GLOBALISATION - toprecommendedwebsites.com€¦ · 2.10.07 nutrition.ppt 2 GLOBALISATION...
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2.10.07 nutrition.ppt 1
DISORDERS OF NUTRITION, OBESITY AND ITS CONSEQUENCES
LECTURES FROM GENERAL
PATHOLOGICAL PHYSIOLOGY
OLIVER RÁCZ, FRANTIŠEK NIŠTIAR,
IWAR KLIMEŠ, ANNA ŠOFRANKOVÁ
DANIELA KUZMOVÁ, ANDREJ JANCO
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GLOBALISATION
❚ Undernutrition, malnutrition - 1/3 of world
❚ Obesity - 1/3 of world (Globesity?)
❚ Obesity combined with malnutrition (micronutrient deficiency, McDonaldisation, Coca-colonisation)
❙ ARE WE LOSING THE BATTLE?
❙ Economical growth and cultural changes in developing regions (South Africa, Japanese in USA, etc.
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Undernutrition, malnutrition
❚ Absolute starvation - with water 2 months❙ glycogenolysis, gluconeogenesis, lipolysis, ketosis
❙ curtailed physiological processes, impaired immunity
❙ weight loss 40-50 % threatens life (protein catabolism)
❙ Blood glucose remains around the lower margin of the normal range!
❚ Kwashiorkor - protein malnutrition❙ manifestation after lactation
❙ weakness, growth retardation, hypalbuniemia, ascites, intercurrent infections, apatia...
EATING DISODERS (ANOREXIA, BULIMIA) PSYCHIATRIC DISEASES?
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Undernutrition in rich
countries??!
Hospitals, hospices, chronic diseases
❚ Decreased oral intake❙ anorexia, nausea, dysphagia, pain, dentition
❙ poverty, old age (tea & toast diet), social isolation, alcohol or drug abuse, depression
❚ Increased losses❙ Diarrhea, malabsorption, bleeding, nephrotic sy….
❚ Increased requirements❙ fever, infection, burns, neoplasma, thyreotoxicosis...
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OBESITYAre we fighting a losing battle ?
BMI = kg/(m)2
norm 19 - 25 (0)
overweight 25 - 30@ (I)
obesity 30 - 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 %
5 8
10 18
15 28
20 45
25 56
30 67
35 81
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
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The obesity pandemic
❚ COUNTRY M/W > BMI 30❚ SLOVAKIA 19/14❚ USA 20/25❚ JAPAN 8/3❚ RUSSIA 11/28❚ SOUTH AFRICA 8/44❚ KUWAIT 32/44❚ GREECE 27/18
❚ BUT!
❚ SIMPLE OVERWEIGHT IS ≈ ≈ ≈ ≈ 30/50 %❚ ALARMING INCREASE IN THE PAST 20 YEARS
❚ ALARMING INCREASE IN CHILDREN
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OBESITY - external factors
❚ PHYSICS❙ no obesity without excess calories (+ 1 % = 10kg in 10 years)
❙ excess calories - not always obesity (substrate cycles, UCP)
❚ Once a day, without breakfast
❚ Infant formulas
❚ Fast food, quick eating
❚ Nibbling (TV)
❚ Stress
❚ Night eating
❚ Binge eating
❚ Alcohol (beer)
◆ Eating disorders - anorexia mentalis & bulimia
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OBESITY - genes & forms
❚ Bodystat (glucostat, lipostat), appetite
❚ Basal output of energy = 75 %; ion transport!
❚ Postprandial output
❚ Spontaneous physical activity
❚ Lipid metabolism (lipases)
❚ Insulin sensitivity
◆ Rare hereditary and/or endocrine diseases formy -hypothalamus, Prader-Willi sy, etc. (connected with hyperphagia)
◆ Gynoid (Renoir) and android [lower & upper body obesity; pear & apple]
◆ sugar & fat eaters ?
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Different types of obesity
❚ Gynoid and android
❙ (female, male, lower and upper body, gluteal and abdominal, Renoir and Rubens)
❚ Mild gynoid – fertility
❚ Mild android – health risk
❚ And visceral – high risk
❚ Diagnosis – waist circumference
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OBEZITA
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OBESITY - which genes?
❚ Ob gene coding leptin (167 AA)
◗ leptin is excreted from fat
◗ binds to its receptor in hypothalamus
◗ through increased activity of SNS (?!) decreases food intake and increases energy output
◗ ob/ob mice are obese, leptin applications helps
◗ obese men are not mice* (receptor mutation?)
*John Steinbeck: About Mice and Men
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Many accelerators, few brakes,
and a lot of other things
❚ Leptin
❚ Resistin
❚ Adiponectin
❚ Adipsin
❚ Agouti related p.
❚ Acylation stimulating p.
❚ ...
❚ TNF αααα❚ Interleukin 6
❚ Complement factors
❚ Apo E
❚ Angiotensinogen
❚ Prostaglandins
❚ ...
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What is obesity ?
❚ Deviation from the normal range of weight?
❚ Pathological condition ?❙ Of metabolism, caused by ???
❙ Of brain ???
❚ Disease(s) - nosological unit(s)❙ If it is a pandemic, it is a disease
❚ Risk factor of many (other) diseases
❚ A phenotype (manifesting if conditions are favourable)
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Genotyp and environment
“The thrifty genotype”
Very thriftygenes
Less thriftygenes
Food shortage
Less thriftygenes
Very thriftygenes
Surplus of food
4 combinations2 fatal
☺ � ☺ �
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Genotype versus environment
It was not so simple:Homo sapiens 1 500 000 yearsEuropean ancestors 50 000 years tall and healthy hunter/gatherersFarming, villages 10 000 years
Increased morbidity (famine, infections) decrease in height. Thrifty metabolism, strong immunity – t2dm and allergy
Very thriftygenes
Less thriftygenes
Food shortage
Less thriftygenes
Very thriftygenes
Surplus of food
4 combinations2 fatal
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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
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OBESITY - consequences
❚ METABOLIC (Insulin resistance, Diabetes mellitus,...)
❚ ENDOCRINE (sex hormones. growth h., glucocorticoids)
❚ CACRDIOVASCULAR (Hypertension*, Coronary artery disease, stroke, varices)
❚ GIT (gallbladder – also in gynoid obesity)
❚ RESPIRATION (Pickwick sy., snoring, sleep apnoea)
❚ ORTOPEDIC
❚ SKIN
❚ PSYCHOSOCIAL
❚ ONCOLOGICAL
*at BMI 30 the risk of hypertension is increased 5 – 13 times
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Risk of diseases at BMI > 27
0,8Fracture of femur2,5Gout
1,2Breast Ca3,1Stroke
1,3Colorectal Ca1,9Myocardial infarction
1,8Arthrosis2,9Diabetes Type 2
2,0Cholecystopatia2,9Hypertension
RRDiseaseRRDisease
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INSULIN RESISTANCE
1. Causes
❚ PRIMARY FORMS (HEREDITARY)
❙ abnormal insulin molecule, insulin receptor gene mutations, mutations of genes of glucose metabolism
❚ SECONDARY
❙ puberty, gravidity, high age
❙ unhealthy life style (lipids, fructose), obesity
❙ nonesterified fatty acids
❙ stress, starvation, hyperglycemia
❙ uremia, cirrhosis, ketoacidosis
❙ glucocorticoids, growth hormone, katecholamines, glucagon
❙ amylin (B cells of Langerhans islets)
Repeat the mechanism of insulin action!
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INSULIN RESISTANCE
2. Consequences - glucose metabolism
GENETIC BACKGROUND + SECONDARY FACTORS
1. HYPERINSULINEMIA, NORMOGLYCEMIA
X-SYNDROME
2. IMPAIRED GLUCOSE TOLERANCE
GLUCOSE TOXICITY, VITIOUS CYCLE
3. TYPE 2 DIABETES MELLITUS
EXHAUSTION OF B CELLS
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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
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INSULIN RESISTANCE
(HYPERINSULINEMIA, METABOLIC SY)
Unanswered questions
❚ Name ? Reaven? Metabolic? X? Z? syndrome
❚ Syndrome or atherogenic constellation of RF ?
❚ Causal interactions ?
❚ The beginning - the thrifty genotype ?
❚ Or is it in the opposite way? - impaired sympathetic regulation?
❚ Or subclinical inflammation ?
❚ Practical implications ? Prevention, education, therapy?