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incisional surgery (e.g., draining fluid collections), extirpative (e.g., resecting tumors), and
reconstructive (e.g., prosthetic hip replacement) were augmented by a new discipline, operating on
putatively normal organs for a metabolic gain.
Three of the most common, major human diseases – atherosclerosis, cancer, obesity – are metabolic
in origin. These three afflictions are not caused by external trauma (accidents, war) or an invasive
species (viruses, bacteria), but are metabolic in origin. They are manifested by innate bodily
processes, governed by genetics, influenced by the environment and personal habits. They consist
of the chemical dualities of anabolism, the conversion of energy to the construction of arterial
plaques, malignant cells, or fat stores; and catabolism, the release of energy by the annihilation of
these tissues of disease. We readily accept the anabolic yin for these three conditions, but the yang
of the body curing itself is a more elusive concept to grasp. The discovery and utilization of the
body’s healing neurohormonal mechanisms to heal itself is the soul of the nouveau discipline of
metabolic surgery.
The partial ileal bypass [6] metabolic surgery procedure, 1962-1963, was a precursor of the
illumination of the cholesterol transport and receptor mechanism of low-density lipoprotein (LDL)
and high-density lipoprotein (HDL) discovered by Joseph Goldstein and Michael Brown, US,
1973-1974 [7] (Nobel Laureates 1985), following the HDL research of Michel Macheboeuf, France, in
1929 [8].
The Program on the Surgical Control of the Hyperlipidemias (POSCH) trial started in 1973, with
results published in 1990 in the New England Journal of Medicine, was the first major NIH-funded
metabolic surgery trial. The partial ileal bypass intervention modality study group of 421, in
comparison to the control group of 417, showed statistically significant reductions in overall
mortality, mortality due to coronary heart disease, reductions in peripheral atherosclerotic disease,
and lowering of overall mortality in the surgery subgroup with an ejection fraction over 50% [9]. In
addition, sequential coronary arteriograms at 0, 3, 5, 7, and 10 years showed statistically significant
actual regression of coronary atherosclerotic plaque lesions [10]. The statin trials of 1992 and
thereafter augmented the metabolic surgery-derived knowledge.

Comparably, the metabolic surgery of endocrine organ resection ushered in pharmaceutical
hormonal cancer therapy. The demonstration of lasting type 2 diabetes (T2D) resolution by gastric
bypass (Walter Pories, US, 1995 [11]) and biliopancreatic diversion (BPD) (Nicola Scopinaro, Italy,
2011 [12]), and the elucidation of the release of the incretin hormone glucagon-like peptide-1
(GLP-1), primarily from the ileum [13], by bariatric surgery research, led to major drug industry
proliferation of GLP-1 analogues for T2D and obesity therapy.
Understanding the definition of metabolic surgery, the major successful outcomes of metabolic
surgery procedures, and the translation of metabolic surgery-derived knowledge to non-operative
surgical advances has inspired metabolic surgery research, within and outside the peritoneal cavity.
This plethora of investigations includes: transfemoral artery bilateral perirenal sympathetic nerve
ablation for T2D, duodenal stimulation for T2D, carotid sinus stimulation for hypertension, single
cervical vagus nerve stimulation for refractory depression, intestinal transposition for obesity and
T2D, islet cell transfer to the liver for T2D, intrathecal implantable pump infusions for pain and
spasticity, implantable insulin pumps for T2D and other utilizations [14].
Bariatric surgery is the most prevalent and successful metabolic surgery of the 21st century [15]. Yet,
at its genesis, it was not recognized as metabolic surgery. There were two physiologic mechanisms
credited for its effectiveness in causing weight reduction, and the weight reduction per se as the
cause of resolution for T2D, hypertension, cardiovascular disease, etc. The procedures were said to
be either restrictive, limiting caloric intake (e.g., gastric banding), or malabsorptive, limiting caloric
absorption (e.g., BPD). This explanation was gradually discarded in favor of neurohormonal
perturbations (e.g., GLP-1 enhancement, gastrin hormone suppression, excitement of the
submucosal nerve syncytium of the intestine, vagal parasympathetic and celiac plexus sympathetic

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