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Gastric Bypass -- for Doctors Only

The information contained here is for physicians who may have a patient with a Gastric Bypass, to aid in managing their care. The terms we use here are medical and technical, and we assume an underlying understanding of anatomy, physiology and pharmacology. We’re sure that with this title, many others will read it, but you’re on your own with the medical words.

Medical Attitudes Toward Obesity Surgery

The value of modern bariatric surgical techniques, in the treatment of serious and life-threatening co-morbid conditions, remains unknown or unrecognized, for many physicians. Many cling to the outmoded concept that "all it needs is a healthy diet and exercise" to solve the lifelong problem of intractable obesity. Numerous studies have refuted this simplistic concept, demonstrating the contribution that genetics and pathophysiology play in this disease process. At the same time, there is not a single scientific study which can show significant and sustained weight loss or health enhancing efficacy, from treatment of clinically severe obesity by dietary means.

Morbid Obesity as a Disease Process

Typically, students of medicine are taught that obesity results from an excess of caloric intake over daily metabolic needs. Conventional wisdom attributes this excess to behavior which is voluntary, and usually associated with some degree of moral deficiency, from want of self-control to unrestrained gluttony. Obese patients are often regarded, even by their physicians, as "lazy, ugly, self-indulging, and immoral", who suffer from a "self-inflicted" problem. This is not true.

The Concept of Disease

Our concept of disease, and its operational definition, is often challenged by expansion of our knowledge. Many physicians, if asked to define the word ‘disease’, would find the meaning of the word to be ineffably complex, while asserting that "I know it when I see it". In fact, our paradigm must continually adapt to increasing knowledge and understanding.

Disease implies some form of physical malfunction or pathophysiology, a causative mechanism such as infection, neoplasm or genetic origin. It is associated with some form of damage to the body, and is usually accompanied by suffering, or by death.

Morbid Obesity easily fits all of these criteria: it has a strong genetic predisposition, it produces malfunction in many organ systems and structures, it leads to indescribable suffering, and results in substantial mortality.

The Genetic Connection

Could variations in the human body habitus, and the quantity and physiology of adipose tissue, be attributable to genetic variability within the human species? This suggestion is often met with skepticism, when suggested as a factor in human obesity. Yet, few informed observers would dispute that slight genetic variations can lead to major changes in body habitus, within other species. The Saint Bernard and the Greyhound, variants of the canine species, demonstrate striking differences in appearance. No one would assert that a Saint Bernard could be made to look like a Greyhound, by placing it on a strenuous diet!

Genetically obese laboratory animals are well-known, and the presence of specific genetic loci, associated with abnormal effector proteins, has been clearly demonstrated. Evidence for a strong genetic connection in humans is abundant, even if less evident to the casual observer. The physician scientist should be aware of numerous carefully structured studies which demonstrate genetic factors to have a strong influence on the occurrence of obesity in humans:

Teleologically, a tendency toward obesity can be understood, when the frequency of starvation in prehistoric populations is considered. Availability of a reserve store of energy considerably enhances survival during episodic starvation, and accumulation of adipose tissue is by far the most efficient means of storing large amounts of energy (several times as efficient as increased muscle mass). Simultaneously, it provides insulation and reduces caloric expenditure for heat production.

While most animal species instinctively regulate energy intake to match consumption, human survival has become detached from instinct, and more dependent upon culture, and intelligence. Human cultures often practice ritualistic feasting during times of plenty, as well as athletic contests which serve to develop muscle mass. Humans who undergo starvation develop a compensatory response of overconsumption when food becomes abundant. This detachment of caloric intake from caloric requirement may be a genetically determined, peculiarly human characteristic, and may explain the behavior of the severely obese, who acknowledge that they can never seem to eat enough.

The belief that Morbidly Obese patients can control their weight by restricted intake and altered behavior is illusory, and leads to a failure of medical therapy, not a failure of will power. The utter failure of dietary and behavioral therapy to produce a beneficial therapeutic effect in the Morbidly Obese demands that medical scientists seek an alternative solution.

 Health Effects of Morbid Obesity

The adverse health effects of Morbid Obesity are protean, and the consequences are concretely expressed in terms of a markedly increased relative risk of mortality, at any age. The following listing catalogs the numerous ways in which obesity adversely affects health:

Atherosclerotic Cardiovascular Disease

Diabetes Mellitus, Type II

Respiratory Disease

Gastrointestinal Disorders

Renal Disease

Metabolic

Orthopedic

Dermatologic

Gonadal Dysfunction

Cancer

Trauma

Social

Mortality

Obesity is uncontrovertibly associated with increased mortality. On any day, the morbidly obese patient suffers an estimated relative risk of mortality which is 2 to 8 times that of the normal-weighted person.

Obesity is the most serious health problem facing Americans today. Yet dietary therapy, which conventional medical wisdom regards as the staple, and which is the most widely recommended treatment, has never been proven, by ordinary scientific criteria, to have long-term efficacy.

When Clinically Severe Obesity threatens life, the only effective and long-term therapy is surgical treatment, and the most effective surgical therapy is Gastric Bypass, Roux en-Y.

 

Results of Obesity Surgery

Weight Loss

We have maintained follow-up with over 90% of the first 300 patients to undergo Laparoscopic Gastric Bypass, Roux en-Y.  The chart below shows average weight loss, as a percentage of Excess Body Weight, for 300 patients between 3 and 48 months following surgery.

Percentage of Excess Body Weight Loss over 3 - 48 Months -- 300 Laparoscopic Gastric Bypasses:

The above graphic shows average weight loss.  It is reasonable, to ask what the results are, in cases where patients do not apply themselves persistently, to the recommended regimen.  Long term weight loss results are shown below, for those patients more than 24 months post-operative:

Percentage excess body weight lost vs. time post-operative - 300 cases:

     < 50% 50 - 60 % 61 - 75%     >75%   Total
 24 Months     3 (5%)    5 (8%)  10 (16%)   44 (71%)    62
 30 Months     6 (13%)    5 (11%)    6 (13%)       29 (63%)    46
 36 Months     4 (14%)    2 (7%)          4 (14%)       19 (66%)    29
 42 Months     1 (6%)    2 (12%)        4 (24%)   10 (59%)    17
 48 Months     0    1 (13%)       2 (25%)        5 (63%)        8

This table shows that weight loss results will vary, depending upon the effectiveness with which the patient makes use of the new physiology created by the Gastric Bypass.   It is here that success depends heavily upon the commitment of both physician and patient to follow-up, and to skillful use of the tool provided by the Gastric Bypass. Nevertheless, overall succcess with Gastric Bypass far exceeds what might be expected from dietary therapy, and the associated health benefits are striking.

Surgical treatment relieves over 96% of co-morbid conditions, within one year – frequently within days:

Pre-Operative vs Post-Operative Co-Morbidities - 300 Cases Laparoscopic Gastric By

  Condition                                                                          Pre-Operative       Post-Operative

  GastroEsophageal Reflux Disease        180        3
  Hypercholesterolemia        176        6
  Hypertriglyceridemia        106        1
  Diabetes Mellitus (Type II)          59        1
  Glucose Intolerance          30        0
  Stress Incontinence        134        4
  Obstructive Sleep Apnea        150        2
  Hypertension          79                       6
  Arthritis (Symptomatic)        249      20
                                                  TOTAL      1163      43

Treatment of Severe Obesity by Surgery was associated with a 96% reduction in Co-Morbidities.

The results of weight-loss surgery, in the treatment of Diabetes Mellitus are particularly striking, and expecially gratifying.  The following table shows effects of surgery in 59 Type II Diabetics undergoing Laparoscopic Gastric Bypass:

                    Parameter                                               Pre-Operative                 Post-Operative

Abnormal Fasting & 2hPP Blood Sugar                   59                    0
On Medicatiion (Oral or Insulin)                   25                    0
Elevated HgbA1C                   41                    1

Indications and Informed Consent for Treatment:

When a patient meets weight criteria for severe obesity, either Body Mass Index (BMI) greater than 40 kgm/m2, or greater than 35 kgm/m2 with a severe co-morbidity, that patient deserves to be informed of the option of bariatric surgery. Gastric Bypass can be accomplished with a risk and morbidity which approximates that of cholecystectomy, and has the potential to revolutionize a patient’s life. Laparoscopic Gastric Bypass requires an average length of stay of 2.9 days, and patients typically return to full activity, even strenuous activity, within 2 weeks.

Body Mass Index = Weight (kgm)/ (Height (meters))2

Anatomy and Physiology of the Operation

Gastric Bypass, Roux en-Y, is performed by different surgeons with numerous anatomic and technical variations, including pouches from 15  to 60 cc, or more, in volume.   Pouch orientation and the small bowel routing chosen also varies.  Results of the procedure, especially long-term weight loss and maintenance, are heavily dependent on both surgical methodology, and comprehensive long-term follow-up and support.

The Gastric Bypass, as we perform it, is a high-gastric transection, forming a lesser curvature proximal pouch of approximately 15 cc capacity. Gastrointestinal continuity is re-established by a Roux en-Y entero-enterostomy. The Roux limb of proximal jejunum is positioned retrocolic and retrogastric, and is anastamosed side-to-side to the proximal gastric pouch, forming a stoma which is 12 mm in diameter. No synthetic band or mesh is employed.

The distal stomach, comprising approximately 90% of the total stomach, is bypassed and defunctionalized, although it continues to secrete mucous and acid, as well as gastrin in response to physiological stimuli, which are markedly reduced. Acid-peptic disease is possible, although it is very unusual, and the distal stomach is very rarely the site of secondary disease. Biliary and pancreatic anatomy and secretion is unchanged by the operation, and bilio-pancreatic secretions meet the foodstream just a few centimeters downstream from their normal site, after which bowel transit is normal, and absorption is unimpaired distally. The physiologic effects, and the side-effects, are similar to those of partial gastrectomy with Billroth II anastamosis.

Gastric Bypass functions to limit intake by restriction of capacity, and by fostering a prominent sense of satiety, which appears to result from early entry of foods, particularly proteins, into the proximal jejunum. Unlike the malabsorptive procedures, nutrient absorption is minimally affected, and nutritional derangement is very unlikely.

Post-Operative Regimen

All of our patients undergo education in nutrition and physiology, and are provided with extensive written instructions, in the form of an "Owners Manual" for their surgery.  Our basic instructions are quite simple:

Weight loss is often profound for 1 - 2 months, and then typically averages 2 - 3 lb per week over the following 8 - 18 months, depending upon the amount of weight available to be lost. 

Nutritional Considerations Following Gastric Bypass

The Gastric Bypass is primarily a restrictive operation, augmented by physiological effects on the sense of satiety. It does not seriously affect absorption of ingested nutrients. The bypassed gut includes the distal 90% of stomach, and the duodenum. The remaining gut, comprised of the jejunum and ileum, as well as the colon, accomplish most of the absorptive function of the intact gastrointestinal tract.

Many physicians, when informed of the small amounts of food ingested after gastric bypass, are moved to recommend frequent small feedings, to increase nutrient intake, and to "avert starvation". This is decidedly the wrong approach. The rapid weight loss which follows Gastric Bypass is almost entirely salutary, while long-term weight loss approximates 2 pounds per week, implying a caloric deficit of approximately 1000 calories per day. This is a healthful rate of loss, when accompanied by adequate intake of protein and essential vitamins. Frequent feedings frustrate weight loss, and more importantly encourage the most self-defeating habitual behavior that the bypass patient can acquire: snacking and eating between meals.

The effects of the Gastric Bypass on nutrition reflect its restrictive effect, and the exclusion of the duodenum from contact with the food stream:

Vitamin Availability

Multivitamins

The markedly reduced intake volume following Gastric Bypass implies that ingestion of vitamins within food will be inadequate. Every patient is therefore ordered to supplement dietary vitamin intake with a high-potency multivitamin supplement. Presently, we recommend one of the following:

Vitamin B-12

Impaired complexing of Vitamin B-12 in the proximal stomach may lead to reduced absorption in the intestine. We recommend that this be replaced by use of exogenous Vitamin B-12, either as a sub-lingual preparation, or by periodic injection. The cost of empiric Vitamin B-12 dosage is far less than that of regular testing of levels, let alone therapeutic repletion of deficiency. Effective supplementation:

Iron

Iron absorption occurs primarily in the duodenum, and is significantly impaired following Gastric Bypass. Iron supplementation is recommended in all menstruating females. The preferred formulation is Ferrous fumarate, with Vitamin C, in a non-enteric coated tablet.

Calcium

Calcium intake is likely to be inadequate in the bypassed patient, due to reduced food intake, and the need to avoid milk ingestion. Calcium absorption is not impaired.   Patients should ingest 1000 - 1500 mgm of Calcium daily. Suitable preparations are numerous.  

Protein

We recommend that each meal contain approximately one-half of its volume as protein-containing foods, such as eggs, chicken, turkey or fish, and we do not require any detailed calculation of required protein intake. Other potential sources include soy protein (tofu), beans, cottage cheese. For those who prefer it, protein intake should approximate 1 - 1.5 gram per kgm of ideal body weight -- adipose tissue is predominantly stored fat, and does not require protein repletion.

Protein intake should be adequate with each meal, since the body's ability to store protein or amino acids is very limited, and they are constantly required for synthesis. Even more significant to the weight-loss process is the very important inhibitory effect which protein has on the desire to continue eating. We recommend that protein be eaten first, to ensure that it is eaten, and to enhance the very important satiety response of the Gastric Bypass, which seems to be most effectively stimulated by protein contact with jejunum.

 

Adverse Effects

Early Post-Operative

Within the first three months following surgery, a small minority of patients experience difficulty complications, or with early adjustment to the physiology of the operation: 

    1. Inadequate chewing of solid foods.  Nearly all cases of nausea begin after institution of the use of solid foods.  Most obese persons habitually ingest their food rapidly, often in large bites, and chew very minimally.  A normal stomach will compensate for this behavior, but the tiny pouch of the Gastric Bypass is easily obstructed, or overwhelmed with volume, and reacts by producing nausea and vomiting.  Patients must conscientiously focus on chewing each morsel until it is essentially liquefied.
    2. Repeated vomiting may cause swelling at the gastroenterostomy stoma, which leads to further vomiting.
    3. Abnormal motility in the Roux limb may cause stasis - occasionally demonstrable by Upper GI series, but probably a rare cause.  
    4. Distention of the Distal Stomach:  When vomiting occurs, there is retrograde peristalsis, which may overfill the distal stomach with what would have been vomitus, had there been any way out.  This overfilling can itself be a stimulus to vomiting, which further fills the distal stomach with each cycle.  Treatment with Reglan or Propulcid may be rapidly effective.
    5. Ketosis.  Nausea and vomiting may lead to ketosis, which can cause nausea and vomiting. The solution may be short-term IV therapy, accompanied by anti-emetics or Propulcid, to promote gastric emptying and break the cycle.
    6. Ulceration at the gastroenterostomy margin - incidence less than 1%..
    7. Psychological factors:  An occasional patient will become so attentive to gastrointestinal function that a conditioned reflex vomiting will supercede and replace an initial stimulus of physical origin.  (A similar effect is often observed with chemotherapy, causing intense nausea simply on entering the office, or hearing the voice of the provider of care.)
    8. Steatohepatitis, manifested by increasing derangement of liver function, and pernicious vomiting.  Although very rare after gastric bypass, this condition requires aggressive management, preferably by establishment of distal gastric access and enteral nutrition with complex diet, as well as vitamin supplementation.

Treatment consists of rehydration, and suppression of vomiting with anti-emetics.  Whenever intravenous fluid therapy is instituted, multivitamins and thiamine should be simultaneously administered.  Patients should return to a clear diet, of water, broth and jello until stabilized.   Prilosec or Propulcid may be tried empirically.  Persistence of symptoms is an indication for Upper GI series, initially with water-soluble contrast.  Endoscopy should be undertaken with great caution during the first 30 days following surgery.

Patients with persistent fatigability should be assessed for anemia, hypoalbuminemia, hypometabolic state, and abnormal liver function.

Side Effects

Exclusion of the pylorus leads to increased symptoms of Dumping Syndrome, which are related to ingestion of foods with a high osmotic load, particularly sugars. Since these foods are undesirable in the weight-control patient, dumping provides negative feedback to limit undesired behavior, and is not considered to be a liability. The rare patient who exhibits dumping symptoms, or reactive hypoglycemia, with other foods should be carefully evaluated for insulinoma.  Glucose Tolerance Testing is contra-indicated following Gastric Bypass:  results will be spurious and uninterpretable, due to the altered anatomy and physiology, and dangerous hypoglycemic reactions, as well as severe dumping syndrome, can occur with ingestion of a large glucose meal.

Iron Deficiency may result from impaired iron absorption combined with iron loss from menstruation, gastrointestinal hemorrhage or chronic blood loss. Ferrous sulfate is poorly absorbed distally, and is quite irritating to the small stomach. Its use should be avoided. Non-enteric-coated ferrous fumarate with Vitamin C (Ferancee HP, Vitron C) provides superior absorption, and is well-tolerated. Enteric-coated iron preparations may not be well absorbed. Parenteral iron therapy is rarely necessary, and failure to improve iron reserves with oral preparations usually implies a continuing occult blood loss.  

Vitamin B-12 absorption may be impaired, in approximately 5 - 10% of patients. We recommend supplemental sub-lingual B-12 to all patients, and maintain very satisfactory blood levels. Deficiency also can readily be corrected by parenteral injection. Absorption of other vitamins is not impaired by the Gastric Bypass operation. 

Other Vitamin Deficiencies may result from inadequate intake in the diet, and all patients should use a high-potency multivitamin preparation daily.  Whenever intravenous fluid therapy is needed, concurrent multivitamin administration is mandatory.

Calcium intake is usually marginal or inadequate after Gastric Bypass, due to reduced intake of foods, not to abnormal absorption. Only the duodenum and a few centimeters of proximal jejunum are bypassed with the operation, and absorptionn of most subtances, including calcium, is unaffected. All patients should consume supplemental calcium, 1000 mgm daily. Hypocalcemia is not a specific complication of Gastric Bypass, and should be evaluated for other causes.

Absorption of Medications is generally normal – we have not identified any which have impaired absorption. Sustained release medications may be less reliably absorbed following Gastric Bypass, due to decrease in transit time. Standard release versions of needed medications are preferred.

Diarrhea is not a side-effect of Gastric Bypass.  Acute diarrhea is likely to be of infectious origin, while chronic diarrhea may be a manifestation of inflammatory bowel disease, which has no known relationship to gastric bypass.  Symptoms of irritable colon are unaffected or improved by Gastric Bypass, while ulcerative colitis is generally unaffected.  Pre-existing Crohn's disease may increase the risk of Gastric Bypass, and may be a relative contraindication.   Suppression of diarrhea of infectious origin with antibiotics (Cipro, Flagyl) is desirable, to avoid dehydration - bypass patients are less able to consume large quantities of liquids.

Constipation may occur, due to reduced food volumes, and reduced fiber intake.  It should preferably be treated with stool softeners, such as Surfak.   Fiber preparations are difficult for the bypass patient to use, due to the restrictive effect.

Reduced metabolic rate and reduced thermogenesis, are recognized compensatory physiological responses to starvation and calorie restriction, and are probably mediated by reduced central stimulus to release of thyroid hormone. Since the operation produces severe calorie restriction, some patients appear to manifest a persistent hypometabolic response following bypass, beginning within 1 - 2 months, and sometimes persisting even when weight has stabilized.  Symptoms may include reduced energy, lethargy, cold intolerance, and slow weight loss. Laboratory evaluation should include evaluation of free-T3.  Patients thus afflicted appear to respond to replacement-level doses of thyroid hormone, instituted in a stepwise dosage regimen.  

Pregnancy, while obviously not a direct consequence of the Gastric Bypass, can occur unexpectedly in patients who do not carefully take contraceptive precautions.  Fertility is often greatly impaired by obesity, and may be greatly enhanced as weight loss progresses.  Many patients know they cannot conceive from years of trying, and fail to protect themselves following surgery.  While early pregnancy can be managed, weight loss and nutrition inevitably suffer.  We recommend that patients carefully avoid pregnancy for 12 - 18 months following surgery.  When weight is stable, successful pregnancy and delivery are easily managed -- we have published information on this issue: 

Pregnancy following gastric bypass for morbid obesity.  Wittgrove AC, Jester L, Wittgrove P, Clark GW  Obesity Surg 1998 Aug;8(4):461-4; discussion 465-6.

Late Complications

Late complications of Gastric Bypass include the usual complications of abdominal surgery, such as intestinal obstruction and hernia. In addition, some are specific to this type of procedure:

Obstruction of the Duodenal Limb, a rare occurrence, may be due to adhesive obstruction, or stenosis at the entero-enterostomy.  It can lead to a symptom picture which mimics acute pancreatitis, with epigastric abdominal pain, and hyperamylasemia. It can be evaluated by CT scan, which will demonstrate a dilated duodenal segment, and by DISIDA scan, showing delay or non-emptying of isotope from the duodenal loop (the radiologist must be advised to observe for this finding, which requires a longer than standard test procedure). This condition can be associated with acute gastric dilatation, and shock. It should be treated as a surgical emergency, with relief of the obstruction and decompression of the stomach as the surgical goals. 

Bowel Obstruction, partial or complete, may be due to internal hernia, or to adhesive obstruction.  In partial obstruction, small bowel follow-through examination may demonstrate bowel loops posterior to the distal stomach, indicative of internal hernia in the lesser peritoneal sac.  Patients who have undergone laparoscopic bypass can be approached initially with laparoscopic exploration and reduction of the obstruction.  The narrow field of view, and distended loops of bowel, can render the anatomy very confusing, even for the experienced laparoscopist.   Conversion to open laparotomy should be considered whenever visualization is uncertain.

Stomal Ulceration occurs in 1 - 2% of patients, at the gastroenterostomy. It is usually manifested by epigastric abdominal pain, with a variable relationship to food ingestion, usually relieved by antacids.  It is often associated with nicotine usage.   It is best evaluated by Esophagogastroscopy, which should demonstrate the ulceration. Treatment with H2-blockers or Prilosec is usually effective, and surgical revision is seldom required. Stomal ulcer may be associated with Stenosis of the Gastroenterostomy. Incidence of this condition is reported to vary between 0.5% (in our series) and 33%. Symptoms include intolerance of solid foods, or even of liquids. Patients may complain of regurgitation of frothy fluid (saliva), and vomiting of ingested solids or liquids. Endoscopy demonstrates a stenotic stoma (normal diameter is 12 mm), which is best treated by balloon dilatation – to a maximum diameter of 15 mm. It is very important to avoid excessive dilatation, which may permanently impair the function and effectiveness of the Gastric Bypass.

Hyperuricemia frequently occurs during the period of rapid weight loss, associated with catabolism of large volumes of tissue. Patients with a prior history of gout, or hyperuricemia, should be maintained on Allopurinol. We believe that prophylactic administration of Allopurinol may also be beneficial, in preventing some occurrences of gouty arthritis, or uric acid urinary calculi.

Cholelithiasis has been reported in over 20% of previously normal gallbladders, within 3 years following bariatric surgery, presumably due to reduced fat intake and diminished stimulus to emptying, which accompany the altered diet.  The use of Actigall, and its accompanying risks, probably is not justified.

 

Diagnostic Examinations of the Duodenum and Biliary Tree

Gastric bypass has no effect on the biliary tree, but the altered upper gastrointestinal anatomy which follows the Gastric Bypass reduces diagnostic access to the duodenum and biliary tree. Esophagogastroduodenoscopy, and endoscopic retrograde cholangiopancreatography are rendered difficult. Examination can often be achieved by retrograde passage of a pediatric colonoscope, via the enteroenterostomy, and we have accomplished ERCP by this route as well. Percutaneous catheterization of the distal stomach may also be performed, allowing antegrade introduction of an endoscope, via a temporary opening into the distal stomach.   During endoscopy, the appropriate caliber of the gastroenterostomy stoma is 12mm.   It should not be dilated in the absence of obstructive symptoms, and should never be dilated to a diameter greater than 15mm.

Symptoms not related to Gastric Bypass

Gastroesophageal Reflux symptoms are not expected after Gastric Bypass. The operation reduces acid-bearing tissue in the proximal pouch to negligible amounts, in most patients, and also diverts bile distally, eliminating bile reflux. Symptoms of reflux should elicit an investigation to determine their cause. Diarrhea is not produced by Gastric Bypass – its effects should not be confused with those of the Intestinal Bypass, which inevitably caused diarrhea, often with electrolyte imbalance. The occurrence of diarrhea requires diagnositc investigation to seek its cause.

Strange and Mysterious Illnesses.  Many physicians, when confronted with a bizarre and unexplained symptom complex, particularly ill-defined complaints such as chronic fatigue syndrome, fibromyalgia, dizziness, postural hypotension, and neurological complaints, reflexively recommend reversal of the Gastric Bypass. This is seldom, if ever, the correct solution. Many thousands of such operations have been performed over the last two decades. The procedure is very similar in physiology to partial gastrectomy for peptic ulcer disease, which has been in use for several decades, and which has a long-established safety record, and an equally well-known complex of side-effects.

Patients who have had a bypass are as susceptible to unrelated disease processes as are any other persons. Speculative reversal subjects the patient to needless risk, inevitable regain of excess body weight, recurrence of co-morbidities, and in all probability, persistence of the precipitating symptom complex. We have over 4000 of our post-operative patients in our database, and offer lifetime follow-up. We stand ready to perform necessary surgery, but have found no indication, and have performed no reversals, in over 5 years.

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