Original articleThe effect of psychological stress on symptom severity and perception in patients with gastro-oesophageal reflux
Introduction
Heartburn and acid regurgitation, caused by the reflux of gastric acid into the oesophagus, are the main symptoms of gastro-oesophageal reflux disease (GORD). It can also present with chest pain, belching, nausea, or nonobstructive dysphagia secondary to GORD [1]. Preclinical levels of gastro-oesophageal reflux (GOR) are increasingly common in Western societies and currently affect up to 40% of the U.S. population [2]. Despite a wealth of recent research, a number of uncertainties surround its aetiology, particularly with symptom perception. Evidence now suggests that psychosocial influences, such as stress or stress-related personality characteristics, may play an important role in the presentation, diagnosis, and treatment of this disease [3], [4], [5].
Stress is believed to exacerbate GOR symptomatology by increasing resting lower oesophageal sphincter (LOS) pressure, impairing sphincter relaxation and thus delaying acid clearance from the oesophagus [6]. However, while the application of psychological relaxation techniques has led to significant reductions in reported heartburn and duration of oesophageal acid exposure [7], clinical evidence for a decisive direct relationship between stress and GOR is still rather uncertain, with results reporting both an increase and decrease in GOR symptomatology during periods of stress [3], [8], [9], [10], [11], [12]. An indirect relationship between stress and GOR is also suggested. For example, using an acid-perfusion test to reproduce reflux symptoms, it has been discovered that some reflux-negative heartburn patients report reflux-related pain [13]. Moreover, the alteration of symptom perception is believed to occur during periods of heightened arousal [14]. This may account for the proportion of patients with normal endoscopy who report the presence of typical reflux symptoms [13], [15]. Further exploration of both these relationships is therefore necessary.
Empirical evidence for the influence of individual differences in stress responses in GOR patients is fairly limited [16]. Johnston et al. [17] report that although a stress task did not produce an increase in reflux, symptom ratings of subjects with low trait anxiety were similar for both stress and neutral tasks, and their ratings were generally consistent with oesophageal pH data. However, a dissociation between symptom self-rating and oesophageal pH data was present for highly anxious subjects. The perceived increase of reflux symptoms, in the absence of actual increased acid reflux, has also been reported in a subset of highly anxious GOR patients exposed to a stressor [18]. Similarly, patients with dyspepsia of unknown origin had significantly higher anxiety and tension scores than symptom-positive dyspepsia subjects [19]. Current literature seems to suggest a pivotal role of anxiety in altered symptom perception, but a wider range of stress-related characteristics needs investigation.
Limitations of previous methods employed may also explain the uncertainties surrounding the relationship between stress and GOR. For example, previous research has often involved very small sample sizes [11], [12]. Investigators frequently used physical or purely cognitive stressors [3], [8], [11], [12], even though more valid ones such as interview scenarios have been shown to increase oesophageal contractions [20]. The measurement of stress is also inconsistent between studies comparing the effect of actual stress (measurement of physiological processes) with that of perceived stress (participant's subjective rating). Control groups are often not employed, and psychological stress resulting from very recent insertion of the pH probe is seldom taken into account.
One major difficulty of work in this area is that, although relationships between psychological stress and gastro-oesophageal function are easily established, the direction of causality is far more difficult to ascertain. The current investigation therefore adopted an experimental design to assess oesophageal acid level at the exact point that a psychological stressor was administered (additionally using cortisol as a biological marker of the stress response). Post hoc, the sample was also divided into high and low state anxiety ratings and high and low biological markers (cortisol) of stress for additional analysis.
In summary, the current literature suggests a correlation between stress and GOR. However, the present evidence surrounding the exact nature of this relationship is contradictory. The investigation reported here had three main aims. First, to determine whether exposure to a psychological stressor is causally related to a change in acid reflux, or whether stress merely acts to alter perception of GOR symptoms; second, to assess whether state anxiety influences the relationship between stress and GOR; and third, to establish whether stress-related personality characteristics could affect the relationship between stress and acid secretion.
Section snippets
Participants
Fifty patients with main symptoms of heartburn and acid regurgitation, referred for 24-h pH monitoring to the Oesophageal Investigation Unit at St. Thomas' Hospital, were recruited. Participants who smoked more than 70 cigarettes per week, who suffered from rheumatoid arthritis, atopic dermatitis, allergic rhinitis, allergic asthma, and depression, who used high doses of glucocorticoids, and could not tolerate a high-fat meal or fast before the investigation were excluded. The reasons for this
Results
There were no significant differences between the experimental and control groups for any baseline demographic or personality questionnaire scores. More importantly, both the control and experimental groups demonstrated similar levels of objective reflux and GOR symptom ratings prior to testing (Table 1). Cortisol analysis revealed that both groups produced almost identical levels of cortisol at Sample 3, immediately prior to the test period (TSST=11.02 nmol/l; control=11.16 nmol/l).
Discussion
The study primarily aimed to investigate the presence of a causal relationship between stress and GOR; four main findings emerged. First, the TSST was confirmed to be a reliable and valid laboratory inducer of acute physiological and psychological stress in patients with GOR symptoms. Second, neither actual exposure to experimental stress (TSST), biological markers of stress (cortisol levels), nor state anxiety was found to be related to objective GOR parameters as assessed in this experiment.
Acknowledgments
The Authors would like to thank the late Mr. Bill Owen for his great interest and encouragement to develop this study.
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