Vagal nerve function in obesity: therapeutic implications

Abstract

The primal need for nutrients is satisfied by mechanisms for sensing internal stores and detecting food; ATP is the most primitive signal. With increasing density of sensory neurons and glia (the primordial brain) and the emergence of autonomic neural activity throughout the endoderm, transmitters and other signaling molecules enable alimentation before the appearance of innate storage functions. Memory and, ultimately, cognition are prerequisites for processing and producing food to facilitate assimilation and safeguard the supply of nutrients. The gut-brain-gut axis via the vagus nerve is the autonomic neurohumoral pathway integrating these elements of energy homeostasis. Humans uniquely override obligate nutrient needs, eating in the absence of deprivation, resulting in pathological chronic overnutrition arising from dysautonomia. Obesity surgery circumvents powerful redundant mechanisms of alimentation and reduces excess stores of body fat from chronic overnutrition while preventing re-accumulation of fat. All bariatric operations, whether purely restrictive, maldigestive and malabsorptive, or combinations, rely on regulatory mechanisms related to autonomic nervous system function and the brain-gut axis. We review the functional anatomy and the importance of the vagus nerve for maintaining maladaptive chronic overnutrition and describe interventions to abrogate its effects. In aggregate, the preponderance of evidence supported by laboratory and clinical mechanistic studies interrupting abdominal bi-directional vagal transmission demonstrates that the majority of patients report less "hunger" and lose weight.