1 Department of Internal Medicine, First trimester nausea is associated with
gastric slow wave dysrhythmias (tachygastria, bradygastria). We tested
the roles of meal composition and caloric content on nausea and slow
wave rhythm in 14 nauseated pregnant women. Electrogastrography
quantified dysrhythmic activity and signal power responses to meals.
Symptomatic women reported mild to moderate nausea and exhibited
increased dysrhythmias during fasting
(P < 0.05).
Protein-predominant meals reduced nausea and dysrhythmic activity to
greater degrees than equicaloric carbohydrate and fat meals and
noncaloric meals (P < 0.05). Meal
consistency did not affect symptom responses, although liquid meals
decreased dysrhythmias more than solids
(P < 0.05). Carbohydrates and fats
increased electrogastrographic power to similar degrees as proteins,
whereas responses to noncaloric meals were less. In conclusion, protein
meals selectively reduce nausea and gastric slow wave dysrhythmias in
first trimester pregnancy. Meal consistency is a limited factor in the
favorable effects of protein. Electrogastrographic power changes do not
explain the symptom response to protein. Thus dietary modulation of
gastric myoelectric rhythm with protein supplementation may provide
symptomatic benefit in nausea of pregnancy.
electrophysiology; gastrointestinal motility; electrogastrography; gastric emptying
NAUSEA AND VOMITING affect 50-80% of women during
the first trimester of pregnancy and produce significant loss of
productivity as well as impaired health status (8-10, 16,
18). Medications and cutaneous stimulation techniques
(acupressure, acupuncture) are advocated for treatment by some
clinicians, but their efficacy is unproven in many instances (1, 5, 12,
20, 24). Because of concerns about adverse medication reactions for the fetus, management of first trimester nausea has relied on modification of dietary intake to provide foods that reduce symptoms (21). Obstetricians commonly recommend ingestion of solid carbohydrate meals,
such as soda crackers, based primarily on anecdotal reports (2, 7, 13,
20). However, more recent investigations indicate that protein meals
may be more beneficial for symptom control and that carbohydrates and
fats either have no effect or worsen nausea (6, 15, 23, 29).
The pathophysiology of nausea in pregnancy is poorly understood, in
part because most technologies for evaluating gastrointestinal motility
are invasive or expose the fetus to ionizing radiation. The technique
of electrogastrography noninvasively measures gastric myoelectric
activity (27). In healthy individuals, the stomach exhibits rhythmic
electrical depolarizations (slow waves) that control gastric motor
function. In some diseases, nausea may be associated with altered
gastric motility and disturbances in slow wave rhythm in which cycling
is too rapid (tachygastria) or too slow (bradygastria) (11, 17, 26,
28). Furthermore, in normal individuals, the electrogastrographic
amplitude or power increases after eating; an absence of this increase
correlates with delays in solid phase gastric emptying (3, 27). A
pathogenic role for slow wave disturbances in generating nausea is
suggested by studies that show that dysrhythmias begin before nausea is experienced, are correctable by treatments that reduce symptoms, and
can be normalized by gastric electrical pacing (4, 14, 22, 26).
Previous investigations have shown that women with first trimester
nausea exhibit slow wave dysrhythmias that resolve after delivery and
that can be mimicked by exogenous progesterone and estrogen
administration to nonpregnant women (19, 30). In contrast, asymptomatic
pregnant women show no rhythm disruptions (25). The acute effects of
different dietary components and their liquid vs. solid consistency on
nausea and slow wave rhythm in first trimester pregnancy have not been
rigorously explored.
The aim of this controlled investigation was to determine which meal
characteristics offer the greatest reduction in symptoms in women with
first trimester nausea and whether these meals have specific effects on
electrogastrographic parameters. We examined whether meals consisting
predominantly of protein, carbohydrate, or fat selectively reduce
nausea and dysrhythmic activity or modify the power responses. We then
compared the effects of solid and liquid nutrient meals to determine
whether meal consistency affects symptom and slow wave responses to
eating. Finally, to assess whether the caloric content is important,
nausea and slow wave activity were measured after ingestion of
noncaloric liquid and solid meals. Through these studies we hoped to
gain insight into dietary modulation of symptoms and gastric
myoelectric activity in patients with nausea of first trimester pregnancy.
Study Population
ABSTRACT
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
MATERIALS AND METHODS
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
Study Design
All studies were performed after overnight fasting. Electrogastrography was performed according to the method of Stern and colleagues (27). Subjects were placed supine in a quiet warm room without visual or auditory distractions. After gentle skin abrasion to enhance electrical conduction, Ag-AgCl electrodes (Accutac diaphoretic electrocardiogram electrodes, NDM, Dayton, OH) were affixed to the abdomen. The first electrode was placed in the mid-clavicular line below the left costal margin. The third electrode was placed midway between the xiphoid and the umbilicus. The second electrode was placed equidistant between the first and third electrodes. A fourth reference electrode was affixed in the right upper abdominal quadrant. Electrodes were connected via direct nystagmus couplers (model 9859, SensorMedic, Anaheim, CA) to a chart recorder for continuous display of slow wave activity. Time constants were set at 10 s and high frequency cutoffs at 0.3 Hz to minimize interference from nongastric signals.Before initiation of electrogastrographic recording, a 15-min equilibration period was provided to ensure a stable fasting tracing. Fasting recording was performed for 15 min, after which each pregnant woman ate a standardized test meal prepared by the University of Michigan Clinical Research Center. Five minutes were allotted for ingestion of each meal. After completion of the meal, postprandial electrogastrographic recording was performed for 45 min. Each subject recorded her level of nausea with an integral scale from 0 (no nausea) to 10 (severe nausea with vomiting) every 10 min throughout the study (twice during fasting and five times postprandially).
Subjects presented on separate days for each test meal and completed
all meal ingestions within 2 wk of study entry. Meals were ingested in
random order, and all studies were completed by the 14th gestational
week. The order of meal ingestion was provided by the dietician service
in the Clinical Research Center and was different for each subject. The
400-kcal caloric meals were formulated to be
single-nutrient-predominant for protein, fat, or carbohydrate and to be
palatable (Table 1). Liquid and solid meals
that were protein-, carbohydrate-, or fat-predominant were given to
determine if the physical consistency of the caloric meal affected
symptom and electrogastrographic responses to nutrient ingestion.
Noncaloric solid and liquid meals of similar volumes assessed the
importance of caloric supplementation in reducing nausea and slow wave
dysrhythmias in first trimester pregnancy.
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Data Analysis
Interpretation of symptom and electrogastrographic data was performed only from those studies in which fasting or postprandial nausea was reported by the pregnant volunteers. Electrogastrographic recordings from the excluded asymptomatic studies showed no increase in dysrhythmic activity and were not different from those in studies of healthy nonpregnant women in the same laboratory that used identical data analysis protocols, similar to findings previously reported (25). Because of this exclusion, data presented for each test meal do not include results from all 14 pregnant volunteers. However, each nutrient test meal is represented by at least 8 recordings in which nausea was reported. Specifically, eight women ingested the liquid protein, liquid carbohydrate, solid carbohydrate, solid fat, and inert meals, whereas nine women ingested the solid protein and liquid fat meals.Nausea scoring. Nausea scores under fasting and postprandial conditions were calculated for pregnant women with first trimester nausea. The fasting nausea score was calculated as the mean of two reports at 10-min intervals. Postprandial nausea at 5, 15, 25, 35, and 45 min after meal ingestion was plotted as the net change (increase or decrease) in the recorded nausea score compared with fasting.
Electrogastrographic analysis. Electrogastrographic recordings from the three leads were analyzed visually to determine which provided the signal most free of motion artifact and respiratory interference. This lead selection and all subsequent electrogastrographic analyses were performed in a blinded fashion, so that the investigator did not know the identity of the volunteer or the test meal condition being studied. This signal was digitized at 4 Hz by the analog-to-digital converter and filtered above 15 cycles per minute (cpm) and below 0.5 cpm to remove high- and low-frequency noise. Commercially available software (Fourier Perspectives III, Alligator Technologies, Fountain Valley, CA) was employed to perform power spectral analysis on 4-min recording segments in the fasting and postprandial periods. A running spectral analysis plot was generated across the frequency range of 0.5-9 cpm at 2-min intervals, so that each successive line in the pseudo-three-dimensional plot represented the mean amplitudes at the different frequencies of the 4-min recording segments acquired every 120 s in overlapping fashion. Data from the power spectral analyses were converted to spreadsheet format (Lotus 1-2-3 2.0, Lotus Development, Cambridge, MA) to quantify gastric slow wave disturbances.
Power spectra were divided into bradygastric (Statistical Analysis
All results are expressed as means ± SE. Repeated measures ANOVA was performed on the nausea scores, dysrhythmic indexes, and postprandial power increases to compare responses to meal consistencies and nutrient subclasses and to test if there were significant interactions between meal consistency and time after eating and between nutrient subclass and time after eating. Repeated measures ANOVA determined that there was no effect of the order of meal ingestion on nausea scores, dysrhythmic indexes, or power increases. Repeated measures ANOVA was performed separately within each meal consistency and nutrient subclass to estimate the magnitudes of the nutrient effects. When the main effect of nutrient subclass was significant within an analysis, the Newman-Keuls multiple range test was employed to identify differences between nutrients. Statistical significance was accepted at a P value of <0.05. ![]() |
RESULTS |
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Effects of Test Meals on Symptoms
The mean fasting nausea score during all studies of pregnant women was 2.8 ± 0.3. Including only those sessions in which fasting symptoms were recorded, the mean fasting nausea score was 3.5 ± 0.3, representing mild to moderate nausea. Meal ingestion produced time-dependent reductions in nausea (F = 5.73, P = 0.0002). Both liquid (F = 3.70, P = 0.01) and solid (F = 2.82, P = 0.03) meals reduced nausea scores in time-dependent fashion, with maximal reductions in nausea score of 1.0 ± 0.3 for each consistency at 45 min after ingestion (Fig. 1A). Comparison of the effects of meal consistency on postprandial changes in nausea scores revealed no differences in responses to liquid and solid meals (F = 0.01, P = 0.91). In contrast, postprandial changes in nausea scores exhibited a significant dependence on nutrient subclass (protein, carbohydrate, fat, or noncaloric; F = 3.39, P = 0.02; Fig. 1B). Analysis of differences between nutrient subclasses detected a significantly greater reduction in postprandial nausea with protein ingestion compared with meals of other subclasses (P < 0.05). Protein ingestion produced significant time-dependent reductions in nausea (F = 9.21, P = 0.0009) with maximal decreases in nausea score of 2.0 ± 0.2 at 45 min, whereas time-dependent decreases in nausea score did not reach statistical significance for carbohydrate, fat, and noncaloric meals. There were no differences in symptom responses to caloric carbohydrate and fat meals and noncaloric meals (P > 0.05).
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Gastric Slow Wave Responses to Meals
Meal effects on slow wave rhythm. During fasting, pregnant women with nausea exhibited dysrhythmic indexes of 61 ± 2%. This was significantly greater than fasting dysrhythmic indexes from a group of young, healthy, asymptomatic, nonpregnant women measured with an identical protocol (30). In contrast to healthy volunteers who show 3-cpm waveforms on visual inspection of electrogastrographic tracings, nauseated women in first trimester pregnancy exhibited prolonged periods of abnormal slow wave activity with slow (bradygastric) or rapid (tachygastric) rhythms interspersed with normal 3-cpm activity.
Measures of dysrhythmic activity were calculated in a time-dependent fashion to correlate with nausea score findings. As with nausea scores, meal ingestion produced time-dependent reductions in dysrhythmic indexes (F = 10.08, P = 0.0001). Both liquid (F = 6.58, P = 0.0004) and solid (F = 3.39, P = 0.02) meals produced improvements in dysrhythmic activity, with maximal 11 ± 3% and 6 ± 3% decreases in dysrhythmic index at 25 min after eating, respectively (Fig. 2A). In contrast to the nausea scoring, decreases in dysrhythmic index were greater with liquid than with solid meals (F = 5.39, P = 0.02). As with the nausea reports, postprandial changes in dysrhythmic index exhibited a significant dependence on nutrient subclass (F = 5.06, P = 0.003; Fig. 2B). Proteins (F = 8.94, P = 0.001), fats (F = 6.26, P = 0.004), and noncaloric meals (F = 4.02, P = 0.03) produced time-dependent changes in dysrhythmic index, whereas carbohydrates evoked no change in dysrhythmias. Analysis of differences between nutrient subclasses detected a significantly greater reduction in postprandial dysrhythmic indexes with protein ingestion compared with meals of other subclasses (P < 0.05), with a maximal 19 ± 3% decrease at 45 min after eating. Analysis between nutrient subclasses detected no differences in dysrhythmic index responses to caloric carbohydrate and fat meals and noncaloric meals (P > 0.05). Visual analysis of electrogastrographic tracings before and after protein ingestion showed normalization of the aberrant slow wave activity to 3-cpm waveforms that were most evident in the final 30 min of the postprandial recording periods (Fig. 3). In contrast, visual analysis of electrogastrographic tracings after ingestion of meals of other nutrient subclass predominance showed persistence of abnormal slow wave activity, with periods of bradygastric and tachygastric activity interspersed between periods of normal 3-cpm waveforms (Fig. 4).
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Meal effects on electrogastrographic power.
Increases in electrogastrographic signal power after test meal
ingestion were quantified to correlate with nausea scoring reports.
Time-dependent increases in power were observed after meal ingestion
(F = 11.02, P = 0.0001). Both liquid
(F = 9.35, P = 0.0002) and solid
(F = 7.64, P = 0.0006) meals increased
electrogastrographic power (Fig.
5A). In
contrast to nausea scores and dysrhythmic indexes, maximal increases in
power were observed within 5 min of eating. There was a trend toward
greater powers with liquid meal ingestion than solids that did not
reach statistical significance (F = 3.57, P = 0.06), with maximal increases to
6.2 ± 1.5- and 3.0 ± 0.7-fold of fasting, respectively. As with
nausea scores and dysrhythmic indexes, postprandial increases in power
showed significant dependence on nutrient subclass
(F = 4.10, P = 0.01; Fig.
5B). Meals in each nutrient subclass
produced time-dependent increases in electrogastrographic power
compared with fasting levels (protein:
F = 7.63, P = 0.003; carbohydrate:
F = 4.62, P = 0.02; fat:
F = 8.92, P = 0.002; noncaloric:
F = 4.06, P = 0.03). However, in contrast to the
nausea and dysrhythmic index findings, analysis of differences between
nutrient subclasses did not show a selective effect for protein meals.
In this analysis, carbohydrate and fat meals produced similar increases
in power to protein-predominant meals
(P > 0.05), especially over the
first 25 min after meal ingestion, which were greater than those
produced by noncaloric meals (P < 0.05).
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DISCUSSION |
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The present study provides controlled data on symptom responses to ingestion of meals of different nutrient composition in nauseated women in first trimester pregnancy. As suggested by others, protein-predominant meals produced quantifiable decreases in nausea, whereas carbohydrate- and fat-predominant meals did not produce statistically significant effects (23, 29). Solid and liquid protein meals reduced nausea to similar degrees, indicating that the physical form of the meal has little relevance to its symptomatic effect. The demonstration that noncaloric meals did not decrease nausea is consistent with the hypothesis that the beneficial effects of proteins stem from a positive effect of that nutrient class rather than the alternate explanation that carbohydrates and fats have adverse symptom effects.
Dysrhythmic activity correlated well with symptom reports in women with first trimester nausea. During fasting, symptomatic pregnant women exhibited slow wave rhythm disruptions that were both bradygastric and tachygastric in morphology. As with nausea scores, protein-predominant meals reduced dysrhythmic activity to significantly greater degrees than did carbohydrates, fats, and noncaloric meals. The time courses for reductions in nausea scores and dysrhythmic indexes after protein ingestion were very similar, with improvements becoming evident ~25 min after eating. Both the nutrient selectivity and the time dependence of the slow wave rhythm responses are consistent with the theory that dysrhythmic gastric myoelectric activity is pathogenic of induction of nausea. The time delay in the dysrhythmic and symptomatic improvements suggests that direct activation of gastric neural pathways does not underlie the beneficial effect of protein ingestion. Rather, it indicates that more slowly activating systems, perhaps involving small intestinal sites or hormonal mediators, are responsible for the slow wave-stabilizing and nausea-reducing effects of the protein test meals. Alternatively, the time dependence of the symptom and electrogastrographic responses may correlate with intragastric meal redistribution from the fundus to the distal stomach before delivery into the intestine.
In contrast to nausea-scoring results, fats and noncaloric meals produced small but significant decreases in dysrhythmic indexes. Furthermore, liquid meals improved dysrhythmic activity to greater degrees than solids. There are several possible explanations for the relatively larger and more broadly based effects of meals on slow wave rhythm disturbances than on symptoms. It is conceivable that there is a threshold reduction in dysrhythmic activity, achieved by protein meals but not by fats or noncaloric meals, that is required to decrease nausea. Alternatively, slow wave rhythm disruption may be one of many cofactors in the production of nausea. With this theory, proteins may have beneficial effects in addition to and separate from their actions on dysrhythmic activity.
The electrogastrographic power responses to meal ingestion did not correlate with reductions in first trimester nausea. In contrast to a previous study that showed blunting of the postprandial power response in asymptomatic pregnant women (25), our investigation demonstrated increases in electrogastrographic power after ingestion of all test meals. Power responses to carbohydrates and fats were not different from responses to proteins. Although lesser in magnitude, power increases also were observed with noncaloric meals, a finding consistent with the accepted criteria for normality (3, 27). Furthermore, the increase in signal power occurred within 5 min with all meals, much sooner than nausea was reported to improve. These nutrient- and time-dependent differences in power response and nausea reports indicate that this electrogastrographic parameter cannot explain the nutrient-specific reductions in symptoms after protein meal ingestion.
There are alternate explanations for our findings. It is possible that meal palatability played a role in symptom reduction and dysrhythmia resolution with protein ingestion. However, the liquid and solid protein meals had very different taste characteristics. Furthermore, the liquid protein, liquid carbohydrate, and solid carbohydrate meals all were sweet, yet only the protein preparation was beneficial. Additionally, patient surveys did not reveal any differences in palatability. Second, it is possible that improvements with protein meals represent responses to a balanced diet, as each meal had carbohydrate and fat components representing 47% of the caloric load. However as part of a prior investigation of women with first trimester nausea, we tested the effects of ingestion of a mixed liquid meal that can be used as a sole enteral nutrition source (30). This supplement, which contains 14% of calories contributed by protein, 64% by carbohydrate, and 22% by fat, did not reduce dysrhythmic activity to any degree, in contrast to the protein-rich meals provided in the current study. Third, this investigation only evaluated single, stereotyped meals given on one occasion. It would be important to administer a diverse range of protein-enriched foodstuffs of differing tastes and seasoning over a period of weeks to confirm the beneficial effects of proteins and to determine that no tolerance to their efficacy developed. Finally, given the relatively small numbers of pregnant women tested, it is conceivable that type II errors may explain the lesser efficacy of carbohydrate, fat, and noncaloric meals in reducing nausea and dysrhythmic activity. In fact, reductions in dysrhythmic indexes and trends to reductions in symptoms were observed with other nutrients. Other studies of gastric myoelectric activity have shown improvement in slow wave stability after meal ingestion, suggesting that these responses may be part of a generalized response to gastric filling (4). Nonetheless, the most striking findings of this investigation relate to the selectively beneficial effects of protein-predominant meals versus the other nutrient classes.
In conclusion, meals consisting predominantly of proteins improve symptoms and gastric slow wave rhythm in women with first trimester nausea to greater degrees than do carbohydrates, fats, or noncaloric meals. Meal consistency is a limited factor in the beneficial effects of proteins. These findings do not support the prevalent recommendation for carbohydrate meals in first trimester nausea but suggest that dietary modulation of gastric myoelectric activity with proteins may provide benefit to symptomatic pregnant women.
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ACKNOWLEDGEMENTS |
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This study was supported in part by National Institute of Diabetes and Digestive and Kidney Diseases Grants RO1 DK-35783 and P30 DK-34933 and General Clinical Research Centers Program Grants MO1 RR-00042 and 3 MO1 RR-00042-32S1.
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: W. L. Hasler, 3912 Taubman Center, Box 0362, Univ. of Michigan Medical Center, Ann Arbor, MI 48109 (E-mail: whasler{at}umich.edu).
Received 25 August 1998; accepted in final form 16 June 1999.
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