Ed Mason at Large-October 2012

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.

Dr. Mason, what is your opinion of bariatric surgery being performed in patients with a BMI between 30 and 35kg/m2?
-Sonny Cavazos, MD
San Antonio, TX
Dr. Mason: It has been approved, but I do not think it is indicated in most patients. Two recent papers[1,2] compared more intensive use of a patient’s standard medical treatment of type 2 diabetes mellitus (T2DM) with operations that stimulate secretion of glucagon-like peptide-1 (GLP-1). Operations that cause dumping of hypertonic solutions containing glucose, bile acid, and other GLP-1 secretory stimulants, which provide endogenous GLP-1, showed markedly better results. These two nearly identical studies showed that medical treatment should be coupled with GLP-1 mimetics, or prolongation of the half-life of the inadequate levels of endogenous GLP-1 by blocking dipeptidyl peptidase-4 (DPP-4) inactivation of GLP-1. GLP-1 also stimulates insulin secretion but only if blood glucose is above normal. Unlike insulin, GLP-1 mimetics are seldom followed by hypoglycemia. Obesity surgery has contributed evidence that surgery is no longer needed for rapid resolution of noninsulin dependent diabetes when body weight is not life threatening. Most of these patients should respond to GLP-1 mimetics or DPP4 blockade, which are available therapies. Thus, there is no indication for surgery. Approval of glucose mimetics that stimulate GLP-1 secretion could resolve the epidemic of T2DM and might guide us to resolution of the obesity epidemic.

What is your opinion on using drugs phentermine and topiramate extended-release (Qsymia) and lorcaserin hydrochloride (Belviq), recently approved for use in the United States, instead of weight loss surgery or with surgery?
-Terrence Fullum, MD
Washington, DC
Dr. Mason: From what I have read about these drugs, I suggest that their use be further studied to prove both safety and effectiveness. More mechanisms of action are needed regarding combined use of surgery and these medications. Are there predictable effects and are they additive or interactive? Are they desirable? These questions require study before considering either substitution for, or combination with, surgery.

We began treating severe obesity with intestinal bypass in 1954, postulating success due to malabsorption. In 1966, we explained that weight loss after gastric bypass was likely due to restriction of intake plus malabsorption. It is now evident that the mechanism of both intestinal and gastric bypass is stimulation of secretion of GLP-1 and other hormones.

We are learning more now about the brain in treatment of obesity. GLP-1 acts both peripherally and by stimulating GLP-1 receptors in the lining of the portal vein located on afferent fibers of the vagus nerve. In the brain, the vagus nerve cells, with signals from the portal vein, secrete GLP-1. There is then neural and hormonal stimulation of cells in the hypothalamus followed by signals to the abdomen in the regulation of body weight.

We know that many individuals with severe obesity have a history of adverse childhood experiences3 and that proper prolonged counseling can result in a return to normal weight without surgery or medication. The future of research in prevention and treatment of obesity involves both the cerebral and abdominal domains (some say brains). It may now be a time for further study of chronic fine-needle stimulation of areas in the hypothalamus, which is not new. Rex Ingram, Chairman of Anatomy at the University of Iowa in the 1930s, used lesions in the hypothalamus to affect body weight and blood sugar.[4] Such effects on weight control can be reversibly accomplished by stimulation instead of destruction.[5] Let’s find out more about how all of this regulation of weight evolved in nature and what humans have done to disrupt it.

What are the biggest factors that continue to energize the obesity epidemic? How, as a society, can we influence this epidemic and manufacture a cure for obesity in the next decade?
-Terrence Fullum, MD
Washington, DC
Dr. Mason: In my opinion we live in an increasingly dysfunctional society. Dysfunction from unrealistic goals, life style, and environment creates stress. Disruptive family life, with both parents working; inappropriate nutrition; inadequate education; and especially, multiple, adverse childhood experiences (ACE) add to risk of obesity.[3] Facilitating movement of lower to middle and middle to upper class with educational preparation for higher paying jobs should help. Eliminating certain chemicals from our environment may be important. Addiction to eating junk food and sugar must also be addressed. More walking, stair climbing, and exercise are essential. Work, hobbies, and interests that occupy time and minds should help decrease or eliminate gourmanding of junk food and drinks. Glucose-sweet drinks and junk food should not be available to children at home, school, or elsewhere. A sufficient tax might be considered or designed as an experiment. Counseling should be expanded as treatment for patients whose obesity appears to be related to ACE. Mechanism trumps empiricism in choice of any operation or other treatment. Beware of personal bias.

What is on the horizon for bariatric surgery? Where will bariatric surgery be in 10 years? Do you foresee new procedures?
-Terrence Fullum, MD
Washington, DC
Dr. Mason: I see a reduction in the number of different procedures, but nothing really new. What should occur in the next 10, 8, or 4 years is education as to why dumping in normal people prevents T2DM, why an operation introduced in 1885 prevents and cures T2DM, and why insulin should not be used to treat T2DM. There will continue to be new discoveries and technical improvements. Sleeve gastrectomy is an irreversible reintroduction of a long tube that eliminates the stomach as a site for dilution and digestion. A long lesser curvature gastroplasty without stabilization of the outlet was introduced by Tretbar in 1976.[6,7] With sleeve gastrectomy there is an intrinsic risk of leak related to staple line length. Lumens that are too small tend to obstruct and cause enlargement above the obstruction. Segments that are too large obey the law of LaPlace, creating enlarged pouches that empty poorly. The stretching of the wall of the pouch is related to the radius. Therefore larger segments increase in size. The outlet becomes the highest narrow area. As a result the functional length of the pouch is unpredictable.

References
1.    Schauer PR, Kahyap SR, Wolske K, et al. Bariatric surgery versus intensive medical therapy in obese patients with diabetes. N Eng J Med. 2012;366:1567–1576.
2.    Mingrone G, Panunzi S, Gaetano A, et al. Bariatric surgery versus conventional medical therapy for type 2 diabetes. N Engl J Med. 2012;366:1577–1585.
3.    Felitti VJ, Anda RF, Nordenberg D et al. The relationship of adult health status to childhood abuse and household dysfunction. Am J Prev Med. 1998;14:245–258.
4.    Barris RW, Ingram WR: The effect of experimental hypothalamic lesions upon blood sugar. Am J Physiol. 1936;114:555–561.
5.    Halpern CH, Wolf JA, Bale TL, Stunkard AJ, et al. Brain stimulation in the treatment of obesity. J Neurosurgery. 2008;109:625–634.
6.    Tretbar LL, Sifers EC. Vertical stapling: A new type of gastroplasty. Int.J Obes. 1981;5:538.
7.    Mason EE. Surgical Treatment of Obesity. W.B. Saunders, Philadelphia 1981:403.

Category: Ed Mason at Large, Past Articles