Test bank for critical care nursing a holistic approach 11th edition morton f...
Approach to a patient of obesity
1. APPROACH TO A PATIENT OF
OBESITY
MODERATOR: Dr Vishvanayak Sir
Professor; Dept. of Medicine
PRESENTED BY: Dr Veeresh Kumar Dhanni
PG Resident IInd year; MD (Medicine)
2. BACKGROUND
• In a world where food supplies are intermittent, the ability to store
energy in excess, of what is required for immediate use, is essential for
survival.
• Fat cells, residing within widely distributed adipose tissue depots, are
adapted to store excess energy efficiently as triglyceride, and when
needed, releases stored energy as free fatty acids for use at other sites.
• However, in the presence of nutritional abundance and a sedentary
lifestyle, and influenced by genetic endowment, this system increases
adipose energy stores & produces adverse health consequences.
• Obesity is a substantial public health crisis in the industrialized world,
whose prevalence is increasing rapidly.
3. • This growing rate represents a pandemic that needs urgent attention if
obesity’s potential toll on morbidity, mortality and economics is to be
avoided.
• Compared with a non-obese person, an obese person incurs more in
medical costs annually (annual cost of lost productivity due to obesity,
spent annually on weight-loss products and services).
• In a 2016 position statement, the American Association of Clinical
Endocrinologists (AACE) and the American College of Endocrinology
(ACE) proposed a new name for obesity, Adiposity-based Chronic
Disease (ABCD).
• They did not introduce the name as an actual replacement for the term
obesity but instead as a means of helping the medical community focus
on the pathophysiologic impact of excess weight.
4. DEFINITION
• Obesity is a state of - excess adipose tissue mass. Although often viewed
as equivalent to increased body weight, but this need not be the case
always, lean but very muscular individuals may be overweight by multiple
standards without having increased adiposity.
• Obesity can be defined as a chronic, multi-factorial, neuro-behavioural
disease, wherein an increase in body fat promotes adipose tissue
dysfunction & abnormal fat mass physical forces, resulting in adverse
metabolic, bio-chemical & psycho-social health consequences.
• Obesity represents a state of excess storage of body fat. Obesity is
therefore defined by assessing its linkage to morbidity or mortality.
5. PREVALENCE
• Data from the National Health and Nutrition Examination Surveys
(NHANES) show that the increasing prevalence of medically significant
obesity raises great concern. Overall, the prevalence of obesity is higher in
women (38%) than in men (34%).
• According to the World Health Organization, global obesity almost
doubled between 1980 and 2008.
• There were >200 million obese men and almost 300 million obese
women, i.e., 11% of adults worldwide, in 2008.
• A majority (65%) of the world’s population lives in countries where being
overweight or obese kills more people than being underweight.
6.
7. • In developing countries, such as India, obesity prevalence is rising (5%)
with a greater tendency to harmful intra-abdominal obesity at lower
BMIs in this population, and the consequences for metabolic and
cardiovascular health are disproportionate to obesity prevalence.
• The causes of increased obesity globally are complicated, and may vary
from country to country, but contributory factors include:
• rising incomes,
• changing food supplies,
• reduced physical activity.
8. PHYSIOLOGY
• Physiologic regulation of body weight depends on:
• Energy balance
• Appetite
• Energy expenditure
• Brown adipose tissue
• Adipocyte
• Leptin
• ENERGY BALANCE
• Body weight is regulated by both endocrine and neural components
that ultimately influence the effector arms of energy intake and
expenditure. Even small imbalances between energy intake and
expenditure will ultimately have large effects on body weight.
9. • For example, a 0.3% positive imbalance over 30 years would result in a
9kg weight gain.
• Alterations in stable weight by forced overfeeding or food deprivation
induce physiologic changes, i.e.;
• with weight loss, appetite increases and energy expenditure
falls;
• with overfeeding, appetite falls and energy expenditure
increases.
• These compensatory mechanism fails, however, permitting obesity to
develop when food is abundant and physical activity is limited.
• APPETITE
• Appetite is desire to eat food, sometimes due to hunger or due to other
neurological or metabolic triggers.
10. • Appetite is influenced by many factors that are integrated by the brain,
most importantly within the hypothalamus. Signals that impinge on
the hypothalamic center include neural afferents, hormones, and
metabolites.
11. • ENERGY EXPENDITURE
• It includes the following components:
• resting or basal metabolic rate;
• the energy cost of metabolizing and storing food;
• the thermic effect of exercise;
• adaptive thermogenesis, which varies in response to long-term
caloric intake (rising with increased intake).
*Basal metabolic rate accounts for ~70% of daily energy
expenditure, whereas active physical activity contributes 5–10%.
• BROWN ADIPOSE TISSUE (BAT)
• Adaptive thermogenesis occurs in BAT, which plays an important
role in energy metabolism in many mammals. In contrast to white
adipose tissue, which is used to store energy in the form of lipids,
BAT expends stored energy as heat.
12. • A mitochondrial uncoupling protein (UCP-1) in BAT dissipates the
hydrogen ion gradient in the oxidative respiration chain and
releases energy as heat.
• The metabolic activity of BAT is increased by a central action of
leptin, acting through the sympathetic nervous system that heavily
innervates this tissue.
• In rodents, BAT deficiency causes obesity and diabetes; stimulation
of BAT with a specific adrenergic agonist (β3 agonist) protects against
diabetes and obesity.
• BAT exists in humans (especially neonates), and although its
physiologic role is not yet established, identification of functional
BAT in many adults using positron emission tomography (PET)
imaging has increased interest in the implications of the tissue for
pathogenesis and therapy of obesity.
13. • Beige fat cells, recently described, resemble BAT cells in expressing
UCP-1. They are scattered through white adipose tissue, and their
thermogenic potential is uncertain.
• THE ADIPOCYTE AND ADIPOSE TISSUE
• Adipose tissue is composed of the lipid-storing adipose cell and a
stromal/vascular compartment in which cells including pre-
adipocytes & macrophages reside.
• Adipose mass increases by enlargement of adipose cells through lipid
deposition, as well as by an increase in the number of adipocytes.
• Hypertrophic V/S Hypercellular Obesity
• Hypertrophic obesity, characterized by enlarged fat cells, is
typical of android abdominal obesity.
• Hypertrophic obesity usually starts in adulthood, is
associated with increased cardiovascular risk, and responds
quickly to weight reduction measures.
14. • Hypercellular obesity is more variable than hypertrophic
obesity; it typically occurs in persons who develop obesity in
childhood or adolescence.
• Hypercellular obesity may find it difficult to lose weight
through nonsurgical interventions.
15. • Adiponectin, an abundant adipose-derived protein whose levels are
reduced in obesity, enhances insulin sensitivity and lipid oxidation
and has vascular-protective effects, whereas RBP4, whose levels are
increased in obesity, may induce insulin resistance.
• LEPTIN
• The product of the ob gene, is peptide leptin, a name derived from the
Greek root leptos, meaning thin.
• Leptin is secreted by adipose cells and acts primarily through the
hypothalamus.
• Its level of production provides an index of adipose energy stores.
• Raising leptin levels can decrease food intake and increase energy
expenditure.
16.
17. ETIOLOGY
• Obesity is a heterogeneous group of disorders.
• Causes:
• Primary causes:
• Physical inactivity
• Eating habits
• Psychological factors (overeating may be a symptom of depression,
anxiety and frustration)
• Genetic factors
• Secondary causes:
• Hypothyroidism
• Cushing's syndrome
18. • Hypothalamic disorders
• Diabetes mellitus
• Pickwickian syndrome
• Laurence-Moon-Biedl syndrome
• Medications-valproic acid, carbamazepine, antidepressants,
corticosteroids, antipsychotics, lithium and glipizide
• Genes Versus Environment
• Obesity is commonly seen in families, and the heritability of body
weight is similar to that for height.
• Inheritance is usually not Mendelian, however, and it is difficult to
distinguish the role of genes and environmental factors.
• Currently, identified genetic variants, both common and rare, account
for <5% of the variance of body weight.
19. • Environment plays a key role in obesity, as evidenced by the fact that
famine limits obesity in even the most obesity-prone individual.
• Undoubtedly, genes influence the susceptibility to obesity in response
to specific diets and availability of nutrition.
• Cultural factors are also important, these relate to both availability
and composition of the diet and to changes in the level of physical
activity.
• Role of diet composition in obesity continues to generate controversy,
it appears that high-fat diets, when combined with simple, rapidly
absorbed carbohydrates, promote obesity.
• Specific genes are likely to influence the response to specific diets,
but these genes are largely unidentified.
20. • Additional environmental factors may contribute to the increasing
obesity prevalence:
• sleep deprivation,
• changes in gut micro-biome,
• viral infections.
• Specific syndromes associated with obesity
• Cushing’s Syndrome
• Obesity may be associated with excessive local reactivation of
cortisol in fat by 11β-hydroxysteroid dehydrogenase 1, an
enzyme that converts inactive cortisone to cortisol.
• Hypothyroidism
• The weight gain that occurs in hypothyroidism is mostly due to
myxedema.
21. • Insulinoma
• Patients with insulinoma often gain weight as a result of overeating
to avoid hypoglycemic symptoms.
• The increased substrate plus high insulin levels promote energy
storage in fat.
• Craniopharyngioma And Other Disorders Involving The
Hypothalamus
• Whether through tumors, trauma, or inflammation,
hypothalamic dysfunction of systems controlling satiety, hunger,
and energy expenditure can cause varying degrees of obesity.
• Specific Genetic Syndromes
• Genetic defects disturbs a defined pathway through which leptin (by
stimulating POMC and increasing α-MSH) restricts food intake and
limits weight.
24. PATHOGENESIS
• Obesity can result from increased energy intake, decreased energy
expenditure, or a combination of the two.
25. • Concept of a body weight set point
• This idea is supported by physiologic mechanisms centered around a
sensing system in adipose tissue that reflects fat stores and a receptor,
or adipostat, that is in the hypothalamic centers.
• When fat stores are depleted, the adipostat signal is low, and the
hypothalamus responds by stimulating hunger and decreasing energy
expenditure to conserve energy.
• Conversely, when fat stores are abundant, the signal is increased,
and the hypothalamus responds by decreasing hunger and increasing
energy expenditure.
• The recent discovery of the ob gene, and its product leptin, and the db
gene, whose product is leptin receptor, provides important elements
of a molecular basis for this physiologic concept.
26. • What Is the Status of Food Intake in Obesity?
• Do the Obese Eat More Than the Lean?
• Many obese individuals believe that they eat small quantities of food,
and this claim has often been supported by the results of food intake
questionnaires.
• However, it is now established that average energy expenditure
increases as individuals get more obese, due primarily to the fact that
metabolically active lean tissue mass increases with obesity.
• Given the laws of thermodynamics, the obese person must therefore
eat more than the average lean person to maintain their increased
weight.
• What Is the State of Energy Expenditure in Obesity?
• The average total daily energy expenditure is higher in obese than
lean individuals when measured at stable weight.
27. • However, energy expenditure falls as weight is lost, due to loss of
lean body mass and to decreased sympathetic nerve activity.
• The physiologic basis for variable rates of energy expenditure (at a
given body weight and level of energy intake) is essentially unknown.
• Another component of thermogenesis, called non-exercise activity
thermogenesis (NEAT), has been linked to obesity.
• It is the thermogenesis that accompanies physical activities other than
volitional exercise such as the activities of daily living, fidgeting,
spontaneous muscle contraction, and maintaining posture.
• The wide variation in fat storage seen in overfed individuals is
predicted by the degree to which NEAT is induced. The molecular
basis for NEAT and its regulation is unknown.
28. • Role of Leptin
• The vast majority of obese persons have increased leptin levels but do
not have mutations of either leptin or its receptor.
• They appear, therefore, to have a form of functional leptin resistance.
• Some individuals produce less leptin per unit fat mass than others or
have a form of relative leptin deficiency that predisposes to obesity are
at present contradictory and unsettled.
29. PATHOLOGY
• Obesity has major adverse effects on health, associated with an increase in
mortality, with a 50-100% increased risk of death from all causes
compared to normal-weight individuals, mostly due to cardiovascular
causes.
• Mortality rates rise as obesity increases, particularly when obesity is
associated with increased intra-abdominal fat. Life expectancy of a:
• moderately obese individual could be shortened by 2-5 years,
• a 20 to 30 year old male with a BMI >45 may lose 13 years of life.
• Insulin Resistance and Type 2 Diabetes Mellitus
• Hyper-insulinemia and insulin resistance are pervasive features of
obesity, increasing with weight gain & diminishing with weight loss.
30. • Insulin resistance is more strongly linked to intra-abdominal fat than
to fat in other depots. Molecular links between obesity and insulin
resistance in fat, muscle, and liver, include:
• insulin itself, by inducing receptor down-regulation;
• free fatty acids that are increased and capable of impairing
insulin action;
• intracellular lipid accumulation;
• several circulating peptides produced by adipocytes, including the
cytokines TNF-α and IL-6, RBP4, and the adipokine-adiponectin,
which have altered expression in obese adipocytes and can modify
insulin action.
• Additional mechanisms:
• obesity-linked inflammation,
• infiltration of macrophages into tissues including fat,
• induction of the endoplasmic reticulum stress response (cause
resistance to insulin action in cells).
31. • Despite the prevalence of insulin resistance, most obese individuals do
not develop diabetes, suggesting that diabetes requires an
interaction between obesity-induced insulin resistance & impaired
insulin secretion.
• Obesity, however, is a major risk factor for diabetes, and as many as
80% of patients with type 2 diabetes mellitus are obese. Weight loss
and exercise, even of modest degree, increase insulin sensitivity and
often improve glucose control in diabetes.
• Reproductive Disorders
• Disorders that affect the reproductive axis in male:
• Hypogonadism;
• in men, whose weight is >160% ideal body weight (IBW),
plasma testosterone and sex hormone binding globulin (SHBG)
are often reduced;
32. • estrogen levels (derived from conversion of adrenal androgens in
adipose tissue) are increased;
• free testosterone may be decreased in morbidly obese men whose
weight is >200% IBW.
• gynecomastia may be seen.
• Disorders that affect the reproductive axis in female:
• menstrual abnormalities;
• increased androgen production;
• decreased SHBG;
• increased peripheral conversion of adrenal androgen to estrogen,
• oligomenorrhea with polycystic ovarian syndrome (PCOS),
with its associated anovulation and ovarian hyperandrogenism
(40% of women with PCOS are obese).
• In obese women with PCOS, weight loss often restores normal
menses.
33. • The increased conversion of androstenedione (adrenal androgen) to
estrogen, which occurs to a greater degree in women with lower body
obesity, may contribute to the increased incidence of uterine cancer
in postmenopausal women with obesity.
• Cardiovascular Disease
• Obesity is an independent risk factor for cardiovascular disease in
men and women (including coronary disease, stroke & congestive
heart failure). The waist-to-hip ratio may be the best predictor of
these risks.
• Hypertension and glucose intolerance associated with obesity, leads
to more adverse impact of obesity.
• Obesity, especially intra-abdominal obesity, is associated with an
atherogenic lipid profile;
• increased low-density lipoprotein cholesterol,
• increased very-low-density lipoprotein,
34. • increased triglyceride;
• decreased high-density lipoprotein cholesterol
• decreased levels of the vascular protective adipokine
adiponectin.
• Obesity-induced hypertension is associated with:
• increased peripheral resistance and cardiac output,
• increased sympathetic nervous system tone,
• increased salt sensitivity,
• increased insulin-mediated salt retention.
• Pulmonary Disease
• Obesity may be associated with:
• reduced chest wall compliance,
• increased work of breathing,
• increased minute ventilation due to increased metabolic rate,
35. • decreased functional residual capacity
• decreased expiratory reserve volume.
• Severe obesity may be associated with:
• obstructive sleep apnea (obesity hypoventilation syndrome),
• hypoxic and hypercapnic ventilatory responses.
• Sleep apnea can be obstructive (most common), central, or
mixed and is associated with hypertension.
• Continuous positive airway pressure has been used with some
success.
*Weight loss (10–20 kg) can bring substantial improvement.
• Hepatobiliary Disease
• Obesity is frequently associated with non-alcoholic fatty liver disease
(NAFLD), one of the most common causes of liver disease in
industrialized countries.
36. • NAFLD + Hepatic Fatty Infiltration inflammatory non-alcoholic
steato-hepatitis (NASH) cirrhosis hepatocellular carcinoma.
• Steatosis typically improves following weight loss, secondary to diet
or bariatric surgery.
• Obesity is associated with:
• enhanced biliary secretion of cholesterol,
• super-saturation of bile,
• higher incidence of gallstones, particularly cholesterol gallstones.
• A person 50% above IBW has about a six-fold increased incidence of
symptomatic gallstones.
• Paradoxically, fasting increases super-saturation of bile by
decreasing the phospholipid component. Fasting-induced
cholecystitis is a complication of extreme diets.
37. • Cancer
• Obesity is associated with:
• increased risk cancer,
• poorer treatment outcomes,
• increased cancer mortality.
• Obesity in males is associated with higher mortality from cancer of:
• esophagus,
• colon,
• rectum,
• pancreas,
• liver,
• prostate.
• Obesity in females is associated with higher mortality from cancer of:
• gallbladder,
38. • bile ducts,
• breasts,
• endometrium,
• cervix,
• ovaries.
• Bone
• Obesity is associated with an increased risk of osteoarthritis, partly
due to the trauma of added weight bearing, but potentially linked to
activation of inflammatory pathways that could promote synovial
pathology.
• Joint
• The prevalence of gout may also be increased.
39. • Cutaneous Disease
• Acanthosis nigricans, darkening and thickening of the skinfolds on
the neck, elbows, and dorsal inter-phalangeal spaces.
• Acanthosis reflects the severity of underlying insulin resistance
and diminishes with weight loss.
• Friability of skin may be increased, especially in skinfolds, enhancing
the risk of fungal and yeast infections.
• Venous stasis is increased in the obese.
43. METABOLIC SYNDROME
• The metabolic syndrome, also known as syndrome X, insulin resistance
syndrome, consists of a constellation of metabolic abnormalities that
confer increased risk of cardiovascular disease (CVD) and diabetes
mellitus.
• The major features of the metabolic syndrome include:
• central obesity,
• hypertriglyceridemia,
• low levels of high-density lipoprotein (HDL),
• hyperglycemia,
• hypertension.
• Higher prevalence in women than men, i.e., 36% vs 30%, respectively.
46. COVID-19 & OBESITY
• The Centers for Disease Control and Prevention (CDC) includes obesity
in the list of conditions that increase the likelihood of severe illness in
persons with COVID-19.
• An international study reported that older age, male sex & obesity is the
greatest risk factor for severe pneumonia.
• The death rate is even higher in the obese COVID-19 patients, as a result
of hypoxia, due to the interplay between adipose tissue hypoxia and
obstructive sleep apnea.
• The discrepancy of manifestations seen in COVID-19 seems to be
mediated by a differential immune response rather than a differential
viral load.
47.
48. HIF
HIF β
HIF α
stable protein in the
nucleus, under hypoxic
changes, its activity is
unaffected
has a short half-life and because of its
degradation by an enzyme known as propyl
hydroxylase; under hypoxic conditions,
propyl hydroxylase gets deactivated, thus
leading to the stabilization of HIFα
HIF 2α
HIF 1α
may act on
hemopoietin genes
(heme-regulating
genes).
HIF-2α is
stimulated by
chronic hypoxia.
acts on EPO
release seems to be
markedly augmented in
obesity due to adipose
tissue hypoxia and
obstructive sleep apnea
resulting in cyclic
hypoxia
can also be secreted
by direct viral
proteolytic effects
exerts detrimental effects on the
immune system, characterized by
unopposed pro-inflammation at
the macrophages, dendritic cells, T
cells, and complement levels
resulting in cytokines’ storm,
which is linked to the poor
outcomes of COVID-19.
role is regulatory
and largely opposes
the actions mediated
by HIF-1α
Inhibiting HIF-1α release or switching its production to HIF-
2α by natural products such as resveratrol or by synthetic
drugs, a good therapeutic strategy can be offered to prevent
COVID-19 worst outcome in infected patients
49. DIAGNOSIS
• Standard laboratory studies in the evaluation of obesity should include the
following:
• Fasting lipid panel
• Liver function studies
• Thyroid function tests
• Fasting glucose and hemoglobin A1c (HbA1c)
• Other tests are performed as indicated by clinical findings.
• For example, the 24-hour urinary free-cortisol test is needed only
when Cushing syndrome or other hypercortisolemic states are
clinically suspected.
• Lipid panel
• At minimum, test fasting cholesterol, triglycerides, and high-density
lipoprotein cholesterol (HDL-C) levels.
50. • These levels may be normal, or the typical dyslipidemia associated
with cardiometabolic syndrome may be found.
• This dyslipidemia is characterized by reduced HDL-C and elevated
fasting triglyceride concentrations.
• Liver and thyroid function tests
• Liver function tests yield normal results in most obese patients.
• However, elevated transaminase levels may indicate non-alcoholic
steatohepatitis (NASH) or fatty infiltration of the liver.
• Thyroid function test results are also typically normal, but checking
them to detect primary hypothyroidism.
• Screening with a serum thyrotropin level is usually sufficient.
• Glucose and Insulin studies
• Obesity is associated with insulin resistance and increased serum
levels of fasting insulin and C-peptide serum levels.
51. • All patients with obesity should be screened for diabetes.
• Evaluation of Degree of Fat
• Five main steps for evaluation of obesity:
• a focused obesity-related history,
• a physical examination to determine the degree and type of
obesity,
• assessment of comorbid conditions,
• determination of fitness level,
• assessment of the patient’s readiness to adopt lifestyle changes.
• The Obesity-Focused History
• Information from the history should address the following seven
questions:
• What factors contribute to the patient’s obesity?
• How is the obesity affecting the patient’s health?
52. • What is the patient’s level of risk from obesity?
• What does the patient find difficult about managing weight?
• What are the patient’s goals and expectations?
• Is the patient motivated to begin a weight management
program?
• What kind of help does the patient need?
• Although the vast majority of cases of obesity can be attributed to
behavioural factors that affect diet and physical activity
patterns, but the history may suggest secondary causes that merit
further evaluation. Disorders to consider include:
• polycystic ovarian syndrome,
• hypothyroidism,
• Cushing’s syndrome,
• hypothalamic disease.
53. • Drug-induced weight gain also should be considered. Common causes
include medications for:
• diabetes (insulin, sulfonylureas, thiazolidinediones);
• steroid hormones;
• antipsychotic agents (clozapine, olanzapine, risperidone);
• mood stabilizers (lithium);
• antidepressants (tricyclics, monoamine oxidase inhibitors,
paroxetine, mirtazapine);
• antiepileptic drugs (valproate, gabapentin, carbamazepine).
• Other medications, such as non-steroidal anti-inflammatory drugs
and calcium channel blockers, may cause peripheral edema but do
not increase body fat.
• The patient’s current diet and physical activity patterns may reveal
factors that contribute to the development of obesity and may identify
behaviors to target for treatment.
54. • Physical examination to determine the degree and type of obesity
• Three key anthropometric measurements are important in evaluating
the degree of obesity:
• weight,
• height,
• waist circumference.
• Body Mass Index (BMI) and Waist Circumference
• Although not a direct measure of adiposity, the most widely used
method to gauge obesity is the:
• Body Mass Index (BMI) (which is equal to weight/height2 (in
kg/m2)),
• In general, BMI correlates closely with the degree of body
fat in most settings; however, this correlation is weaker at low
BMIs.
55. • The BMI is used to classify weight status & risk of disease.
BMI provides an estimate of body fat & is related to disease
risk. At a similar BMI, women have more body fat than
men.
• A BMI of 30 is most commonly used as a threshold for
obesity in both men and women.
• All-cause, metabolic, cancer, and cardiovascular morbidity
begin to rise when BMIs are ≥25.
• Most authorities use the term overweight to describe
individuals with BMIs between 25 and 30.
• Lower BMI thresholds for overweight & obesity have been
proposed for the Asia-Pacific region since this population
appears to be at risk for glucose & lipid abnormalities at
lower body weights.
56.
57. • The surgical literature often uses a different classification to
recognize particularly severe obesity. The categories are as follows:
• Severe obesity- BMI >40 kg/m2
• Morbid obesity- BMI of 40-50 kg/m2
• Super obese- BMI >50 kg/m2.
• Ideal body weight for height
• Calculated by multiplying square of height in meters by 22.5.
• Overweight: More than 10% of ideal body weight.
• Obesity: More than 20% of ideal body weight.
• Underweight: Less than 20% of ideal body weight.
• Waist circumference and waist to hip ratio
• Measurement of the waist circumference is a surrogate for visceral
adipose tissue and should be performed in the horizontal plane above
the iliac crest, specifically, at the narrowest segment between ribcage
and iliac crests.
58. • Waist circumference >80 cm in females and >90 cm in males
indicate abdominal obesity.
• Maximum measurement over buttocks as hip measurement.
• Waist:hip ratio <0.8 in females and <0.9 in males-normal.
• Waist:hip ratio >0.8 in females and >0.9 in males-obesity.
• The distribution of adipose tissue in different anatomic depots also
has substantial implications for morbidity.
• Specifically, intra-abdominal and abdominal subcutaneous fat
have more significance than subcutaneous fat present in the
buttocks and lower extremities.
• Excess abdominal fat, assessed by measurement of waist
circumference or waist-to-hip ratio, is independently associated with
a higher risk for diabetes mellitus and cardiovascular disease.
59. • Many of the most important complications of obesity, such as insulin
resistance, diabetes, hypertension, hyperlipidemia, and hyper-
androgenism in women, are linked more strongly to intra-abdominal
and/or upper body fat than to overall adiposity.
• The mechanism underlying this association is unknown but may relate
to the fact that intra-abdominal adipocytes are more lipo-lytically
active than those from other depots.
• Release of free fatty acids into the portal circulation has adverse
metabolic actions, especially on the liver. Adipokines and cytokines
that are differentially secreted by adipocyte depots may play a role in
the systemic complications of obesity.
• Other procedures that are used in few clinical centers include the following:
• Skin fold thickness
• Estimated by using special calipers.
60. • Skin fold thickness measured over triceps, biceps, subscapular
and supra-iliac regions.
• Normal triceps skin fold thickness in males-12.5 mm.
• Normal triceps skin fold thickness in females-16.5 mm.
• A person’s body fat percentage can be indirectly estimated by using
the Deurenberg equation, as follows:
• body fat percentage = 1.2(BMI) + 0.23(age) - 10.8(sex) - 5.4
• with age being in years and sex being designated as 1 for males and
0 for females.
• Normally, healthy men have a body fat percentage of 15-20%,
while normal healthy women have a body fat percentage of 25-
30%.
• This equation has a standard error of 4% and accounts for
approximately 80% of the variation in body fat.
61. • Dual-energy radiographic absorptiometry (DEXA) (measure body
composition, particularly fat mass and fat-free mass, but cannot
distinguish between subcutaneous and visceral abdominal fat deposits)
• The current standard techniques for measuring visceral fat volume are
abdominal computed tomography (CT) scanning and magnetic
resonance imaging (MRI) techniques.
• Bioelectrical impedance analysis
• Ultrasonography to determine fat thickness
• Less expensive techniques for direct measurement of visceral fat
include abdominal ultrasonography and abdominal bioelectrical
impedance.
• Underwater weighing.
62.
63. • Assessment of comorbid conditions
• Obesity-Associated Comorbid Conditions
• The evaluation of comorbid conditions should be based on
presentation of symptoms, risk factors, and index of suspicion.
• For all patients, a fasting lipid panel should be performed and a
fasting blood glucose level and blood pressure must be
determined.
• Patients at very high absolute risk include those with the
following:
• established coronary heart disease,
• presence of other atherosclerotic diseases (peripheral arterial
disease, abdominal aortic aneurysm),
• symptomatic carotid artery disease,
• type 2 diabetes,
• sleep apnea.
64. • Identifying the High-Risk Patient
• The American Society of Clinical Endocrinologists (AACE) and
the American College of Endocrinology (ACE) have proposed an
obesity disease staging system that is based on ethnic-specific
BMI cutoffs in conjunction with assessment for adiposity-related
complications.
• Stage 0 is assigned to individuals who are overweight or obese by
BMI classification but have no complications, whereas stages 1
and 2 are defined as individuals who are overweight or obese by
BMI classification and have one or more mild-moderate
complications (stage 1) or at least one severe complication
(stage 2).
• A different functional staging system for obesity, called the
Edmonton Obesity Staging System (EOSS), classifies individuals
with obesity into five graded categories (0–4), based on their
morbidity and health-risk profile along three domains-medical,
functional, and mental, independent of BMI.
65.
66. • Determination of fitness level (physical fitness)
• Several prospective studies have demonstrated that physical fitness,
reported by questionnaire or measured by a maximal treadmill
exercise test, is an important predictor of all-cause mortality rate
independent of BMI and body composition.
• These observations highlight the importance of taking a physical
activity and exercise history during examination as well as
emphasizing physical activity as a treatment approach.
• Assessing the Patient’s Readiness to Change
• Assessment includes patient motivation and support, stressful life
events, psychiatric status, time availability and constraints, and
appropriateness of goals and expectations.
• Readiness can be viewed as the balance of two opposing forces:
• motivation or the patient’s desire to change,
• resistance or the patient’s resistance to change.
67. • A helpful method to begin a readiness assessment is to use the
motivational interviewing technique of anchoring the patient’s
interest and confidence to change on a numerical scale.
• With this technique, the patient is asked to rate on a scale from 0 to
10, with 0 being not so important or confident and 10 being very
important or confident, his or her level of interest in and confidence
about losing weight at this time.
68.
69. TREATMENT
• The Goal of Therapy
• Primary goals of treatment are:
• to improve obesity-related comorbid conditions,
• reduce the risk of developing future comorbidities.
• The decision of how aggressively to treat the patient and which
modalities to use is determined by:
• patient’s risk status,
• expectations,
• available resources.
• Not all patients who are obese by BMI alone, need to be treated, as
exemplified by the concepts of obesity paradox or the metabolically
healthy obese.
70. • Depending on BMI risk category, modality/therapy recommended
for obesity management:
• lifestyle management,
• Pharmacotherapy,
• surgery.
• An initial weight-loss goal should be of 8–10% of present weight
over 6 months, it is a realistic target as well, and should be affirmative
about maintenance of weight loss.
71.
72. LIFESTYLE MANAGEMENT
• Obesity care involves attention to three essential elements of lifestyle:
• dietary habits,
• physical activity,
• behavior modification.
• Because obesity is fundamentally a disease of energy imbalance, all
patients must learn:
• how and when energy is consumed (diet),
• how and when energy is expended (physical activity),
• how to incorporate this information into their daily lives
(behavioral therapy).
73. • DIET THERAPY
• The primary focus of diet therapy is to reduce overall calorie
consumption.
• Guidelines from the American Heart Association/American College of
Cardiology/The Obesity Society (AHA/ACC/TOS) recommend
initiating treatment with:
• a calorie deficit of 500–750 kcal/d compared with the patient’s
habitual diet,
• alternatively, a diet of 1200–1500 kcal/d for women and 1500–
1800 kcal/d for men (adjusted for the individual’s body weight)
can be prescribed.
*This reduction is consistent with a goal of losing ~0.5-1 kg/week.
• The calorie deficit can be instituted through dietary substitutions or
alternatives. Examples include choosing
• smaller portion sizes,
74.
75. • eating more fruits and vegetables,
• consuming more whole-grain cereals,
• selecting leaner cuts of meat and skimmed dairy products,
• reducing consumption of fried foods and other foods with added
fats and oils,
• drinking water instead of sugar-sweetened beverages.
• It is important that dietary counseling remains patient centered and
that the selected goals are SMART, i.e.;
• Specific,
• Measurable,
• Agreed upon,
• Realistic,
• Timely.
76. • The macronutrient composition of the diet, the 2015 U.S. Department
of Agriculture Dietary Guidelines for Americans, which focus on
health promotion and risk reduction, for treatment of patients who
are overweight or obese, recommends:
• a diet rich in whole grains, fruits, vegetables, and dietary fiber;
• decreasing sodium intake to <2300 mg/d;
• consuming fat-free or low-fat dairy products;
• keeping added sugars and saturated fat intake to <10% of daily
calories.
• The macronutrient composition will ultimately be determined by
the:
• patient’s taste preferences, cooking style, and culture.
• patient’s underlying medical problems.
• patient’s metabolic profile and risk factors.
• Application of these guidelines to specific calorie goals can be found
on the website www.choosemyplate.gov.
77. • Another dietary approach to consider is based on the concept of
energy density, which refers to the number of calories (i.e., amount
of energy) a food contains per unit of weight.
• Foods with low-energy density include soups, fruits, vegetables,
oatmeal, and lean meats.
• Foods with high-energy density include dry fruits and high-fat
foods such as cheese, egg yolks, potato chips, and red meat.
*Diets containing low-energy-dense foods have been shown to
control hunger and thus to result in decreased caloric intake and
weight loss.
• Occasionally, very low-calorie diets (VLCDs) are prescribed as a form
of aggressive dietary therapy. The primary purpose of a VLCD is to
promote a rapid and significant (13- to 23-kg) short-term weight
loss over a 3 to 6 month period.
• The proprietary formulas designed for this purpose typically supply
≤800 kcal, 50–80 g of protein, and 100% of the recommended
daily intake for vitamins and minerals.
78. • According to a review by the National Task Force on the Prevention
and Treatment of Obesity, indications for initiating a VLCD include:
• involvement of well-motivated individuals who are moderately to
severely obese (BMI, >30 kg/m2),
• have failed at more conservative approaches to weight loss,
• have a medical condition that would be immediately improved
with rapid weight loss. These conditions include:
• poorly controlled type 2 diabetes,
• hypertriglyceridemia,
• obstructive sleep apnea,
• symptomatic peripheral edema.
• The risk for gallstone formation increases exponentially at rates of
weight loss >1.5 kg/week. Prophylaxis against gallstone formation
with urso-deoxycholic acid (600 mg/d) is effective in reducing this
risk.
79. • VLCDs should be used only in limited circumstances and only when
provided by trained practitioners in a medical care setting where
medical monitoring and high intensity lifestyle intervention can be
provided.
• PHYSICAL ACTIVITY
• Although exercise alone is only moderately effective for weight loss,
while the combination of dietary modification and exercise is the
most effective lifestyle approach for the treatment of obesity.
• The most important role of exercise appears to be in the maintenance
of the weight loss.
• Recommendation is, adults should engage in 150 min of moderate-
intensity or 75 min a week of vigorous-intensity aerobic physical
activity per week, performed in episodes of at least 10 min and
preferably spread throughout the week.
80. • We should focus on simple ways to add physical activity into the
normal daily routine like:
• brisk walking,
• using the stairs,
• doing housework and yard work,
• engaging in sports.
• Moreover, ask the patient to wear a pedometer or accelerometer to
monitor total accumulation of steps or kcal expended as part of the
activities of daily living, its is a useful strategy.
• BEHAVIORAL THERAPY
• Cognitive behavioral therapy is used to help change and reinforce
new dietary and physical activity behaviors. Strategies include:
• self-monitoring techniques (e.g., journaling, weighing, and
measuring food and activity);
• stress management;
81. • stimulus control (e.g., using smaller plates, not eating in front of
the television or in the car);
• social support;
• problem solving;
• cognitive restructuring to help patients develop more positive
and realistic thoughts about themselves.
• When recommending any behavioral lifestyle change, the patient
should be asked to identify what, when, where, and how the
behavioral change will be performed.
• The patient should keep a record of the anticipated behavioral
change so that progress can be reviewed at the next visit. Because
these techniques are time consuming to implement, their supervision
is often undertaken by ancillary office staff, such as a nurse-clinician
or registered dietitian.
82.
83. PHARMACOTHERAPY
• Adjuvant pharmacologic treatments should be considered for:
• patients with a BMI ≥30 kg/m2,
• patients with a BMI ≥27 kg/m2 who have concomitant obesity-related
diseases,
• patients for whom dietary and physical activity therapy has not been
successful.
• When an anti-obesity medication is prescribed, patients should be
actively engaged in a lifestyle program that provides the strategies and
skills needed to use the drug effectively, since such support increases total
weight loss.
• Anti-obesity medications approved by the U.S. Food and Drug
Administration (FDA), have traditionally fallen into two categories:
84. • Centrally acting appetite suppressants/anorexiants:
• phentermine,
• phentermine/topiramate (PHEN/TPM) extended release,
• lorcaserin,
• naltrexone sustained release (SR)/bupropion SR,
• liraglutide.
• Peripherally acting gastrointestinal fat blockers:
• orlistat.
• Centrally Acting Anorexiant Medications
• Anorexiants affect satiety (the absence of hunger after eating) and
hunger (the biologic sensation that prompts eating). By increasing
satiety and decreasing hunger, these agents help patients reduce
caloric intake without a sense of deprivation.
• The target site for the actions of anorexiants is the ventromedial and
lateral hypothalamic regions of brain.
85. • The biologic effect of these agents on appetite regulation is produced
by augmentation of the neurotransmission of three monoamines:
• norepinephrine;
• serotonin (5-hydroxytryptamine [5-HT]);
• to a lesser degree, dopamine.
• Sympathomimetic adrenergic agents function by stimulating
norepinephrine release or by blocking its reuptake.
1. Phentermine is the most commonly prescribed anorexiants.
Phentermine dosage:
• 8 mg PO TDS (30 min before meal),
• 15-37.5 mg PO OD (before breakfast or 1-2 hours after breakfast).
• The most common side effects are restlessness, insomnia, dry
mouth, constipation, increased blood pressure and heart rate.
86. 2. PHEN/TPM is a combination drug that contains a catecholamine
releaser (phentermine) and an anticonvulsant (topiramate).
• Topiramate is an anticonvulsant for the treatment of epilepsy and
for the prophylaxis of migraine headaches. Weight loss was
identified as an unintended side effect of topiramate. The
mechanism responsible for weight loss is uncertain but is thought
to be mediated through the drug’s modulation of γ-amino-butyric
acid receptors, inhibition of carbonic anhydrase, and
antagonism of glutamate.
• PHEN/TPM dose is 7.5mg/46mg to 15mg/92mg. The most
common side effects are paresthesias, dry mouth, constipation,
dysgeusia, and insomnia.
• Because of an increased risk of congenital fetal oral-cleft
formation from topiramate, women of childbearing age should
have a negative pregnancy test before treatment and monthly
thereafter, and use effective contraception consistently during
medication therapy.
87. 3. Lorcaserin is a selective 5-HT2C receptor agonist is thought to
decrease food intake through the pro-opiomelanocortin (POMC)
system of neurons.
• Lorcaserin dose is 10 mg BD. The most common side effects are
headache, dizziness, and nausea.
4. Naltrexone SR/bupropion SR (NB) is a combination of an opioid
antagonist and a mild reuptake inhibitor of dopamine and
norepinephrine, respectively.
• Naltrexone is used for treatment of alcohol dependence and for
blockade of effects of exogenously administered opioids,
whereas bupropion is an antidepressant and smoking cessation
aid.
• As a combination drug,
• bupropion stimulates secretion of α-melanocyte stimulating
hormone (MSH) from POMC,
88. • naltrexone blocks the feedback inhibitory effects of opioid
receptors activated by the β-endorphin released in the
hypothalamus, thus allowing the inhibitory effects of MSH to
reduce food intake.
• Naltrexone SR/bupropion SR (NB) dose is 8 mg/90 mg two
tablets BD. Medication may lead to slight increased blood
pressure and smaller decrease in pulse. The most common side
effect are nausea, constipation, headache, vomiting, dizziness,
diarrhea, insomnia, and dry mouth.
5. Liraglutide is a glucagon-like peptide-1 (GLP-1) analogue, was
previously approved for the treatment of type 2 diabetes at doses up
to 1.8 mg once daily.
• In addition to its effect as an incretin hormone (glucose-induced
insulin secretion), liraglutide inhibits both gastric emptying and
glucagon secretion and stimulates GLP-1 receptors in the
arcuate nucleus of the hypothalamus to reduce feeding.
89. • Liraglutide dose is up to 3.0 mg sc daily. There is a small increase
in heart rate with this medication. The most common side effects
are nausea, diarrhea, constipation and vomiting.
• GLP-1 agonists should not be prescribed in patients with a family
or personal history of medullary thyroid cancer or multiple
endocrine neoplasia.
• FDA introduced a prescription trial period to assess effectiveness or
response to these medications, i.e., effect should be assessed after 12
weeks of treatment for PHEN/TPM and lorcaserin or 16 weeks for
naltrexone SR/bupropion SR and liraglutide.
• For PHEN/TPM, if the patient has not lost at least 3% of body
weight at 3 months, the clinician can either escalate the dose and
reassess progress at 6 months or discontinue treatment entirely.
90. • For lorcaserin and naltrexone SR/bupropion SR, the medication
should be discontinued if the patient has not lost at least 5% of body
weight at 4 months.
• For liraglutide, the medication should be discontinued if the patient
has not lost at least is a 4% body weight at 4 months.
• Peripherally Acting Medications
• Orlistat is a synthetic hydrogenated derivative of a naturally
occurring lipase inhibitor, lipostatin, that is produced by the mold
Streptomyces Toxytricini.
• This drug is a potent, slowly reversible inhibitor of pancreatic,
gastric, and carboxyl-ester lipases and phospholipase A2, which
are required for the hydrolysis of dietary fat into fatty acids and
monoacyl-glycerols.
• Orlistat acts in the lumen of the stomach and small intestine by
forming a covalent bond with the active site of these lipases.
91. • Taken at a therapeutic dose of 120 mg TDS with meal, orlistat
blocks the digestion and absorption of ~30% of dietary fat. After
discontinuation of the drug, fecal fat content usually returns to
normal within 48–72 hours.
• Because orlistat is minimally (<1%) absorbed from the
gastrointestinal tract, it has no systemic side effects. Adverse
gastrointestinal effects, including flatus with discharge, fecal
urgency, fatty/oily stool, and increased defecation.
• When taken concomitantly, psyllium mucilloid is helpful in
controlling orlistat-induced gastrointestinal side effects.
• Because serum concentrations of the fat-soluble vitamins D and E
and β-carotene may be reduced by orlistat treatment, vitamin
supplements are recommended to prevent potential deficiencies.
92. • OTHER DRUGS USED
• Imcivree (setmelanotide)
• This drug is FDA approved for chronic weight management
(weight loss and weight maintenance for at least one year) in
patients six years and older with obesity due to three rare genetic
conditions:
• pro-opiomelanocortin (POMC) deficiency,
• proprotein subtilisin/kexin type 1 (PCSK1) deficiency,
• leptin receptor (LEPR) deficiency.
• Imcivree is the first FDA-approved treatment for these genetic
conditions, but not approved for obesity likely benign or other
types of obesity, including obesity associated with other genetic
syndromes and general (polygenic) obesity.
• Medications used off-label
• These include several antidepressants, such as selective serotonin
reuptake inhibitors (SSRIs), include the following:
93. • Methylphenidate
• Zonisamide
• Octreotide
• Diabetes Medications
• Metformin does not have an indication for obesity, but it is
useful in preventing diabetes and improving insulin resistance in
conditions such as polycystic ovary syndrome. Its use was
associated with weight neutrality or mild weight loss.
• The first glucagon like peptide (GLP)-1 analogue, exenatide
(Byetta), although not FDA approved for obesity management, has
been associated with modest weight loss in subjects with type 2
diabetes.
• Pramlintide (Symlin), which is a synthetic analogue of the
pancreatic hormone amylin, not FDA approved for obesity
management.
94. • Higher doses (240 mcg before main meals) than those approved
for the management of type 2 diabetes (60-120 mcg before main
meals) have produced modest weight loss in obese or overweight
patients with or without diabetes.
• Once weekly injectable Semaglutide at a dose 2.4 mg/week is
very effective in causing significant weight loss of 14-15 kg in a
year in obese people without Diabetes. Semaglutide dose for
diabetic control in diabetic patients is 7 to 14 mg daily.
• Antidepressants
• Although not all are FDA approved for this purpose, several SSRIs
may cause anorexia as one of their major adverse effects.
• Fluoxetine was associated with some weight loss, although this
effect appeared to be limited to the acute phase of treatment.
95. • Ephedrine & Caffeine
• Ephedrine and caffeine are second-line options in the medical
management of obesity. They both act by increasing energy
expenditure, but they are associated with tachycardia,
hypertension, and palpitations.
• These medications are associated with greater weight loss when
used in combination than when used alone. They cause 25-40% of
their weight loss by inducing thermogenesis, but they also
decrease food intake, which accounts for 60-75% of the weight-
loss effect.
• Cannabinoid-receptor Antagonists
• The central cannabinoid system has an increasingly recognized role in
appetite and feeding disorders.
• Activation of the cannabinoid type 1 (CB1) receptor is associated
with increased appetite.
96. • Rimonabant, the most-developed CB1-receptor antagonist, caused a
mean weight loss of 3-6 kg over a 1-year follow-up at doses of 5-20
mg/day. Adverse effects included dizziness, depression and suicidal
ideation, headaches, nausea, vomiting, and diarrhea.
• The drug was rejected by the FDA because of side effects of
depression and suicidal ideation; in Europe, it was approved but later
recalled.
• Catechin
• Catechin, a flavonoid found in green tea, may aid in preventing
obesity. Patients who had type 2 diabetes mellitus, can take orally
either 582.8 mg or 96.3 mg per day by drinking green tea.
• Participants receiving the higher catechin dose may undergo a
significantly greater reduction in waist circumference than did
patients receiving the lower dose.
97. • Agents in early phases of investigation that may yet prove useful against
obesity include the following:
• Ghrelin antagonists,
• Alpha–melanocyte-stimulating hormone analogs
• Enterostatin
• Neuropeptide YY antagonists
• β3-adrenergic agonists.
• Leptin is still used in cases of the rare obesity subclass of leptin-deficient
obesity and lipodystrophy, but a study of the leptin analogue
metreleptin in obese patients with diabetes found that metreleptin did not
alter body weight. The combination of metreleptin with pramlintide,
however, led to enhanced weight loss in one study, but a more recent
randomized clinical trial on the combination of these 2 drugs was stopped
because of safety concerns.
• Peptide YY (3-36) is being developed as a nasal inhaler. Ongoing,
preliminary phase 1 and 2 trials yielded encouraging results.
98. • Various nutra-ceuticals and herbal products have shown great effect. For
example, an extract from the African cactus Hoodia Gordonii may cause
clinically significant appetite suppression.
• Tagatose, preliminary reports suggest the potential utility of agents that
impede dietary carbohydrate absorption, is undergoing trials.
• Lisdexamfetamine dimesylate, treat binge eating disorder.
• Flouxetin treat bulimia nervosa.
• Drugs no longer used
• Amphetamine, meth-amphetamine and phenmetrazine, were all
withdrawn because of their high potential for abuse.
• Thyroid hormone - Hyperthyroidism, with its sequelae.
99. • The combination of fenfluramine and phentermine (fen-phen),
fenfluramine was withdrawn in 1997 (along with D-fenfluramine)
because of its potential for adverse cardiac, valvular and
pulmonary hypertensive effects.
• Rainbow pills (a mixture of digitalis and diuretics) - Fatal
arrhythmias and electrolyte derangements.
• Di-nitro-phenol - Cataracts and neuropathy.
• Aminorex - Pulmonary hypertension.
• Phenylpropanolamine - Increased risk of myocardial infarction and
stroke.
• Sibutramine - severely increases heart rate and blood pressure.
• Rimonabant - severe psychological symptoms, suicidal tendencies.
100. SURGERY
• Bariatric surgery can be considered for:
• patients with severe obesity (BMI ≥ 40 kg/m2),
• patients with moderate obesity (BMI, ≥35 kg/m2) associated with a
serious medical condition.
• Weight-loss surgeries have traditionally been classified into three
categories on the basis of anatomic changes:
• restrictive,
• restrictive-malabsorptive,
• malabsorptive.
• The clinical benefits of bariatric surgery in achieving weight loss and
alleviating metabolic comorbidities have been attributed largely due to
changes in:
101. • the physiologic responses of gut hormones, bile acid metabolism, the
microbiota, and in adipose tissue metabolism,
• metabolic effects resulting from by-passing the foregut include
altered responses of ghrelin, glucagon-like peptide 1, peptide YY3-
36, and oxyntomodulin,
• additional effects on food intake and body weight control may be
attributed to changes in vagal signaling,
• loss of visceral fat, is associated with multiple metabolic, adipokine,
and inflammatory changes that include:
• improved insulin sensitivity and glucose disposal,
• reduced free fatty acid flux,
• increased adiponectin levels,
• decreased interleukin 6, tumor necrosis factor α, and high-
sensitivity C-reactive protein levels.
102. • Restrictive surgery
• Restrictive surgeries limit the amount of food the stomach can hold
and slow the rate of gastric emptying.
• Laparoscopic adjustable gastric banding is the prototype of this
category.
• These bands have diameters that are adjustable by way of their
connection to a reservoir that is implanted under the skin.
• Injection of saline into the reservoir and removal of saline from
the reservoir tighten and loosen the band’s internal diameter,
respectively, thus changing the size of the gastric opening.
• The mean percentage of total body weight lost at 5 years is
estimated to be 20-25%, longer-term follow-up has been more
disappointing leading to near abandonment of the procedure.
103. • In the laparoscopic sleeve gastrectomy, the stomach is restricted by
stapling and dividing it vertically, removing ~80% of the greater
curvature and leaving a slim banana-shaped remnant stomach along the
lesser curvature. This procedure is superior to that after laparoscopic
adjustable gastric banding.
• Restrictive-malabsorptive Surgery
• Restrictive-malabsorptive bypass procedures combine the elements of
gastric restriction and selective malabsorption:
• Roux-en-Y gastric bypass,
• biliopancreatic diversion,
• biliopancreatic diversion with duodenal switch.
• Roux-en-Y is the most commonly undertaken and most accepted
bypass procedure. These procedures generally produce a 30-35%
average total body weight loss at 5 years.
104. • Significant improvement in multiple obesity-related comorbid
conditions, including type 2 diabetes, hypertension, dyslipidemia,
obstructive sleep apnea, quality of life and long-term
cardiovascular events, has been reported.
• The rapid improvement seen in diabetes after restrictive-
malabsorptive procedures is thought to be due to caloric restriction,
reduced insulin resistance, and surgery-specific effects on glucose
homeostasis brought about by alteration of gut hormones.
• The mortality rate from bariatric surgery is generally <1% but varies
with the procedure, the patient’s age and comorbid conditions, and
the experience of the surgical team.
• The most common surgical complications include stomal stenosis or
marginal ulcers (occurring in 5-15% of patients) that present as
prolonged nausea and vomiting after eating or inability to advance
the diet to solid foods.
105. • These complications typically are treated by endoscopic balloon
dilation and acid suppression therapy.
• Malabsorptive Surgery
• Intraluminal Gastric Balloons, two gastric balloon devices for
weight loss that can be placed in the stomach endoscopically are
approved, i.e.,
• the RESHAPE device consists of two silicone balloons attached to
a central silicone shaft,
• the ORBERA is a single-balloon device.
• Mean weight loss of 7.2 kg and 8.8 kg, respectively; both systems are
approved only for up to 6 months of use in adults with a BMI of 30–
40 kg/m2.
• Adverse effects include nausea, vomiting, and abdominal pain.
106. • For patients who undergo laparoscopic adjustable gastric banding, there
are no intestinal absorptive abnormalities other than mechanical
reduction in gastric size and outflow. Therefore, selective deficiencies are
uncommon unless eating habits become unbalanced.
• In contrast, the restrictive-malabsorptive procedures carry an increased
risk for micronutrient deficiencies of vitamin B12, iron, folate, calcium,
and vitamin D. Patients with restrictive-malabsorptive procedures require
lifelong supplementation with these micronutrients.
• Liposuction
• Cosmetic surgery, or plastic surgery, basically a fat removal
procedure, done to shape the contour of specific area of body.
107. PROGNOSIS
• Data from insurance databases and large, prospective cohorts, such as
findings from the Framingham and National Health and Nutrition
Examination Survey (NHANES) studies, clearly indicate that obesity is
associated with a substantial increase in morbidity and mortality rates.
• For a person with a BMI of 25-28.9 kg/m2, the relative risk for coronary
heart disease is 1.72. The risk progressively increases with an increasing
BMI, i.e, with BMIs greater than 33 kg/m2, the relative risk is 3.44.
• Overall, obesity is estimated to increase the cardiovascular mortality
rate 4-fold and the cancer-related mortality rate 2-fold, whereas,
severely obese have a 6 to 12 fold increase in the all-cause mortality
rate.
108. • For persons with severe obesity (BMI ≥40), life expectancy is reduced by
as much as 20 years in men and by about 5 years in women.
• The greater reduction in life expectancy for men is consistent with the
higher prevalence of android (i.e., predominantly abdominal) obesity
and the biologically higher percentage of body fat in women.
• The risk of premature mortality is even greater in obese persons who
smoke.
• Factors that modulate the morbidity and mortality associated with
obesity include the following:
• Age of onset and duration of obesity
• Severity of obesity
• Amount of central adiposity
• Comorbidities
• Gender
109. • Level of cardiorespiratory fitness
• Race.
• Patient Education
• In studies among low-income families; adults and adolescents noted
caloric information when reading labels. However, this information
did not affect food selection by adolescents, but parental food
selections for children differed.
• NHANES found that patients who received a formal diagnosis of
overweight/obese from a healthcare provider demonstrated a higher
rate of dietary change and/or physical activity than did persons
whose overweight/obese condition remained undiagnosed.
• These marking/labelling are important for any clinician caring for
overweight/obese patients.
110. WORLD OBESITY DAY
• World Obesity Day was established by the World Obesity Federation in
2015 as an annual campaign. It is celebrated on October 11th, with the goal
of initiating and supporting practical actions that will help people
achieve and maintain a healthy weight and reverse the global obesity
crisis.
• The objectives of World Obesity Day are to:
• Increase knowledge and understanding of the challenge of obesity,
and what can and should be done to overcome it.
• Encourage governments to take urgent action to meet their
commitment to halt the rise in obesity by 2025.
• Share national experiences of campaigning to enable the spread of
best practices.
• Encourage member associations and supporters to get involved with
advocacy and campaigning on obesity related issue.
