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Physicians

OBESITY

EPIDEMIOLOGY:

Approximately 78 million adults above age 20 (37.5 million men and 40.6 million women) and 12.5 million children and adolescents (5.5 million boys and 7 million girls) in the United States are obese. In 2009-2010, the prevalence of obesity among men and women was almost 36%.(1) The prevalence in children and adolescents was 16.9%.

According to World Health Organization (WHO) estimates, 26 % of women and 19% of men in Pakistan are obese (Body Mass index (BMI) > 25) but only 4% of women and 1 % of men are recognized as obese using the standard criteria (BMI > 30). The prevalence of obesity is even higher in urban areas (56% in men and 67% in women) when Asian specific definition for obesity is used.(2)

PATHOPHYSIOLOGY:
HYPERTROPHIC VS. HYPERCELLULER OBESITY:

The adipocyte, which is the cellular basis for obesity, may be increased in size or number in obese persons. Hypertrophic obesity, characterized by enlarged fat cells, is typical of android abdominal obesity. Hypercellular obesity is more variable than hypertrophic obesity; it typically occurs in persons who develop obesity in childhood or adolescence, but it is also invariably found in subjects with severe obesity.

Hypertrophic obesity usually starts in adulthood, is associated with increased cardiovascular risk, and responds quickly to weight reduction measures. In contrast, patients with hypercellular obesity may find it difficult to lose weight through nonsurgical interventions.

ADIPOCYTE PRODUCTS:

The adipocyte is increasingly found to be a complex and metabolically active cell. At present, the adipocyte is perceived as an active endocrine gland producing several peptides and metabolites that may be relevant to the control of body weight; these are being studied intensively.

Many of the adipocytokines secreted by adipocytes are proinflammatory or play a role in blood coagulation. Others are involved in insulin sensitivity and appetite regulation. However, the function of many of these identified cytokines remains unknown or unclear.

Proinflammatory products of the adipocyte include the following:(3)

  • Tumor necrosis factor–alpha (proinflammatory)
  • Interleukin 6 (proinflammatory)
  • Monocyte chemoattracting protein–1 (MCP-1)

Other adipocyte products include the following:(3)

  • Lipotransin
  • Plasminogen activator inhibitor-1 (PAI-1) - Associated with cardiovascular risk
  • Adipocyte lipid-binding protein
  • Acyl-stimulation protein
  • Prostaglandins - Coagulation role
  • Adipsin
  • Perilipins
  • Lactate
  • Leptin - Appetite regulator
  • Adiponectin - Major role in insulin sensitivity
  • Monobutyrin
  • Phospholipid transfer protein

METABOLISM AND FUNCTION:

Critical enzymes involved in adipocyte metabolism and function include the following:

  • Endothelial-derived lipoprotein lipase - Lipid storage
  • Hormone-sensitive lipase - Lipid elaboration and release from adipocyte depots
  • Acyl-coenzyme A (acyl-CoA) synthetases - Fatty acid synthesis

In addition, a cascade of enzymes is involved in beta-oxidation and fatty acid metabolism. The ongoing flurry of investigation into the intricacies of adipocyte metabolism has not only improved our understanding of the pathogenesis of obesity but has also offered several potential targets for therapy.

DEVELOPMENT:

Another area of active research is investigation of the cues for the differentiation of preadipocytes to adipocytes. The recognition that this process occurs in white and brown adipose tissue, even in adults, has increased its potential importance in the development of obesity and the relapse to obesity after weight loss.

Among the identified elements in this process are the following transcription factors:

  • Peroxisome proliferator-activated receptor–gamma (PPAR-gamma)
  • Retinoid-X receptor ligands
  • Perilipin
  • Adipocyte differentiation–related protein (ADRP)
  • CCAAT/enhancer-binding proteins (C/EBP) alpha, beta, and delta

PPAR-gamma agonists increase the recruitment, proliferation, and differentiation of preadipocytes (healthy fat) and cause apoptosis of hypertrophic and dysfunctional adipocytes (including visceral fat). This results in improved fat function and improved metabolic parameters associated with excessive fat–related metabolic diseases (EFRMD), including type 2 diabetes mellitus, hypertension, and dyslipidemia.

HORMONAL INFLUENCES ON APPETITE:

In addition to neurotransmitters and neurogenic signals, many hormones affect appetite and food intake. Endocannabinoids, through their effects on endocannabinoid receptors, increase appetite, enhance nutrient absorption, and stimulate lipogenesis. Melanocortin hormone, through its effects on various melanocortin receptors, modifies appetite.

Several gut hormones play significant roles in inducing satiety, including glucagonlike peptide-1 (GLP-1), neuropeptide YY (PYY), and cholecystokinin. Leptin and pancreatic amylin are other potent satiety hormones. On the other hand, ghrelin, which is secreted from the stomach fundus, is a major hunger hormone.

ODOR DETECTION THRESHOLD:

Smell plays an important role in feeding behavior. Differences in the odor detection threshold (i.e. the lowest concentration of a substance detectable by the human olfactory sense) were found in a study that measured thresholds in 8 lean, fasted individuals before and during a 2-hour hyperinsulinemic euglycemic insulin clamp.(4)

Increased insulin led to reduced smelling capacity, potentially reducing the pleasantness of eating. Therefore, insulin action in the olfactory bulb may be involved in the process of satiety and may be of clinical interest as a possible factor in the pathogenesis of obesity.(4)

GENETICS:

Mutations resulting in defects of the leptin receptor in the hypothalamus may occur. These mutations result in early onset obesity and hyperphagia despite normal or elevated leptin levels, along with hypogonadotropic hypogonadism, and defective thyrotropin secretion.

Murray et al first reported on a sequence variant within the leptin gene that enhances the intrinsic bioactivity of leptin, but which was associated with reduced weight rather than obesity.(5) This sequence variant within the leptin gene is also associated with delayed puberty.

NATURAL HISTORY:

It results from a complex interaction of biological, psychological, behavioral and environmental factors where the consumption of calories exceeds caloric expenditure leading to an accumulation of body fat, hence the obese state. Obesity is associated with a significant increase in mortality and with risk of many disorders, including diabetes mellitus, hypertension, dyslipidemia, heart disease, stroke, sleep apnea, cancer, and others.

SIGN AND SYMPTOMS:

Although several classifications and definitions for degrees of obesity are accepted, the most widely accepted classifications are those from the World Health Organization (WHO), based on body mass index (BMI). The WHO designations are as follows:(6)

  • Grade 1 overweight (commonly and simply called overweight) - BMI of 25-29.9 kg/m 2
  • Grade 2 overweight (commonly called obesity) - BMI of 30-39.9 kg/m 2
  • Grade 3 overweight (commonly called severe or morbid obesity) - BMI ≥40 kg/m 2

Some authorities advocate a definition of obesity based on percentage of body fat, as follows:

  • Men - Percentage of body fat greater than 25%, with 21-25% being borderline
  • Women - Percentage of body fat great than 33%, with 31-33% being borderline

RATIONALE FOR SCREENING:

The U.S. Preventive Services Task Force (USPSTF) recommends that health care providers screen all adult patients for obesity, and the American Academy of Family Physicians agrees. In 2012, the USPSTF published an updated recommendation that clinicians offer or refer obese patients to intensive behavioral interventions, which can lead to weight loss as well as improve glucose tolerance and other CVD risk factors.

Calculating a person's body mass index (BMI) can be useful for assessing their body fat. It is a screening tool for determining if someone has a weight problem. For adults, the following formula used:

BMI = body weight (in kg) ÷ height squared, in meters

DIAGNOSTIC TESTS:

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)

LIPID PANEL:

At minimum, test fasting cholesterol, triglycerides, and high-density lipoprotein cholesterol (HDL-C) levels. 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; however, increased low-density lipoprotein cholesterol (LDL-C) and normal to marginally increased total cholesterol are not uncommon among obese individuals.

LIVER AND THYROID FUNCTION TEST:

Liver function tests yield normal results in most obese patients. However, elevated transaminase levels may indicate nonalcoholic steatohepatitis (NASH) or fatty infiltration of the liver.

Thyroid function test results are also typically normal, but checking them to detect primary hypothyroidism (characterized by increased serum thyrotropin and normal or reduced thyroxine and / or triiodothyronine levels) is worthwhile. Screening with a serum thyrotropin level is usually sufficient. Of importance, hypothyroidism itself rarely causes more than mild obesity.

GLUCOSE AND INSULIN STUDIES:

Obesity is associated with insulin resistance and increased serum levels of fasting insulin and C-peptide serum levels. However, insulin levels are normal in many persons who are obese.

All patients with obesity should be screened for diabetes. Additional information is gained by using glucose and HbA1c tests together if the patient is fasting. The American Diabetes Association currently recommends using the HbA1c test not only to screen for diabetes, but also to follow patients who already have the diagnosis.(7) In contrast, the American Association of Clinical Endocrinologists recommends that HbA1c be considered an additional, optional diagnostic criterion.(8)

Prediabetes is indicated by impaired fasting glucose (fasting plasma glucose levels of 100-125 mg / dL [5.6-6.9 mmol / L]) or impaired glucose tolerance (2-h oral glucose tolerance test values of 140-199 mg / dL [7.8-11.0 mmol / L]). Patients with these findings are at relatively high risk for the future development of diabetes. Type 2 diabetes is diagnosed when the fasting glucose is 126 mg / dL or greater or HbA1c is 6.5% or higher.(9)

EVALUATION FOR DEGREE OF FAT:

Body mass index (BMI) calculation, waist circumference, and waist / hip ratio are the common measures of the degree of body fat used in routine clinical practice. Other procedures that are used in few clinical centers include the following:

  • Caliper-derived measurements of skin-fold thickness
  • Dual-energy radiographic absorptiometry (DEXA)
  • Bioelectrical impedance analysis
  • Ultrasonography to determine fat thickness
  • Underwater weighing

The standard techniques for measuring visceral fat are magnetic resonance imaging (MRI) and computed tomography (CT) scanning. Less expensive techniques for direct measurement of visceral fat include abdominal ultrasonography and abdominal bioelectrical impedance.

PATIENT SELECTION FOR TREATMENT:

The goal of therapy is to prevent, reverse, or ameliorate the complications of obesity. Thus, the selection of patients for treatment is based upon initial risk assessment. Assessment of an individual's overall risk status includes determining the degree of overweight (body mass index [BMI]), the presence of abdominal obesity (waist circumference), and the presence of cardiovascular risk factors (e.g. hypertension, diabetes, dyslipidemia) or comorbidities (e.g. sleep apnea, nonalcoholic fatty liver disease). The relationship between BMI and risk allows identification of patients to target for weight loss intervention.

  • A BMI of 20 to 25kg / m2 is associated with little or no increased risk unless waist circumference is high (a marker of increased cardiometabolic risk), or the subject has gained more than 10 kg since age 18 years.
  • Individuals with a BMI of 25 to 29.9kg/m2, who do not have risk factors for cardiovascular disease (CVD) or other obesity related comorbidities, may be described as having low risk. They should receive counseling on prevention of weight gain. This includes advice on dietary habits and physical activity.
  • Individuals with a BMI between 25 and 29.9kg/m2 and with one or more risk factors for CVD (diabetes, hypertension, dyslipidemia), or with a BMI of 30 to 34.9kg/m2, are at moderate risk. They should be counseled about weight loss interventions (diet, physical activity, behavioral modification, and for some patients, pharmacologic therapy).
  • Individuals with a BMI of 35 to 40kg/m2 are at high risk, and those with a BMI above 40 kg/m2 are at very high risk from their obesity. Individuals in the highest risk categories should receive the most aggressive treatment (lifestyle intervention, pharmacologic therapy, bariatric surgery).

BMI is calculated as follows:

BMI   =   body weight (in kg) ÷ height squared, in meters

THERAPY CONSIDERATIONS:

In January, 2015, the Endocrine Society released new guidelines on the treatment of obesity to include the following:(10,11)

  • Diet, exercise, and behavioral modification should be included in all obesity management approaches for body mass index (BMI) of 25 kg/m2 or higher. Other tools, such as pharmacotherapy for BMI of 27 kg/m 2 or higher with comorbidity or BMI over 30 kg/m2 and bariatric surgery for BMI of 35 kg/m 2with comorbidity or BMI over 40 kg/m 2, should be used as adjuncts to behavioral modification to reduce food intake and increase physical activity when this is possible.
  • Drugs may amplify adherence to behavior change and may improve physical functioning such that increased physical activity is easier in those who cannot exercise initially. Patients who have a history of being unable to successfully lose and maintain weight and who meet label indications are candidates for weight loss medications.
  • To promote long-term weight maintenance, the use of approved weight loss medication (over no pharmacological therapy) is suggested to ameliorate comorbidities and amplify adherence to behavior changes, which may improve physical functioning and allow for greater physical activity in individuals with a BMI of 30 kg/m2 or higher or in individuals with a BMI of 27 kg/m 2 and at least one associated comorbid medical condition (e.g. hypertension, dyslipidemia, type 2 diabetes mellitus, and obstructive sleep apnea).
  • If a patient's response to a weight loss medication is deemed effective (weight loss of 5% or more of body weight at 3 month and safe, it is recommended that the medication be continued. If deemed ineffective (weight loss less than 5% at 3 month or if there are safety or tolerability issues at any time, it is recommended that the medication be discontinued and alternative medications or referral for alternative treatment approaches be considered.
  • In patients with type 2 diabetes mellitus who are overweight or obese, antidiabetic medications that have additional actions to promote weight loss (such as glucagon-like peptide-1 [GLP-1] analogs or sodium-glucose-linked transporter-2 [SGLT-2] inhibitors) are suggested, in addition to the first-line agent for type 2 diabetes mellitus and obesity, metformin.
  • In obese patients with type 2 diabetes mellitus who require insulin therapy, at least one of the following is suggested: metformin, pramlintide, or GLP-1 agonists to mitigate associated weight gain due to insulin. The first-line insulin for this type of patient should be basal insulin. This is preferable to using either insulin alone or insulin with sulfonylurea.
  • Angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and calcium channel blockers, rather than beta-adrenergic blockers, should be considered as first-line therapy for hypertension in patients with type 2 diabetes mellitus who are obese.
  • In women with BMI of more than 27 kg/m2 with comorbidities or BMI of more than 30 kg/m 2 seeking contraception, oral contraceptives are suggested over injectable medications because of weight gain with injectables, provided that women are well informed about risks and benefits (i.e. oral contraceptives are not contraindicated).

TREATMENT OPTIONS:

Treatment of obesity starts with comprehensive lifestyle management (i.e. diet, physical activity, behavior modification).(12) The 3 major phases of any successful weight-loss program are as follows:

  • Preinclusion screening phase
  • Weight-loss phase
  • Maintenance phase - This can conceivably last for the rest of the patient's life but ideally lasts for at least 1 year after the weight-loss program has been completed

LIFE STYLE MODIFICATION: A comprehensive lifestyle intervention (combined diet, exercise, and behavioral treatment) is the most important strategy for weight management. The behavioral component facilitates adherence to diet and exercise regimens. It includes regular self-monitoring of food intake, physical activity, and body weight.

One example of a successful lifestyle intervention program is the Diabetes Prevention Program (DPP).(13) The two major goals of the DPP lifestyle intervention were a minimum of 7 percent weight loss and a minimum of 150 minutes of exercise per week (such as brisk walking). Several behavioral components were used to help achieve these goals, including behavioral self-management training, individual case managers, group and/or individual sessions, individualized adherence strategies, and a network of training, feedback, and clinical support.

BEHAVIOR MODIFICATION: Behavior modification or behavior therapy is one cornerstone in the treatment for obesity. The goal of behavioral therapy is to help patients make long-term changes in their eating behavior by modifying and monitoring their food intake, modifying their physical activity, and controlling cues and stimuli in the environment that trigger eating. These concepts are usually included in programs conducted by psychologists or other trained personnel as well as many self-help groups.

DIETARY THERAPY: Many types of diets produce modest weight loss. Options include balanced low-calorie, low-fat low-calorie, moderate-fat low-calorie, low-carbohydrate diets, and the Mediterranean diet. Dietary adherence is an important predictor of weight loss, irrespective of the type of diet. Thus, we suggest tailoring a diet that reduces energy intake below energy expenditure to individual patient preferences, rather than focusing on the macronutrient composition of the diet. The addition of dietary counseling may facilitate weight loss, particularly during the first year.

No adult who has been studied in a metabolic chamber has needed fewer than 1000 kcal/day for weight maintenance. Thus, even subjects who claim to be "metabolically resistant" to weight loss should lose weight if they comply with a diet of 800 to 1200 kcal/day. If subjects claim to eat less than 1200 kcal/day and yet do not lose weight, one can conclude they are recording intake erroneously and suggest that they reduce by half what they claim to eat. More severe caloric restriction might be expected to induce weight loss more quickly, but a comparison with 400 versus 800 kcal/day diet formulas showed no difference in weight loss. We thus recommend diets with >800kcal/day.

EXERCISE: Increasing energy expenditure through physical activity has particular attractiveness in efforts at long-term maintenance of a lower body weight.

PHARMACOLOGICAL:
GASTROINTESTINAL AGENTS:

ORLISTAT: Orlistat is a gastrointestinal and pancreatic lipase inhibitor that induces weight loss by inhibiting dietary fat absorption. Orlistat should be taken during or up to 1 hour after a meal containing fat. Its effectiveness in producing weight loss does not depend on systemic absorption. Orlistat is available over the counter in a half-strength dose and as a prescription drug as a full-strength dose.

Orlistat may reduce absorption of some fat-soluble vitamins (A, D, E, K) and beta carotene. Administer a multivitamin supplement containing fat-soluble vitamins orally daily, 2 hours before or 1 hour after a meal. Orlistat may also affect the absorption of some medications. In particular, patients on warfarin need closer monitoring because of the potential for malabsorption of vitamin K.

At the full dose of 120 mg 3 times daily, Orlistat is frequently associated with such adverse GI events as flatulence, oily stool, diarrhea, and stool incontinence. Frequently, these adverse events result from the common misconception that because Orlistat blocks fat absorption, people can consume more fat. It is important to advise patients to reduce total fat intake while on Orlistat to reduce the frequency and severity of adverse events.

Doses of the over-the-counter form of Orlistat (60 mg), are associated with fewer adverse events. However, this dosage is less effective for weight loss.

CNS STIMULANTS; ANOREXIANTS:

LORCASERIN: Lorcaserin is indicated as an adjunct to a reduced-calorie diet and exercise for long-term weight management in patients with an initial BMI of more than 30 kg/m2(obese) or in those with a BMI of more than 27 kg/m2 (overweight) who have at least 1 weight-related comorbid condition (e.g. hypertension, dyslipidemia, type 2 diabetes mellitus).

The exact mechanism of action of lorcaserin is unknown, but this agent is thought to decrease food consumption and promote satiety by selectively activating 5-HT2C receptors on anorexigenic pro-opiomelanocortin neurons located in the hypothalamus.

PHENTERMINE/TOPIRAMATE: This low-dose combination of phentermine, a sympathomimetic amine anorectic, and extended-release topiramate, an antiepileptic drug that possibly suppresses appetite and enhances satiety. The drug combination is indicated as an adjunct to a reduced-calorie diet and increased physical activity for long-term weight management in adults.

PHENTERMINE: Phentermine is a sympathomimetic amine that increases the release and reuptake of norepinephrine and dopamine. Its anorexiant effect occurs as a result of satiety-center stimulation in hypothalamic and limbic areas of the brain.

As a pharmacologic component of a comprehensive weight-reduction program (including behavioral modification, caloric restriction, and exercise), phentermine is intended for patients with an initial BMI of more than 30 kg/m2. It is also appropriate for patients with a BMI of between 27 and 30 kg/m2 who have other risk factors (e.g. diabetes, hyperlipidemia, and hypertension).

Phentermine is indicated for use in patients older than 16 years. It is available in capsules, tablets, and orally disintegrating tablets. This medication is contraindicated for use in pregnant women.

DIETHYLPROPION: Diethylpropion is indicated for use as a short-term adjunct in the management of obesity. It is a sympathomimetic amine that reduces appetite, an effect that appears to be secondary to CNS effects. It is available in a 24-hour controlled-release formulation that should be taken at midmorning. It is indicated for use in patients older than 16 years.

PHENDIMETRAZINE: Phendimetrazine is indicated for use as a short-term adjunct in the management of obesity in patients older than 17 years. It is a sympathomimetic amine that reduces appetite, an effect that appears to be secondary to CNS effects.

This agent is available in a 24-hour slow-release 105 mg capsule, which should be taken in the morning 30-60 minutes before breakfast. It is also available in 17.5-35 mg tablets, which should be taken 2 or 3 times daily and an hour before a meal. The maximum recommended dose is 70 mg 3 times daily. Phendimetrazine is contraindicated during pregnancy

BENZPHETAMINE: Benzphetamine is a sympathomimetic amine that reduces appetite, an effect that appears to be secondary to CNS effects. It is used as a short-term adjunct to caloric restriction in exogenous obesity. It is indicated for use in patients older than 12 years; the maximum dose is 50 mg 3 times daily. This medication is contraindicated during pregnancy.

GLUCAGON LIKE PETIDE-1 INHIBITOR:

LIRAGLUTIDE: Liraglutide is a glucagonlike peptide-1 (GLP-1) analog. GLP-1 is a physiological regulator of appetite and calorie intake, and the GLP-1 receptor is present in several areas of the brain involved in appetite regulation. It is indicated for chronic weight management as an adjunct to diet and exercise in adults with a BMI of ≥30 (obese) or adults with a BMI of ≥27 (overweight) who have at least 1 weight-related condition (e.g. hypertension, type 2 diabetes, dyslipidemia).

ANTIDEPRESSANTS, DOPAMINE REUPTAKE INHIBITORS, OPIOID ANTAGONISTS:

BUPROPION: Increases dopamine activity in the brain, which appears to lead to a reduction in appetite and increase in energy expenditure by increasing activity of pro-opiomelanocortin (POMC) neurons.

NALTREXONE: Blocks opioid receptors on the POMC neurons, preventing feedback inhibition of these neurons and further increasing POMC activity.

Combination may regulate activity in the dopamine reward system of the brain that helps control food cravings and overeating behaviors.

SURGICAL:

Among the standard bariatric procedures are the following:

  • Roux-en-Y gastric bypass
  • Adjustable gastric banding
  • Gastric sleeve surgery
  • Vertical sleeve gastrectomy
  • Horizontal gastroplasty
  • Vertical-banded gastroplasty
  • Duodenal-switch procedures
  • Biliopancreatic bypass
  • Biliopancreatic diversion

GOALS OF THERAPY:

The goal of any treatment, including drug therapy, for overweight subjects must be realistic.

  • The ideal outcome is a return to normal body weight, but this is usually unrealistic. In one study, as an example, subjects were asked about their dream weight, and this was later compared with the actual weight loss achieved; no subject achieved their dream weight and few were happy with the weight loss they achieved. Thus, the clinician and the patient need to come to a mutual understanding of the realities of weight loss.
  • Success may be measured by the degree of weight loss and improvement in associated risk factors. Weight loss should exceed 2 kg during the first month of drug therapy (one pound per week), fall more than 5 percent below baseline between three to six months, and remain at this level to be considered effective. A weight loss of 5 to 10 percent can significantly reduce the development of diabetes in those with pre-diabetes.(14) and reduce blood pressure and risk factors for cardiovascular disease in higher risk patients(15). Improvement in baseline risk factors after weight loss is an important criterion in the determination of whether to continue therapy.(16)
  • In drug trials, weight loss of 10 to 15 percent using both drug and behavioral intervention is considered a very good response, and weight loss exceeding 15 percent is an excellent response. This degree of weight loss generally has substantial benefits, including lowering blood pressure and improving serum lipid concentrations, increasing insulin sensitivity, and reducing hyperglycemia, with reversion to normal glucose tolerance in some early onset diabetics, and may reduce risk of mortality. However, a drug may produce side effects that can reduce its overall benefits.
  • The maximal duration of published treatment results is four years for(17) If patient response is good, using the criteria noted above, and the patient wishes to continue Orlistat, this may be considered after acknowledging the lack of longer term data and obtaining the patient's willingness to continue.
  • Drug therapy does not cure obesity. Patients with obesity given drugs should be advised that when the maximal therapeutic effect is achieved, weight loss ceases. When drug therapy is discontinued, weight is expected to rise.
  • When overweight patients have diabetes, depression, behavioral problems, or cardiovascular disease, it is important to select drugs for these diseases which produce weight loss, rather than weight gain, when benefits in total outweigh risks of adverse effects. Several drugs are well known to produce weight gain and should be avoided if good alternatives are available.(18) Although weight loss is always desirable, it must be balanced against other factors (ability to achieve desired glycemic control, other side effects and risks of meds, and expense).

Achieving and maintaining weight loss is made difficult by the reduction in energy expenditure that is associated with weight loss. In one report, as an example, maintenance of body weight at 10 percent below the baseline weight in patients with obesity was associated with an 8 kcal/kg reduction in total energy expenditure.

GUIDELINES:

Treatment for obesity is based on guidelines from the prestigious societies such as Endocrine Society.

To review the Endocrine Society guidelines, click on the link below.

http://press.endocrine.org/doi/abs/10.1210/jc.2014-3415

LONG TERM MONITORING:

As with the management of other chronic medical conditions (e.g. diabetes mellitus, hypertension, bronchial asthma), long-term success in the management of obesity is contingent on long-standing follow-up with the weight-loss program. Experience obtained from the lifestyle intervention group of patients in the Diabetes Prevention Program and information drawn from the ongoing Diabetes Prevention Program Observation study have borne out the importance of regular follow-up.

Patient visits may not need to occur as frequently during follow-up as during the initial weight-loss phase. Nevertheless, they are paramount if the lessons learned regarding diet, exercise habits, and behavioral patterns are to be maintained.

CONSULTATION AND COUNSELING:

The following consultations are recommended in the treatment of obesity:

  • Dietitians
  • Exercise and physical therapists
  • Behavioral scientists and/or psychologists
  • Bariatric surgeon - In appropriate setting

In select cases, consultation with a psychiatrist may be indicated. Psychiatric consultation should be sought for patients with psychiatric disorders and personality disorders (e.g. severe depression, mania, obsessive disorders) that may be worsened by attempts at weight loss if not adequately treated and controlled.

PRECAUTIONS:

Offer following preventions to patients:

  • Don't try to lose weight fast, without first checking with your doctor.
  • Don't waste your precious time trying to achieve the impossible. The speed at which you can lose weight (without regaining it) is dependent on various factors. Including your present weight, your general lifestyle, how active you are, how regular your lifestyle is, your health & family history, the amount of stress in your life.
  • Make sure you follow a sensible balanced diet. Avoidfad diets as they will ruin your metabolism and choose a sensible diet plan that allows you lots to eat and offers a balanced menu.
  • Never go hungry. Remember, hunger is the biggest diet killer. Most dieters still think that the less they eat, the faster they lose weight. This is nonsense. The less we eat the more uptight and miserable we get. This results in your diet failing.
  • Eat good food. We eat too much restaurant-food, junk food, instant snacks and processed foods. These foods are usually very high in the two most-fattening ingredients: fat and sugar. This is why obesity is becoming such a problem, especially in America where an estimated 1 in 3 children are overweight.
  • Start with the attitude that this is serious and your good health is the ultimate goal. Get professional help. Professional help might come from any of the following: a dietician, medical doctor, nutritionist, hypnotherapist, cognitive therapist, fitness instructor or any other person with training in the health and weight loss fields. Remember, you are ultimately responsible for your own health.

REFERENCES:

  • Flegal KM, Carroll MD, Kit BK, Ogden CL. Prevalence of obesity and trends in the distribution of body mass index among US adults, 1999-2010.JAMA. 2012 Feb 1. 307(5):491-7.
  • WHO/IASO/ITO.Asia Pacific Perspective: Redefing obesity and its treatment   World Health Organization, Western Pacific  Region;2000.
  • Hamdy O. The role of adipose tissue as an endocrine gland.Curr Diab Rep. 2005 Oct. 5(5):317-9
  • Ketterer C, Heni M, Thamer C, Herzberg-Schäfer SA, Häring HU, Fritsche A. Acute, short-term hyperinsulinemia increases olfactory threshold in healthy subjects.Int J Obes (Lond). 2011 Aug. 35(8):1135-8
  • Murray PG, Read A, Banerjee I, Whatmore AJ, Pritchard LE, Davies RA, et al. Reduced appetite and body mass index with delayed puberty in a mother and son: association with a rare novel sequence variant in the leptin gene.Eur J Endocrinol. 2011 Apr. 164(4):521-7
  • http://apps.who.int/bmi/index.jsp?introPage=intro_3.html
  • Tan CE, Ma S, Wai D, Chew SK, Tai ES. Can we apply the National Cholesterol Education Program Adult Treatment Panel definition of the metabolic syndrome to Asians?.Diabetes Care. 2004 May. 27(5):1182-6.
  • American Association of Clinical Endocrinologists Statement on the Use of A1C for the Diagnosis of Diabetes. Available athttp://emedicine.medscape.com/article/117853-workup. Accessed: August 6. 2012.
  • [Guideline] Diagnosis and classification of diabetes mellitus.Diabetes Care. 2010 Jan. 33 Suppl 1:S62-9.
  • Tucker ME. New US obesity guidelines. Treat the weight first. Medscape Medical News. Available athttp://www.medscape.com/viewarticle/838285.
  • Apovian CM, Aronne LJ, Bessesen DH, et al. Pharmacological management of obesity: an endocrine society clinical practice guideline.J Clin Endocrinol Metab. 2015 Feb. 100(2):342-62.
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  • Diabetes Prevention Program Research Group, Knowler WC, Fowler SE, et al. 10-year follow-up of diabetes incidence and weight loss in the Diabetes Prevention Program Outcomes Study. Lancet 2009; 374:1677.
  • Douketis JD, Macie C, Thabane L, Williamson DF. Systematic review of long-term weight loss studies in obese adults: clinical significance and applicability to clinical practice. Int J Obes (Lond) 2005; 29:1153.
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  • Torgerson JS, Hauptman J, Boldrin MN, Sjöström L. XENical in the prevention of diabetes in obese subjects (XENDOS) study: a randomized study of orlistat as an adjunct to lifestyle changes for the prevention of type 2 diabetes in obese patients. Diabetes Care 2004; 27:155.
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