Abstract
The excitation of vagal mechanoreceptors located in the stomach wall directly contributes to satiation. Thus, a loss of gastric innervation would normally be expected to result in abrogated satiation, hyperphagia, and unwanted weight gain. While Roux-en-Y-gastric bypass (RYGB) inevitably results in gastric denervation, paradoxically, bypassed subjects continue to experience satiation. Inspired by the literature in neurology on phantom limbs, I propose a new hypothesis in which damage to the stomach innervation during RYGB, including its vagal supply, leads to large-scale maladaptive changes in viscerosensory nerves and connected brain circuits. As a result, satiation may continue to arise, sometimes at exaggerated levels, even in subjects with a denervated or truncated stomach. The same maladaptive changes may also contribute to dysautonomia, unexplained pain, and new emotional responses to eating. I further revisit the metabolic benefits of bariatric surgery, with an emphasis on RYGB, in the light of this phantom satiation hypothesis.
Highlights
Satiation in Health and ObesityA wide range of sensations can be evoked from the gastrointestinal (GI) tract including, but not limited to, pain and warmth (Cervero, 1994; Mulak et al, 2008)
Regardless of technical details, the phantom satiation hypothesis predicts that an effective alternative strategy to bariatric surgery would consist in mimicking, as closely as possible, the patterns of denervation and dysautonomia observed after Rouxen-Y-gastric bypass (RYGB)
The phantom satiation hypothesis appears consistent with a large body of literature and provides a complementary explanation to already existing hypotheses on how GI surgeries modify metabolism and behaviors
Summary
Satiation in Health and ObesityA wide range of sensations can be evoked from the gastrointestinal (GI) tract including, but not limited to, pain and warmth (Cervero, 1994; Mulak et al, 2008). According to the hypothesis presented here, phantom sensations of satiation are evoked when food is traversing GI segments above and below the denervated or truncated stomach, including the esophagus and lower intestines (Figure 1). One would expect lesions in brain regions involved in processing vagal sensory information including, but not limited to the insula, to be associated with satiation and weight loss.
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