Bitter taster status predicts susceptibility to vection-induced motion sickness and nausea

Background Sensitivity to bitter taste and susceptibility to nausea are both protective mechanisms that guard against toxin ingestion, and both these traits vary within and between populations. Thus, we postulated that they may have co‐evolved, such that they are associated. Methods Bitter taster status was determined in 40 subjects (13 men, 27 women) by measuring the differential perceived taste intensity between salt and n‐propylthiouracil using a labeled magnitude scale; susceptibility to vection‐induced motion sickness and nausea was assessed using an optokinetic drum, a validated multi‐symptom scoring scale, and electrogastrography. Key Results Taster status distribution was 25% non‐tasters (NT), 40% tasters (T), and 35% supertasters (ST). Gender had no impact on this distribution, but females had a higher mean maximum symptom score than males (12.4 ± 1.4 vs 7.3 ± 2.0). Non‐tasters displayed a faster and larger increase in mean symptom scores, had a higher percentage of subjects with high maximum symptom scores, and had a higher mean maximum score than T or ST, (14.8 ± 2.6 vs 7.1 ± 1.8, vs 9.8 ± 2.0). Taster status did not affect the gastric myoelectric frequency response to vection. Conclusions & Inferences Non‐tasters are more susceptible to vection‐induced motion sickness and nausea than T or ST, suggesting these two traits may have co‐evolved in a reciprocal manner: in environments where the NT trait conferred an evolutionary advantage by enabling intake of fruits and vegetables containing bitter, yet beneficial, phytonutrients, increased nausea susceptibility may have arisen to maintain protection against ingested toxins.     

Effects of fentanyl on gastric myoelectrical activity: a possible association with polymorphisms of the μ‐opioid receptor gene?

Background: Opioids have inhibitory effects on gastric motility, but the mechanism is far from clear. Electrical slow waves in the stomach determine the frequency and the peristaltic nature of gastric contractions. The primary aim of this study was to investigate the effects of the opioid fentanyl on gastric myoelectric activity. As there were large variations between the subjects, we investigated whether the variation was correlated to single nucleotide polymorphisms (SNP) of the μ-opioid receptor (MOR) gene.
Methods: We used cutaneous multichannel electrogastrography (EGG) to study myoelectrical activity in 20 patients scheduled for elective surgery. Fasting EGG was recorded for 30 min, followed by intravenous administration of fentanyl 1 μg/kg and subsequent EGG recording for 30 min. Spectral analysis of the two recording periods was performed and the variables assessed were dominant frequency (DF) of the EGG and its power (DP). Genetic analysis of the SNP A118G and G691C of the MOR gene was performed with the polymerase chain reaction technique.
Results: There was a significant reduction in DF and DP after intravenous fentanyl. However, there was a large variation between the patients. In eight subjects EGG was unaffected, five subjects had a slower DF (bradygastria) and in six subjects the slow waves disappeared. We found no correlation between the EGG outcome and the presence of A118G or G691C in the MOR gene.
Conclusions: Fentanyl inhibited gastric myoelectrical activity in about half of the subjects. The variation could not be explained by SNP in the MOR gene. Because of small sample size, the results must be regarded as preliminary observations.     

Cholinergic effects on human gastric motility

BACKGROUND: Cholinergic regulation of chronotropic (frequency) and inotropic (force) aspects of antral contractility and how these impact on gastric emptying are not well delineated. AIMS: To determine the effects of cholinergic stimulation and inhibition on myoelectric, contractile, and emptying parameters of gastric motility. METHODS: Ten normal subjects underwent three studies each, using simultaneous electrogastrography (EGG), antroduodenal manometry, and gastric emptying with dynamic antral scintigraphy (DAS). After 30 minutes of baseline fasting manometry and EGG, subjects received saline intravenously, atropine (0.6 mg then 0.25 mg/hour intravenously), or bethanechol (5 mg subcutaneously). This was followed by another 30 minutes' recording and by three hours of postprandial recording after ingestion of a technetium-99m labelled solid meal. RESULTS: During fasting, atropine decreased, whereas bethanechol increased, the antral manometric motility index and EGG power. Postprandially, atropine decreased the amplitude of antral contractions by DAS, decreased the postprandial antral manometric motility index, and slowed gastric emptying. Atropine caused a slight increase in postprandial frequency of antral contractions by DAS and gastric myoelectrical activity by EGG. Bethanechol slightly increased the amplitude, but slightly decreased the frequency of antral contractions by DAS and decreased the frequency of gastric myoelectrical activity by EGG, with no significant increase in the motility index or gastric emptying. CONCLUSIONS: Cholinergic antagonism with atropine reduces antral contractility and slows gastric emptying. Cholinergic stimulation with bethanechol increases antral contractility, but decreases the frequency of antral contractions, without altering the antral motility index or gastric emptying.     

Revised spectral metrics for body surface measurements of gastric electrophysiology

Background

Electrogastrography (EGG) non-invasively evaluates gastric function but has not achieved common clinical adoption due to several technical limitations. Body Surface Gastric Mapping (BSGM) has been introduced to overcome these limitations, but pitfalls in traditional metrics used to analyze spectral data remain unaddressed. This study critically evaluates five traditional EGG metrics and introduces improved BSGM spectral metrics, with validation in a large cohort.

Methods

Pitfalls in five EGG metrics were assessed (dominant frequency, percentage time normogastria, amplitude, power ratio, and instability coefficient), leading to four revised BSGM spectral metrics. Traditional and revised metrics were compared to validate performance using a standardized 100-subject database of BSGM tests (30 min baseline; 4-h postprandial) recorded using Gastric Alimetry® (Alimetry).

Key Results

BMI and amplitude were highly correlated (r = −0.57, p < 0.001). We applied a conservative BMI correction to obtain a BMI-adjusted amplitude metric (r = −0.21, p = 0.037). Instability coefficient was highly correlated with both dominant frequency (r = −0.44, p < 0.001), and percent bradygastria (r = 0.85, p < 0.001), in part due to misclassification of low frequency transients as gastric activity. This was corrected by introducing distinct gastric frequency and stability metrics (Principal Gastric Frequency and Gastric Alimetry Rhythm Index (GA-RI)^TM) that were uncorrelated (r = 0.14, p = 0.314). Only 28% of subjects showed a maximal averaged amplitude within the first postprandial hour. Calculating Fed:Fasted Amplitude Ratio over a 4-h postprandial window yielded a median increase of 0.31 (IQR 0–0.64) above the traditional ratio.

Conclusions & Inferences

The revised metrics resolve critical pitfalls impairing the performance of traditional EGG, and should be applied in future BSGM spectral analyses.