Discussion
Gastroparesis, bloating, nausea, nonpurging, increases gastric motility, illness, self-induced vomiting, eating disorders, vomiting, Camilleri, upper gastrointestinal symptom, PD, gastrointestinal distress, gastroparesis, eating disorder, DSM-5
GASTROPARESIS, TARDIVE DYSKINESIA, DYSFUNCTION, SAID, MITCHELL, GASTROPARESIS, PATHOLOGY, DELAYED GASTRIC EMPTYING, PURGING
We sought to determine whether delayed gastric emptying was associated with purging, binge eating, or both, and results supported a specific association with purging. In addition, delayed gastric emptying was associated with greater postprandial gastrointestinal distress, suggesting that a mechanical disruption in the digestive process may contribute to urges to self-induce vomiting. Combined with prior findings of significantly greater postprandial release of PYY and insulin (Keel et al., Very limited research has been dedicated to understanding self-induced vomiting in eating disorders despite the presence of this feature in PD, AN, and BN. Indeed, the DSM-5 eliminated the DSM-IV's distinction between purging and nonpurging BN subtypes due to a lack of empirical support (van Hoeken, Veling, Sinke, Mitchell, & Hoek, In addition to providing novel insight into factors that may contribute to purging, current results may explain why efforts to alter gastric emptying proved ineffective in alleviating symptoms in BN. Devlin et al. (That said, specifying a link between self-induced vomiting and gastric emptying and using a pharmacological manipulation to eliminate group differences in gastric emptying did not open a promising avenue for developing an intervention for PD. Instead, findings provide a cautionary tale regarding the challenges in identifying and isolating a dysfunction within complex systems. Physiologically, metoclopramide increases gastric motility but it also enhances the release of gut peptides that impact feelings of satiation, satiety, and, at high levels, malaise, by increasing how quickly food enters the intestinal tract. In the case of PD, a medication that increases gastric motility may alleviate one cause of gastrointestinal distress while exacerbating another source – exaggerated PYY response. Exploratory analyses identified an association between gastric emptying and PYY release and demonstrated that medication robustly increased PYY response across participants. After the study was funded, the FDA released a black box warning regarding possible serious side effects associated with metoclopramide, which is a dopamine receptor antagonist that crosses the blood-brain barrier and has been linked to tardive dyskinesia. As such, the possible but unlikely anti-emetic benefits appear outweighed by the risks associated with extended treatment. These conclusions align with those regarding the management and treatment of gastroparesis in which delayed gastric emptying causes bloating, excessive fullness, nausea, and vomiting (Camilleri, Parkman, Shafi, Abell, & Gerson, Our novel use of a 2 × 2 factorial design dissociated effects linked to bingeing Our study enjoyed several strengths. Our rigorous inclusion and exclusion criteria eliminated several common confounds. Our use of a double-blind, placebo-controlled cross-over design permitted stronger inferences regarding group differences in gastric emptying and their downstream effects on subjective and gut peptide responses to food intake. Our measures included structured clinical interview assessments and self-report questionnaires that were selected based on their strong psychometric properties, which were further supported in our current study. Finally, our sample size is the largest in the published literature on gastric emptying in BN, including nearly twice the number of participants included in prior studies, is the first study of gastric emptying in PD, and used a rigorous analytic approach. Moreover, part of this study reflects an independent and successful replication of delayed gastric emptying in purging BN compared to healthy controls.Despite these strengths, limitations warrant consideration. First, despite our best efforts and a one-year no cost extension, we were unable to secure our target sample of 25 participants with BN who relied solely on nonpurging compensatory behaviors. This produced an unbalanced design in which a majority of those with binge eating were also purging and a majority of those who were not purging were healthy controls. To avoid biased estimates of the main effects of binge eating and purging, we reported results from models with all main and interaction effects and utilized an analytic approach that is well-suited to unbalanced designs. Second, our study utilized a combination of a cross-sectional and experimental design but does not permit causal inferences regarding associations with symptoms. All eating disorder participants were studied during the state of illness and compared to controls who never experienced eating pathology. Thus, we cannot determine whether delayed gastric emptying contributes to self-induced vomiting, is a consequence of self-induced vomiting, or is related to self-induced vomiting through an underlying third variable. Indeed, although our design shares some features with a clinical trial, it reflects a case-control observational design. Prior to comparing groups in the placebo condition, we did not know whether delayed gastric emptying would be associated with bingeing, purging, or their combination. In addition, our use of a single 10 mg dose of metoclopramide was not intended to produce meaningful changes in symptom levels. Instead, it was used to produce its FDA-approved effect on gastric motility to probe downstream consequences on differences in gastric emptying and gastrointestinal distress. We did not employ the current standard, a 4 h scintigraphy of a solid-phase meal, to measure delayed gastric emptying, or standard measures of upper gastrointestinal symptom severity, such as the Gastroparesis Cardinal Symptom Index (Camilleri et al., In conclusion, delayed gastric emptying is linked to purging and may further contribute to gastrointestinal distress described by individuals with PD. Future work may benefit from the use of wireless motility capsule assessment and standard assessments of upper gastrointestinal symptom severity (Camilleri et al., 