6.
Rationale For the Surgical Treatment of Morbid Obesity

Introduction

There is considerable misinformation concerning the validity of bariatric surgery in the management of morbid obesity. The following "Rationale for Surgery" covers the field in general. References are provided to allow the interested reader to obtain more detailed information along with the opportunity to examine the original data on which these statements are based.

Bariatric surgery is a recognized sub-interest in the field of General Surgery. It has been endorsed by the National Institutes of Health Consensus Conference, 1992.[1] The American Society for Bariatric Surgery (ASBS) has a representative on the American College of Surgeons Board of Governors and is a specialty surgical society in the Specialty & Service Society section of the American Medical Association. Regular members of the ASBS are all Board Certified Surgeons who have a special interest in surgical treatment of hugely obese patients. It must be emphasized that these procedures are in no way to be considered as cosmetic surgery, and, as you read on, this should become abundantly clear.

Among recent articles of interest included in the references are the paper from Pories et al. from the University of East Carolina, a group with the finances and personnel to enable follow-up of their entire obesity surgery population, some 600 patients, achieving a patient follow-up of 96% at 14 years after surgery. This paper, while particularly emphasizing the beneficial effects of surgically induced weight loss in Type II diabetics, also includes follow-up data on other aspects of their series.[2] Other papers detailing the results of bariatric surgery in the younger and older age groups and noting improvement in co-morbidities not generally appreciated include results in adolescents,[3-5], those over 55 years of age,[6, 7] and the remarkable improvements in asthmatics which follows surgically induced weight loss.[8, 9] The introduction of the laparoscopic approach to bariatric surgery has achieved dramatic improvement in patient discomfort and length of hospital stay.[10, 11]

Rationale For the Surgical Treatment of Morbid Obesity

Morbid obesity (this term is synonymous with "clinically severe obesity") is a disease of excess energy stores in the form of fat. Morbid obesity correlates with a Body Mass Index (BMI) of 40 kg/m2 or with being 100 pounds overweight. Being overweight is associated with real physical problems which are now well recognized. The most obvious is an increased mortality rate directly related to weight increase.[12] In a 12 year follow-up of 336,442 men and 419,060 women, it was found that the mortality rates for men 50% above average weight were increased approximately two fold. In the same weight group the mortality was increased five fold for diabetics and four fold for those with digestive tract disease. In women, the mortality was also increased two fold, while in female diabetics the mortality risk increased eight fold and three fold in those with digestive tract disease. It is clear that overweight people of both sexes, especially young overweight people, tend to die sooner than their lean contemporaries. [13-15] While obesity, of itself, is a risk factor,[16] most mortality and morbidity is associated with the co-morbid conditions. This applies to non-operated as well as peri-operative mortality and morbidity. These conditions have been outlined in the 1985 National Institutes of Health Consensus Conference and include hypertension, hypertrophic cardiomyopathy, hyperlipidemia, diabetes, cholelithiasis, obstructive sleep apnea, hypoventilation, degenerative arthritis and psychosocial impairments.[16, 17]

A Veterans Administration study of 200 morbidly obese men aged 23 to 70 years, with an average weight of 316 lbs (143.5 kg) showed a twelve fold increase in mortality in the 25-34 year age group and a six fold increase in the 35-44 year age group. During the average follow-up period of 7 ½ years, 50 of the original group had died.[18] An interesting ongoing study in this regard is the Swedish Obesity Study (SOS) in which 2000 patients have been randomized to diet therapy and gastric restrictive surgery.[19] The study is still incomplete but indicates reduction in diabetes, hypertension and lipid disturbances in the surgically treated group.[20]

The Nurses Health Study has reported obesity related health risks in women at much less impressive degrees of obesity. Weight gain after the age of 18 years was shown to be a strong predictor of cardiovascular risk. This large prospective cohort study involving 115,886 women apparently healthy at baseline, showed a strong association between BMI and cardiovascular disease. As compared with women whose BMI was less than 21 kg/m2, the age and smoking adjusted relative risk of non-fatal myocardial infarction and fatal coronary artery disease for women with BMI of 25-29 was 1.8 (95%CI: 1.2-2.5), and that for women with BMI >29 was 3.3 (95%CI:2.3-4.5).[21]

The Framington study noted that the first cohort to terminate because of demise of all participants was the morbidly obese. Finally, in this litany of risk, the Guinness Book of Records memorializes the worlds heaviest individuals. Note that none of these lived over 40 years of age. Recent work suggests that the significantly increased mortality risk of morbid obesity reverts to normal following successful weight loss surgery.[22]

Obesity is dangerous to health because of the associated increased prevalence of cardiovascular risk factors such as hypertension, diabetes mellitus, hypertriglyceridemia, hyperinsulinemia and low levels of high density lipoprotein (HDL) cholesterol. Statistically significant improvements have been observed in both diabetes and hypertension, with >10 percent weight loss, and in cardiovascular conditions, with 5 percent weight loss.[23] Data from the Framingham study support the estimate that a ten percent reduction in body weight corresponds to a twenty percent reduction in the risk of developing coronary heart disease.[24] Serious consequences of severe obesity are well documented and include cardiac dysfunction, pulmonary problems, digestive diseases, and endocrine disorders as well as obstetric, orthopedic, and dermatologic complications.

The association between average weight of population groups and the prevalence of non-insulin-dependent diabetes has been repeatedly observed.[25, 26] The risk for diabetes has been reported to be about twofold in the mildly obese, fivefold in moderately obese and tenfold in severely obese persons.[27] The duration of obesity is also an important determinant of the risk for developing diabetes.[28] In cross-sectional studies, obesity has been shown to be associated with an increased prevalence of non-insulin-dependent diabetes in both men and women.[29] The NHANES II data found that the overall relative risk of developing diabetes was 2.9 times higher for obese persons who are 20-75 years old.[30] The risk of developing diabetes also increases with age,[31, 32] if a family history is present [33] and if the obesity is central.[34] A prospective study in Scandinavia showed that moderate obesity was associated with a 10 fold increase in the risk of diabetes. This risk increased sharply as obesity became more severe.[34] In patients who are morbidly obese and candidates for surgical treatment, diabetes and hypertension are highly correlated with body weight and waist-hip ratio.[35]

Cancer mortality rates are increased in severely obese females; e.g. endometrium (5.4 times), gallbladder (3.6 times), uterine cervix (2.4 times), ovary (1.6 times), breast (1.5 times). Cancer mortality rates are increased in severely obese males; e.g., colorectum (1.7 times), and prostate (1.3 times). [36]

The 2000 US Census estimates the adult population ³ 20 years and < 70 years at 185,634,000 persons. Prevalence estimates, using NHANES III data obtained a few years previously, are 2.8% for US adults with a body mass index (BMI) ³ 40 kg/m2 and 8% for those with a BMI>=35 kg/m2,[37] These numbers approximate to six million morbidly obese adults and another 9.6 million (8.0-2.8 =5.2%) with BMI >35 but <40. The relative risk for all cause mortality is increased at BMI levels ³ 30 kg/m2. [37, 38]

Health care for the six million morbidly obese adults in the United States of America, [37, 39] eighty percent of whom are women of childbearing age,[40] has been hampered by the misconception that body weight is not a physiologically regulated variable, but rather determined by acquired food habits and conscious and unconscious desires. Obesity represents a management challenge for physicians and a psychological and biological challenge for patients.

Lack of respect for the morbidly obese is an issue of concern. A survey of severely obese individuals found that nearly eighty percent reported being treated disrespectfully by the medical profession.[41, 42] There are widespread negative attitudes that the morbidly obese adult is weak-willed, ugly, awkward, self-indulgent and immoral. This intense prejudice cuts across age, sex, religion, race, and socioeconomic status. Numerous studies have documented the stigmatization of obese persons in most areas of social functioning. This can promote psychological distress and increase the risk of developing a psychological disorder. The morbidly obese patient is at risk for affective, anxiety and substance abuse disorders. The obese often consider their condition as a greater handicap than deafness, dyslexia or blindness.[43, 44]

Non-Operative Patient

Published scientific reports document that non-operative methods alone have not been effective in achieving a medically significant long-term weight loss in severely obese adults. It has been shown that the majority of patients regain all the weight lost over the next five years.[45, 46] The average medical weight reduction trial is a 10-12 week study with average weight loss of 2.5 kg [47] The use of anorectic medications has recently been advocated as a long-term therapeutic modality in management of what is clearly a chronic disease. In a nearly four year study, utilizing a two drug regimen of Phentermine and Fenfluramine, behavior modification, diet and exercise, the initial optimistic results have not been sustained, with a one third drop out rate and a final average weight loss of only three pounds in those who were followed for the four years of the study.[48] This drug combination appears to have an unacceptably high association with cardiac valvular disease and has been withdrawn from therapeutic use because of these potentially life threatening sequelae. Dietary weight loss attempts often cause depression, anxiety, irritability, weakness and preoccupation with food [49]. The treatment goal for morbid obesity should be an improvement in health achieved by a durable weight loss that reduces life threatening risk factors and improves performance of activities of daily living. Temporary fluctuations of body weight from calorie-restricted diets should be avoided.

Surgical Treatment Goals

Surgical treatment is medically necessary because it is the only proven method of achieving long-term weight control for the morbidly obese. Surgical treatment is not a cosmetic procedure. Surgical treatment of severe obesity does not involve the removal of adipose tissue (fat) by suction or excision. Bariatric surgery involves reducing the size of the gastric reservoir, with or without a degree of associated malabsorption. Eating behavior improves dramatically.[50] This reduces caloric intake and ensures that the patient practices behavior modification by eating small amounts slowly, and chews each mouthful well. Success of surgical treatment must begin with realistic goals and progress through the best possible use of well designed and tested operations. These have been worked out over the last thirty years, and are now standardized, clearly defined procedures, with well recognized and documented outcome results.

Prevention of secondary complications of morbid obesity is an important goal of management. Therefore, the option of surgical treatment is a rational one supported by the time honored principle that diseases which harm call for therapeutic intervention that, while vigorous, is less harmful than the disease being treated. The biological basis for morbid obesity is unknown, though recent work has demonstrated a genetic component of between 25 and 50%.[51] Several studies confirm the influence of genetically determined proteins produced by the fat cell[52, 53] to be among the many mechanisms which have a place in the control of satiety.[54] These studies confirm that morbid obesity is a disease, not a disorder of willpower, as sometimes implied. The physiologic, biochemical and genetic evidence is overwhelming that morbid obesity is a complex disorder. Contributing causes include inheritance and environmental, cultural, socioeconomic and psychological factors.

Patient Selection

The option of surgical treatment should be offered to patients who are morbidly obese, well informed, motivated, and acceptable operative risks. The patient should be able to participate in treatment and long-term follow-up. Some patients with manifest psychopathology that jeopardizes an informed consent and cooperation with long term follow up may need to be excluded. A decision to elect surgical treatment requires an assessment of the risk and benefit in each case. Increased abdominal fat or "central obesity" (apple shaped as opposed to pear shaped) is an important risk factor associated with the major complications of obesity. Functional impairments associated with obesity are also important deciding factors for surgical treatment. An important conclusion of the 1991 National Institutes Consensus Development Conference Statement on the surgical treatment of obesity was that "patients judged by experienced clinicians to have a low probability of success with non-surgical measures, as demonstrated, for example, by failure in established weight control programs or reluctance by the patient to enter such a program, may be considered for surgical treatment".[1]

Patients whose BMI exceeds 40 are potential candidates for surgery if they strongly desire substantial weight loss, because obesity severely impairs the quality of their lives. They must clearly and realistically understand how their lives may change after operation.

In certain circumstances, less severely obese patients (with BMI's between 35 and 40) also may be considered for surgery. Included in this category are patients with high risk co-morbid conditions such as life threatening cardiopulmonary problems (e.g., severe sleep apnea, Pickwickian syndrome, obesity-related cardiomyopathy, or severe diabetes mellitus). Other possible indications for patients with BMI's between 35 and 40 include obesity-induced physical problems that are interfering with lifestyle (e.g., musculoskeletal or neurologic or body size problems precluding or severely interfering with employment, family function and ambulation).

End stage obesity syndrome: Some candidates for surgical treatment of severe obesity have such impaired health that they must be hospitalized pre-operatively and undergo treatment to improve their operative risk.

Risks of Surgical Treatment

Assessing the risks of surgical treatment of obesity involves operative, perioperative and long term complications. Available published series report that the immediate operative mortality rate for both vertical banded gastroplasty and Roux-en-y gastric bypass is relatively low. Morbidity in the early postoperative period, i.e., wound infections, dehiscence, leaks from staple breakdown, stomal stenosis, marginal ulcers, various pulmonary problems, and deep thrombophlebitis may be as high as ten percent or more. Splenectomy is necessary in 0.3% of patients to control operative bleeding. However, the aggregate risk of the most serious complications of gastrointestinal leak and deep venous thrombosis is less than one per cent. In the late postoperative period, other problems may arise and may require reoperation. The mortality and morbidity rates of reoperation are higher than those of primary operations.

Childbearing

Women of childbearing age who elect to have weight reduction operations must use secure birth control methods during the period of rapid weight loss. They should be informed that maternal malnutrition may impair normal fetal development. This is particularly important to those who may have previously failed to conceive, since fertility may increase following weight loss. Indeed, failure to conceive in the face of morbid obesity is yet another positive indication for weight loss surgery. Women who become pregnant after these surgical procedures need specific attention from the surgical care team. However, there are several reports in the literature of pregnancy outcomes following gastric bypass without evidence of fetal impairment.[72, 73]

Nutritional Consequences of Gastric Restrictive Surgery for Obesity

Gastric restrictive surgery in the motivated, cooperative patient, who has been educated in the nutritional requirements to maintain adequate protein/calorie/mineral/vitamin intake, routinely results in a smooth post-operative course, with some protein deficit in the first 3 postoperative months, which is completely restored 18 months after surgery, by which time the patient will have re-established a lean body mass appropriate to the total body weight.

Pure gastric restrictive procedures such as vertical banded gastroplasty (VBG), silastic ring gastroplasty (SRG) and adjustable silastic gastric banding (AGB) all achieve weight loss by restricting volume of intake. Intake becomes a function of the patient's motivation to chew well and eat slowly. Failure to do so may result in repeated vomiting and isolated cases of protein and vitamin deficiency have been reported in these circumstances. Careful patient follow up is therefore mandatory, with particular emphasis on the first three postoperative months. Adjustable silastic gastric banding (AGB) approved in 2001 for use in the USA following FDA trials can be considered functionally similar to vertical banded gastroplasty.

Gastric bypass with Roux-y (RGB) results in ingested food bypassing the gastric fundus, body, antrum, duodenum and a variable length of proximal jejunum. In consequence, these patients are at risk to develop iron deficiency secondary to lack of contact of food iron with gastric acid and consequent reduced conversion of iron from the relatively insoluble ferrous to the more absorbable ferric form. In addition, vitamin B12 deficiency may result in consequence of food no longer coming in contact with gastric intrinsic factor. Vitamin D and calcium absorption may also be reduced since the duodenum and proximal jejunum, which are the preferential sites of absorption, are bypassed by this procedure. Life long supplements of multivitamins, vitamin B12 iron and calcium are mandatory following this procedure. A corollary of this is the need for long -erm follow-up for physical, nutritional and metabolic evaluation and counseling.

Biliopancreatic diversion (BPD) and Biliopancreatic Diversion with Duodenal Switch (BPDS) are procedures designed to incorporate a maximum of malabsorption along with a degree of gastric restriction while at the same time reducing the incidence of complications which were previously associated with the outdated jejuno-ileal bypass procedure. These procedures induce extensive weight loss, but still have a significant incidence of metabolic consequences which make careful long-term nutritional supplementation, biochemical monitoring and clinical follow-up absolutely essential.

FDA Approves Implanted Stomach Band to Treat Severe Obesity

FDA today approved a new surgically implanted device to help severely obese people lose weight. The product, the Lap-Band Adjustable Gastric Banding System, made by BioEnterics Corporation of Carpinteria, Calif., is an inflatable band that is placed around the upper stomach to create a small gastric pouch. This limits food consumption and creates an earlier feeling of fullness.

The band is implanted by laparoscopic "keyhole" surgery and is then adjusted over time either tightened or loosened to meet individual patient needs. Once the band is in place, it is inflated with saline. Subsequent adjustments are made through a portal under the skin.

The Lap-Band is intended for severely obese people those at least 100 lbs. overweight or who are at least twice their ideal body weight who have failed to reduce their weight by other methods such as a supervised diet, exercise and behavior modification programs. Severely obese people usually have serious health problems such as hypertension, gall bladder disease, and diabetes, resulting from their excess weight. For them, being overweight is a serious health issue, not just a cosmetic problem.

The Lap-Band is intended to remain in place permanently, but it can be surgically removed, if necessary. People who get the Lap-Band will need to diet and exercise in order to maintain their weight loss. Previously the only surgical treatments available for severe obesity were more invasive procedures such as stomach stapling and gastric bypass.

FDA approved the Lap-Band based on a review of clinical studies of safety and effectiveness conducted by the manufacturer.

BioEnterics studied 299 patients age 18 to 55 who were implanted with the Lap-Band at eight medical centers in the United States. Patients were required to follow a severely restricted diet after the device was implanted and to exercise at least 30 minutes a day.

During the course of the three-year study, most patients steadily lost weight, and by 36 months had lost an average of 36% of their excess weight. Sixty two percent of patients lost at least 25% of their excess weight; 52% lost at least 33%; 22% lost at least 50%; and 10% lost at least 75%. Two percent of patients gained some weight, and 5% neither lost nor gained.

Eighty nine percent of patients experienced at least one side effect. These included nausea and vomiting (51%), heartburn (34%), abdominal pain (27%), and band slippage or pouch enlargement (24%). Nine percent of patients needed to have another operation to correct a problem with the device. Twenty five percent had their entire Lap-Band Systems removed, mostly because of adverse side effects. In about one-third of those patients, insufficient weight loss was also reported as a contributing factor to the decision to have the Lap-Band removed.

Source: FDA Talk Paper
U.S. Food and Drug Administration
June 5, 2001

What Specific Recommendations Can Be Made For the Treatment of Severe Obesity?

Patients seeking therapy for the first time should be evaluated by a knowledgeable physician and provided with sufficient information on which to make a reasonable choice for therapy.

In spite of the failure of medical therapy by drugs, diet, behavior modification and exercise to achieve documented long-term weight loss in the morbidly obese, it is accepted practice to require that the potential candidate for surgical treatment have made good faith attempts to achieve weight loss by dietary means. Although the segment of the morbidly obese population able to lose significant weight by non-surgical means is miniscule, candidates for surgery must be given the opportunity to try, a proposition which justifies insistence on at least one attempt at dietary weight loss prior to acceptance into a bariatric surgery program.

Decisions on what therapy to recommend to patients with morbid obesity should depend on their wishes for outcomes, on the need for therapy, and on the physician's explanation of options for therapy and the current information on probable safety, efficacy, advantages and risks. The need for close nutritional monitoring during rapid weight loss and the need for lifelong medical surveillance after surgical therapy should be made clear to the prospective patient and their relatives.

The operation should be carried out by a surgeon substantially experienced with the appropriate procedures and working in a clinical setting with adequate support for all aspects of perioperative assessment and management. These include hospital facilities geared to care for the morbidly obese patient, medical specialty availability, psychological support, dietary and nutritional counseling, and patient support groups.

Preoperative Psychological Testing

There are two possible reasons for preoperative psychological testing prior to bariatric surgery. One is to weed out those with significant psychopathology in whom surgery would be contra-indicated, the other to pre-select those in whom the surgery is likely to be a success. Unfortunately psychologic evaluation has proven of limited value in both these situations.

Studies of severely overweight persons conducted before their undergoing anti-obesity surgery have shown a) that there is no single personality type that characterizes the severely obese; b) that this population does not report greater levels of psychopathology than do average-weight control subjects; and c) that the complications specific to severe obesity include body image disparagement and binge eating. Studies conducted after surgical treatment and weight loss have shown 1) that self esteem and positive emotions increase; 2) that body image disparagement decreases; 3) that marital satisfaction increases, but only if a measure of satisfaction existed before surgery; and 4) that eating behavior is improved dramatically. The results of surgical treatment are superior to those of dietary treatment alone. Practitioners should be aware that severely obese persons are subjected to prejudice and discrimination and should be treated with an extra measure of compassion and concern to help alleviate their feelings of rejection and shame. [74]

In addition, numerous studies in the literature attempting to identify patient characteristics related to outcome have been reported, but no reliable psychological predictors of success have been identified. (See Vallis and Ross 1993[75] for a comprehensive review of this area). Only two general recommendations emerge from this study. (1) The more distressed patients are by their obesity , (reflected by exogenous depression) the more likely they are to lose weight; and (2) Serious psychiatric disturbance, to the extent that psychiatric treatment or admission is required, appears to be a negative predictor of outcome. While other psychological variables have been shown to be associated with post-surgical weight loss, none have been replicated in independent studies. [75]

Accordingly, routine preoperative psychological evaluation should be required in patients who have a history of severe psychiatric disturbance or who are currently under the care of a psychologist/psychiatrist. Such patients, and those under the age of 18 years, should be required either to have psychiatric clearance in writing from their counselor or to undergo psychiatric evaluation before surgery. Other patients who wish to have the benefit of psychologic counseling before surgery should be encouraged to do so. Postoperative support can be extremely important, especially for those with preoperative psychological difficulties, and should be actively pursued by patient, surgeon and psychologist/psychiatrist.

For more information contact:
American Society for Bariatric Surgery
7328 West University Avenue, Suite F
Gainesville, FL 32607 (U.S.A.)
(352) 331-4900 (Phone)
(352) 331-4975 (Fax)
E-mail: info@asbs.org

References

  1. Gastrointestinal surgery for severe obesity. Proceedings of a National Institutes of Health Consensus Development Conference. March 25-27, 1991, Bethesda, MD. Am J Clin Nutr, 1992. 55(2 Suppl): p. 487S-619S.
  2. Pories, W.J., et al., Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Ann Surg, 1995. 222(3): p. 339-50; discussion 350-2.
  3. Rand, C.S. and A.M. Macgregor, Adolescents having obesity surgery: a 6-year follow-up. South Med J, 1994. 87(12): p. 1208-13.
  4. Breaux, C.W., Obesity surgery in children. Obes Surg, 1995. 5(3): p. 279-284.
  5. Strauss, R.S., L.J. Bradley, and R.E. Brolin, Gastric bypass surgery in adolescents with morbid obesity. J Pediatr, 2001. 138(4): p. 499-504.
  6. Macgregor, A.M. and C.S. Rand, Gastric surgery in morbid obesity. Outcome in patients aged 55 years and older. Arch Surg, 1993. 128(10): p. 1153-7.
  7. Murr, M.M., M.R. Siadati, and M.G. Sarr, Results of bariatric surgery for morbid obesity in patients older than 50 years. Obes Surg, 1995. 5(4): p. 399-402.
  8. Macgregor, A.M.C., Effect of surgically induced weight loss on asthma in the morbidly obese. Obes Surg, 1993. 3: p. 15-21.
  9. Dixon, J.B., L. Chapman, and P.O. O'Brien, Marked improvement in asthma after Lap-Band surgery for morbid obesity. Obes Surg, 1999. 9: p. 385-389.
  10. Wittgrove, A.C. and G.W. Clark, Laparoscopic gastric bypass, roux-en-Y- 500 patients: technique and results, with 3-60 month follow-up. Obes Surg, 2000. 10(3): p. 233-9.
  11. Higa, K.D., K.B. Boone, and T. Ho, Complications of the laparoscopic Roux-en-Y gastric bypass: 1,040 patientswhat have we learned? Obes Surg, 2000. 10(6): p. 509-13.
  12. Lew, E.A. and L. Garfinkel, Variations in mortality by weight among 750,000 men and women. J Chronic Dis, 1979. 32: p. 563-576.
  13. Build and blood pressure study. 1959, Chicago Society of Actuaries.
  14. Blair, D.F. and L.W. Haines, Mortality experience according to build at higher durations. Society of Actuaries, 1966. 18: p. 35-46.
  15. Stevens, J., et al., The effect of age on the association between body-mass index and mortality [see comments]. N Engl J Med, 1998. 338(1): p. 1-7.
  16. Hubert, H.B., et al., Obesity as an independent risk factor in gross obesity. Circulation, 1983. 67: p. 968-977.
  17. Health Implications of Obesity. NIH Consensus Development Conference Statement. Ann Int Med, 1985. 103: p. 1073-77.
  18. Drenick, E.J., et al., Excessive mortality and causes of death in morbidly obese men. JAMA, 1980. 243: p. 443-5.
  19. Sjostrom, L., et al., Swedish obese subjects (SOS). Recruitment for an intervention study and a selected description of the obese state. Int J Obes Relat Metab Disord, 1992. 16(6): p. 465-79.
  20. Sjostrom, C.D., et al., Reduction in incidence of diabetes, hypertension and lipid disturbances after intentional weight loss induced by bariatric surgery: the SOS Intervention Study. Obes Res, 1999. 7(5): p. 477-84.
  21. Willett, W.C., et al., Weight, weight change and coronary heart disease in women. Risk within the "normal" weight range. JAMA, 1995. 273: p. 461-5.
  22. Benotti, P.N., et al., Gastric restrictive operations for morbid obesity. Am J Surg, 1989. 157(1): p. 150-5.
  23. Kanders, B.S., et al., Weight loss outcome and health benefits associated with the Optifast program in the treatment of obesity. Int J Obes, 1989. 13: p. 131-134.
  24. Kannel, W.B. and T. Gordon, Obesity and cardiovascular disease. Obesity, ed. W.Burland, P.D. Samuel, and J. Yudkin. 1974, London: Churchhill Davidson.
  25. Rimm, A.A., et al., Disease and obesity in 73, 532 women. Obes Bariat Med, 1972. 1: p. 77-84.
  26. Keen, H., The incomplete story of obesity and diabetes, in Proceedings of the First International Congress on Obesity, A. Hayward, Editor. 1975, Newman Publishing Co Ltd: London. p. 116-127.
  27. Report of the United States National Commission on Diabetes to the Congress of the United States, in Publication Number 76-1021. 1975, U.S. Department of Heath, Education and Welfare: Bethesda, Maryland.
  28. Beirman, E.L., J.D. Bagdade, and D.J. Porte, Obesity and diabetes. The odd couple. Am J Clin Nutr, 1968. 21: p. 1434-7.
  29. Colditz, G.A., et al., Weight as a risk factor for clinical diabetes in women. Am J Epidemiol, 1990. 132: p. 501-13.
  30. Van Itallie, T.B., Health implications of overweight and obesity in the United States. Ann Intern Med, 1985. 103(6, Pt 2): p. 983-988.
  31. Hartz, A.J., et al., Relationship of obesity to diabetes: influences of obesity level and body fat distribution. Prev Med, 1983. 12: p. 351-7.
  32. Bennett, O.H., et al., Epidemiologic studies of diabetes in the Pimaindians. Rec Prog Horm Res, 1976. 32: p. 333-6.
  33. Kalkoff, R.K., et al., Relationship of body fat distribution to blood pressure, carbohydrate tolerance, and plasma lipids in healthy obese women. J Lab Clin Med, 1974. 102: p. 621-7.
  34. Westlund, K. and R. Nickolaysen, 10 year mortality and morbidity related to serum cholesterol. A follow-up of 3751 men aged 40-49. Scand J Clin Lab Invest, 1992. 30(Suppl 127): p. 1-24.
  35. Mason, E.E., K. Renquist, and D. Jiang, Predictors of Two Obesity Complications: diabetes and hypertension. Obes Surg, 1992. 2(3): p. 231-237.
  36. Garfinkel, L., Overweight and cancer. Ann Intern Med, 1985. 103: p. 1034-6.
  37. Kuczmarski, R.J., et al., Varying body mass index cutoff points to describe overweight prevalence among US adults: NHANES III (1988 to 1994). Obesity Research, 1997. 5(6): p. 542548.
  38. Calle, E.E., M.J. Thun, and J.M.e.a. Petrelli, Body mass index and mortality in a prospective cohort of U.S. adults. N Eng J Med, 1999. 341: p. 1097-1105.
  39. Flegal, K.M., et al., Overweight and obesity in the United States; prevalence and trends. Int J Obes, 1998. 22: p. 39-47.
  40. Kuczmarski, R.J., Prevalence of overweight and weight gain in the United States. Am J Clin Nutr, 1992. 55: p. 495S-502S.
  41. Maddox, G.L. and J.V. Leiderman, Overweight as a social disability with medical implications. J Med Ed, 1968. 44: p. 214-20.
  42. Kurland, H.D., Obesity: an unfashionable problem. Psychiatric Opinion, 1970. 7: p. 20-4.
  43. Rand, C.S. and A.M. Macgregor, Morbidly obese patients' perceptions of social discrimination before and after surgery for obesity. South Med J, 1990. 83(12): p. 1390-5.
  44. Rand, C.S. and A.M. Macgregor, Successful weight loss following obesity surgery and the perceived liability of morbid obesity. Int J Obes, 1991. 15(9): p. 577-9.
  45. Perri, M.G. and P.R. Fuller, Success and failure in the treatment of obesity: where do we go from here? Med Exerc Nutr Health, 1995. 4: p. 255-272.
  46. National Task Force on the Prevention and Treatment of Obesity: Very low calorie diets. JAMA, 1993. 270: p. 967-974.
  47. Safer, D.J., Diet, behaviour modification and exercise. A review of obesity treatments from a long term perspective. South Med J, 1991. 84(12): p. 1470-4.
  48. Weintraub, M., et al., Long-term weight control study. IV (weeks 156-190). The second double-blind phase. Clin Pharmacol Ther, 1992. 51: p. 608-614.
  49. Powers, P.S., Conservative treatments for morbid obesity, in Surgery for the morbidly obese patient, M. Deitel, Editor. 1989, Lea & Febiger: Philadelphia. p. 27-37.
  50. Rand, C.S., A.M. Macgregor, and G.C. Hankins, Eating behavior after gastric bypass surgery for obesity. South Med J, 1987. 80(8): p. 961-4.
  51. Bouchard, C., The genetics of obesity. 1994, Boca Raton: CRC Press. 245.
  52. Francke, S., et al., Genetic studies of the leptin receptor gene in morbidly obese French Caucasian families. Hum Genet, 1997. 100(5-6): p. 491-6.
  53. Freidman, J. and J. Halaas, Leptin and the Regulation of body weight in mammals. Nature, 1998. 395: p. 763-770.
  54. York, D.A., Peripheral and central mechanisms regulating food intake and macronutrient selection. Obes Surg, 1999. 9(5): p. 471-9.
  55. IBSR, IBSR 2000-2001 Winter Pooled Report. 2001, International Bariatric Surgery Registry: Iowa City. p. 19.
  56. Sugerman, H.J., et al., Gastric bypass for treating severe obesity. Am J Clin Nutr, 1992. 55(2 Suppl): p. 560S-566S.
  57. Linner, J.H. and R.L. Drew, Why the Operation We Prefer is the Roux-Y Gastric Bypass. Obes Surg, 1991. 1(3): p. 305-306.
  58. Mason, E.E., Gastric surgery for morbid obesity. Surg Clin North Am, 1992. 72(2): p. 501-13.
  59. Yale, C.E., Gastric surgery for morbid obesity. Complications and long-term weight control. Arch Surg, 1989. 124(8): p. 941-6.
  60. MacLean, L.D., B.M. Rhode, and R.A. Forse, Late results of vertical banded gastroplasty for morbid and super obesity [see comments]. Surgery, 1990. 107(1): p. 20-7.
  61. Hall, J.C., et al., Gastric surgery for morbid obesity. The Adelaide Study. Ann Surg, 1990. 211(4): p. 419-27.
  62. Charuzi, I., et al., Bariatric surgery in morbidly obese sleep-apnea patients: short- and long-term follow-up. Am J Clin Nutr, 1992. 55(2 Suppl): p. 594S-596S.
  63. Sugerman, H.J., et al., Long-term effects of gastric surgery for treating respiratory insufficiency of obesity. Am J Clin Nutr, 1992. 55(2 Suppl): p. 597S-601S.
  64. Benotti, P.N., et al., Heart disease and hypertension in severe obesity: the benefits of weight reduction. Am J Clin Nutr, 1992. 55(2 Suppl): p. 586S-590S.
  65. Brolin, R.E., Results of obesity surgery. Gastroenterol Clin North Am, 1987. 16(2): p. 317-38.
  66. Gleysteen, J.J., Results of surgery: long-term effects on hyperlipidemia. Am J Clin Nutr, 1992. 55(2 Suppl): p. 591S-593S.
  67. MacDonald, K.G., Jr., et al., The Gastric Bypass Operation Reduces the Progression and Mortality of Non-Insulin-Dependent Diabetes Mellitus. J Gastrointest Surg, 1997. 1(3): p. 213-220.
  68. Kral, J.G., L.V. Sjostrom, and M.B. Sullivan, Assessment of quality of life before and after surgery for severe obesity. Am J Clin Nutr, 1992. 55(2 Suppl): p. 611S-614S.
  69. Rand, C.S., A. Macgregor, and G. Hankins, Gastric bypass surgery for obesity: weight loss, psychosocial outcome, and morbidity one and three years later. South Med J, 1986. 79(12): p. 1511-4.
  70. Macgregor, A.M. and C.S. Rand, Revision of Staple Line Failure Following Roux-en-Y Gastric Bypass for Obesity: a follow-up of weight loss. Obes Surg, 1991. 1(2): p. 151-154.
  71. Linner, J.H. and R.L. Drew, Reoperative surgeryindications, efficacy, and long-term follow-up. Am J Clin Nutr, 1992. 55(2 Suppl): p. 606S-610S.
  72. Rand, C.S. and A.M. Macgregor, Medical care and pregnancy outcome after gastric bypass surgery for obesity [letter]. South Med J, 1989. 82(10): p. 1319-20.
  73. Wittgrove, A.C., et al., Pregnancy following gastric bypass for morbid obesity. Obes Surg, 1998. 8(4): p. 461-4; discussion 465-6.
  74. Stunkard, A.J., An overview of current treatments for obesity, in Treatment of the seriously obese patient, T.A. Wadden and T.B. VanItallie, Editors. 1992, New York. p. 34.
  75. Vallis, J.M. and M.A. Ross, The role of psychological factors in bariatric surgery for morbid obesity: Identification of psychological predictors of success. Obes Surg, 1993. 4: p. 346-359.
  76. National Institutes of Health Consensus development statement. Health implications of obesity. 1985.

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