February 2012: Ed Mason at Large

| February 16, 2012 | 0 Comments

This ongoing column is dedicated to sharing with readers the life and experiences of Dr. Edward Mason.

Column Editor: Tracy Martinez, RN, BSN, CBN
Ms. Martinez is the Program Director for Wittgrove Bariatric Center in La Jolla, California.

Currently, the American Society for Metabolic and Bariatric Surgery (ASMBS) has 1,621 integrated health members. They include nurses, physician assistants (PAs), nurse practitioners, dieticians, psychologists, exercise coordinators, and obesity medicine specialists (bariatricians). When did you feel, as a bariatric surgeon, these disciplines were important in the care of the bariatric patient?

-Tracy Martinez, RN, BSN, CBN

Dr. Mason: The need for help in the care of these patients was one of the first requirements when I began using gastric bypass in 1966. I asked our surgery department manager for someone to assist me. She knew a graduate student who was working in the outpatient clinic who was willing to manage the program. Then, we needed someone to help with patient education preoperatively and help patients with questions that arose during follow ups. Eva, the wife of one of the faculty memebers, was a volunteer Spanish translator in the hospital. She was hired as a social worker and remained on the job for 27 years. Patients told her about things no one else knew, such as adverse childhood events. Now, practioners use a tool called the Adverse Childhood Experiences or ACE Study.[1] which analyzes the relationship between multiple categories of childhood trauma and health and behavioral outcomes later in life.1 Whenever there was a problem that might require a physician, she contacted one of us. Eva provided continuity and availability of care that was far beyond any specific job description. This is an answer to your question about the local history, but it does not address the situation for 2012.

For years, bariatric surgeons have stressed the importance of long-term follow up. Obviously, as time goes on, the number of postoperative patients grows immensely. What is your feeling about the role of bariatricans? Do you feel a fellowship should be created for optimal care?

-Tracy Martinez, RN, BSN, CBN

Dr. Mason: I assume that such questions are being addressed by the ASMBS. It is complex because there are so many specialties that each have the need for help with their patients, and with decreasing payment, for the care provided. I attempted to provide a registry for collection and analysis of follow-up data for many years and had to abandon it for lack of financing. This was voluntary on the part of surgeons. Now, it is mandatory and the American College of Surgeons (ACS) and the ASMBS are cooperating in answering a part of your question. I might ask what is the difference between a medical and a surgical bariatrician? To what extent is the answer patient based as opposed to specialty based? I suspect it comes down to financing. The whole conundrum could be solved by eliminating obesity and now type 2 diabetes. I believe this is possible by finding and eliminating the causes. There is rapid progress in this direction. Education, paradigm shifts, and translation of what we learn to patient care is the ultimate solution and part of the important salvation of humans on earth.

There are always amazing patient stories. Surgeons sometimes talk about a challenging surgical procedure or an amazing postoperative course and recovery. What is one of your most memorable bariatric patients and why?

-Tracy Martinez, RN, BSN, CBN

Dr. Mason: There was a young man who had obesity and was a chain smoker who lost a leg, including the hip, as a child in a farm machine accident. He lost weight after a gastric bypass. He regained weight and asked a surgeon in another hospital to add an intestinal bypass. This resulted in malnutrition, which I managed by surgery, restoring some of the bypassed bowel to function. The obesity never returned but cigarette smoking continued. He led a very active life for many years. I retired and do not know whether he is still alive. We never did find a way to obtain the needed counseling for our patients. There are not enough people who can provide counseling or are even aware of the need. The financing is not available to train and support enough counseling which is quite time consuming. Felitti recommends that every severely obese patient be asked two questions: 1) When did you become obese? and 2) Why did you begin to gain weight at that time? If this uncovers an adverse childhood event, the patient needs counseling. A surgical procedure may be needed as well although it might be avoided. Either way, the underlying cause of potentially fatal, risky behavior needs to be resolved. We could at least add this education to our armamentarium and try to address the fundamental etiology. The most important part of counseling is listening and letting the patient discover the basis for inappropriate and risky self treatment. Maybe we can help the patients find the listener they can rely upon to listen and wait for them to find their own answers.

I would like to ask a follow-up to the question last month regarding type 2 diabetes and the use of gastric bypass in patients with BMIs less than 40kg/m2. It is true that the drug companies have developed glucagon-like peptide-1 (GLP1) mimetics but that does not seem to be the entire story. Are not there patients with type 2 diabetes who do not respond to the GLP 1 medications who are still potential responders to surgery? Do you think there are “foregut” factors also involved?

-Alan C. Wittgrove, MD, FASMBS
Medical Director
Wittgrove Bariatric Center

La Jolla, California

Dr. Mason: These are very important questions. There are patients whose diabetes fails to respond to obesity surgery because they have both type 1 and type 2 diabetes. The type 1 develops due to destruction of the beta cells by prolonged hyperglycemia. E.T. Bell, Chairman of Pathology at the University of Minnesota, told me in 1945 about an experiment in the animal laboratory that he performed in which continuous intravenous (IV) glucose destroyed the beta cells in the pancreas. The longer the patient has been a type 2 diabetic, the greater the risk of type 1 diabetes. While the insulin-producing beta cells can be destroyed by excessive stimulation, the L-cells continue to respond. This occasionally results in hyperinsulinemic hypoglycemia. Patients like me with type 2 diabetes treated with GLP-1 mimetics may lose use of their L-cells from disuse atrophy. I wish I could obtain glucose mimetics to at least keep my L-cells stimulated.

I do not see any reason why God would provide a foregut hormone when the hindgut hormone is so nicely stimulated by normal dumping. She must have provided the hormone 200 million years ago in order that it could be functioning in the salivary glands of Heloderma suspectum before GLP-1 was moved to the hind gut of mammals more like us. Sarr recently told us about a patient with post-Roux-en-Y gastric bypass (RYGB) noninsulinoma pancreatogenous hypoglycemia (NIPHS), who had been treated unsuccessfully by removal of the excluded stomach. Another operation was performed in which the alimentary (Roux) limb of the RYGB was used to replace the missing stomach (a Henle limb) and to restore duodenal perfusion. The normal sequence of intestinal flow was also restored. The article stated, “At follow up four months postoperatively, her glycopenic symptoms gradually improved markedly (although not totally disappeared).” Sarr concluded that “using the existing Roux limb to divert the ingested food back into the proximal duodenum should in theory reverse (over time) NIPHS. But one must be patient, because the reversal of the pancreatic islet dysfunction likely takes a significant amount of time.” If pre- and postprandial serum GLP-1 had been measured before and after the restoration of duodenal perfusion, I am sure it would have been evident that the last operation had eliminated stimulation of GLP-1 secretion. This could have resulted from slowing intestinal transit enough so that GLP-1 agonists no longer reached the ileum (or rectum, where there are many GLP-1 receptors). So let’s find an explanation for slowing intestinal transit by this operation. In the 1980s, there was a plethora of literature about stasis of the jejunum after Roux-en-Y gastrectomy in which it was concluded that interruption of the intestine and anastomosis caused the stasis. Sarr and his colleagues at the Mayo Clinic contributed to these studies.

One of the reasons that so much is written about the foregut hypothesis is that, in addition to never revealing the putative foregut hormone, the writers never report failure to find a rise in serum GLP-1, the hindgut hormone. There needs to be an appropriate response of one hormone. We only have a hindgut hormone to study. There is no need for two hormones and two hypotheses. In the meantime, GLP-1 gains more and more scientific study and the foregut hypothesis takes us on more mythical reasoning. Do I think there are “foregut” factors also involved? Yes, but they are the factors of dumping, not of yet-to-be-discovered hormones.

I firmly believe that type 2 diabetes is GLP-1 dependent diabetes, just as type 1 diabetes is insulin-dependent diabetes. As we age, we develop GLP-1 dependent diabetes, which I have had for several years and would like to have treated with a glucose-mimetic but could have treated with RYGB. Both provide the most physiologic treatment. I had a medical school classmate who died years ago with kidney failure and leg gangrene due to type 2 diabetes. He and I were the same weight and habitus. He gave the anesthesia for many of my operations for obesity.

I could easily eat enough to qualify for an adjustable gastric band (AGB), but I cannot obtain a glucose mimetic that has been in use for a decade as a sweetener for soda and candy but is not approved as a pharmaceutical. I would like to stimulate my L-cells so that they do not undergo disuse atrophy. The AGB operation does not stimulate secretion of GLP-1. I reduced my weight to 135 pounds by swimming a half mile daily and eating less. That did not help so now I have returned to 150 pounds. We are physicians who operate but we can use the knowledge obtained from our surgery to help millions who can never be reached by surgery because they are not sufficiently obese and because epidemics cannot be treated with surgery. In the process, we can greatly reduce the cost of medical care. Then, maybe we can hire more people with special training to take care of the patients who live longer with bariatric surgery, in further answer to the first questions this month.

1.    Felitti VJ, Anda RF, Nordenberg D, et al. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. The Adverse Childhood Experiences (ACE) Study. Am J Prev Med. 1998;14(4):245–258.
2.    Sarr M G. Noninsulinoma pancreatic hypoglycemia after Roux-en-Y gastric bypass: A more simple operative treatment. Bariatric Times. 2011;8(10):8–9.

Category: Ed Mason at Large, Past Articles

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