The History of Bariatric Surgery: My 50 Years with Surgical Treatment of Diabesity

| December 1, 2015

by John G. Kral, MA, MD, PhD, FACS

Professor of Surgery, Medicine and Cell Biology, SUNY Downstate Medical Center, College of Medicine and School of Graduate Studies, Brooklyn, New York.

Dr. Kral is Professor of Surgery, Medicine and Cell Biology and former Director of Surgery at Kings County Hospital, Brooklyn, New York. He is past president of New York State Society of Surgeons and advisor to IPRO and Blue Cross Blue Shield. He is currently on the Advisory Board of an FDA Devices Panel. Dr. Kral is charter member of the New York Academy of Sciences Sackler Institute for Nutrition Science, New York, New York, where he chaired the Obesity, Diabetes and Nutrition-related Diseases Working Group until 2015.

Dr. Kral has had published more than 150 peer-reviewed papers and 80 chapters and reviews. He is associate editor of several journals and a reviewer for high-impact journals. In 2013, The Obesity Society awarded him the Stunkard Life-Time Achievement Award. His current clinical research includes studying the relationships between maternal environmental stress and pediatric obesity.

Bariatric Times. 2015;12(12):14–17.

This column is dedicated to telling the stories of leaders who have helped shape the field of bariatric surgery through their discoveries, teaching, and stewardship.

Column Editor: George L. Blackburn, MD, PhD, FACS
S. Daniel Abraham Professor of Nutrition; Associate Director, Division of Nutrition Harvard Medical School; Director, Center for the Study of Nutrition Medicine, Department of Surgery, Beth Israel Deaconess Medical Center, Boston, Massachusetts

Column Editor: Daniel B. Jones, MD, MS, FACS
Professor of Surgery, Harvard Medical School, Vice Chair, Beth Israel Deaconess Medical Center, Boston, Massachusetts

A Message from the Column Editors
Dear Readers of Bariatric Times:
Bariatric surgery has many leaders who have shaped the field by their discoveries, teaching, and stewardship. In this column, we invite leaders to tell us about their most significant accomplishment(s). Here, we will hear from leaders about their visions, hurdles, collaborations, and, ultimately, what impact their accomplishments have had on the field of bariatric surgery. We will also learn how they set goals and have turned ideas into reality, as well as what was anticipated and what was not expected throughout their journeys.
We are very excited about this project and hope it will help to inspire the next generation of leaders as they evaluate new devices and technology and consider novel procedures and treatments in an era of cost containment. We hope you enjoy these stories.

Drs. George L. Blackburn and Daniel B. Jones

My academic life started in Sweden with behavioral neuroscience, followed by pharmacology studying metabolic effects of adrenergic stress with Dr. Per Björntorp, an expert on lipid and carbohydrate metabolism and obesity. For my PhD, he had me lipectomize rats on adipose tissue metabolism and energy balance,[1] and I formulated my concepts of a “metabolic sink”’ and a “critical cell size” driving adipogenesis. Concomitantly, the surgery department started an intestinal bypass program with strong interdisciplinary research interests in liver, adipose tissue metabolism, and vascular biology. I coordinated the program with the aim of it entailing “personalized” surgery— learning from patients, their tissues, and their needs—antithetical to assembly-line transactional proceduralism, outsourcing care and caring to ancillary staff unable to emulate surgeons’ bonds with patients, which I believe is the current model of “bariatric” surgery in the United States.

We learned that jejuno-ileal bypass affected ingestive behavior, liver metabolism, foregut physiology, body composition, and insulin resistance, finding relationships between hyperinsulinemia and hepatic lipid synthesis underlying fatty liver and downregulation of protein synthesis, the basis of a “metabolic syndrome.”[2] In the 1970s, myself, Dr. Björntorp, and others demonstrated that JIB improved insulin resistance,[3,4] but more than 20 years later, the important “fathers of foregut hypotheses” somehow forgot history, a practice I feel was common in ASBS’ hagiography. My observations of reduced appetite, delayed gastric emptying, and increased acid and histamine excretion piqued my interest to investigate vagal nerve function—both efferent and afferent. Cognizant of hypothalamic regulation of energy balance, I believed complete abdominal truncal vagectomy would increase sympathetic tone, slow gastric emptying of solids, increase liquid emptying, and abrogate release of insulin and other gastrointestinal neuroendocrine hormones. It worked.[5] Patients started requesting that I cut the “hunger nerve,” although I had never mentioned hunger. More than 25 years follow up has demonstrated that truncal vagectomy potentiated weight loss and metabolic improvement after VBG,[6] a principle embodied in the recently approved vBloc® vagal blocking therapy (EnteroMedics, St. Paul, Minnesota).

Gastric bypass, which has been erroneously considered a “restrictive” operation, was proliferating while purely restrictive gastroplasties were ubiquitous, being almost as simple as entero-anastomoses, although all open procedures were cumbersome in severe obesity. In 1980, I re-emigrated to New York and began work at Columbia University and St. Luke’s Roosevelt Hospital Center, which was the first National Institutes of Health (NIH) Obesity Research Center. Here, I helped to establish a division of metabolic surgery. I operated a small series of VBG and adopted a diversionary operation modeled on ileal interposition devised by Dr. Howard Dorton of Lexington Kentucky. During this time, Dr. Nicola Scopinaro and I organized the first surgical satellite meeting of the International Congress of Obesity in Genoa, Italy. After meeting Dr. Dorton’s patients and studying their charts, we described duodeno-ileal bypass (DIB) to differentiate from the maligned JIB.[7] DIB anastomosed ultra-short jejunum (~5 cm) functionally end-side to relatively long 50cm of terminal ileum, creating an anti-reflux mechanism in the blind loop. I used it as a rescue operation for the numerous failing VBGs, a “staged approach”[8] similar to the one my grad student in Sweden and I were using with VBG to rescue vagectomy in patients dissatisfied with relatively slow weight loss. These experiences demonstrated that restrictive operations alone were less effective than truly metabolic diversionary ones, similar to recent findings with two-staged BPD-DS with failing sleeve gastrectomy owing to regeneration of resected neuroendocrine mucosa.

Moving to St. Luke’s enabled me to extend my studies on body composition and perform laboratory studies of eating behavior related to obesity operations using the Universal Eating Monitor with Harry Kissileff.[9] We discovered significant sex differences in eating behavior, with eating rate differentially influencing short-term outcomes related to type of operation.[10] These differences eroded over time, particularly as gastroplasties were failing. However, we demonstrated the association between eating rate, central adiposity, and nonalcoholic fatty liver disease (NAFLD),[11,12] work that was later continued with Drs. Picard Marceau and Simon Biron in BPD patients in Quebec City. We confirmed my earlier findings of the relationship between NAFLD and the insulin-resistant metabolic syndrome,[13] finding an association with liver fibrosis and full-blown cirrhosis, fully reversible after BPD[14] and challenging hepatology dogma.

During the first-ever Nutrition Week in 2002 (predecessor of Obesity Week), I met endocrinologist Fritz Horber whose group presented associations between appetite regulatory gene variants, disordered eating, and outcomes of adjustable banding.[15,16] Our collaboration extended to patients with mechanistically different operations followed more than 72 months with links to my earlier findings on eating.

My collaboration with Picard Marceau and his team studied offspring discordant for maternal fitness during pregnancy before versus after BPD, comparing pregnancies, deliveries, and offspring fitness.[17–19] We found significant differences in metabolic parameters and their trajectories over the life-cycle (indeed >25 years), associated with differential methylation of inflammatory and insulinotropic genes implying epigenetic mechanisms and explaining transgenerational transmission of diabesity,[20] altogether representing pre-emptive or primordial preventive capacity of effective metabolic operations.

Dr. Ed Mason, to whom we all are grateful for unfailing scholarship, generosity of teaching, and commitment to quality assurance, historically initiated “Bariatric Surgery Symposia” in Iowa City, Iowa, to which a small band of co-conspirators made pilgrimage. At the 1983 symposium, I sat at a pub eating lunch with Drs. Pat O’Leary, John Halverson, and Harvey Sugerman. There, we decided that it was time to expand the horizon of the symposia, emulating professional academic sub-specialty organizations with program committees, invited speakers, members, and peer review. We proposed this to the always gracious Ed. That afternoon the American Society for Bariatric Surgery (ASBS) was founded, with Ed, appropriately, as its first president. Subsequently, I have learned that he coincidentally had had the same idea at that time, demonstrating that “great minds think alike.”

The term “bariatric” derives from the Greek words “baros” and “iatros.” Baros and barys are the Greek words for “weight” and “heavy.” Iatros translates to “physician” and “healer.” I was very critical of the term. Using a term that means “one who cures” creates an oxymoron because there is no need to cure something that is not a disease (at that time, obesity was not classified as a disease).

The catch-all term “bariatric,” originally conceived to add prestige to an organization of practitioners earning their livelihood through weighing patients and prescribing remedies that were unproven, unscientific, and questionably ethical in ill patients, was adopted by surgeons impressed by the jargon. The word has since come to signify all activities related to weight-loss and has become a new branch of medicine. The disease of “obesity” is more than simply being obese (i.e., having a body mass index [BMI] over 35kg/m2) It encompasses other diseases, including the following: hypertension (definable elevation of blood pressure), dyslipidemia (abnormality of blood lipids), and diabetes (elevatation of levels of blood glucose sometimes exceeding renal filtration capacity). These disease phenotypes are often primary in contrast to being heavy. Although BMI is a relatively convenient metric to adjust weight for height and is correlated with body fat, it is an amalgam of two phenotypes, where height has a stronger, thus narrower, genetic component (logically). As we know so well, threshold levels of BMI determining eligibility for needed treatment are deeply flawed.

In 1985, I was the only surgeon to present at the NIH Consensus Development Conference titled “Health Implications of Obesity” During this time“obesity” was declared a disease by the Centers foe Disease Control and Prevention (CDC). The American Medical Association later recognized it as a disease in 2013. My topic at the NIH conference was “morbid obesity.” I was displeased with this term because obesity is intrinsically morbid as are all diseases. Adding the word morbid implied that obesity itself was not morbid and that obesity in other forms might not be diseases. I acquiesced, describing morbid obesity as “malignant,” impairing quality of life (first study in severe obesity) and justifying surgical treatment.[21]

I convinced the NIH that another consensus conference on surgical treatment was overdue, after the 1978 conference on JIB. They gave me remarkable freedom to design a new conference, picking topics, defining criteria for speakers, and selecting speakers ultimately approved by an advisory board and NIH functionaries. They also tasked me with chairing the conference. A crisis over perceived conflicts of interest of experts chairing consensus conferences at NIH intervened (a surgeon chairing a meeting on breast cancer had raised sharp criticism). They suggested calling our meeting a “workshop.” I determined that a workshop would not have sufficient authority to engender meaningful change as compared to the consensus format, so I ceded the chairmanship to Dr. Scott Grundy, a highly respected metabolic physician/scientist, who did a great job in 1991.22 Later, during an ASBS meeting in Boston, I enlisted Dr. Bob Brolin to co-organize an Obesity Biology Club at the annual meetings of The Society for Surgery of the Alimentary Tract (SSAT) and The American Gastroenterological Association (AGA). This filled the need to enlighten gastroenterologists by having a scientific dialogue that extended beyond the narrow practice interests of the ASBS. We had a good run of one decade, which is the time it took for the leadership of SSAT and AGA to understand the magnitude of the obesity problem and its ability to attract attendees to their meetings.

In aggregate, I believe I helped to bring people in the medical profession (internists and surgeons) to recognize the value of surgical treatment of obesity at a time when it was seriously questioned, an effort that was replicated by Dr. Francesco Rubino in bringing diabetologists and endocrinologists into the fray of understanding the value of metabolic operations for “their” patients. The recent founding of Obesity Week by Phil Schauer and others embodies this union. Ironically, when “obesity” has become accepted, it is time to retire it, just as the term morbid obesity is being phased out in civilized discourse. With recognition of a dysmetabolic state associated with impaired fitness or poor health, obesity and its treatment should be replaced by amelioration of “diabesity,” as suggested by Ethan Sims in 1973.[23,24]

As physicians who operate, we should be the standard-bearers for ethical use of our tools. The term “bariatric” has served us well in the device industry and those of us who have jumped on the band-wagon (laughing all the way to the bank) because band outcomes have piggy-backed on the superior outcomes of truly metabolic operations when they are lumped together. We should educate our patients, our colleagues, and society by honestly differentiating between restriction alone and metabolic operations. Not only are they mechanistically different, they exhibit very different trajectories of weight loss and, more importantly, metabolic outcomes over time. Editors and reviewers should insist on stratifying for type of operation.

Something needs to be done about the rush-to-publish premature results. The majority of bariatric papers fail to provide clinically relevant long-term outcomes with a semblance of steady state, contravening a fundamental scientific principle. As surgeons we can uniquely provide meaningful long-term studies, without resorting to the trickery of describing follow up with an average long-term duration to characterize a range including one-year results and a decimated long-term cohort with fewer patients operated and many lost (i.e., the follow-up defect). Most drug studies get published after only one year. I believe that we can do so much better.
Stop obsessing about weight loss. We’ve always objected when obesity surgery was called cosmetic while at the same time we invented a new biologically flawed “excess body weight” term, implying that it is all about the weight and that failure to get below BMI 30 was failure of the operation or worse, failure of the patient.

Consider the following: Eighty percent of bariatric surgical candidates are women; a significant number of patients who undergo bariatric surgery do it for cosmetic benefit rather than health benefits; and men who present for bariatric surgery are typically less metabolically fit than women and are typically older. However, study outcomes are expressed as weight, sometimes lumping together the waist circumference of both sexes. Why not stratify all outcomes by sex?
The nonincentivized Swedish social security system provided patients and physicians who operate the luxury of optimizing care and enabling clinical research, a truly holistic approach. In Sweden, we did not replicate the devastating long-term outcomes of JIB surgery, which led to its condemnation: no liver cirrhosis, minimal urolithiasis, no marasmus or macro- or micro-nutrient or vitamin deficiencies, which I believe was attributable to universal healthcare in Sweden. Let’s face it. A thorough work up, taking the time to know your patient, operating, and then following your patient long enough to adequately monitor supplementation and ancillary care during a lengthened life-span, costs a lot of money. This might explain the outcome differences between countries with universal healthcare and those without.
I propose the following recommendations for scientific editing in our field:
1.    “Bariatric” means treating weight, which is not a disease. Do not report studies of postoperative weight change alone—they are of minor medical value.
2.    All operations termed “bariatric” are not the same. Discriminate between operations with different mechanisms.
3.    All abdominal operations cause acute metabolic changes of varying duration altering homeostasis. Weight loss per se also alters homeostasis. Metabolic outcomes should be reported at steady state.
4.    Mechanistically different gastrointestinal operations have different postoperative trajectories for achieving steady state (as do open vs. laparoscopic approaches and excisional, resective, anastomotic and implantation procedures). Beware of reports and studies comparing outcomes of different gastrointestinal operations at fixed time points (e.g., 12, 24 and 36 months).
5.    Baseline metabolic diseases, parameters, and active medications significantly affect outcomes of gastrointestinal operations. All reports and studies should characterize and report metabolic patient characteristics at baseline.
6.    Men and women differ in metabolic physiology and body composition, in their responses to trauma and stress, and in their changes over the life cycle (especially gonadal hormone status). Always stratify for sex and age in studies of metabolic outcomes.
7.    Gastric restriction, whether by reduction of volume and/or stoma size, significantly alters meal size and consistency, at least transiently, depending on operation and pre-existing as well as postoperative host factors. For example, it is physically impossible to “binge” or gorge during the period of effective gastric restriction, thus invalidating or at least complicating diagnosis of binge eating disorder and its psychological correlates. Reports and studies of postoperative eating behavior and its psycho-social implications should consider mechanisms or effects on meal volume and transit and their time-course caused by the operation.
8.    Rodent foregut anatomy differs morphologically and functionally from human. Quadruped foregut motility also differs from ambulatory human foregut motility. Gastrointestinal operations on non-primates are inadequate models of human foregut operations treating the dysmetabolic diathesis of obesity.
9.    Foregut operations affect eating behavior as do psycho-social and socio-economic factors, context, prior experience, supply and demand, and diurnal and seasonal variations. No experiment on sub-primate species adequately replicates sufficient or necessary factors to “model” outcomes of clinical operations.
10.Genetically engineered, precocial rodents by design exhibit altered phenotypes appearing in utero and/or within 21 days post-natally, active throughout the animals’ life-cycle; whereas most human obesities are expressed conditionally and at varying time-points relatively late during development. Engineered rodents are scientifically valuable for studying gene function, but of limited value for understanding foregut operations in people.

1.    Kral JG. Surgical reduction of adipose tissue in the male Sprague-Dawley rat. Am J Physiol. 1976; 231:1090–1096.
2.    Kral JG, Lundholm K, Sjöström L, Björntorp P, Schersten T. Hepatic lipid metabolism in severe human obesity. Metabolism. 1977;26:1025–1031.
3.    Rehfeld JF, Juhl E, Quaade F. Effect of jejunoileostomy on glucose and insulin metabolism in ten obese patients. Metabolism. 1970;19:529–538.
4.    Kral JG, Björntorp P, Schersten T, Sjöström L. Body composition and adipose tissue cellularity before and after jejunoileostomy in severely obese subjects. Eur J Clin Invest. 1977;7:413–419.
5.    Kral JG. Vagotomy as a treatment for severe obesity. Lancet. 1978;I:307-308.
6.    Kral JG, Paez W, Wolfe BM. Vagal nerve function in obesity: therapeutic implications. World J Surg. 2009;33:1995–2006.
7.    Kral JG. Obesity surgery—State of the art. In: Van Itallie TB, Hirsch J, eds. Recent Advances in Obesity Research IV. London: John Libbey and Co.; 1985: 237–246.
8.    Kral JG. Overview of surgical techniques for treating obesity. Am J Clin Nutr. 1992; 55:552S–555S.
9.    Kissileff HR, Klingsberg G, Van Itallie TB. Universal eating monitor for continuous recording of solid or liquid consumption in man. Am J Physiol. 1980;238(1):R14–22.
10.    Kral JG, Kissileff HR.  Surgical approaches to the treatment of obesity. Ann Behav Med. 1987;9:15–19.
11.    Kral JG, Schaffner F, Pierson Jr RN, Wang J. Body fat topography as an independent predictor of fatty liver. Metabolism. 1993;42:548–551.
12.    Kral JG, Buckley MC, Kissileff HR, Schaffner F. Metabolic correlates of eating behavior in severe obesity. Int J Obes. 2001; 25:258–264.
13.    Marceau P, Biron S, Hould FS, Marceau S, Simard S, Thung SN, Kral JG. Liver pathology and the metabolic “Syndrome X” in severe obesity. J Clin Endo Metab. 1999;84:1513–1517.
14.    Kral JG, Thung SN, Biron S, Hould FS, Lebel S, Marceau S, Simard S, Marceau P. Effects of surgical treatment of the metabolic syndrome on liver fibrosis and cirrhosis. Surgery. 2004;135:48–58.
15.    Branson R, Potoczna N, Kral JG, Lentes KU, Hoehe MR, Horber FF.  Binge eating is a major phenotype of melanocortin 4 receptor gene mutations. N Engl J Med. 2003;348:1096–1103.
16.    Potoczna N, Branson R, Piec G, Steffen R, Ricklin T, Kral JG, Hoehe MR, Luentes KU, Horber FF. Gene variants and binge eating as predictors of comorbidity and outcome of treatment in severe obesity. J Gastroint Surg. 2004;8:971–982.
17.    Marceau P, Kaufman D, Biron S, Hould F-S, Lebel S, Marceau S, Kral JG. Outcome of pregnancies after biliopancreatic diversion. Obes Surg. 2004; 14:318–324.
18.    Kral JG, Biron S, Simard S, Hould FS, Lebel S, Marceau S, Marceau P. Large maternal weight loss from obesity surgery prevents transmission of obesity to children followed 2-18 years. Pediatrics. 2006; 118(6):e1644–e1649.
19.    Smith J, Cianflone K, Biron FS, Hould S, Lebel S, Marceau S, Lescelleur O, Biertho L, Simard S, Kral JG, Marceau P. Effects of maternal surgical weight loss in mothers on intergenerational transmission of obesity. J Clin Endocrinol Metab. 2009;94:4275–4283.
20.    Guénard, F, Deshaies Y, Cianflone K, Kral JG, Marceau P, Vohl M-C.  Differential methylation in glucoregulatory genes of offspring born before vs. after maternal gastrointestinal bypass surgery. Proc Natl Acad Sci USA. 2013:110(28):11439–11444.
21.    Kral JG. Morbid obesity and related health risks. Ann Int Med. 1985;103:1043–1047.
22.    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):487S–619S.
23.    Sims EA, Danforth E Jr, Horton ES, Bray GA, Glennon JA, Salans LB.Endocrine and metabolic effects of experimental obesity in man. Recent Prog Horm Res. 1973;29:457–496.
24.    Kral JG. Diabesity: Palliating, curing or preventing the dysmetabolic diathesis. Maturitas. 2014; 7:243–248.

FUNDING: No funding was provided.

FINANCIAL DISCLOSURES: The author reports no conflicts relevant to the content of this article.

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Category: Past Articles, The History of Bariatric Surgery

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