Obesity and diseases of civilization

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Obesity and Being Overweight

By Amr
Abdelmonem,MD. Assistant professor of anesthesia
,surgical intensive care and clinical nutrition
in faculty of medicine, Cairo university Member
of North American Association For The Study Of
Obesity Member of the American society of
regional anesthesia and pain medicine
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The O WordObesity

• 1998, world health organization defined
  overweight and obesity based on
• Body Mass Index
• ( BMI Kg / m2)
• Over weight 25.0 to 29.9
• Class 1 obesity 30.0 to 34.9
• Class 2 obesity 35.0 to 39.9
• Class 3 obesity 40.0 or greater
• BMI is not a measure of body composition
• BMI is an important correlate of impaired
• HRQL(health related quality of life)

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National institutes of health of the US have
recently recommended weight Management based on
Standardized cut- offs for BMI at 25 and 30 Kg/m2
and

• On waist circumference ( action levels)
• Minimum circumference between lower rib margin
  and iliac crest
• Action level 1 at 94 cm in men and 80 cm in women
• Action level 2 at 102 cm in men and 88 cm in
  women
• Greater than action level 1 individuals are at
• increased health risk ,should avoid weight gain
• Greater than action level 2 are at high health
  risk ,
• should seek Professional help

NICK CIRCUMFERENCE measurement is a simple and
time-saving screening measure that can be used to
identify overweight and obese patients. Men with
NC lt37 cm and women with NC lt34 cm are not to be
considered overweight
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The Pathophysiology of Obesity

• Cultural Influences on Eating and Activity
  Patterns
• Biologic Factors
• Genetic Factors
• Effects of Certain Medications
• Medical Causes of Obesity

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Cultural Influences on Eating and Activity
Patterns

• Both leisure and working time are increasingly
  sedentary as people move from one seated position
  to another in their use of the automobile, the
  television, video games, and the computer

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The simplistic solution of eat less and
exercise more does it always work?
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Biological factors

• Three primary neuroendocrinal components
• Afferent signals (orexigenic and anorexigenic
  peptides )
• CNS processing unit VMH-PVN-LHA
• Efferent system complex of effectors
• Appetite and its motor component ( medullary NTS)
• Autonomic nervous system ,with its 2 pathways
• a. sympathetic limb b. parasympathetic limb
• 3.Three components of total energy expenditure
• Resting energy expentiture (50 to 65 )
• Thermal effect of food
• Voluntary energy expentiture

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Afferent signals

• Ghrelin hormone
• Cholecystokinnin hormone
• Bombesin hormone
• Leptin hormone
• Melanocortins

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Central processing unit and hypothalamic obesity
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Efferent system
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1.Appetite and its motor components

• Nucleus tractus solitarius (NTS) is the central
  integratorthat control appetite and satiety

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2.Autonomic nervous system

• 1.Sympathetic nervous system (SNS)
• Activation of the adrenergic beta 3 receptors in
  adipocytes
• 2. Parasympathetic nervous system (PNS)
• Activation of muscarinic M3 receptors
  ?acetylcholine ? depolarization of beta cell
  ?calcium influx ? hyperinsulinemia

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3.Components of energy expenditure

• Resting energy expenditure
• Determined by fat free mass(60-80 variability)
• Developmental regression of RMR(?muscle-organ
  ratio)
• 79.2kcal/Kg 0-2.5 years-36kcal/Kg4-7
  years-28.3kcal/Kg during adolescence-21kcal/Kg in
  adulthood)
• ?fat mass-age-sex-physical activity can affect
  RMR
• Measured by indirect calorimetry (Vo2-CO2)
• Thermal effect of food
• Energy cost is 10 of energy ingested
• Voluntary energy expenditure
• (Non-exercise Associated Thermogenesis (30 of
  TEE)
• Volitional physical activity)

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Genetic Factors

• The human obesity gene map 2003 update identified
  more than 430 gene mutation affecting BMI, body
  fat mass ,percentage of body fat ,abdominal fat
  ,fat-free mass , skin folds , RMR and
  neuroendocrinal components of energy balance

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Effects of Certain Medications

• Antacid pills
• Anti-inflammatory
• Beta blockers
• Contraceptive pills
• Statins
• Cough drops
• Antihistaminics

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Medical Causes of Obesity

• Hypothroidism
• Cushing disease and syndrome
• Polycystic ovarian syndrome

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The world of lipid
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Lipid metabolism
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Lipids

1. Triglycerides (neutral fat)
2. Phospholipids
3. Cholesterol
4. Few others less important

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Transportation of lipids
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Triglycerides fat globules
Bile
Emulsified fat
Pancreatic lipase
Fatty acids and 2-monoglycerides
Resynthesis
Venous system
Triglycerides
Aggregate
Chylomicrons
Thoracic duct
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Chylomicrons in the venous blood
Capillaries of liver and adipose tissue
Lipoprotein lipase
Hydrolysis of triglycerides
Fatty acids glycerol
Fat cells
Resynthesis
Triglycerides
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Release of fat from fat cells

• Hydrolysis of triglycerides
• into FA glycerol by
• Low carbohydrate load to fat cells
• Hormone sensitive lipase (HSL)
• On leaving fat cells ? FA ionize in the plasma ?
  immediately combines with albumin molecules (FFA
  or NEFA)

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Free fatty acid (FFA )

• Concentration of FFA in the plasma during resting
  conditions is 15mg/ dl of total FA of .5gm
• This small amount is the physiologically active
  because
• Every 2-3 minutes half of the plasma FFA is
  replased with new FA
• ?almost all energy requirements of the body can
  be provided by oxidation of the transported FFA
  without using CHO or proteins
• 2. All the conditions that increase the rate
  of FA utilization also increase FFA conc up to 5
  to 8 folds

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The Fat Depots

• Large quantities of fat are stored in 2 major
  tissues
• Adipose tissue and liver
• Adipose tissue is called fat depots

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Adipose Tissue vs. Fat
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Total body adipose tissue percentage
Age Males Females
10-30 12-18 20-26
31-40 13-19 21-27
41-50 14-20 22-28
51-60 16-20 22-30
61 17-21 22-31
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Traditional Adipose Tissue Classification

• Classical anatomy was mainly organ-centered,
  without recognizing the specialized organ-like
  functions of different tissues
• This was especially true of adipose tissue, which
  only recently has been recognized as an
  "endocrine organ
• N Engl J Med .20013451345
• Simple anatomic adipose tissue groupings
  subcutaneous adipose tissue, organ-surrounding
  adipose tissue, interstitial adipose and adipose
  tissue in bone marrow
• Adipose tissue is also named according to special
  biological functions, such as white, mammary
  gland, brown, and bone marrow adipose tissues

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Recent proposed Classification of total body
adipose tissue Shen et al,Obes Res.2003111
Subcutaneous
Internal
Superficial
Visceral
Non- visceral
Deep
Intramuscular Perimuscular Orbital
Intrathoracic
Intraabdominopelvic
Intrapricardial
Intraperitoneal
Extrapritoneal
Extrapricardial
Intraabdominal
Intrapelvic
Parametrial Retropubic Paravesical Retrouterine
Pararectal Retrorectal
Preperitoneal
Retrroperitoneal
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Dynamic state of storage fat

• Exchange of fat between adipose tissue and blood
  
• Because of rapid exchange of FFA
• Triglycerides in the fat cells are renewed
  approximately once every 2 to 3 weeks

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Use of triglycerides for energy

1. Hydrolysis of triglycerides ? FA glycerol
2. Entry of FA into mitochondria by carnitine
   shuttle system
3. Splitting of acetyl CoA from FA
4. Oxidation of acetyl CoA in citric acid cycle

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The liver lipids

• The principal functions of liver in lipid
  metabolism
• Degradation of fatty acids
• Synthesize triglycerides from carbohydrates
• Synthesize other lipids (cholesterol and
  phospholipids )

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Formation of acetoacetic acid in the liver

• Large share in the initial degradation of FA
• FA? acetyl CoA ? 2 acetyl CoA H2O ?acetoacetic
  acid ? other cells for energy
• Acetoacetic acid can also be converted to
  B-hydroxybuteric acid and acetone
• Acetoacetic acid and B-hydroxybuteric acid
  diffuses through liver cell membranes to blood to
  other tissues for energy
• Their transport is so rapid not more than 3 mg/dl
  except in!

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Ketosis

• The name acetoacetic acid consist of keto acid
  and 3 compounds called ketone bodies
• Excess FA ? excess acetoacetic acid ? ketosis
• Low carbohydrate load (DM,starvation or high fat
  diet)
• Tremendous quantities of FA become available to
  liver for degradation ? excess keto acid and
  ketone bodies

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Synthesis of triglycerides from carbohydrates

• CHO either used for energy or stored as glycogen
• However excess CHO will be converted to
  triglycerides (liver) to be trasported by VLDL to
  adipose tissue
• Average person has almost 150 times as much
  energy stored in the form of fat as stored in the
  form of CHO
• Each gram of fat gives 2.5 times calories as CHO

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Fat sparing effect of carbohydrates

• Excess of carbohydrates ? preffered metabolic
  fuel because
• ?a-glycerophosophate ?shift metabolism toward fat
  storage
• FA synthesized more rapidly than they are
  degraded because of the vailabilty of acetyl CoA
  carboxylase ? converts acetyl CoA to FA
• ?excess CHO in diet not only spares fat but also
  increases fat synthesis

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Upper and Lower Body Adipose Tissue Function A
Direct Comparison of Fat Mobilization in males
between 22 to 43years.
Garry .Obes Res,2004

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• Objectives
• Fat in the lower body is not associated with
  the same risk of cardiovascular disease as fat in
  the upper body. Is this explained by differences
  in the physiological functioning of the two
  depots? This study had two objectives
• to determine whether fat mobilization and blood
  flow differ between gluteal and abdominal adipose
  tissues in humans, and
• 2) to develop a new technique to assess gluteal
  adipose tissue function directly.

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• Research Methods and Procedures
• They performed detailed in vivo studies of
  adipose tissue function involving the assessment
  of fat mobilization by measurement of adipose
  tissue blood flows, arterio-venous differences of
  metabolites across each depot, and gene
  expression in tissue biopsies in a small-scale
  physiological study.

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• Results
• Gluteal adipose tissue has a lower blood flow
  (67 lower, p lt 0.05) and lower hormone-sensitive
  lipase rate of action (87 lower, p lt 0.05) than
  abdominal adipose tissue. Lipoprotein lipase rate
  of action and mRNA expression are not different
  between the depots.
• This is the first demonstration of a novel
  technique to directly investigate gluteal adipose
  tissue metabolism.

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• Discussion
• Direct assessment of fasting adipose tissue
  metabolism in defined depots show that the
  buttock is metabolically "silent" in terms of
  fatty acid release compared with the abdomen.

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• Another study done by dora and published in
  obesity research journal confirned
• Abdominal adipocytes are more sensitive and
  responsive to beta adrenergic stimulation of
  lipolysis than gluteal adipocytes
• Gluteal lipocytes have higher LPL activity than
  abdominal lipocytes
• This study was done on post menopausal females

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Metabolic syndrome
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What is metabolic syndrome?

• Metabolic syndrome is a collection of health
  risks that increase the chance of developing
  heart disease, stroke, and diabetes.
• The condition is also known by other names
  including Syndrome X, insulin resistance
  syndrome, and dysmetabolic syndrome.

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What are these health risks? ATP III
Guidelines
WHO Guidelines Abdominal
Obesity   Waist Circumference
Waist/Hip
Ratio  Men gt 40 inches (102 CM)
 gt0.90  Women gt 35
inches (88 CM)
 gt0.85 Other Variables   Triglycerides ?150
mg/dL
? 150 mg/dL HDL-Cholesterol  Men lt 40 mg/dL

lt35 mg/dL  Women lt 50 mg/dL

lt39 mg/dL Blood Pressure ?130/ ?85 mm Hg
gt140/gt90 mm Hg Fasting
Glucose ?110 mg/dL
110 mg/dL WHO guidelines also
include microalbuminuria (gt20 µg/min or
albumincreatinine ratio gt30 mg/g).
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The pathogenesis of metabolic
syndrome
Complex interplay of a still largely unknown
genetic background with environmental lifestyle-
related factors
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Environmental lifestyle-related factors
When we eat ,our bodies break down the food into
its basic components ( protein- carbohydrates-
fat), and absorbs them into blood stream ? rise
in blood sugar ? pancreas will release insulin?
moves sugar into cells? either burned for energy
or stored away as fat in fat cells or glycogen
in liver and muscles
Years of dietery abuse in susceptible patients ?
malfunctioning of insulin sensors ?
hyperinsulinemia
Continued dietery abuse ? insulin sensors to
sluggish ? insulin resistance
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Markers of insulin resistance

• Hypertriglyceridemia
• HDL
• Hypertension
• Hyperinsulinemia
• Abdominal obesity
• Hyperglycemia
• Recently Marjo etal , proven liver fat
  accumulation as an important marker
• ( Obes Res
  2002 10 859)

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Obesity
Lets walk through the fat metabolism pathway and
follow the flow of fat molecules
Fat travels in the form of triglycerides ? at
cells ? ezymatic breakdowen ? fatty acids enter
the cells ?mitochondria ? breakdowen fat ? in
order to enter mitochondria ,fats need carnitine
? insulin inhibitsFat- carnitine shuttle system
? fats move back into blood Glucagon accelerates
this shuttle system
Muscle ,liver, kidney, lung, heart and other
cells break down fat
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Fat cells merely store the fat molecules !
Two enzyme systems on the surface of fat cells
regulated by insulin and glucagon
Insulin stimulates lipoprotein lipase that
transports fatty acid into fat cells
Glucagon stimulates hormone sensitive lipase
that releases the fat from fat cells into the
blood
Although we cannot control lipoprotein lipase
directly, we can control It indirectly by
cotrolling the metabolic hormones ,insulin and
glucagon
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DYSLIPIDEMIA

• Functions of Cholesterol
• Adrenal hormones and sex hormones
• Main component of bile acids
• Essential for normal growth and development of
  brain and nervous tissue
• Gives the ability of skin to shed water
• Precursor of vitamine D3 in the skin
• Normal growth and repair of tissues
• Transportation of triglycerides

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Where does cholesterol come from?
80 comes from the body itself , every cell in
the body is capable of making its own
cholesterol , most dont and rely instead on
that made in the liver and skin.
Cholesterol and triglycerides are insoluble in
blood
Lipoproteins are envelops that enclose
cholesterol and triglycerides Making them
soluble in blood,so that they can be transported
to tissues
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Sequence of events in the life of lipoproteins
Liver
Makes and release VLDL
HDL
Released to tissues Deposited in coronary
arteries
TRIGLYCERIDES WITH CHOLESTEROL
Scavenges cholesterl From tissues carries Through
blood Hands it off to VLDL
Removed by liver
TRI AND CHOLES
CholesteroL rich
MATURE VLDL
Triglycerides Released to blood And tissues
LDL
Cholesterol Bulk tri
LDL
More triglycerides release
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When the level of cholesterol inside the cells
falls ? LDL receptors Attach to the surfaces of
the hepatic cells? invaginate LDL cholesterol By
endocytosis
Obese patients with insulin resistance have LDL
receptors dysfunction
Cholesterol synthesis inside the cells depends
on an enzyme named 3- hydroxy-3
methyl-glutaryl-coenzyme A reductase
Couple of hormones affect the activity of the
rate limiting enzymeHMG-CoA reductase
INSULIN AND GLUCAGON
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Diet and cholesterol quiz
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Patient with the following
findingTotal cholesterol 240 LDL 160
HDL35Total/ HDL 6.85 LDL/HDL 4.57
Diet 1 Diet 2
Total cholesterol 159 mg/dl 191 mg/dl
LDL 111 mg/dl 139 mg/dl
HDL 32 mg/dl 42 mg/dl
Total /HDL 4.97 4.55
LDL/HDL 3.47 3.31
Which is better?
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Hypertension
Data from NHANES III show that the (age
adjusted prevalence) Of high blood pressure
increases progressively with higher levels Of
BMI in men and women
High blood pressure is defined as
SBP? 140 mm Hg or MBP ? 90 mm Hg or currently
taking antihypertensives
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What is the etiology that connects obesity and
hypertension?
Hyperinsulinemia and insulin resistance
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• Mechanism
• Increased sodium retention
• Increased sympathetic nervous system activity
• Alteration in the mechanics of blood vessels

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The precise mechanism whereby weight loss
results in a decrease in Blood pressure is
unknown .

• However
• It is known that weight loss is associated with
• ? vascular resistance,total blood volume and
  cardiac output
• Improvement in hyperinsulinemia and insulin
  resistance
• ? sympathetic nervous system activity
• Suppression of the activity of renin angiotensin
  aldosterone system
• Recently ,serum angiotensin converting enzyme
  activity declines with modest weight loss.

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Type II Diabetes mellitus

• It represents 90 of all cases of diabetes.
• Requires years of underlying metabolic
  disturbance before symptoms become apparent
• The development and diagnosis usually follows
  weight gain
• In Type I and Type II diabetes blood sugar is
  elevated but for different reasons

• Type I there is no insulin to hold it down by
  moving it into cells

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• Type II the cells become resistant to insulin
  that even large amounts cant adequately move the
  sugar into cells
• In early stages there is hyperinsulinemia ,later
  pancreatic beta cells wear out from constantly
  producing insulin under stimulation of
  hyperglycemia

• Resistin is a protein secreted by fat cells as a
  signal from adipose tissue linking obesity to
  insulin resistance and type II diabetes
• Liese et al,
  Eur J Nutr.200140282
• Increased White blood cell count is correlated
  with insulin resistance in diabetic obese females
• 
  Pannacciulli et al,Obes Res.2003111232

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Coronary artery disease

• Observational studies have shown that
  overweight,obesity, and VAT are directly related
  to cardiovascular risk factors
• ( ? cholesterol , ? LDL, ? triglycerides,
  hypertension, ? fibrinogen,hyperinsulinemia , ?
  HDL, ?plasminogen activator inhibitor )

The term "Syndrome X" refers to a heart condition
where chest pain and electrocardiographic changes
that suggest ischemic heart disease are present,
but where there are no angiographic findings of
coronary disease.
RECENTLY Complement 3 and acute phase proteins is
the immunological link between central obesity
and CHD
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• Recent studies have shown that risks of nonfatal
  myocardial infarction and CHD death increase with
  increasing levels of BMI
• In British, Swedish, Japanese and US populations
  , CHD incidence increased at BMIs above 22 and an
  increase of 1 BMI unit was associated with
• 10 increase in the rate of coronary events
• Recent study has found that obese CHD patients
  are younger and and are hospitalized more
  frequently during the first 10 years of their
  illness than the non-obese

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Obesity and cardiac dysrhythmias(prolonged Q-T
interval)

• Q-T interval is usually measured in lead II , and
  is corrected for heart rate .
• Q-Tc measured Q-T ? square root of R-R interval
• Prolonged Q-T interval reflects prolonged
  repolarization of the ventricle
• Proposed mechanism is increased SNS activity
• Recent study had found that Prolonged Q-T
  interval is associated with abnormal WHR ,higher
  levels of FFA and hyperinsulinemia in obese women
  .
• Wight loss leads to normalization of Q-Tc with
  attenuation of hyperinsulinemia
• Esposito et al,Obes Res.200311653-659

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Oxidant Stress
Imbalance
Between
Formation Of Reactive
oxygen/nitrogen species
(ROS/RNS) And
Antioxidants
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Pathologic stress ?
Induces monocytes to release mediators
(TNF? and interleukins 1-6-8) ?
Activates PMNs ?
Release ROS(superoxide (O2-), hydrogen peroxide,
hypochlorite, nitric oxide (NO), hydroxyl radical
?
Induce tissue injury by

• damaging DNA
• Cross linking cellular proteins
• Peroxidation of membrane lipids ?
• Diminishing membrane fluidity
• Increasing membrane permeability

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Oxidant Stress and Obesity

• Adipocytes and preadipocytes have been identified
  as sources of inflammatory cytokines
• including TNF? , interleukin (IL)1-ß, and IL-6.
• Stimuli capable of inducing cytokine release from
  adipocytes may include
• lipopolysaccharides, intracellular
  triglycerides, and catecholamines

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We could predict that
The accumulation of intracellular triglycerides
or tissue adiposity promotes increased oxidant
stress Therefore reduction of total body fat
through diet and/or exercise may be an effective
means of reducing systemic inflammation and
oxidant stress.
Consistent with this prediction
Reductions in plasma markers of oxidant stress
and in ROS generation by isolated leukocytes have
been observed after 4 weeks of energy
restriction and weight loss. Dandona et al. J
Clin Endocrinol Metab,2001 86355-363
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Good news
Physical activity ? Decreases adipose derived
inflammatory mediators Activates signaling
pathways that lead to increased synthesis of
intracellular antioxidants and antioxidant
enzymes and decreased ROS production
Miyazaki et al, Eur Appl Physiol.2001 841-6
Pischon et al, Obes Res.2003111055
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A novel pathway to the manifestations of
metabolic syndrome
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Obesity And Diseases
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Obesity and cancer

• Strong risk factor for esophageal cancer
• Uterine and gall bladder cancer in obese women
• High risk for colon and prostate cancer in obese
  males
• Breast cancer for obese postmenopausal women

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What is the link between obesity and cancer

1. Hyperinsulinemia and insulin resistance
2. Oxidant stress

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Obesity and osteoarthritis

• Degenerative process affecting articular
  cartilage
• Predisposing factors advancing age genetic
  predisposition obesity
• Common affected sites knees and hips then
  cervical spine and lower lumbar area
• Pathogenesis
• Forces across the hip and knee during walking and
  stair climbing are 2 to 4 times normal body
  weight and each extra weight will multiply these
  forces on the joints
• NHNES showed that adults with BMIgt30 have 4 folds
  higher prevalence than those lt30
• Leptin overexpression in arthritic joint is
  related to cartilage destruction and correlated
  with BMI

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Obesity and gout

• Is a metabolic disorder of purine metabolism
• Either primary genetic defect in purine
  metabolism
• Or secondary to chemotherapeutic drugs, renal
  impairment , thiazide diuretics ,alcohol abuse
  and purine rich foods (liver,kidney,peas,lentils,r
  ed meat)
• Clinical picture crystals of uric acid (tophi)
  build up forming large deposits in
  metatarsophalyngeal joints, wrist,elbow,knee,and
  extraarticular tissues(nephrolithiasis,
  myocardium, aortic valve and extradural spinal
  region.
• Recently insulin resistance is the precursor of
  gout (journal of american medical association
• Diet regimens that lead to gout any regimen that
  results in a rapid weight loss will increase uric
  acid 2-3 folds

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Obesity and gallstones

• The incidence of gallstones is significantly
  higher in obese women and men
• The risk of stone formation is also high if a
  person loses weight too quickly

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Obesity and lungs

• Strong risk factor for adult onset asthma
  (imbalance between good eicosanoids and bad
  eicosanoids)
• Increased risk of hypoxemia and detrimental work
  of breathing
• Pickwickian syndrome

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Obesity and sleep apnea and sleep disorders

• Obese tend to fall asleep faster and sleep longer
  during the day
• At night ,it takes them longer to fall asleep
  they sleep less than others.
• When the upper airways relaxes and collapses at
  intervals during sleep ,thereby temporary
  blocking the passage of air (sleep apnea)
• Symptoms morning headach, fatigue and
  irritability
• Side effects dysrhythmias,stroke ,right sided
  heart failure and car accidents
• Sleep apnea deprives patients from REM sleep
• REM sleep the dreaming phase of sleep, necessry
  for emotional wellbeing
• Obesity leads to sleep apnea which leads to loss
  of REM sleep which leads to raising of BMI

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OBESITY AND EATING DISORDERS

• Binge eating about 30 of obese are binge
  eaters ,who typically consume 5000 to 15000
  calories in one sitting
• To be diagnosed as a binge eater ,person has to
  binge twice a week for 6 months
• Bulimia binge eating followed by purging in
  order to lose weight
• Anorexia severe weight loss and is life
  threatening

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Types and approaches to obesity treatment
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• Do it yourself programs
• Non-clinical programs
• Clinical programs
• Individual heath care professional
• Multidisciplinary group of professionals
  (physician ,dietitian ,exercise and psychological
  counselors )

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Evaluation of the program by the physician

• The match between the program and the consumers
• The soundness and safety of the program
• Assessment of physical health and psychological
  status
• Attention to diet and pharmacotherapy
• Attention to physical activity
• Program safety
• Outcome of the program
• Long-term weight loss
• Improvement in obesity related comorbidities
• Improved heath practice
• Monitoring adverse effects that might result from
  the program

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Caloric restriction

• Normal caloric intake 20-25 calories for each Kg
  of the body weight or
• According to Harris-Benedict equation
• for males RMR 66.4 13.8 W 5H 6.8A
• for females RMR 665 9.6W 1.8H 4.7A
• Wweight (kg), H height (cm), and A age (yr)
• e.g. weight 120 kg H 175 A35
• RMR 66.4 13.8(120)5(175) 6.8(35)2359.5
• Less than 500 calories deficit per day? weight
  loss of .5 Kg per week

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Side effects of very low caloric diets lt RMR

• Rebound effect ( leptin)
• Insufficient vitamines (ADEK) and minerals
  (Ca,zinc,iron and folic acid)
• Fatigue ,intolerance to cold,hair loss, gall
  stone formation ,gout , and menstrual
  irregularities
• Hypokalemia due to diuresis ?arrhythmias
• Hyponatremia ? fatigue, dizziness , confusion and
  coma
• Constipation (absence of insoluble fibres)

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Macronutrient composition of diets
91
Traditionally ,a low fat high carbohydrate diet
has been recommended to help obese patients lose
weight National institute of health ,national
heart ,lung and blood institute ,and national
institutes of diabetes and digestive and kidney
diseases .clinical guidelines on the
identification ,evaluation ,and treatment of
overweight and obesity in adults
.Bethesda,MDNIH1998
92
Data from a recent meta analysis that evaluated
randomized clinical trials that compared
fat-restricted and calorie restricted diets has
found no difference in weight loss between diet
groups Pirozzo S,etal.Cochrane Database Syst
Rev.20022Cd003640
93
The results from four randomized controlled
trials that compared the effect of low
carbohydrate diet with a low fat diet on body
weight in adult obese subjects have recently been
published Brehm, et al . (2003) A randomized
trial comparing a very low carbohydrate diet and
a calorie-restricted low fat diet on body weight
and cardiovascular risk factors in healthy women
J Clin Endocrinol Metab. 88,1617-1623 Samaha, et
al (2003) A low-carbohydrate as compared with a
low-fat diet in severe obesity N Engl J Med.
348,2074-2081 Foster, et al (2003) A randomized
trial of a low-carbohydrate diet for obesity N
Engl J Med. 348,2082-2090 Yancy, WS,et al.
(2004) A low-carbohydrate, ketogenic diet versus
a low-fat diet to treat obesity and
hyperlipidemia a randomized, controlled trial
Ann Intern Med. 140,769-777 Stern, et al (2004)
The effects of low-carbohydrate versus
conventional weight loss diets in severely obese
adults one-year follow up of a randomized trial
Ann Intern Med. 140,778-785
94

• A consistent difference in weight loss at 6
  months has been observed between groups across
  studies subjects randomized to the
  low-carbohydrate diet lost 4 to 5 kg more weight
  than those randomized to the low-fat diet.
• However, weight loss was no different between
  groups at 1 year .
• In addition, in subjects who had type 2
  diabetes, there were greater improvements in
  fasting blood glucose concentrations and insulin
  sensitivity with a low-carbohydrate than with a
  low-fat diet.
• The data from these studies has also found
  greater improvements in serum triglyceride and
  high-density lipoprotein-cholesterol
  concentrations,
• but not in serum low-density lipoprotein-choleste
  rol concentrations, in the low-carbohydrate than
  the low-fat group .

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Mitochondrial uncouplings

• All UCPs may lower mitochondrial ATP production
  through respiratory uncoupling ,thus stimulating
  substrate oxidation in mitochondria
• Ricquier D, etal. Biochem J.2000345161-
  Fink BD,etal. J Biol Chem.20022773918
• In transgenic mice ,high fat diet stimulates
  respiratory uncoupling in white adipose tissue
  and may lower plasma lipids by inducing fat
  oxidation .
• Martin R,etal.Obes Res.200513835.

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Energy Density

• Definition the energy (kilocalories) present in
  a certain weight (grams) of food.
• It can affect the total caloric intake .
• Energy-dense foods are usually high in fat
  (e.g.,butter) and/or are dry (e.g.,fruits)
• Moreover, the results of short-term studies have
  suggested that manipulating energy density might
  be a useful approach to noncognitively regulate
  total energy intake

97

• At present, it is unlikely that one diet is
  optimal for all overweight or obese persons, and
  dietary guidance should be individualized to
  allow for specific food preferences and
  individual approaches to reducing weight.

98

• Walking is metabolically expensive for obese
• Greater body mass and heavier legs
• Decreased stability ,wider stance and wider
  lateral leg swing.
• Energy cost of walking is 20-100greater for
  obese
• Walking slower for a set distance is an
  appropriate exercise recommendation for weight
  management prescription in obese adults
• Raymond ,etal. Obes Res
  .200513891

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Spot reduction

• Mentioned to be condemned

100
Why treat overweight and obesity?

• Not only
• to improve the BODY IMAGE
• But also
• to reduce the
• OBESITY RELATED COMORBIDITIES

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