ReviewPhysiology & behavior2008
De-stabilization of the positive vago-vagal reflex in bulimia nervosa.
Review in Physiology & behavior, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 37 citations in OpenAlex.
- When the Locus Coeruleus Speaks Up in Sleep: Recent Insights, Emerging Perspectives.International journal of molecular sciences · 2022Review
- Altered physiology of gastrointestinal vagal afferents following neurotrauma.Neural regeneration research · 2021Review
- Multi-method assessment of palatable food exposure in women with and without eating disorders.European eating disorders review : the journal of the Eating Disorders Association · 2020Article
- CCK response in bulimia nervosa and following remission.Physiology & behavior · 2013Article
- Vagal afferent controls of feeding: a possible role for gastrointestinal BDNF.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2013Review
- Molecular anatomy of the gut-brain axis revealed with transgenic technologies: implications in metabolic research.Frontiers in neuroscience · 2013Article
- Early postnatal overnutrition: potential roles of gastrointestinal vagal afferents and brain-derived neurotrophic factor.Physiology & behavior · 2012Review
- The effect of right vagus nerve stimulation on focal cerebral ischemia: an experimental study in the rat.Brain stimulation · 2012Article
- Plasticity of vagal brainstem circuits in the control of gastrointestinal function.Autonomic neuroscience : basic & clinical · 2011Review
- Plasticity of vagal brainstem circuits in the control of gastric function.Neurogastroenterology and motility · 2010Article
- Conceptualizing the role of estrogens and serotonin in the development and maintenance of bulimia nervosa.Clinical psychology review · 2010Review
- Cranial Nerves IX, X, XI, and XII.Psychiatry (Edgmont (Pa. : Township)) · 2010Article
- Purdue Ingestive Behavior Research Center symposium 2007: influences on eating and body weight over the lifespan--childhood and adolescence.Physiology & behavior · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Bulimia nervosa is characterized by consuming large amounts of food over a defined period with a loss of control over the eating. This is followed by a compensatory behavior directed at eliminating the consumed calories, usually vomiting. Current treatments include antidepressants and/or behavioral therapies. Consensus exists that these treatments are not very effective and are associated with high relapse rates. We review evidence from literature and present original data to evaluate the hypothesis that bulimia involves alterations in vago-vagal function. Evidence in support of this include (1) laboratory studies consistently illustrate deficits in meal size, meal termination, and satiety in bulimia; (2) basic science studies indicate that meal size and satiation are under vagal influences; (3) anatomical, behavioral and physiological data suggest that achieving satiety and the initiation of emesis involve common neural substrates; (4) abnormal vagal and vago-vagal reflexive functions extend to non-eating activational stimuli; and (5) studies from our laboratory modulating vagal activation have shown significant effects on binge/vomit frequencies and suggest a return of normal satiation. We propose a model for the pathophysiology of bulimia based upon de-stabilization of a bi-stable positive vago-vagal feedback loop. This model is not meant to be complete, but rather to stimulate anatomical, psychobiological, and translational neuroscience experiments aimed at elucidating the pathophysiology of bulimia and developing novel treatment strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.