6 z Complement factors z Apo E z Angiotensinogen z Prostaglandins z...
2.10.07nutrition.ppt18 What is obesity ? zDeviation from the normal range of weight? zPathological condition ? yOf metabolism, caused by ??? yOf brain ??? zDisease(s) - nosological unit(s) yIf it is a pandemic, it is a disease zRisk factor of many (other) diseases zA phenotype (manifesting if conditions are favourable)
2.10.07nutrition.ppt19 Genotyp and environment “The thrifty genotype”
2.10.07nutrition.ppt20 Genotype versus environment It was not so simple: Homo sapiens1 500 000 years European ancestors50 000 years tall and healthy hunter/gatherers Farming, villages10 000 years Increased morbidity (famine, infections) decrease in height. Thrifty metabolism, strong immunity – t2dm and allergy
2.10.07nutrition.ppt21 Genes (polymorphisms of genes) are responsible for diet induced obesity is about 67 % They are permissive Most of them (600 !) are involved in appetite regulation Appetite is not the same as hunger There is a broad field for intervention Healthy life style – everybody Pharmacology – small portion Surgery - exceptionally
2.10.07nutrition.ppt22 OBESITY - consequences zMETABOLIC (Insulin resistance, Diabetes mellitus, Gout) zENDOCRINE (sex hormones. growth h., glucocorticoids) zCACRDIOVASCULAR (Hypertension*, Coronary artery disease, stroke, varices) zGIT (gallbladder – also in gynoid obesity) zRESPIRATION (Pickwick sy., snoring, sleep apnoea) zORTOPEDIC zSKIN zPSYCHOSOCIAL zONCOLOGICAL *at BMI 30 the risk of hypertension is increased 5 – 13 times
2.10.07nutrition.ppt23 Risk of diseases at BMI > 27 DiseaseRRDiseaseRR Hypertension2,9Cholecystopatia2,0 Diabetes Type 22,9Arthrosis1,8 Myocardial infarction 1,9Colorectal Ca1,3 Stroke3,1Breast Ca1,2 Gout2,5Fracture of femur0,8
2.10.07nutrition.ppt24 INSULIN RESISTANCE 1. Causes zPRIMARY FORMS (HEREDITARY) yabnormal insulin molecule, insulin receptor gene mutations, mutations of genes of glucose metabolism zSECONDARY ypuberty, gravidity, high age yunhealthy life style (lipids, fructose), obesity ynonesterified fatty acids ystress, starvation, hyperglycemia yuremia, cirrhosis, ketoacidosis glucocorticoids, growth hormone, katecholamines, glucagon yamylin (B cells of Langerhans islets) Repeat the mechanism of insulin action!
2.10.07nutrition.ppt26 INSULIN RESISTANCE (HYPERINSULINEMIA) 3. Consequences for the whole body DYSLIPOPROTEINEMIA TAG, small dense LDL, HDL-CH, postprandial hyperlipidemia HYPERTENSION Sodium & water resorption, ion transport, activity of SNS (?!) HEMOCOAGULATION DISORDER fibrinogen, fibrinolysis, hemorrheologic abnormalities HYPERURICEMIA HYPERANDROGENISM IN WOMEN ENDOTHELIAL DYSFUNCTION (INSULIN IS A GROWTH FACTOR) ATHEROSCLEROSIS
2.10.07nutrition.ppt27 INSULIN RESISTANCE (HYPERINSULINEMIA, METABOLIC SY) Unanswered questions zName ? Reaven? Metabolic? X? Z? syndrome zDefinition – WHO 2009 zSyndrome or atherogenic constellation of RF ? zCausal interactions ? zThe beginning - the thrifty genotype ? zOr is it in the opposite way? - impaired sympathetic regulation? zOr subclinical inflammation ? zPractical implications OK: Prevention, education, therapy
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