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‫بسم هللا الرحمن الرحيم‬
The Obesity Pandemic: Where have we
been and Where are we going?
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
The O Word:Obesity
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 (severely
obese)
BMI is not a measure of body composition
BMI is an important correlate of impaired
HRQL(health related quality of life)
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 timesaving screening measure that can be used to identify
overweight and obese patients.
Men with NC <37 cm and women with NC <34 cm are not to
be considered overweight
The Pathophysiology of Obesity
• Cultural Influences on Eating and
Activity Patterns
• Biologic Factors
• Genetic Factors
• Effects of Certain Medications
• Medical Causes of Obesity
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
The simplistic solution of
“’eat less and exercise more’”
does it always work?
Biological factors
Three primary neuroendocrinal components :
•
•
•
1.
2.
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
a. Resting energy expentiture (50 to 65% )
b. Thermal effect of food
c. Voluntary energy expentiture
Afferent signals
Orixegenic peptides
Ghrelin
NPY
VMH
AGRP
VMH
Anorexigenic peptides
Orexin A-B
LHA
leptin
UCPs
Cholecyto
kinnin
Cummings et al.showed that ghrelin rise preprandially
And fall postprandially in healthy subjects
Diabetes 2001;50:1714
In obese subjects ,lower preprandially
And higher postprandially
Shiiya T,et al. J Clin Endocrin Metab.2002;87:240
Ghrelin H does not influence gastric
Empyting in obese subjects
Maria E,et al.Obes Res.2005;13:739
Nobel prize winner Yalow demonstrated
The effect of cholecystokinnin as a
Neurotransmitter acting on the
Hypothalamus and on the vagus nerve
Inviting the sense of fullness
Central processing unit
Location
Ventromedial hypothalamus [VMH;consisting of ventromedial
And arcuate nuclei], Para ventricular nucleus [PVN] and
Lateral Hypothalamus [LHA]
Damage to the CPU: hypothalamic obesity
Hypothalamic damage from a tumor, surgery , or
radiation results in unrelenting weight gain that is not
amenable to diet regimens
However ,not all patients with HO suffer from hyperphagia!!
Efferent system
1.Appetite
• Bridge between energy intake and energy expenditure
• Divided into 3 components
[Hunger –Satiation – Satiety]
• Biomarkers
[glucose – ghrelin- cholecystokinnin-meal size and
components - vagus n- GLP1-leptin –others]
• Afferent pathways(biomarkers) + efferents from
VMH and LHA all meet within NTS
(central integrator that determines satiety versus appetite)
2.Autonomic nervous system
1.Sympathetic nervous system (SNS)
Stimulation of the adrenergic beta 3 receptors in adipocytes
➞lipolysis
2. Parasympathetic nervous system (PNS)
Activation of muscarinic M3 receptors ➞acetylcholine ➞
depolarization of beta cell ➞calcium influx ➞
hyperinsulinemia
3.Components of energy expenditure
1.
Resting energy expenditure [50-65%of total daily EE]
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
2.Thermal effect of food [10% of total daily EE]
The thermal effect is higher for protein and CHO than for fat
3.
Voluntary energy expenditure [5-50%of total daily EE]
Non-exercise Associated Thermogenesis [NEAT](30% of TEE)
•
(involuntary muscle contraction)
•
Volitional physical activity !!!
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
The world of lipid
Lipid metabolism
Lipids
1.
2.
3.
4.
Triglycerides (neutral fat)
Phospholipids
Cholesterol
Few others less important
Transportation of lipids
Triglycerides fat globules
Bile
Emulsified fat
Pancreatic lipase
Fatty acids and 2-monoglycerides
Resynthesis
Venous system
Triglycerides
Aggregate
Chylomicrons
Thoracic duct
Chylomicrons in the venous blood
Capillaries of liver and adipose tissue
Lipoprotein lipase
Hydrolysis of triglycerides
Fatty acids +glycerol
Fat cells
Resynthesis
Triglycerides
Release of fat from fat cells
Hydrolysis of triglycerides
into FA + glycerol by
1. Low carbohydrate load to fat cells
2. Hormone sensitive lipase (HSL)
On leaving fat cells ➞ FA ionize in the
plasma ➞ immediately combines with
albumin molecules (FFA)
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:
1. 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
The Fat Depots
• Large quantities of fat are stored in 2 major
tissues
Adipose tissue and liver
Adipose tissue is called fat depots
Adipose Tissue vs. Fat
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
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 .2001;345:1345
• 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
Recent proposed Classification of total body adipose tissue
Shen et al,Obes Res.2003;11:1
Internal
Subcutaneous
Superficial
Visceral
Deep
Intrathoracic
Intrapricardial
Extrapricardial
Intraabdominopelvic
Intraperitoneal
Intraabdominal
Preperitoneal
Non- visceral
Intramuscular
Perimuscular
Orbital
Extrapritoneal
Intrapelvic
Retrroperitoneal
Parametrial
Retropubic
Paravesical
Retrouterine
Pararectal
Retrorectal
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
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
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 )
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 Bhydroxybuteric 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!
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
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
Fat sparing effect of carbohydrates
•
Excess of carbohydrates ➞ preffered
metabolic fuel because :
1. ↑α-glycerophosophate ➞shift metabolism
toward fat storage
2. FA synthesized more rapidly than they are
degraded because of the availabilty of acetyl
CoA carboxylase ➞ converts acetyl CoA to FA
◎excess CHO in diet not only spares fat but
also increases fat synthesis
Upper and Lower Body Adipose Tissue Function:
A Direct Comparison of Fat Mobilization in males
between 22 to 43years.
Garry .Obes Res,2004
• 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:
1) 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.
• 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 smallscale physiological study.
• Results:
Gluteal adipose tissue has a lower blood
flow (67% lower, p < 0.05) and lower
hormone-sensitive lipase rate of action
(87% lower, p < 0.05) than abdominal
adipose tissue. Lipoprotein lipase rate of
action and mRNA expression are not
different between the depots.
This was the first demonstration of a
novel technique to directly investigate
gluteal adipose tissue metabolism.
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.
Another study done by Dora B and his colleagues
demonstrated that :
1. Abdominal adipocytes are more sensitive and
responsive to beta adrenergic stimulation of
lipolysis than gluteal adipocytes
2. Gluteal lipocytes have higher LPL activity than
abdominal lipocytes
This study was done on post menopausal females
Dora B, et al. regulation of lipolysis and lipoprotein lipase after weight loss in obese ,postmenopausal women .Obes Res .2004;12:32
Metabolic syndrome
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.
What are these health risks?
ATP III Guidelines
WHO Guidelines
Abdominal Obesity
Waist Circumference
Men > 40 inches (102 CM)
Women > 35 inches (88 CM)
Other Variables
Triglycerides 150 mg/dL
HDL-Cholesterol
Men < 40 mg/dL
Women < 50 mg/dL
Blood Pressure 130/ 85 mm Hg
Fasting Glucose 110 mg/dL
Waist/Hip Ratio
>0.90
>0.85
 150 mg/dL
<35 mg/dL
<39 mg/dL
>140/>90 mm Hg
110 mg/dL
WHO guidelines also include microalbuminuria (>20 µg/min or albumin:creatinine ratio
>30 mg/g).
The pathogenesis of metabolic
syndrome
Complex interplay of a still largely
unknown genetic background with
environmental lifestyle- related
factors
Environmental lifestyle-related factors:
When we eat ,our bodies break down the food
into its basic components ( proteincarbohydrates- 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
Markers of insulin resistance :
Hypertriglyceridemia
HDL
Hypertension
Hyperinsulinemia (>15µu/ml)
Marc C,et al. Obes Res.2005;13:703
Abdominal obesity
Hyperglycemia
Marjo etal , proven liver fat accumulation as an important
marker Obes Res 2002; 10: 859
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
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
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
Where does cholesterol come from?
80 % comes from the body itself , every cell in the
body is capable of making its own cholesterol ,
most don’t 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
Sequence of events in the life of lipoproteins
Liver
Makes and release VLDL
HDL
Released to tissues
Deposited in coronary
arteries
TRIGLYCERIDES
WITH CHOLESTEROL
Removed by liver
CholesteroL
rich
VLDL
TRI AND CHOLES
LDL
More triglycerides release
Scavenges cholesterl
From tissues carries
Through blood
Hands it off to
Cholesterol
Bulk +tri
LDL
MATURE
VLDL
Triglycerides
Released to blood
And tissues
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
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
What is the etiology that connects
obesity and hypertension?
Hyperinsulinemia and insulin resistance
Mechanism
1. Increased sodium retention
1. Increased sympathetic nervous system
activity
1. Alteration in the mechanics of blood
vessels
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.
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
•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.2001;40:282
•Increased White blood cell count is correlated with
insulin resistance in diabetic obese females
Pannacciulli et al,Obes Res.2003;11:1232
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
•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
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.2003;11:653-659
Oxidant Stress
Imbalance
Between
Formation
Of
Reactive oxygen/nitrogen species
(ROS/RNS)
And
Antioxidants
Pathologic stress 
(TNF
Induces monocytes to release mediators
and interleukins 1-6-8) 
Activates PMNs 
Release ROS(superoxide (O2·-), hydrogen
peroxide, hypochlorite, nitric oxide (NO),
hydroxyl radical 
Induce tissue injury by:
1.
2.
3.
•
•
damaging DNA
Cross linking cellular proteins
Peroxidation of membrane lipids 
Diminishing membrane fluidity
Increasing membrane permeability
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
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; 86:355-363
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; 84:1-6
Pischon et al, Obes Res.2003;11:1055
A novel pathway to the manifestations of
metabolic syndrome(2004)
Obesity And Diseases
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
What is the link between obesity and cancer
1. Hyperinsulinemia and insulin resistance
2. Oxidant stress
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 BMI>30 have 4 folds higher
prevalence than those <30
• Leptin overexpression in arthritic joint is related to
cartilage destruction and correlated with BMI
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,red 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)
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
Obesity and lungs
• Increased risk of intrapulmonary
shunts and ventilation perfusion
mismatching
• Pickwickian syndrome
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
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
Types and approaches to
obesity treatment
1. Do it yourself programs
2. Non-clinical programs
3. Clinical programs
•
Individual heath care professional
•
Multidisciplinary group of professionals
(physician ,dietitian ,exercise and
psychological counselors )
Evaluation of the program by the physician
•
•
The match between the program and the consumers
The soundness and safety of the program:
1.
2.
3.
4.
Assessment of physical health and psychological status
Attention to diet and pharmacotherapy
Attention to physical activity
Program safety
•
Outcome of the program
1.
2.
3.
4.
Long-term weight loss
Improvement in obesity related co morbidities
Improved heath practice
Monitoring adverse effects that might result from the program
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
W=weight (kg), H = height (cm), and A= age (yr)
e.g. weight : 120 kg H= 175 A=35
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
Side effects of very low caloric diets < RMR
• Increase NPY
• 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
• Hypernatremia ➞ fatigue, dizziness , confusion
and coma
• Constipation (absence of insoluble fibres)
Glycemic Index
• In 1981 Jenkins and his collegues developed
the GI.
• The GI for a food was defined relative to a
standard food (glucose or white bread).
• Over a 2-hour period, the area under the
glucose response curve after consuming 50
grams of carbohydrate from the test food was
compared with the area under the glucose
response curve after consuming 50 grams of
carbohydrate from the reference food.
• Both levels were given as the difference from
fasting blood glucose levels .
• The tests have been done in both healthy
people and people with diabetes.
Jenkins and his colleagues have
proposed that
• All carbohydrates are not equivalent and
that the rate of absorption of
carbohydrate foods into the bloodstream
is a critical factor in hyperinsulinemia.
• Slowly absorbed foods would be
beneficial because they trigger less of a
rise and fall in blood glucose and, thus,
less of a rise and fall in insulin levels
Supportive researches
• The Food and Agriculture Organization of the United
Nations and the World Health Organization have issued
an extensive report on various aspects of carbohydrate
in the diet that endorsed using the GI as an
appropriate guide for preventing obesity (1998)
• Other organizations have followed suit, particularly in
Europe (1998) , Canada, and Australia (2002) ..
• Writing in support of statements from the European
Association for the Study of Diabetes, Ha and Lean
(1998) have endorsed the use of the GI as one method
of assuring that carbohydrate foods with slower
absorption times be encouraged to assist in glycemic
control.
• In the U.S., Bell and Sears (2003) have similarly
encouraged the use of the GI to create a diet that
features low-GI carbohydrates as a way of reducing the
rising levels of both obesity and type 2 diabetes in the
U.S.
The Glycemic load
• Definition :The GI multiplied by the grams of
carbohydrate in a specific portion of a
carbohydrate-containing food.
• Because it slows absorption and lessens
hyperinsulinemia, a low–glycemic-load diet
would promote appropriate weight loss, improve
cardiovascular health, and reduce diabetes
• e.g., Carrots illustrate the leveling effect of using glycemic load
• it has a high glycemic index, but because it contains relatively little
carbohydrate, it ends up with a modest glycemic load
Salmeron, J, Manson, JE, Stampfer, MJ, Colditz, GA, Wing, AL, Willett, WC. (1997) Dietary fiber, glycemic load, and the risk of noninsulin-dependent diabetes mellitus in women JAMA 277,472-477
Bell, SJ, Sears, B. (2003) Low-glycemic-load diets: impact on obesity and chronic diseases Crit Rev Food Sci Nutr. 43,357-377
Alternative food pyramid
Ludwig, DS. (2000) Dietary glycemic index and obesity J Nutr. 130,280S-283S
• Ludwig in 2000 has developed an
alternative food pyramid based on the GI.
• The base (low-GI foods) is vegetables and
fruits
• The second tier is reduced-fat dairy, lean
protein, nuts, and legumes
• The third tier is unrefined grains and pasta
• and the top level, which should be the
most restricted in diet planning, is refined
grains, potatoes, and sweets.
Obstetric and Pediatric studies
Brand-Miller, JC, Holt, SHA, Pawlak, DB, McMillan, J. (2002) Glycemic index and
obesity Am J Clin Nutr. 76(suppl),281S-285S
• Weight gain was also lessened with a lowGI diet in a small study (n = 12) of
pregnant women.
• In a retrospective pediatric study, greater
weight loss has been seen with a low-GI
diet compared with a conventional low-fat
diet, although these do not seem to have
been isoenergetic diets
A more recent review by Brand-Miller et al.
(2003) has reviewed 14 studies of glycemic
control in people with diabetes using highvs. low-GI diets.
Although most of the studies were on small
numbers of people, and the usual dietary
compliance problems in free-living
individuals can be assumed, a slight, but
significant, benefit in glycemic control with
low-GI diets was detected.
Brand-Miller, J, Hayne, S, Petocz, P, Colagiuri, S. (2003) Low-glycemic index diets in the management
of diabetes: a meta-analysis of randomized controlled trials Diabetes Care 25,2261-2267
Criticisms of the GI
• As is immediately apparent from examination of
the GI table
Foster-Powell, K, Holt, SHA, Brand-Miller, JC. (2002) International table of glycemic index and glycemic load values: 2002 Am J
Clin Nutr. 76,5-56 )
• Values for the GI of foods can be rather broad.
• Published GI for boiled white rice, for instance,
varied from 45 to 112 .
• Bananas ranged from 30 to 70, partially
depending on their degree of ripeness.
• White durum-wheat semolina spaghetti varied
from 46 to 65, depending on length of cooking
time.
Judwith et al. Obes Res.2004
Energy Density
• Definition
Amount of energy in a given weight of food
(kcal/g)
• For the same amount of energy ,a greater
weight of food can be consumed when the
food is low in energy density than when
its energy density is high
Barbara j ,et al. J Am Diet Assoc.2005;105:S89
Components that have greatest impact
on energy density
1.Water : has the greatest impact because
it adds substantial weight without energy
2.Fat :because of its high caloric content
(9kcal/g)
! not all high fat foods have high energy
density ,water lowers ED even of high fat
food e.g., cheese has same ED of fat free
but dry pretzels
3.Fiber : modest influence as only limited
amount of fibers can be added to food
Researches on energy density
• Studies by Rolls and Bell (2000) have shown that
people often select food quantity by weight, so
that when low-energy-dense foods are selected,
calorie content is often decreased
• More recent work by Rolls et al. (2004) has
shown that modifying meals to increase the
amounts of fruits and vegetables, which are
generally not particularly energy dense, increases
satiety and leads people to select meals with a
lower total calorie content
• However, they have also found that instructing subjects to
increase the fruits and vegetables in their diet was not sufficient
for weight loss to occur, unless the added fruits and vegetables
also displaced high-energy-dense foods
American Society for Clinical Nutrition, has
noted that a number of diet strategies exist
for weight loss and that different individuals
may find different strategies useful.
Although they do not specifically endorse
either the GI or energy density as methods
for choosing foods, they have noted that
both have some support in the literature
and that further research into them is
warranted
Klein, S, Sheard, NF, Pi-Sunyer, X, et al (2004) Weight management through lifestyle modification for the
prevention and management of type 2 diabetes: rationale and strategies. A statement of the American
Diabetes Association, the North American Association for the Study of Obesity, and the American Society for
Clinical Nutrition Am J Clin Nutr. 80,257-263
Jeff S,et al.cardiovascular and hormonal
aspects of very low Carbohydrate
ketogenic diet.Obes Res.2004;S12:11s5
• The design was a parallel
,randomized ,clinical intervention
study of an energy restricted (deficit
of 500 kcal/d) CLCKD and low fat
diet (< 30%total energy from fat) in
29n healthy over-weight /obese men
and premenopausal women for 8
weeks.
TC
VLCD
Low Fat Diet
-11%
-15%
LDL NO CHANGE
-18%
HDL -3%
-7%
TG
-15%
-44%
VLCD
Low Fat Diet
-775 g/w
-384 g/w
TRUNKAL MASS -505 g/w
-157 g/w
INSULIN
- 29%
-12%
LEPTIN
- 50%
-17%
FREE T3
No significant changes
No significant changes
GLUCAGON
No significant changes
No significant changes
Inflammation
Biomarkers
REE
(kilojoules/Kg)
Same significant
reductions
Not significantly
affected
Same significant
reductions
Not significantly
affected
FAT LOSS
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,MD:NIH;1998
Data from a recent meta analysis that evaluated
randomized clinical trials that compared fatrestricted and calorie restricted diets has found
no difference in weight loss between diet groups
Pirozzo S,etal.Cochrane Database Syst Rev.2002;2:Cd003640
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
• 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 lowcarbohydrate 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-cholesterol
concentrations, in the low-carbohydrate than the lowfat group .
Mitochondrial uncouplings
All UCPs may lower mitochondrial ATP
production through respiratory uncoupling
,thus stimulating substrate oxidation in
mitochondria
Ricquier D, etal. Biochem J.2000;345:161- Fink BD,etal. J Biol Chem.2002;277:3918
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.2005;13:835.
• 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.
• Walking is metabolically expensive for obese :
1. Greater body mass and heavier legs
2. Decreased stability and wider lateral leg swing.
Energy cost of walking is 20-100%greater for obese
• Walking slower for a set distance is an
appropriate exercise recommendation
for weight management prescription in
obese adults
Raymond ,etal. Obes Res .2005;13:891
Why treat overweight and obesity?
Not only
to improve the BODY IMAGE
But also
to reduce the
OBESITY –RELATED COMORBIDITIES