Download Chapter Sonia CSI 2014

Chapter for ‘Cardiology update 2014”
Management of Obesity: by Optimizing Nutrition?
Dr. Sonia Arora, MBBS, DNHE,
Senior Consultant, Diet and Nutrition, Kishori Ram Hospital and Diabetes Carte Centre, Bathinda, Punjab.
Email: [email protected]
Dr. Vitull K. Gupta MD (Medicine),
Associate Professor, Adesh Institute of Medical Sciences and Research, Bathinda, Punjab.
Senior Consultant Physician, Kishori Ram Hospital and Diabetes Carte Centre, Bathinda,
Meghna Gupta MBBS (Std),
Adesh Institute of Medical Sciences and Research, Bathinda, Punjab.
Weight control is a journey, not a destination.
The second half of twentieth century witnessed major health transitions in the world, propelled by socio-economic and
technological changes. Dietary deficits and excesses and lifestyle changes that accompany industrialization and
urbanization with economic development make a significant contribution to the most globally pervasive change of rising
burden of obesity and non-communicable diseases (NCDs).
Obesity was identified as a disease 35 years ago when, World Health Organization (WHO) listed obesity as a disease
condition in its International Classification of Diseases in 1979. The epidemic of rapid nutritional transition and its adverse
health consequences in the Asian region are now beginning to get noticed. These include insulin resistance, type 2 diabetes,
hypertension (HTN), coronary artery disease (CAD), hyperlipidemia, metabolic syndrome (Syndrome X), stroke and
certain cancers. The economic and health consequences of obesity epidemic can spell disaster for the nation unless
immediate remedial measures are instituted.1
What is Obesity?
Obesity is a state of excess adipose tissue mass that imparts health risk. (20% >Ideal Body Weight). Lean but very
muscular individuals may be overweight by arbitrary standards without having increased adiposity. Obesity is effectively
defined by assessing its linkage to morbidity or mortality. Obesity is a metabolic condition best described as a defense of
an expanded adipose tissue mass.2
Methods to Calculate Obesity:

Body Mass Index (BMI): weight in Kg / height in meter 2 (kg/m2),

Skin-fold thickness,

Densitometry (underwater weighing),

Computed tomography (CT) or MRI,

Waist to Hip Ratio (Central Obesity),

Ideal Body Weight (Kg) = {(Height in cm-100) X 0.9}.
BMI: BMI is recommended as a practical approach for assessing body fat in the clinical setting and provides a more
accurate measure of total body fat compared with the assessment of body weight alone.3 BMI overestimates body fat in
persons who are very muscular and it can underestimate body fat in persons who have lost muscle mass.
Classification of BMI:4 5
 Underweight (<18.5Kg/m2).{ Mildly thin (17.0- 18.4Kg/m2) Moderately/ severely thin (<17.0 Kg/m2) }
 Normal (18.5-24.9 Kg/m2).
 Overweight (25-29.9kg/m2)
 Obese (30- 34.9 Kg/m2).
 Sever Obesity ( 35- 39.9Kg/m2)
 Morbid Obesity (>40Kg/m2)
Indians tend to have excess body fat, abdominal and truncal adiposity. For any given waist circumference (WC), Indians
have increased body fat accumulation and for any given body fat, Indians have increased insulin resistance.6
7
These
features have been referred to as “Asian Indian Phenotype or Paradox”.8 WC or waist-to-hip ratio measures the excess
abdominal fat and is a surrogate for visceral adipose tissue which is independent risk factor for diabetes mellitus and
cardiovascular diseases. Cut points that define higher risk for Asian men is >90cm and women >80cm. WHO has revised
the BMI cut-off for Asian Indians and suggested a BMI of >25kg/m2 to define obesity against the >30kg/m2 recommended
for Europeans.9
Pathophysiology of Obesity:
Obesity is a complex, multifactorial disease influenced by several factors like genetic, environmental, cultural,
neuroendocrine and metabolic factors. Our understanding of how and why obesity occurs is incomplete.10 The
pathophysiology of obesity seems simple: a chronic excess of nutrient intake relative to the level of energy expenditure.
However, due to the complexity of the neuroendocrine and metabolic systems that regulate energy intake, storage and
expenditure, it has been difficult to quantitate all the relevant parameters (e.g., food intake and energy expenditure) over
time in human subjects.11
There is increased interest in the concept of a body weight "set point" a physiologic sensing system in adipose tissue that
reflects fat stores and a receptor or "adipostat," in the hypothalamic centers. When fat stores are depleted, the adipostat
signal is low and hypothalamus responds by stimulating hunger and decreasing energy expenditure to conserve energy and
vice versa. The discovery of ‘ob’ gene and its product leptin provides a molecular basis for this physiologic concept.
Signals that impinge on the hypothalamic center include neural afferents, hormones, and metabolites. Vagal inputs
bringing information from viscera. Hormonal signals include leptin, insulin, cortisol, gut peptides including ghrelin,
peptide YY (PYY) and cholecystokinin. These diverse hormonal, metabolic and neural signals act by influencing the
expression and release of various hypothalamic peptides that are integrated with serotonergic, catecholaminergic,
endocannabinoid and opioid signaling pathways. In general, majority of energy expenditure is accounted for by the
basal/resting metabolic rate (55% to 70%), with the smallest contribution from thermogenesis (5% to 10%) and the most
variable form from physical activity (20% to 40%). 12 The physiologic basis for variable rates of energy expenditure (at a
given body weight and level of energy intake) is essentially unknown. One newly described component of thermogenesis,
called non exercise activity thermogenesis (NEAT) has been linked to obesity.11 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. NEAT accounts for about two-thirds of the increased daily energy expenditure
induced by overfeeding. 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.
Causes of Obesity epidemic in India:13
Obesity epidemic in India has its roots in urbanization, industrialization and drastic change in the life style especially urban
and rich who have urbanized to western levels. Indians are genetically susceptible to weight accumulation especially
around the waist.
The important components of life style changes are:
• Unhealthy eating patterns, wrong choices of food: Traditional micronutrient rich foods are being replaced by energy
dense highly processed micronutrient poor foods with greatly increased portions ‘Dil Mange More’. High calorie snacks,
junk food revolution, cool cola (‘thanda matlab’) colonization and food as rewards or demonstration of love are all part of
new life styles. All celebrations and festivals seem to be centered around rich foods.
• Sedentary pursuits: TV and movie watching, video games, internet gazing and telephone gossip sessions are now
important activities of children. TV also affects by heavy marketing of colas and other fatty foods. The number of TV sets
and telephone connections are touted as indices of development!
• ‘Obesogenic schools’ and Tuition classes: An important factor for obesity in India is the intense competition for
admissions to schools and colleges with flourishing tuition classes’ right from nursery levels! Children are forced to use
their play time for additional studies. Games or physical training sessions are restricted or non existent in many schools.
Some schools do not have any playgrounds at all.
• Inadequate play areas: Due to unsafe roads (traffic, crime) children are discouraged form walking or cycling to school.
Motorized vehicles are popular and they are perceived to be quicker and safer for transport. Erosion of open spaces for
exercise and lack of parental time to supervise play are all part of new obesogenic lifestyles. As against food as rewards,
ironically exercise is meted out as a punishment - ‘100 sit ups,’ ‘run round the field.’
Secondary causes of obesity: relate to diseases like Cushing's Syndrome, Hypothyroidism, Insulinoma
Craniopharyngioma and other disorders involving the hypothalamus and male hypogonadism,
How to Manage Obesity:
Treatment of an overweight or obese person incorporates a two step process:

Assessment.

Management.
Assessment includes determination of the degree of obesity and overall health status. Management involves not only
weight loss and maintenance of body weight but also measures to control other risk factors. The U.S. Preventive Services
Task Force recommends screening of all adult patients for obesity and offer intensive counseling and behavioral
interventions to promote sustained weight loss.11 14
Management of Obesity by Optimizing Nutrition:
The primary goal of treatment is to improve obesity-related co-morbid conditions and reduce future risk of co-morbidities.
Management strategies are determined by the patient's history, physical examination, investigations, risk status,
expectations and available resources. Effective weight control involves multiple techniques and strategies including life
style management (dietary therapy, physical activity, behavior therapy), pharmacotherapy and surgery as well as
combinations of these strategies. Life style modifications are essential part of obesity management and all patients must
learn how and when energy is consumed (diet), how and when energy is expended (physical activity) and how to
incorporate this information into their daily life (behavior therapy). National Institutes of Health guidelines suggest that
non-pharmacological therapies should be attempted for 6 months and drugs should be considered if weight loss is
unsatisfactory that is <0.45kg/month.
The concept that “a calorie is a calorie” underlies most conventional weight loss strategies by optimizing nutrition because
of the principle that obesity results from an imbalance between energy intake and expenditure. Management of obesity by
optimizing nutrition requires modifications to the type, quantity and/or frequency of food and drink consumed to achieve
and maintain a hypocaloric intake. Overall reduced caloric intake is the cornerstone of obesity treatment. A weight loss of
approximately 0.5 kg/week results from a loss of adipose tissue that entails an energy deficit of 3,500 kcal/week. This
requires a daily energy deficit of at least 500 kcals/day.15 To ensure this deficit it is standard practice to aim for 600 kcal
deficit. Approaches to achieving a hypocaloric energy (600 kcal deficit) prescription vary:

Reducing energy intake,

Food composition,

Low or very low calorie diets,

Commercial diets,

Glycaemic load/glycaemic index diets,

Mediterranean diet,

Protein sparing modified fast and low carbohydrate low-fat diets.
Reducing Energy Intake:
The rate of weight loss on a given caloric intake is related to the rate of energy expenditure. With chronic caloric
restriction, metabolic rate diminishes and slows the rate of weight loss on a constant diet. The NHLBI guidelines16
recommend initiating treatment with a calorie deficit of 500–1000 kcal/d compared to the patient's habitual diet is
consistent with losing approximately 1–2 lb/week. It is important that the dietary counseling remains patient-centered and
that the goals are practical, realistic and achievable. The NICE guideline17 compares various dietary interventions (600
kcal/day deficit diets and low-fat diets together) largely based on a comprehensive health technology assessment (HTA)
which systematically reviewed RCTs of dietary interventions in overweight and obese patients with a minimum of 12
months follow up. Median weight change across 12 comparisons was a loss of 4.6 kg (range –0.60kg to –7.20kg) for a 600
kcal deficit diet or low-fat diet and a gain of 0.60 kg (range +2.40 kg to –1.30 kg) for usual care. There were clear benefits
with regard to clinical outcomes such as prevention of diabetes and improvement in hypertension. These effects appeared
to persist for up to three years. 18
Food Composition:
The macronutrient composition of diet will vary depending on the patient's preference and medical condition, but should
include a diet rich in whole grains, fruits, vegetables and dietary fiber consisting 45–65% of calories from carbohydrates,
20–35% from fat and 10–35% from protein. Daily fiber intake of 38g (men) and 25g (women) for persons >50 years of age
and 30g (men) and 21 g (women) for those <50 is recommended. Both low carbohydrate (<30g/day) and low-fat (<30% of
total daily energy) diets are associated with modest weight loss at 12 months. A meta-analysis comparing low
carbohydrate/high protein (LC/HP) diets with low-fat/high carbohydrate (LF/HC) diets found that the LC/HP diets were
more effective for weight loss at six months but that the difference between strategies was not significant at 12 months. 19 20
A large RCT with follow up to two years concluded that reduced calorie diets result in clinically meaningful weight loss
regardless of which macronutrients they emphasize.21
Another dietary approach is the concept of energy density, which refers to the number of calories a food contains per unit
of weight. Adding water or fiber to a food decreases its energy density by increasing weight without affecting caloric
content. Examples of foods with low-energy density include soups, fruits, vegetables, oatmeal and lean meats. Diets
containing low-energy dense foods have been shown to control hunger and result in decreased caloric intake and weight
loss. Alcohol consumption provides unneeded calories and displaces more nutritious foods so it not only increases the
number of calories in a diet but has been associated with obesity in epidemiologic studies as well as in experimental
studies.22
23
The impact of alcohol calories on a person’s overall caloric intake needs to be assessed and appropriately
controlled.
A World Cancer Research Fund systematic review developed a range of evidence based conclusions on the associations
between dietary components and obesity. 24

Low energy-dense foods: whole grains, cereals, fruits, vegetables and salads. (probably protect against weight
gain, overweight and obesity).

High energy-dense foods: foods containing animal fats, other high fat foods, confectionery and sugary drinks.
(probably a cause of weight gain, overweight, and obesity, particularly when large portion sizes are consumed
regularly).

Sugary drinks probably cause weight gain, overweight, and obesity.

‘Fast foods’ probably cause weight gain, overweight, and obesity.
Adults are more likely to maintain a healthy weight if they reduce consumption of high energy dense foods through
selection of a low-fat, high fiber diet, consuming fewer take-aways, eating more fruit, whole-grains, vegetables and salads,
minimizing alcohol intake and consuming less confectionery and fewer sugary drinks.17 25 26
Low and Very Low Calorie diets:
Low calorie diets (LCD, 800-1800 kcal/day) and very low calorie diets (VLCD, <800 kcal/day) are associated with modest
weight loss (5-6%) at 12 months follow up. Although VLCD are associated with greater weight loss in short term (3 to 4
months) this difference is not sustained at 12 months. 27 VLCDs are prescribed as a form of aggressive dietary therapy to
promote a rapid and significant (13–23 kg) short-term weight loss over a 3–6 month period.11 These propriety formulas
typically supply 800 kcal, 50–80 g protein and 100% of the recommended daily intake for vitamins and minerals.
Indications include well-motivated individuals who are moderately to severely obese (BMI >30), have failed at more
conservative approaches to weight loss and have a medical condition like poorly controlled type 2 diabetes,
hypertriglyceridemia, obstructive sleep apnea and symptomatic peripheral edema that would be immediately improved
with rapid weight loss. Contraindications include pregnancy, cancer, recent myocardial infarction, cerebrovascular disease,
hepatic disease or untreated psychiatric disease. Side effects are fatigue, constipation or diarrhea, dry skin, hair loss,
menstrual irregularities, orthostatic dizziness and difficulty in concentrating. Because of the need for close metabolic
monitoring, the British Dietetic Association specialist group recommends close medical and dietary supervision for
VLCDs.28
Commercial Diets:
No medical condition has generated as many dietary remedies as obesity. All diets have their followers, but hard data on
the efficacy of the diets are scarce. A current area of controversy is the use of low-carbohydrate, high-protein diets for
weight loss. Most low-carbohydrate diets (e.g., South Beach, Zone and Sugar Busters!) recommend a carbohydrate level of
approximately 40–46% of energy. The Atkins diet contains 5-15% carbohydrate, depending on the phase of the diet. Metaanalysis of trials20 found
low-carbohydrate, non-energy-restricted diets appear to be at least as effective as low-fat,
energy-restricted diets in inducing weight loss for up to 1 year. Several randomized, controlled trials 29
30
of these low-
carbohydrate diets have demonstrated greater weight loss at 6 months with improvement in CAD risk factors, including an
increase in HDL cholesterol and a decrease in triglyceride levels. A variety of commercial weight reduction programmes
(Atkins, low carbohydrate; Ornish, LEARN, very low fat; and Zone macronutrient ratios), are associated with a modest
reduction in body weight and a reduction in several cardiac risk factors in overweight and obese premenopausal women at
12 months. Zone, LEARN and Ornish produce comparable results. Atkins was associated with significantly greater weight
loss and more favorable metabolic effects at 12 months than Zone. 31 In an RCT of commercial weight loss programmes in
the UK (Dr Atkins’ new diet revolution, Slim-Fast plan, Weight Watchers pure points programme and Rosemary Conley’s
eat yourself slim diet and fitness plan), all groups lost weight and body fat at six months compared to control (average
weight loss 5.9 kg) but there was no difference between groups. At 12 months follow up all diets resulted in a clinically
useful weight loss of around 10% in participants who had kept to their original diet. 32 In adults with known hypertension,
dyslipidemia, or fasting hyperglycemia, a range of commercial weight reduction programmes (Atkins, Weight Watchers,
Ornish, Zone) is associated with a modest reduction in body weight and a reduction in several cardiac risk factors at one
year. Increased adherence resulted in more weight loss and a greater reduction in cardiac risk factors. 29
Glycaemic load (GL)/glycaemic index (GI) diets:
The application of the GI to weight regulation is relatively recent but already vigorously debated. 33
34
There is increasing
evidence that several features of low-GI foods are potentially beneficial for weight control including ability to promote
satiety and delay hunger, higher metabolic rate, reduced postprandial glycemia and/or insulinaemia and higher fat
oxidation. Over the past two decades, higher carbohydrate intake, particularly of refined and high-GI carbohydrate, has
accompanied increases in obesity, type 2 diabetes and the metabolic syndrome.35
36
A review of 16 studies concluded that
low-GI solid foods induce greater satiety than their high-GI counterparts and are followed by less energy intake at
subsequent meals.37 Exchanging high for low-GI foods, without changing the macronutrient ratio, may be optimal because
it is simple, cost-effective and often associated with higher intake of whole grains, abundant quantities of vegetables, fruits
and legumes, moderate amounts of protein and healthful fats and decreased intake of refined grain products, potato and
concentrated sugars. Such a diet bears a close resemblance to that consumed by human ancestors over the last several
hundred thousand years38 and can be easily adapted for individuals of different ethnicities, vegetarians and low-income
groups. Population studies provide further evidence that the glycaemic effect of the diet might influence body fat stores in
humans.39 In a comparison of three reduced-energy diets varying in GI and GL (high-GI/high-GL, low-GI/low-GL and
high-fat/low-GL/high-GI), weight loss was found to be independent of diet composition.40 Unscientific terminology such
as ‘sugar-highs, sugar-lows,’ ‘fuller for longer,’ ‘slow-release energy,’ ‘sustained energy,’ may be scorned by scientists but
are concepts that have intrinsic appeal to members of the public. Low-GI diets appear to ‘press the right emotional
buttons,’ motivating individuals to adopt a diet that not only ‘controls’ blood glucose levels but is coincidentally healthy.
Clinicians and health professionals remain skeptical, calling for greater scientific evidence on which to base advice to
patients.41
Mediterranean diet (MD):
There's no one "Mediterranean" diet. At least 16 countries border the Mediterranean Sea and diets vary between these
countries and also between regions within a country. Many differences in culture, ethnic background, religion, economy
and agricultural production result in different diets. But the common Mediterranean dietary pattern has following
characteristics:42

High consumption of fruits, vegetables, bread and other cereals, potatoes, beans, nuts and seeds,

Olive oil is an important monounsaturated fat source,

Dairy products, fish and poultry are consumed in low to moderate amounts and little red meat is eaten,

Eggs are consumed zero to four times a week,

Wine is consumed in low to moderate amounts.
In systematic review, the MD group lost significantly more weight than control group who were given either information
on a healthy diet or prescribed a low-fat diet. The need for a consistent universal definition of the MD was highlighted.43
The long-term results of RCTs show that Low Fat Diet and MD could be similarly effective strategies for weight loss,
particularly when applied with equal intensity interventions with calorie deficit. The studies demonstrating effective
weight loss with energy-restricted MD.44 45 Weight loss observed in the studies reviewed was due to the energy deficits in
the diets rather than the type of diet. Another meta-analysis of randomized controlled trials concluded that MD may be a
useful tool to reduce body weight, especially when the MD is energy-restricted, associated with physical activity and >6
months in length.46
There is insufficient evidence on which to base a recommendation for patients.
Physical Activity Therapy:
Exercise is an important component of the overall approach to treating obesity. Increased energy expenditure is the most
obvious mechanism of exercise. The impact of an exercise regimen as a sole therapy of obesity has been difficult to
document but the combination of dietary modification and exercise is the most effective behavioral approach for the
treatment of obesity. A meta-analysis of RCTs found that exercise combined with diet resulted in a greater weight
reduction than diet alone.47 The most important role of exercise appears to be in the maintenance of the weight loss.
Recommendation is 30 min of moderate intensity physical activity on most and preferably all days of the week. Examples
include walking, using the stairs, doing home and yard work and engaging in sport activities. The American College of
Sports Medicine recommends that overweight and obese individuals progressively increase to a minimum of 150 min of
moderate intensity physical activity per week as a first goal. However, for long-term weight loss, a higher level of exercise
(e.g., 200–300 min or 2000 kcal/week) is needed. Other advantages of exercise include increases fitness, increases insulin
sensitivity, decreases blood pressure, lipids, and calcium loss along with improving mental and physical wellbeing.
Behavioral Therapy:
The principles of behavior modification provide the underpinnings for many current programs of weight reduction used to
help change and reinforce new dietary and physical activity behaviors. Typically, the patient is requested to monitor and
record the circumstances related to eating and rewards are designed to modify maladaptive behaviors.
Behavioral
treatments help obese persons to develop adaptive thinking, eating and exercise habits that enable them to decrease their
weight and avoid regaining weight. When recommending any behavioral lifestyle change, have the patient identify what,
when, where and how the behavioral change will be performed. The practitioner must assess the patient’s motivation to
enter weight loss therapy and the patient’s readiness to implement the plan and then take appropriate steps to motivate the
patient for treatment. Because these techniques are time-consuming to implement, they are often provided by ancillary
office staff such as a nurse clinician or registered dietitian. The importance of individualizing behavioral strategies to the
needs of the patient and behavior therapy must be emphasized, as it was for diet and exercise strategies.48
Diet plus Physical Activity plus Behavioral Therapy:
A combination of physical activity, behavior therapy and optimization of diet is more effective for weight loss compared
with diet alone. In a meta-analysis of five studies, median weight change was –4.60 kg (range –3.33 kg to –5.87 kg) for the
combined intervention and –0.48 kg (range 0.53 kg to –2.40 kg) for diet alone.17
Drug Therapy:11 16
A majority of patients who lose weight regain it.49 So the challenge to the patient and the practitioner is to maintain weight
loss. Because of the tendency to regain weight after weight loss, the use of long-term medication to aid in the treatment of
obesity may be indicated for carefully selected patients. Drug therapy is used only as part of a program that includes diet,
physical activity and behavior therapy in carefully selected patients with a BMI
30 (>25 in Indians) or
27 (>23.5 in
Indians) with other risk factors or diseases. Not every patient responds to drug therapy. Trials have shown that initial
responders tend to continue to respond, whereas initial non-responders are less likely to respond, even with an increase in
dosage.50 There are several potential targets of pharmacologic therapy for obesity including suppression of appetite, drugs
increasing energy expenditure, decreasing absorption of selective macronutrients from the gastrointestinal (GI) tract, such
as fat and selective blocking of the endocannabinoid system and other investigational compounds.
Detailed discussion on pharmacological management is out of preview of this chapter.
But Orlistat needs mention as it is presently the only drug specifically licensed for use in the treatment of obesity. Orlistat
should be considered as an adjunct to lifestyle interventions (diet, physical activity and behavioral changes) in the
management of weight loss. Patients with BMI ≥28 kg/m2 (>23.5 in Indians) (with comorbidities) or BMI ≥30 kg/m2 (
>25 in Indians) should be considered on an individual case basis following assessment of risk and benefit. Orlistat reduces
the absorption of energy-dense fat by inhibiting pancreatic and gastric lipases. NICE guideline meta-analysis of 15 RCTs
and found that Orlistat (120 mg three times a day) in combination with a weight-reducing diet is more effective for weight
loss maintenance than placebo and diet at 12 months. 17
Orlistat treatment is associated with increased rates of
gastrointestinal events. These are usually mild and transient.
Weight Loss Surgery:
Weight loss surgery is an option for weight reduction in patients with clinically severe obesity, i.e., a BMI >40, or a BMI
>35 with comorbid conditions (BMI >35, or a BMI >30 with comorbid conditions for Indians). Weight loss surgery should
be reserved for patients in whom other methods of treatment have failed and who have clinically severe obesity.16 Bariatric
surgical procedures reduce caloric intake by modifying the anatomy of the gastrointestinal tract classified as either
restrictive or malabsorptive. Restrictive procedures limit intake by creating a small gastric reservoir with a narrow outlet to
delay emptying. Malabsorptive procedures bypass varying portions of the small intestine where nutrient absorption occurs.
These procedures generally produce a 30–35% average total body weight loss that is maintained in nearly 60% of patients
at 5 years. In general, mean weight loss is greater after the combined restrictive-malabsorptive procedures compared to the
restrictive procedures. An abundance of data supports the positive impact of bariatric surgery on obesity-related morbid
conditions, including diabetes mellitus, hypertension, obstructive sleep apnea, dyslipidemia and nonalcoholic fatty liver
disease.11 51 52 Types of surgery, anaesthetic practice and immediate postoperative care are out of the scope of this chapter.
Conclusion:
India is in the midst of an escalating epidemic of life style disorders like obesity and NCDs. The important causes of the
epidemic in India appear to be: - unhealthy eating patterns, reduced physical activity, increased sedentary pursuits and
possibly `constitutional predispositions'/early origins'. Standard treatment approaches for obesity must be tailored to the
needs of people or patients. There is, therefore, no “cookbook” or standardized set of rules to optimize weight reduction in
a given patient. Treatment of obesity incorporates a two-step process: assessment and management. Obesity is a chronic
disease; patient and practitioner must understand that successful treatment requires a lifelong effort. Therapy for obesity
always begins with lifestyle management and may include pharmacotherapy or surgery; depending on BMI risk category
Effective weight control involves multiple techniques and strategies including dietary therapy, physical activity, behavior
therapy, pharmacotherapy and surgery as well as combinations of these strategies.
Dietary interventions which produce a 600 kcal/day deficit result in sustainable modest weight loss so dietary interventions
should be calculated to produce a 600 kcal/ day energy deficit. Programmes should be tailored to the dietary preferences of
the individual patient. VLCDs are indicated for rapid weight loss and should be conducted under medical supervision.
Weight management should include advise to reduce: intake of energy-dense foods (including foods containing animal
fats, other high fat foods, confectionery and sugary drinks) by selecting low energy-dense foods (for example whole-grains,
cereals, fruits, vegetables and salads), reduce consumption of ‘fast foods’ and alcohol intake. There is no scientific
evidence to validate the utility of specific "fad diets." The main stress should be on: Restriction, Moderation and Selection
of food. The optimal diet for the prevention and treatment of obesity, if one exists, remains to be determined.
References:
1
Murray CJL, Lopez AD. Global Comparative Assessments in the Health Sector. Geneva: World Health Organization,
1994
2
Eckel R. Obesity: a disease or a physiologic adaptation for survival. In:Eckel RH, ed. Obesity Mechanisms and Clinical
Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2003:3–30.
3
Heymsfield SB, Allison DB, Heshka S, Pierson RN Jr. Assessment of human body composition. In: Allison DB, ed.
Handbook of Assessment Methods for Eating Behaviors and Weight Related Problems: Measures, Theory, and Research.
Thousand Oaks, CA: Sage Publications; 1995:515-560.
4
World Health Organization. Technical report series 894: "Obesity: preventing and managing the global epidemic.”
Geneva: World Health Organization, 2000
5
National Family Health Survey (NFHS-3), 2005–06: India
6
Ramachandran A, Snehalatha C, Viswanathan V, Viswanathan M, Haffner SM. Risk of noninsulin dependent diabetes
mellitus conferred by obesity and central adiposity in different ethnic groups: a comparative analysis between Asian
Indians, Mexican Americans and Whites. Diabetes Res Clin Pract 1997; 36: 121-5.
7
Chandalia M, Abate N, Garg A, Stray-Gundersen J, Grundy SM. Relationship between generalized and upper body
obesity to insulin resistance in Asian Indian men. J Clin Endocrinol Metab 1999; 84: 2329-35.
8
Joshi SR. Metabolic syndrome – Emerging clusters of the Indian Phenotype. J Assoc Physicians India 2003; 51: 445-6.
9
The Asia Pacific perspective: Redefining obesity and its treatment. Regional Office for the Western Pacific of the World
Health Organization. World Health Organization, International Association for the Study of Obesity and International
Obesity Task Force. Health Communications Australia Pty Limited, St Leonards, Australia; 2000 p. 22-9.
10
National Research Council. Committee on Diet and Health. Implications for reducing chronic disease risk. Washington,
DC: National Academy Press; 1989
11
Harrison's Principles of Internal Medicine, 17th edition, 2008
12
Ravussin E, Bogardus C. A brief overview of human energy metabolism and its relationship to essential obesity. Am J
Clin Nutr. 1992; 55: 242S–245S.
13
IAP National Task Force for Childhood Prevention of Adult Diseases: Childhood Obesity Indian Pediatrics 2004;
41:559-575
14
McTigue KM et al: Screening and interventions for obesity in adults: Summary of the evidence for the U.S. Preventive
Services Task Force. Ann Intern Med 139:933, 2003
15
Lean ME, James WP. Prescription of diabetic diets in the 1980s. Lancet 1986; 1(8483):723-5.
16
National Heart, Lung, and Blood Institute, North American Association for the Study of Obesity: Practical guide:
Identification, evaluation, and treatment of overweight and obesity in adults. Bethesda, MD, National Institutes of Health
pub number 00- 4084, Oct. 2000.
17
National Institute for Health and Clinical Excellence (NICE). Obesity: the prevention, identification, assessment and
management of overweight and obesity in adults and children. London: NICE; 2006. [cited 16 Dec 2009] Available from
url: http://guidance. nice.org.uk/CG43
18
Avenell A, Broom J, Brown TJ, Poobalan A, Aucott L, Stearns SC, et al. Systematic review of the long-term effects and
economic consequences of treatments for obesity and implications for health improvement. Health Technology Assess
2004;8(21).Available from url: http://www.hta.ac.uk/fullmono/ mon821.pdf
19
Hession M, Rolland C, Kulkarni U, Wise A, Broom J. Systematic review of randomized controlled trials of lowcarbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities. Obes Rev 2009; 10(1):3650.
20
Nordmann AJ, Nordmann A, Briel M, Keller U, Yancy WS, Jr., Brehm BJ, et al. Effects of low-carbohydrate vs low-fat
diets on weight loss and cardiovascular risk factors: a meta-analysis of randomized controlled trials. Arch Intern Med
2006; 166(3):285- 93.
21
Sacks FM, Bray GA, Carey VJ, Smith SR, Ryan DH, Anton SD, et al. Comparison of weight-loss diets with different
compositions of fat, protein, and carbohydrates. N Engl J Med 2009; 360(9):859-73.
22
Tremblay A, Buemann B, Theriault G, Bouchard C. Body fatness in active individuals reporting low lipid and alcohol
intake. Eur J Clin Nutr. 1995; 49:824-831.
23
Tremblay A, Wouters E, Wenker M, St- Pierre S, Bouchard C, Despres JP. Alcohol and a high-fat diet: a combination
favoring overfeeding. Am J Clin Nutr. 1995; 62:639-644.
24
World Cancer Research Fund, American Institute for Cancer Research. Food, Nutrition, Physical Activity and the
Prevention of Cancer: a Global Perspective. London; WCRF. Washington DC, AICR; 2009. [cited 22 Dec 2009].
Available from url: http://www. dietandcancerreport.org/
25
Malik VS, Schulze MB, Hu FB. Intake of sugar-sweetened beverages and weight gain: a systematic review. Am J Clin
Nutr 2006; 84(2):274-88.
26
Maskarinec G, Takata Y, Pagano I, Carlin L, Goodman MT, Le Marchand L, et al. Trends and dietary determinants of
overweight and obesity in a multiethnic population. Obesity 2006; 14(4):717-26.
27
Gilden Tsai A, Wadden TA. The evolution of very-low-calorie diets: an update and meta-analysis. Obesity 2006;
14(8):1283-93.
28
Dietitians in Obesity Management UK. Position Statement on Very Low Energy Diets in the Management of Obesity.
Middlesbrough: DOM UK; 2007. [cited 22 Dec 2009]. Available from url: http:// domuk.org/wpcontent/uploads/2007/02/very-low-energy-diets. pdf
29
Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ. Comparison of the Atkins, Ornish, Weight Watchers,
and Zone Diets for weight loss and heart disease risk reduction: A randomized trial. JAMA 2005; 293(1):43-53.
30
Halton TL, Willett WC, Liu S, et al (2006). "Low-carbohydrate-diet score and the risk of coronary heart disease in
women". N. Engl. J. Med. 355 (19): 1991-2002.
31
Gardner CD, Kiazand A, Alhassan S, Kim S, Stafford RS, Balise RR, et al. Comparison of the Atkins, Zone, Ornish,
and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z
Weight Loss Study: a randomized trial. JAMA 2007; 297(9):969-77.
32
Truby H, Baic S, deLooy A, Fox KR, Livingstone MB, Logan CM, et al. Randomised controlled trial of four commercial
weight loss programmes in the UK: initial findings from the BBC “diet trials”.Br Med J 2006;332(7553):130933
Ebbeling C, Ludwig D. Treating obesity in youth: should dietary glycemic load be a consideration? [in process citation].
Adv Pediatr 2001; 48: 179–212.
34
Raben A. Should obese patients be counselled to follow a low glycaemic index diet? No Obes Rev 2002; 3: 245–256.
35
Liu S, Willett W, Manson J, Hu F, Rosner B, Colditz G. Relation between changes in intakes of dietary fiber and grain
products and changes in weight and development of obesity among middle-aged women. Am J Clin Nutr 2003; 78: 920–
927.
36
McKeown N, Meigs J, Liu S, Saltzman E, Wilson P, Jacques P. Carbohydrate nutrition, insulin resistance, and the
prevalence of the metabolic syndrome in the Framingham offspring cohort. Diabetes Care 2004; 27: 538–546.
37
Ludwig D. Dietary glycemic index and obesity. J Nutr 2000; 130:280S–283S.
38
Eaton, S. B. & Konner, M. (1985) Paleolithic nutrition. A consideration of its nature and current implications. N. Engl. J.
Med. 312:283-289
39
Ma Y, Olendzki B, Chiriboga D, Hebert JR, Li Y, Li W et al. Association between dietary carbohydrates and body
weight. Am J Epidemiol 2005; 161: 359–367.
40
Raatz SK, Torkelson CJ, Redmon JB, Reck KP, Kwong CA, Swanson JE et al. Reduced glycemic index and glycemic
load diets do not increase the effects of energy restriction on weight loss and insulin sensitivity in obese men and women. J
Nutr 2005; 135: 2387–2391.
41
J McMillan-Price and J Brand-Miller. Low-glycaemic index diets and body weight regulation. International Journal of
Obesity (2006) 30, S40–S46. doi:10.1038/sj.ijo.0803491
42
Garcia-Closas R, Berenguer A, Gonzalez CA. Changes in food supply in Mediterranean countries from 1961 to
2001. Public Health Nutr. 2006; 9:53–60.
43
Buckland G, Bach A, Serra-Majem L. Obesity and the Mediterranean diet: a systematic review of observational and
intervention studies. Obes Rev 2008; 9(6):582-93.
44
Esposito K, Marfella R , Ciotola M, Di Palo C, Giugliano F, Giugliano G, Armiento M, D’Andrea F, Giugliano D.
Effect of a Mediterranean-style diet on endothelial dysfunction and markers of vascular inflamation in the metabolic
syndrome. JAMA 2004; 292: 1440-1446.
45
Shai I, Schwarzfuchs D, Henkin Y, Shahar DR, Witkow S, Greenber I et all. Weight loss with a low-carbohydrate,
Mediterranean, or Low- Fat diet. N Engl J Med 2008; 359: 229-241.
46
Esposito K, Kastorini CM, Panagiotakos DB, Giugliano D. Mediterranean diet and weight loss: meta-analysis of
randomized controlled trials. Metab Syndr Relat Disord. 2011 Feb; 9(1):1-12. doi: 10.1089/met.2010.0031. Epub 2010
Oct 25.
47
Shaw K, Gennat H, O'Rourke P, Del Mar C (2006). "Exercise for overweight or obesity". Cochrane database of
systematic reviews
48
Wadden TA, Foster GD. Behavioral assessment and treatment of markedly obese patients. In: Wadden TA, VanItallie
TB, eds. Treatment of the Seriously Obese Patient. New York: Guilford Press; 1992:290-330
49
Methods for voluntary weight loss and control. NIH Technology Assessment Conference Panel. Ann Intern Med.
1992;116:942-949.
50
Weintraub M, Sundaresan PR, Madan M, et al. Long-term weight control study. I (weeks 0 to 34). The enhancement of
behavior modification, caloric restriction, and exercise by fenfluramine plus phentermine versus placebo. Clin Pharmacol
Ther. 1992; 51:586-594.
51
Buchwald H et al: Bariatric surgery: A systematic review and meta-analysis. JAMA 292:1724, 2004
52
DeMaria EJ: Bariatric surgery for morbid obesity. N Engl J Med 356:2176, 2007