Keep it simple, surgeon

Keep it simple, surgeon

Surgery for Obesity and Related Diseases 11 (2015) 286–287 ASMBS Executive Committee interview of Dr. Mason Keep it simple, surgeon “How did you bec...

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Surgery for Obesity and Related Diseases 11 (2015) 286–287

ASMBS Executive Committee interview of Dr. Mason

Keep it simple, surgeon “How did you become interested in bariatric surgery?” My research interest in 1965 was not obesity, but to design a simple and reversible operation to replace gastric resection. My sudden interest in obesity in 1966 was for a disease to treat with gastric bypass. In 1966, after showing in the laboratory that gastric bypass would decrease the secretion of hydrochloric acid and not cause ulcers, I began 2 studies in patients. In 1 study of 8 patients with duodenal ulcer, only 1 was cured. He was also morbidly obese and lost a significant amount of excess weight. A simultaneous second study of using a loop gastric bypass to treat morbid obesity was more successful, as you know. “How did you know that a loop bypass would lead to a desirable weight loss procedure?” Many patients with peptic ulcer, treated with subtotal gastrectomy and a loop gastroenterostomy lost weight, even when they had a normal weight. They learned to eat smaller meals more frequently and to avoid fattening foods that caused dumping symptoms. Gastric bypass made a virtue out of milder dumping, which for lean patients with ulcer had been an undesirable, weight-losing side effect. My mentor, Owen H. Wangensteen, told patients they would live longer at a lower weight. “What drove you to organize the ASBS and ASBSR?” I had been considering establishing an American Society for Bariatric Surgery, because I had hosted an obesity surgery postgraduate course, the University of Iowa Obesity Surgery Colloquium, for 7 years beginning in 1977. We were obesity surgeons and physicians teaching each other. We knew gastric bypass was curing diabetes in 1977, just as had been observed following the introduction of intestinal bypass in 1953. No obesity surgeon could fail to think about such a benefit. The mechanism finally became evident. The common denominator between intestinal and gastric bypass in resolving type 2 diabetes mellitus (T2DM) was endogenous GLP-1 secretion by L-cells as a result of short-circuiting the intestine and with dumping symptoms.

Glucose and other stimulants reached the L-cells before they could be absorbed. The American Society for Bariatric Surgery Registry (ASBSR) was begun in 1985. It was voluntary and provided for surgeons who wished to achieve continuous improvement in patient care. William Edwards Deming’s early failure in the United States and success in Japan with the “Statistical Product Quality Administration,” which is thought to have been the system that was responsible for the postwar Japanese “miracle” [1], was a stimulus to create the ASBSR. “What do you envision the future of bariatric surgery will be?” Sleeve gastrectomy is becoming the current operation of choice. Unfortunately, sleeve gastrectomy is more complex and irreversible. Epidemics of obesity and type 2 diabetes have spread to adolescents and children. Fortunately, Elias [3], and co-workers [2,3] have shown in rodent and growing porcine models that the ballooning portion of the stomach can be invaginated rather than resected [2,3]. The invaginated fundus is anastomosed internally to the antrum, Fundic invagination could be called a sleeve gastrotomy, since it is to sleeve gastrectomy as gastric bypass is to gastric resection. My goal for gastric bypass was to “Keep it simple, surgeon” and be reversible. I envision sleeve gastrotomy as the operation of choice for all ages and times. However, this procedure has not yet been evaluated in humans. There have been a number of studies, mostly from Iran, evaluating a gastric plication that may also be a reversible weight loss procedure; however, longterm evaluation of this procedure is still needed [4]. Lifelong follow-up is a goal that remains to be met for all operations for obesity and T2DM. This will be addressed as physicians, patients, and the curious learn about dumping for T2DM and stimulation of GLP-1 secretion. Record keeping is no longer optional. You will learn how to make scientific use of these data while preserving patient privacy. This will require permission of the patient and participation with special protection, perhaps for lifelong prospective research. As always, prospective studies based upon

http://dx.doi.org/10.1016/j.soard.2015.01.008 1550-7289/r 2015 American Society for Metabolic and Bariatric Surgery. All rights reserved.

Editorial / Surgery for Obesity and Related Diseases 11 (2015) 286–287

hypotheses will require collection of pertinent data. These data may change with increasing knowledge of mechanisms and consequences. You will explain to patients the normal and therapeutic importance of dumping for stimulation of GLP-1 secretion. You will explore and explain resolution of T2DM with glucose mimetics that are poorly absorbed and resolve T2DM when obesity is not a concern. The surgical viewpoint will help resolve the obesity and T2DM epidemics in adults, adolescents, and children. You will understand why only type 1 diabetes is insulin dependent. T2DM is GLP-1 and dumping dependent. Some patients with T2DM develop type 1 diabetes, and will then need treatment for both types 1 and 2. This meeting is an important step toward agreeable, science- supported viewpoints and optimal patient care. Severe obesity and T2DM will, perhaps, be treated with surgery without stomach resection if fundic invagination (sleeve gastrotomy) becomes the standard of care. Further scientific laboratory and translational clinical study is urgent and will be ongoing to save kidneys and eyes, limbs and lives. The future is based upon the past. The elimination of need for treatment of T2DM after gastric bypass was reported at the first University of Iowa Obesity Surgery Colloquium in 1977. You will know how hyperosmotic flushing (also known as dumping) exposes distal bowel to glucose and other stimulants of L-cell secretion of GLP-1. GLP-1 is the hormone required to decrease insulin resistance. Insulin resistance is normal. It is not the cause of diabetes. GLP-1 deficiency is the cause. Normal insulin resistance makes it possible for GLP-1 to regulate insulin action. Both hormones are required. Hyperinsulinemia will be avoided by providing the missing hormone. T2DM is GLP-1 dependent diabetes. T2DM is a disease of the digestive tract. Bariatric and Metabolic Surgeons will understand normal dumping and how glucose mimetics or other poorly absorbed L-cell stimulants can reach the Lcells in distal bowel and prevent or resolve T2DM without surgery. Dumping is required for an immediate effect of a

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surgical procedure upon T2DM. You will understand that without dumping, we would all have T2DM. Dorido’s sleeve gastrotomy (fundic invagination) should be as successful as sleeve gastrectomy. My original goal of decreasing the need for stomach resection will again be fulfilled. Complete stomachs will remain available by a simple reversal operation if needed later in life to provide digestion, dilution and perhaps normal dumping with greater knowledge and the cohesion of paradigms. “Scientific Discipline Will Replace Empiric Craft.” My mentors, Owen and Sara Wangensteen, used this in a subtitle for their history of surgery in 1978 [5]. Thank you for the honor of speaking at this meeting and thanks to all of those who made this possible. A special thanks to Elias Darido and coworkers for their imagination of invagination with internal anastomosis of the fundus to the antrum. Save the stomach, using education, scientific study and clinical translation. Keep it simple, surgeon. Edward E. Mason, M.D., F.A.C.S. Emeritus Professor of Surgery, University of Iowa School of MedicineIowa City, Iowa References [1] W. Edwards Deming [page on the internet]. Wikipedia [updated 2014 January 2015; cited 2014 December 15]. Available from: http://en. wikipedia.org/wiki/W._Edwards_Deming. [2] Darido E, Overby DW, Brownley KA, Farrell TM. Evaluation of gastric fundus invagination for weight loss in a porcine model. Obes Surg 2012;22(8):1293–7. [3] Darido E, Moore JR. Comparison of gastric fundus invagination and gastric greater curvature plication for weight loss in a rat model of dietinduced obesity. Obes Surg 2014;24(6):897–902. [4] Adelbaki TN, Huang CK, Ramos A, Neto MG, Talebpour M, Saber AA. Gastric plication for morbid obesity: a systematic review. Obes Surg 2012;22(10):1633–9. [5] Wangensteen O, Wangensteen S. The rise of surgery. From empiric craft to scientific discipline. London: Dawson Company, 1978.