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Disease Diagnosis:

The year 2000 was the first in recorded history in which the percentage of people worldwide who are obese exceeded the percentage of people who are starving or malnourished.  Americans are getting heavier just as the rest of the world.  Although obesity is common in all races, ages, and both genders, African-American women are heavier than white or Mexican-American women, Mexican-American men are heavier than white men, and white men are heavier than African-American men.  Men, as a group, are more overweight than women in every age group but two, the 55-64 and 65-70 year old age groups.  Women however, still tend to be more obese than men on average. 

The average weight gain for the most Americans is about 5 pounds per year starting in the third or fourth decade of life, which amounts to about 50 extra kilocalories/day per year over the energy requirement.  This gain usually occurs during the winter and holiday season and is not reversed during the warmer months.  Thus, it means that for the individual to lose the weight, they would have to increase their energy output by an average of 50 kcal/day (This is the amount expended by a 150 pound person walking 2 mph for 15 minutes/ day.)

Weight related disease or overweight and obesity are known risk factors for Diabetes, heart disease, stroke, hypertension, gallbladder disease, osteoarthritis, sleep apnea and uterine, breast, colorectal, kidney, and gallbladder cancers.  Obesity is associated with High blood cholesterol, complications of pregnancy, menstrual irregularities, hirsutism, stress incontinence, depression and increased surgical risk. 

Obese patients require a compete physical examination to rule out signs of secondary causes of obesity, such as Cushing’s syndrome, hypothyroidism, or other pituitary abnormalities.   Obesity is a state of excess adipose tissue mass.  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/heightin (kg/m2 ).  Other approaches to quantifying obesity include anthropometry (skin-fold thickness), densitometry (underwater weighing), computed tomography (CT) or magnetic resonance imaging (MRI), and electrical impedance. 

Measurement of the waste circumference is also important.  This measurement is made at the narrowest point between the rib cage and the umbilicus.  The waist  circumference is an indirect measure of abdominal fat.  High risk levels are a waist circumference of >102 cm (40 inches) for men with other risk factors, and >88 cm (35 inches) for women with other risk factors.  These waist measurements are less predictive for risk in patients with a BMI ≥35 kg/m2. 

Using data from the Metropolitan Life Tables, BMIs for the midpoint of all heights and frames among both men and women range form 19-26 kg/m2.   Based on unequivocal data of substantial morbidity, a BMI of 30 is most commonly used as a threshold for obesity in both men and women.  Large scale epidemiological studies suggest that all cause, metabolic, cancer, and cardiovascular morbidity begin to rise when BMIs are ≥ 25, suggesting that the cut-off for obesity should be lowered.  Some authorities use the term overweight (rather than obesity) to describe individuals with BMIs between 25 and 30.  A BMI between 25-30 should be viewed as medically significant and worthy of therapeutic intervention, especially in the presence of risk actors, that are influenced by adiposity, such as hypertension and glucose intolerance. 

Underweight < BMI=18.5, Normal 18.5-24.9, Overweight 25.0-29.9 with an increased risk for disease, Obesity 30.0-34.9 which is considered a Class 1 Obesity and a high to very high risk for disease, 35.5-39.9 Class 2 Obesity with very high risk for disease across categories, and ≥40 for extreme obesity also known as a Class 3 Obesity with an extremely high risk for diseases for both men and women.

Finally since Obesity is a known risk factor for cardiovascular disease and diabetes mellitus, patients should undergo serum testing for hyperlipidemia and hyperglycemia. 

It must be noted that distribution of adipose tissue in different anatomic depots has substantial implications for morbidity.  Intraabdominal and abdominal subcutaneous fat have more significance than subcutaneous fat present in the buttocks and lower extremities.  Many of the most important complications of obesity, such as insulin resistance, diabetes, hypertension, hyperlipidemia (Often hypertension is concomitant and interlinked with hyperlipidemia), and hyperandrogenism in women, are linked more strongly to Intraabdominal and/or upper body fat than to overall adiposity.  It is thought that Intraabdominal adipocytes are more lipolytically active than those from other depots.  Release of free fatty acids into the portal circulation has adverse metabolic actions, especially on the liver.                                                                                               

Initial Evaluation:

The initial evaluation must include evaluation of potential obesity related diseases noted within the history, physical examination, and laboratory tests.  Always obtain a weight history, eating and activity behaviors.  Search for triggering factors, including medications (many medications can cause obesity!), measure weight, height, and calculate body mass index.  Please categorize obesity classifications and the patient’s health risk.  Determine the patient’s readiness to lose weight.  Always spend time discussing patient goals and expectations setting achievable goals. The initial office visit should determine the aggressiveness and scope of therapy by evaluating the severity of obesity, the presence of concurrent co morbidities, and risk of future obesity-related medical complications

As noted above, certain medications can cause weight gain and increase body fat, thereby making weight loss more difficult.  These drugs differ in their propensity to increase body weight; some medications, such as the anticonvulsant valproic acid, can cause considerable weight gain of 15–20 kg, whereas other medications, such as the ß-adrenergic receptor blocker propranolol, are associated with small and probably clinically insignificant weight gain. The mechanism responsible for medication-induced weight gain has not been carefully studied for most of these agents, but must be related to an increase in energy intake (e.g. antipsychotics and steroid hormones), a decrease in energy expenditure (e.g. ß-adrenergic receptor blockers), a decrease in energy loss (e.g. decreased glucosuria from diabetes therapy), or a combination of these factors. Weight loss therapy can be facilitated by decreasing the dose or substituting the medication with another drug that has less weight gain potential, if possible.

In summary, medications that can cause weight gain are Psychotropic medications such as Tricyclic antidepressants, Monoamine oxidase inhibitors, Specific SSRIs, Atypical antipsychotics, Lithium, Specific anticonvulsants, ß-adrenergic receptor blockers, Diabetes medications such as Insulin, Sulfonylureas, Thiazolidinediones, Highly active antiretroviral therapy, Tamoxifen, and Steroid hormones such as Glucocorticoids and Progestational steroids. 

1.        Pijl H, Meinders AE. Bodyweight changes as an adverse effect of drug treatment. Drug Safety 1996;14:329-342.



Patient motivation, commitment, and compliance are critical for weight loss success. Therefore, knowledge of the patient’s readiness to lose weight will help in developing an appropriate treatment strategy. Good candidates for treatment are patients who decide they want to lose weight for appropriate reasons, are not currently experiencing major life stressors, do not have psychiatric or medical illnesses that prevent effective weight loss, and are willing to devote the time needed to make lifestyle changes.  In addition, the patient’s work, social, and family environment should be considered in deciding if it is a good time to implement weight loss therapy.  If the patient is considered to be ready to lose weight, weight loss therapy should be initiated. If the patient is not ready to lose weight, the immediate goal is to prevent further weight gain and explore barriers to weight reduction.  For example the patient should be able to devote 15-30 min/day to weight control for a 26 consecutive week period.

The cornerstone of obesity treatment involves consuming fewer calories that are expended to mobilize and oxidize endogenous triglycerides as fuel.  Approximately 75%–85% of weight that is lost by dieting is composed of fat, and 15%–25% is fat-free mass. Most, if not all, of the loss of fat is due to a decrease in adipocyte triglyceride content. It is also possible that long-term weight loss can decrease the number of fat cells by stimulating apoptosis (programmed cell death) or morphologic reversion of mature adipocytes to preadipocytes. However, these possibilities have not been evaluated in obese subjects. Later in this section, an overview of the key therapeutic principles involved in obesity management is presented.

Weight loss is associated with an increased risk of gallstones because weight loss increases bile cholesterol super saturation, enhances cholesterol crystal nucleation, and decreases gallbladder contractility. The incidence of new gallstones is approximately 25%–35% in obese patients who experience rapid weight loss after treatment with a very-low-calorie, low-fat diet (<600 kcal/d; 1–3 g fat/d) or gastric surgery.  The risk of gallstone formation increased markedly when the rate of weight loss exceeded 1.5 kg (~1.5% of body weight) per week.

Ursodeoxycholic acid therapy can prevent gallstone formation during rapid weight loss. In a randomized controlled trial of 1004 patients enrolled in a 16-week, 520 kcal/d weight loss program, ursodeoxycholic acid caused a decrease in gallstone formation from 28% in those receiving placebo to 3% in those receiving 600 mg/d of drug. In 233 patients who had gastric bypass surgery; 600 mg/d of ursodeoxycholic acid decreased the incidence of new gallstones from 32% to 2%. This data indicates that 600 mg/d ursodeoxycholic acid is the optimal dose for effective prophylaxis of gallstone formation during rapid weight loss.

1.        Shiffman ML, Kaplan GD, Brinkman-Kaplan V, Vickers FF. Prophylaxis against gallstone formation with ursodeoxycholic acid in patients participating in a very-low-calorie diet program. Ann Intern Med 1995;122:899-905.

2.        Sugerman HJ, Brewer WH, Shiffman ML, et al. A multicenter, placebo-controlled, randomized, double-blind, prospective trial of prophylactic ursodiol for the prevention of gallstone formation following gastric-bypass-induced rapid weight loss. Am J Surg 1995;169:91-96.

The clinical management of obesity involves identifying patients who need treatment, developing a realistic treatment plan, and implementing a structured treatment strategy that includes long-term surveillance and the ability to modify therapy based on the clinical response and chronic evaluation.  It can be a life commitment to “live” for some patients.  Since the factors for weight gain can be age related concomitant with factors discussed, those who can incorporate simple weight consciousness to their daily lives, in time perhaps they could re-teach their children for healthy lifestyle absent obesity based on unconsciously bad life habits, and thus will regain weight control based on unconsciously good life habits.

Additional support (such as enlistment of a family member, enrollment in a community weight loss program, referral for behavioral therapy, or referral to a dietician) and frequently scheduled follow-up visits should be arranged.


Dietary fat is composed primarily of triglycerides, which increase food palatability and energy-density. Therefore, low-fat diets often are prescribed for obese patients because these diets facilitate energy restriction.

The key to weight loss is burning more calories than you consume.  It is known that a diet with a deficit of 500-1,000 kcal/day will achieve weight loss of 1-2 lb/weekWhy?  if you cut 500 calories from your typical diet each day, you'd lose about 1 pound a week (500 calories x 7 days = 3,500 calories).  If you need to calculate this 3,500 calories equals about 1 pound (0.5 kilogram) of fat, thus you need to burn 3,500 calories more than you take in to lose 1 pound.

Sound Medical Nutritional Therapy calls for a low calorie diet and reduced fat for achieving the goals of reducing body mass, waist circumference, and overall weight loss.  The MNT diet calls for begining your day correctly.  Thus begin with a healthy breakfast and try to eat at least four servings of vegetables, three servings of fruits daily, and stick to the healthy oils (fats) such as vegetable oil, olive oils and nut butters.  Of course sugar is reduced and meat consumption is limited to a 3- once portion  which could thus fit into the palm of your hand.  Eating a diet of fruits, vegetables and whole grains or plant-based foods help you to lose weight while keeping you healthy and strong.  Finally, try to eat fresh fish at least twice a week again the serving portion should fit into the palm of an average persons hand.

Most importantly check with your Doctor of Medicine before making dietary changes.  If you have any health risks or other diseases, this may modify any quality diet plan you undertake.  Even the DASH diet must be reviewed first by your physician to make sure it will only help you.


A good MNT eating plan combined with exercise is key to aiding weight loss and maintaining the weight you lose.  Picture in your minds eye that there are calories you can't cut with a good MNT program, but that exercise can help to burn off those difficult calories as well as strengthening your heart and blood vessels while reducing your blood pressure.  What has been proven scientifically through double blind studies are that folks who were able to maintain their weight loss over the long term, all exercised to some degree regularly (Try to spend 25-30 minutes/day at least four days a week).  Examples are aerobic exercise which may be brisk walking.  Let's say you usually take the elevator up to your office, use the steps up and down and when shopping don't be afraid to park at the end of the lot.  Walking, walking, walking can be a very good supplement to your MNT plans.


Behavioral Therapy

Behavior therapy is an integral part of the overall treatment regime.  Behavior therapy acts as an adjunct to diet in promoting weight loss and weight maintenance, assessment of the patient’s motivation and readiness to implement a plan. 

Finally, after therapy or successful weight loss, maintenance programs consisting of low calorie diets, physical activity, and behavior therapy, should be continued indefinitely.


Medicinal Therapeutics

Relative to medicinal therapeutics, today there are only two medications approved for long term care and four relative to short-term care.  Of course, Orlistat-Xenical, a non schedule long term medication was approved in 1999.  Sibtramine-Meridia, a schedule 4 medication approved in 1997, is our other long term care medication.  Short term approved medications include Diethypropion-Tenuate (1973), a schedule 4 with adverse affects preventing long term utility.  Phentermine-Adipex, lonamin, approved in 1973, is a schedule 4 medication.  Phendimetrazine-Bontril/Prelu-2, and Benzpelamine-Didrex, are schedule 3 drugs approved in 1961 and 1980 respectively, for short term use.

In conclusion, only sibutramine (Meridia) and orlistat (Xenical) have been approved for long-term use. All the approved medications act as anorexiants, with the exception of orlistat, which blocks the absorption of dietary fat. Anorexiants increase satiation (level of fullness, which regulates the amount of food consumed during a meal) or satiety (level of fullness after a meal, which determines frequency of eating), or both. Methamphetamine is also approved by the FDA for short-term use, but it is a schedule II drug and should be avoided because of its abuse potential. Three anorexiant medications have been removed from the marketplace because of increased risks of either valvular heart disease (fenfluramine and dexfenfluramine) or hemorrhagic stroke (phenylpropanolamine) associated with their use.


1.        Khan MA, Herzog CA, St Peter JV, et al. The prevalence of cardiac valvular insufficiency assessed by transthoracic echocardiography in obese patients treated with appetite-suppressant drugs. N Engl J Med 1998;339:713-718.

2.        Kernan WN, Viscoli CM, Brass LM, et al. Phenylpropanolamine and the risk of hemorrhagic stroke. N Engl J Med 2000;343:1826-1832.


Lifestyle modifications combined with Pharmacotherapy can be a useful adjunctive measure for properly selected patients.  



Surgery is considered an option for patients with a BMI of ≥ 40 kg/m2 , or ≥ 35kg/m2  with cardiovascular risk factors.  Two procedures available are placing a restrictive band around the stomach in order to reduce capacity or bypassing the stomach altogether.  If medical weight loss treatment has failed and are suffering from complications of extreme obesity, surgical procedures are a consideration.  However, absent multidisciplinary care, with attention to diet, activity, behavioral and social supports, surgical weight loss procedures have limited permanent success due to the bowel and stomach stretching to the former size and absorption of food often returns to previous quantities. 


Chronic Evaluation:

Obesity is on the rise around the world.  It is increasing in every group; that it is today’s reliance on others for most everything, an absence of control of the little things in life, out of control overeating energy requirements above expenditure needs, absent science defined sound life habits.   Thus, to correct this mechanism, it is now clear that a commitment for subtle changes in behavior over time, and for life, will make all the difference in the world for those whose lives may be cut short through obesity.

Obesity is a chronic disease that requires long-term therapy for successful long-term weight management. Often, patients who are able to lose weight with obesity therapy regain their lost weight after therapy is discontinued.  In a recent study, 76 obese women (mean body mass index 39.4 kg/m2) who were randomly assigned to one of three treatment groups: 4 months of a very-low-calorie diet (VLCD) of 400–500 kcal/d, 6 months of behavior therapy and a 1000–1200 kcal/d balanced deficit diet, or 6 months of a combination of a VLCD and behavior therapy.  Each treatment program was effective in achieving short-term weight loss. However, most subjects regained a considerable amount of weight by 1 year and had returned to their pretreatment weight at 5 years.

1.  Drent ML, van der Veen EA. Lipase inhibition: A novel concept in the treatment of obesity. Int J Obes Relat Metab Disord 1993;17:241-244.

Thus, it has become clear that maintenance therapy is important for long-term weight management success after initial weight loss is achieved by diet and behavior therapy.  In another recent study, Perri and colleagues randomized obese subjects who lost weight after 5 months of diet and behavior modification therapy to “no maintenance” or a “maintenance program” that involved biweekly contact.  At 1 year after initial weight loss was achieved, participants who received maintenance therapy maintained long-term weight loss, whereas those who did not receive maintenance therapy regained half of their lost weight.

1.        Perri MG, McAllister DA, Gange JJ, et al. Effects of four maintenance programs on the long-term management of obesity. J Consult Clin Psychol 1988;56:529-534.

In conclusion, after the initial treatment plan duration return for Chronic Evaluation has been proved by the evidence to help the patient maintain their weight loss plan, whereas absent these procedures and protocol, most patients regained weight to their detriment.

Medical Text References:

  1. Sloane, Philip D et al, Essentials of Family Medicine, 4th Edition, Lippincott-Williams & Wilkins, pages 783-801
  2. Andreoli Thomas E et al, Cecil Essentials of Medicine, 4th Saunders, pages 434-437.
  3. Kasper Dennis L et al, Harrison’s Principles of Internal Medicine, 16th edition, Mc Graw Hill, pages 422-429

Medical Research References:

1.        Ballor DL, Poehlman ET. Exercise-training enhances fat-free mass preservation during diet-induced weight loss: a meta-analytical finding. Int J Obes Relat Metab Disord 1994;18:35-40.

2.        Knittle JL, Ginsberg-Fellner F. Effect of weight reduction on in vitro adipose tissue lipolysis and cellularity in obese adolescents and adults. Diabetes 1972;21:754-761.

3.        Naslund I, Hallgren P, Sjostrom L. Fat cell weight and number before and after gastric surgery for morbid obesity in women. Int J Obes 1988;12:191-197.

4.        Hay DW, Carey MC. Pathophysiology and pathogenesis of cholesterol gallstone formation. Semin Liver Dis 1990;10:159-170.

5.        Broomfield PH, Chopra R, Sheinbaum RC, et al. Effects of ursodeoxycholic acid and aspirin on the formation of lithogenic bile and gallstones during loss of weight. N Engl J Med 1988:319:1567-1572.

6.        Liddle RA, Goldstein RB, Saxton J. Gallstone formation during weight-reduction dieting. Arch Intern Med 1989;149:1750-1753.

7.        Shiffman ML, Sugerman HJ, Kellum JM, et al. Gallstone formation after rapid weight loss: a prospective study in patients undergoing gastric bypass surgery for treatment of morbid obesity. Am J Gastroenterol 1991;86:1000-1005.

8.        Weinsier RL, Wilson LJ, Lee J. Medically safe rate of weight loss for the treatment of obesity: a guideline based on risk of gallstone formation. Am J Med 1995;98:115-117.

9.        Shiffman ML, Kaplan GD, Brinkman-Kaplan V, Vickers FF. Prophylaxis against gallstone formation with ursodeoxycholic acid in patients participating in a very-low-calorie diet program. Ann Intern Med 1995;122:899-905.

10.     Sugerman HJ, Brewer WH, Shiffman ML, et al. A multicenter, placebo-controlled, randomized, double-blind, prospective trial of prophylactic ursodiol for the prevention of gallstone formation following gastric-bypass-induced rapid weight loss. Am J Surg 1995;169:91-96.

11.     Wadden TA, Sternberg JA, Letizia KA, et al. Treatment of obesity by very low calorie diet, behavior therapy, and their combination: a five-year perspective. Int J Obes 1989;13 (suppl 2):39-46.

12.     Perri MG, McAllister DA, Gange JJ, et al. Effects of four maintenance programs on the long-term management of obesity. J Consult Clin Psychol 1988;56:529-534.

13.     Khan MA, Herzog CA, St Peter JV, et al. The prevalence of cardiac valvular insufficiency assessed by transthoracic echocardiography in obese patients treated with appetite-suppressant drugs. N Engl J Med 1998;339:713-718.

14.     Kernan WN, Viscoli CM, Brass LM, et al. Phenylpropanolamine and the risk of hemorrhagic stroke. N Engl J Med 2000;343:1826-1832.

15.     Drent ML, van der Veen EA. Lipase inhibition: A novel concept in the treatment of obesity. Int J Obes Relat Metab Disord 1993;17:241-244.


By Scott David Neff for Family Medicine September 25, 2006

"The most acceptable service to God is doing good to man"   Ben Franklin

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