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Metabolic, That’s All

| June 1, 2016

A Message from Dr. Henry Buchwald

Henry Buchwald, MD, PhD, is from the University of Minnesota, Minneapolis, Minnesota. He has been elected to the presidency of five organizations, including the American Society for Metabolic and Bariatric Surgery (ASMBS), International Federation for the Surgery of Obesity and Metabolic Disorders (IFSO)


Dear Readers:
Katz’s landmark delicatessen was established in New York’s lower east side in 1888. In 1919, a storefront sign maker asked one of the partners, Harry Tarowsky, what the sign he had been commissioned to execute should read. Harry replied, “Katz’s, (pause) that’s all.” The sign maker misunderstood and dutifully painted “Katz’s, that’s all” on the side of the building, where it stands today.

Metabolic surgery was inscribed in the annals of surgery, also without specific intent, in 1896, when regression of metastatic breast carcinoma was induced by bilateral oophorectomy. During the late 19th and early 20th centuries, surgery for peptic, primarily duodenal, ulcer disease was in its hayday, and consisted of gastric and vagal procedures without any attack on the ulcer itself. The partial ileal bypass was introduced in 1962-1963 for the treatment of hypercholesterolemia, and served as the interventional modality for the National Heart, Lung, and Blood Institute (NHLBI)-funded Program on the Surgical Control of the Hyperlipidemias (POSCH). Initiated in 1972, POSCH was the first randomized controlled trial to utilize metabolic surgery. In 1978, Richard Varco and I in a book we titled, Metabolic Surgery, defined this discipline as “the operative manipulation of a normal organ or organ system to achieve a biological result for a potential health gain.”

Bariatric surgery was originated in 1953 and for the past 60 plus years has struggled to gain unqualified recognition as a specialty field. Recently, bariatric surgery has declared metabolic surgery to be an integral part of bariatric surgery, in particular in the management of type 2 diabetes mellitus (T2DM). This emphasis is good but not reasonable or realistic because it reverses the natural order of rank. Bariatric surgery has, and always will be, a manifestation of the larger phylum of metabolic surgery. Thus, when we speak of the advantageous metabolic consequences of bariatric surgery for T2DM, hypertension, hyperlipidemia, etc., we are actually giving credence to the fact that we are performing metabolic surgery. Further, the primary goal and effect of bariatric surgery—weight loss—is, in itself, metabolic in origin and mechanisms.
It is, or at least was, common practice to describe bariatric procedures as being restrictive or malabsorptive based on their gross anatomic alterations, and relegating electronic stimulation procedures to the designation of other. I would propose that all restrictive procedures are malabsorptive and all malabsorptive procedures are restrictive, making that distinction meaningless. A so-called restrictive operation (e.g., laparoscopic adjustable gastric banding), limits food intake (restriction), which results in caloric malabsorption, the ultimate basis for the desired weight loss. So-called malabsorptive operations (e.g., biliopancreatic diversion and duodenal switch) limit the intestinal absorptive surface (malabsorption), which results in caloric restriction, and, once again, weight loss. We should, therefore, look instead for mechanisms of action on a metabolic basis, rather than in the verbal repetition of the altered anatomy of the operation performed.

The intestinal tract is rich in parasympathetic and sympathetic innervation. Up to 90 percent of vagal nerve fibers are afferent, not efferent, and carry signals from the gut to the brain, in particular the hypothalamus. Intestinal sympathetic nerve impulses are primarily mediated via the celiac axis and are involved, among other functions, in glucose production and release. In addition to these communicating networks to and from cerebral centers, there is a dense intrinsic nerve syncytium in the submucosal layer of the intestine extending from the esophagus to the anus. And, finally, there is a fundic gastric pacemaker that regulates gastric contractions. All these neural networks surely must be involved in the regulation of eating behavior and probably in nutrient, particularly in glucose, metabolism. Every one of our metabolic/bariatric operations impinges on these networks by dividing, excising, transposing, or stimulating them.

The literature has become replete, though not clear, about the role of intestinal and other hormones on the eating/satiety process and T2DM. There are up to 100 gut hormones, among which GLP-1, PYY, GIP, and ghrelin have received the greatest attention, as has adipocyte-derived leptin. These hormones interact, complement, and oppose in a mosaic of activity. The equation(s) that governs these relationships has, as yet, proven to be elusive. They are, however, at the heart of the metabolic processes that explain the mechanisms of metabolic/bariatric surgery, especially in their known and unknown interactions with the gut neural-cerebral network.
Bile acids and their relationship not only to digestion but to the metabolism of obesity and T2DM have recently achieved attention. Our metabolic/bariatric operations interrupt the normal enterohepatic bile acid cycle and change their particular oxidative biomedical structure. Hypotheses of causative mechanisms have also emphasized the relationship of the human intestinal bacterial microbiome to who we are, what we do, and what diseases we are susceptible or resistant to. Time will ascertain the causative relationships of bile acids and the microbiome to obesity and its associated metabolic diseases.

Why is metabolic/bariatric surgery superior to today’s pharmaceuticals for both weight loss and resolution of T2DM? Drugs are designed with as unifocal an action as possible to either generate, enhance, or block a metabolic process; any deviation could in effect elicit injurious side effects or complications. Surgery, however, has, in essence, a shotgun effect on metabolic processes, influencing several of them simultaneously by the automedication induced by neurohormonal and other bodily processes. Because obesity and probably T2DM are multifactorial diseases with a great capacity to choose alternate inciting pathways and develop resistance to therapy, multiple-pronged therapy is more likely to be effective and even lasting. The challenge at this time is to understand these pathways, and, in elucidating them, discover the pathologic, metabolic core of the two diseases that dominate global epidemics today and that are perplexing all of science. Metabolic surgery may offer hope for that understanding, an opportunity that obligates metabolic surgeons to unravel the origins, and, in the process, to ascertain therapies, for these universal plagues of the 21st century.

Metabolic, That’s All.

Sincerely,

Henry Buchwald, MD, PhD

Category: Editorial Message, Past Articles

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