Relationship between gastroesophageal reflux disease and objective sleep quality

Abstract

Study Objectives:

To objectively characterize (1) the relationship between gastroesophageal reflux disease (GERD) and sleep quality, and (2) the influence of sleep position on this relationship, using in-laboratory polysomnography.

Methods:

We retrospectively analyzed first-night diagnostic in-laboratory polysomnography data for 3411 patients (median age 55 years; 48% male). Medication use and medical condition data were obtained through self-reported questionnaires. Associations between sleep quality and the presence of GERD, and the influence of sleep position on these associations, were analyzed using multivariable linear regression models.

Results:

After adjusting for age, sex, body mass index, and relevant comorbidities, GERD was associated with a 3.0% decrease in sleep efficiency, 8.8-minute increase in wake after sleep onset, 24.4-minute increase in rapid eye movement (REM) latency, 13.4-minute decrease in total sleep time, 1.4% decrease in %REM sleep, and 1.5% increase in %N3 sleep. Having both GERD and the majority of sleep on the right side was associated with an 8.6% decrease in sleep efficiency, 27.5-minute increase in wake after sleep onset, 35.6-minute decrease in total sleep time, 2.1% decrease in %REM sleep, and 3.5% increase in %N3 sleep. Having both GERD and the majority of sleep on the left side was associated with an 8.7-minute increase in sleep onset latency.

Conclusions:

GERD is associated with an impairment in objective sleep quality. These associations were more pronounced in right-sided sleep and mostly ameliorated in left-sided sleep. Physicians should recognize the potential for poor sleep quality in patients with GERD and the effect of body position on this relationship.

Citation:

Gurges P, Murray BJ, Boulos MI. Relationship between gastroesophageal reflux disease and objective sleep quality. J Clin Sleep Med. 2022;18(12):2731–2738.

BRIEF SUMMARY

Current Knowledge/Study Rationale: Gastroesophageal reflux disease (GERD) is a common disorder characterized by recurring reflux of stomach contents into the esophagus. GERD is exacerbated during sleep and can have a detrimental effect on sleep quality. Yet, the effects of GERD on objectively measured sleep quality remains underexplored.

Study Impact: Using in-laboratory polysomnography, we show that GERD is associated with several impairments in objective sleep quality. Furthermore, this relationship is dependent on body position; the effects of GERD on sleep are more severe in patients who primarily sleep on their right side, and are mostly ameliorated in patients who primarily sleep on their left side. These findings reinforce the need for physicians to recognize the potential for poor sleep quality in patients with GERD.

INTRODUCTION

Gastroesophageal reflux disease (GERD) is a common disorder affecting 18.1%–27.8% of the North American population¹ and accounts for approximately 4% of primary care visits. GERD is characterized by recurring reflux of stomach contents into the esophagus,² causing symptoms of heartburn and chest discomfort.^3,4 Chronic GERD can lead to complications such as esophagitis⁵ and Barrett’s esophagus, which predispose individuals with GERD to esophageal cancer.^6,7

The relationship between sleep and GERD is the subject of current research. During sleep, several physiologic changes occur that prolong acid-contact time in the esophagus and exacerbate GERD symptoms.^8,9 Esophageal peristalsis, which normally clears refluxed contents back into the stomach, is reduced during sleep as a result of a reduction in saliva production and swallowing.^10,11 Furthermore, lying in the recumbent position eliminates the beneficial effects of gravity in keeping refluxed contents in the stomach.^12,13 Finally, reflexes that act to restrict passage of stomach contents into the esophagus and larynx are reduced in sleep, specifically in stage N3 sleep.¹⁴

Evolving evidence suggests that the presence of GERD may have a negative effect on sleep quality.¹⁵ Patients with GERD are at increased risk for self-reported reduced sleep quality^16,17 and are susceptible to consequences of sleep disruption, such as functional impairment and a reduced quality of life.^18–21

Body position during sleep is a well-studied factor affecting reflux. Sleep in the right lateral decubitus position is associated with an increase in esophageal acid exposure compared to left lateral decubitus sleep,^22–25 due to an increase in transient relaxations of the lower esophageal sphincter. Supine sleep is also associated with more frequent reflux events in patients with GERD.^13,25 Sleeping with the head of the bed at an incline has been shown to reduce reflux events, with a combination of incline and left-lateral decubitus sleep being most effective.^26,27 The American Family Physician clinical guidelines recommend a left lateral decubitus sleep position for infant or adolescent patients with GERD,²⁸ but no recommendations are made for adults.^29,30

Despite the present knowledge on the relationship between GERD and sleep, the impact of GERD on objectively assessed parameters of sleep quality remains underexplored. Previous literature examining the link between GERD and sleep quality has primarily relied on self-reported sleep quality questionnaires or involved small sample sizes. Accordingly, the goal of this study was to objectively characterize the relationship between GERD and sleep quality using a cohort of patients who had completed in-laboratory polysomnography. Secondarily, we sought to examine the role of sleep body position in this relationship.

METHODS

Research ethics approval

This study was approved by the local research ethics board for a retrospective analysis of the polysomnographic and clinical data examined in this study.

Study population

Patients who underwent diagnostic overnight in-laboratory polysomnography at the Sunnybrook Health Sciences Centre Sleep Laboratory (Toronto, Canada; ClinicalTrials.gov identifier: NCT03383354) between 2010 and 2017 were included in this study. Participants were given a questionnaire that asked about medical comorbidities and sleep habits during the night of their in-laboratory polysomnography. Medication logs were also collected by a sleep technologist on the night of the in-laboratory polysomnography. The following patients were excluded from analysis: patients who underwent therapeutic in-laboratory polysomnography (eg, continuous or bilevel positive airway pressure titration), those who were less than 18 years of age, or those in whom medication logs or medical comorbidity questionnaires were missing.

In-laboratory polysomnography

As previously described,³¹ participants underwent level 1, technologist-monitored in-laboratory polysomnography (Compumedics Neuroscan, Victoria, Australia), using standard recording and scoring methods.³² Sleep was staged manually and all events were scored by a registered polysomnographic technologist using criteria from the American Academy of Sleep Medicine.³² All studies were interpreted by a certified sleep specialist.

Study design

A participant was considered to have GERD if they both reported GERD on their medical history questionnaire and were also using either a proton-pump inhibitor (PPI) or an H2-antagonist. Controls were those patients who did not report GERD on their medical history questionnaire. Those who reported GERD in the absence of concomitant PPI/H2-antagonist use (ie, nonclinically significant GERD) were excluded from analysis. Our outcomes were the following markers of sleep quality derived from overnight in-laboratory polysomnography: percentage of time spent in each sleep stage (N1, N2, N3, and rapid eye movement [REM] sleep), sleep efficiency (proportion of total time in bed spent asleep), wake after sleep onset (length of periods of wakefulness occurring after sleep onset), sleep onset latency (time from full wakefulness to sleep onset), REM latency (time from sleep onset to REM onset), total sleep time, and arousal index (number of arousals per hour), as previously described.³³

Statistical analyses

Descriptive statistics were computed for the total sample, as well as for patients in the GERD and non-GERD groups. Categorical variables were summarized as frequency counts, normally distributed continuous variables were summarized as means and standard deviations, and nonnormally distributed continuous variables were summarized as medians and interquartile ranges.

For our analyses, we constructed multivariable linear regression models to explore the relationship between the presence of GERD and sleep quality. In the first minimally adjusted model, demographic factors commonly known to independently impact sleep quality, such as age,³³ sex,³³ and body mass index (BMI),^34,35 were included as covariates in our regression analyses. In the second fully adjusted model, medical conditions known to impact sleep quality, such as sleep apnea severity (measured by the apnea-hypopnea index [AHI]),^36–38 periodic limb movements,³⁹ insomnia,⁴⁰ depression,^41–44 fibromyalgia,⁴⁵ and neuropathic pain,^46,47 were included as covariates in addition to age, sex, and BMI.

In our third model, we assessed the influence of sleep position on the relationship between GERD and sleep quality. Interaction terms were computed by multiplying the presence of GERD (assessed as a binary outcome) by the presence of sleeping > 50% of the night on the right or left side (also assessed as binary outcomes). These interaction terms were individually added as independent variables in the fully adjusted model to assess the influence of right- or left-sided sleep.

Prior to modeling, all variables were assessed for multicollinearity (tolerance statistic value < 0.4); if multicollinearity was found, only 1 member of a correlated set of variables was retained in the model. The final model was assessed for any potential violations to linear regression modeling using residual plots to ensure the requirement of normality was met.

Statistical significance was set to P < .05. All data analyses were performed using SPSS (version 26; IBM, Armonk, NY).

RESULTS

Study population

A flowchart of the study population is shown in Figure 1. A total of 7511 polysomnography reports collected between January 2010 and December 2017 were obtained for this study. After removing those with missing questionnaires, therapeutic sleep reports (ie, continuous or bilevel positive airway pressure titrations, split-night studies, adaptive servo-ventilation, and expiratory positive airway pressure), those from patients < 18 years of age, or those from patients who reported GERD without concomitant PPI/H2-antagonist treatment, 3411 patient polysomnography reports (median age = 55 years [interquartile range = 25]; 48% male) were included for analysis. Self-reported GERD with concomitant PPI/H2-antagonist use was reported by 7.2% of patients (244/3411; median age = 61 years [interquartile range 19]; 38% male). Table 1 shows various characteristics of the study population.

Figure 1. Flowchart of the study population.

*Therapeutic studies included continuous or bilevel positive airway pressure titrations, split-night studies, adaptive servo-ventilation, and expiratory positive airway pressure.

Table 1.

Characteristics of study population.

	All Patients (n = 3,411)	GERD (n = 244)	Non-GERD (n = 3,167)
Age in year, median (IQR)	55 (25)	65 (19)	55 (25)
% Male sex	48%	36%	49%
BMI in kg/m2, median (IQR)	27.8 (7.7)	29.5 (8.7)	27.7 (7.7)
Apnea-hypopnea index, median (IQR)	4.2 (13.9)	6.1 (14.9)	4.1 (13.8)
Periodic limb movement index, median (IQR)	0.0 (14.0)	0.7 (21.1)	0.0 (13.5)
Insomnia, n (%)	652 (19.1%)	80 (32.8%)	572 (18.1%)
Depression, n (%)	716 (21.0%)	75 (30.7%)	641 (20.2%)
Fibromyalgia/neuropathic pain, n (%)	81 (2.4%)	17 (7%)	64 (2.0%)

BMI = body mass index, GERD = gastroesophageal reflux disease, IQR = interquartile range.

GERD and sleep parameters

In our first model, age, sex, and BMI were used as covariates (Table 2). The presence of GERD was significantly associated with a 3.7% decrease in sleep efficiency (95% confidence interval [CI]: −6.00 to −1.36, P = .002), 9.1-minute increase in wake after sleep onset (95% CI: 1.07 to 17.10, P = .026), 4.3-minute increase in sleep onset latency (95% CI: 0.29 to 8.39, P = .036), 27.2-minute increase in REM onset latency (95% CI: 15.82 to 38.49, P < .001), 16.8-minute decrease in total sleep time (95% CI: −27.34 to −6.17, P = .002), 1.6% increase in %N3 sleep (95% CI: 0.24 to 2.87, P = .021), and a 1.7% decrease in %REM sleep (95% CI: −2.68 to −0.65, P = .001). There were no significant associations between GERD and %N1 sleep (95% CI: −2.63 to 1.30, P = .51), %N2 sleep (95% CI: −0.91 to 2.66, P = .34), or arousal index (95% CI: −2.66 to 1.60, P = .63).

Table 2.

Linear regression models examining the impact of GERD on sleep quality, while controlling for the impact of various covariates.

	Minimally Adjusted			Fully Adjusted
	β (95% CI)	R2	P	β (95% CI)	R2	P
N1 sleep (%)	−0.67 (−2.63 to 1.30)	.183	.51	−0.37 (−2.09 to 1.34)	.392	.67
N2 sleep (%)	0.88 (−0.91 to 2.66)	.014	.34	0.48 (−1.22 to 2.18)	.118	.58
N3 sleep (%)	1.55 (0.24 to 2.87)	.172	.021*	1.46 (0.15 to 2.77)	.192	.03*
REM sleep (%)	−1.67 (−2.68 to −0.65)	.071	.001*	−1.40 (−2.40 to −0.41)	.132	.006*
Sleep efficiency (%)	−3.67 (−6.00 to −1.36)	.165	.002*	−3.01 (−5.33 to −0.77)	.197	.009*
Wake after sleep onset (minutes)	9.08 (1.07 to 17.10)	.169	.026*	8.77 (0.80 to 16.73)	.191	.031*
Sleep onset latency (minutes)	4.34 (0.29 to 8.39)	.022	.036*	2.81 (−1.23 to 6.85)	.044	.17
REM latency (minutes)	27.15 (15.82 to 38.49)	.023	< .001*	24.43 (13.25 to 35.61)	.061	< .001*
Total sleep time (minutes)	−16.75 (−27.34 to −6.17)	.172	.002*	−13.41 (−23.87 to −2.95)	.205	.012*
Arousal index	−0.53 (−2.66 to 1.60)	.122	.63	0.13 (−1.59 to 1.85)	.438	.88

Minimally adjusted model: covariates include age, sex, BMI. Fully adjusted model: covariates include age, sex, BMI, AHI, periodic limb movements, insomnia, depression, neuropathic pain, and fibromyalgia. *P < .05. CI = confidence interval, REM = rapid eye movement.

In our second model, we accounted for several other covariates that could influence sleep quality, including sleep apnea severity (as assessed by the AHI), depression, insomnia, periodic limb movements, fibromyalgia, and neuropathic pain, in addition to age, sex, and BMI (Table 2). The presence of GERD was significantly associated with a 3.0% decrease in sleep efficiency (95% CI: −5.33 to −0.77, P = .009), 8.8-minute increase in wake after sleep onset (95% CI: 0.80 to 16.73, P = .031), 24.4-minute increase in REM latency (95% CI: 13.25 to 35.61, P < .001), 13.4-minute decrease in total sleep time (95% CI: −23.87 to −2.95, P = .012), 1.5% increase in %N3 sleep (95% CI: 0.15 to 2.77, P = .03), and a 1.4% decrease in %REM sleep (95% CI: −2.40 to −0.41, P = .006). In this model, there were no significant associations between GERD and sleep onset latency (95% CI: −1.23 to 6.85, P = .17), %N1 sleep (95% CI: −2.09 to 1.34, P = .67), %N2 sleep (95% CI: −1.22 to 2.18, P = .58), and arousal index (95% CI: −1.59 to 1.85, P = .88).

Sleep position analysis

Right-sided sleep

In our study population, 747 (21.9%) participants spent > 50% of the night on their right side, and of those, 58 (7.8%) had GERD. Having both GERD and a majority of sleep on the right-side was significantly associated with an 8.6% decrease in sleep efficiency (95% CI: −13.04 to −4.09, P < .001), 27.5-minute increase in wake after sleep onset (95% CI: 11.85–43.06, P = .001), 26.7-minute increase in REM latency (95% CI: 3.21 to 50.22, P = .026), 35.6-minute decrease in total sleep time (95% CI: −56.15 to −15.14, P = .001), 3.5% increase in %N3 sleep (95% CI: 0.88 to 6.02, P = .009), and a 2.1% decrease in %REM sleep (95% CI: −2.68 to −0.65, P = .035) (Table 3).

Table 3.

Linear regression models examining the interaction of GERD and sleep position on sleep quality using a fully adjusted model.

	Right-Sided Sleep			Left-Sided Sleep
	β (95% CI)	R2	P	β (95% CI)	R2	P
N1 sleep (%)	−0.13 (−3.49 to 3.24)	.392	.94	0.45 (−3.16 to 4.06)	.392	.81
N2 sleep (%)	−1.06 (−4.40 to 2.28)	.118	.53	0.02 (−3.56 to 3.60)	.118	.99
N3 sleep (%)	3.45 (0.88 to 6.02)	.193	.009*	−0.21 (−2.97 to 2.55)	.191	.88
REM sleep (%)	−2.10 (−2.68 to −0.65)	.131	.035*	−0.14 (−2.23 to 1.95)	.130	.90
Sleep efficiency (%)	−8.56 (−13.04 to −4.09)	.199	< .001*	−4.01 (−8.81 to 0.79)	.196	.10
Wake after sleep onset (minutes)	27.45 (11.85 to 43.06)	.193	.001*	2.68 (−14.08 to 19.44)	.190	.75
Sleep onset latency (minutes)	5.50 (−2.44 to 13.43)	.044	.17	8.66 (0.16 to 17.15)	.044	.046*
REM latency (minutes)	26.71 (3.21 to 50.22)	.057	.026*	0.70 (−22.52 to 23.92)	.055	.95
Total sleep time (minutes)	−35.64 (−56.15 to −15.14)	.206	.001*	−16.54 (−38.55 to 5.47)	.204	.14
Arousal index	1.54 (−1.83 to 4.91)	.439	.37	0.25 (−3.37 to 3.86)	.438	.89

Fully adjusted model: covariates include age, sex, BMI, AHI, periodic limb movements, insomnia, depression, neuropathic pain, and fibromyalgia. *P < .05. CI = confidence interval, REM = rapid eye movement.

Left-sided sleep

In our study population, 592 (17.4%) participants spent > 50% of the night on their left side, and of those, 51 (8.6%) had GERD. Having both GERD and the majority of sleep on the left-side was significantly associated with an 8.66-minute increase in sleep onset latency (95% CI: 0.16 to 17.15, P = .046). No other changes in objective sleep quality were observed (Table 3).

DISCUSSION

The goal of this study was to objectively assess the impact of GERD on objectively assessed sleep quality using various sleep parameters obtained through in-laboratory polysomnography. On both our minimally and fully adjusted models, there was a significant association between the presence of GERD and a decrease in sleep efficiency, total sleep time, and duration of REM sleep. Furthermore, the presence of GERD was associated with an increase in time awake after sleep onset, REM latency, and duration of N3 sleep. GERD was also associated with an increase in sleep onset latency when controlling for age, sex, and BMI; however, this association was lost when controlling for other medical comorbidities in the fully adjusted model. Moreover, we demonstrated that the association between GERD and sleep quality was more pronounced in patients who spent > 50% of the night on their right-sides. Conversely, the associations between GERD and poorer sleep quality were not seen in patients who spent > 50% of the night on their left side.

We demonstrated that the presence of GERD was significantly associated with a 16.8- and a 13.4-minute decrease in total sleep time in the minimally and fully adjusted regression models, respectively. This is consistent with a large population-based study by Jansson et al that showed a positive association between GERD and self-reported sleeplessness,⁴⁸ which is moderately correlated with and often linked to total sleep time.⁴⁹ Our results show a modest reduction in total sleep time in patients with GERD. Reductions in sleep duration are associated with many adverse health outcomes, such as obesity, hypertension, type II diabetes, and cardiovascular disease, highlighting the importance of detecting and alleviating sleep problems in this patient population.⁵⁰

Our results showed a 3.7% and a 3.0% decrease in sleep efficiency in the minimally and fully adjusted regression models, respectively. We also demonstrated 9.1- and 8.8-minute increases in wake after sleep onset in the minimally and fully adjusted models, respectively. These results are supportive of previous research assessing the relationship between GERD and self-reported sleep quality. Chen et al showed that reflux symptoms were significant risk factors for poor sleep quality.¹⁶ Furthermore, Dickman et al showed that patients who reported more awakenings per night had GERD symptoms that were more frequent and severe.¹⁵

In the present study, GERD was not significantly associated with changes in arousal index, both in the minimally and fully adjusted models. There may be several reasons for this. Prior studies have shown a temporal relationship between reflux events and arousals using concurrent polysomnography/actigraphy and esophageal pH monitoring.^15,51 However, reflux-mediated arousals have been identified to occur more frequently in patients with increasing severity of obstructive sleep apnea (OSA),⁵² suggesting a greater likelihood of associating reflux to arousals when there is a greater baseline level of arousals from OSA.^8,9 Furthermore, there has been conflicting evidence regarding the effect of PPIs on arousals, with studies both showing a reduction⁵³ and showing no effect.⁵⁴ To our knowledge, there have been no large studies reporting an increase in the arousal index in patients with GERD. Thus, the relationship between arousals and GERD remains unproven.⁸ Despite this, we have shown an association between GERD and both sleep efficiency and wake after sleep onset after controlling for several potential confounders, including AHI. This may suggest a possibly greater effect on arousal duration vs the number of arousals, or yet another potential mechanism by which GERD affects sleep quality, independent of arousals. Further research should explore other potential pathophysiological links between GERD and sleep that are not arousal-mediated.

We further analyzed the effects of GERD on sleep architecture. Our results show that GERD was associated with a 1.7% and a 1.4% decrease in REM sleep, with a reciprocal 1.6% and 1.5% increase in N3 sleep, in the minimally and fully adjusted regression models, respectively. Furthermore, we show that GERD was significantly associated with a 27.2- and 24.4-minute increase in latency to REM sleep in the minimally and fully adjusted models, respectively. In support of these findings, 1 previous study showed that PPI treatment led to an increase in REM sleep time, suggesting possible suppressive effects of GERD on REM sleep.⁵⁵ Here we also show that sleeping primarily on the left side is associated with a reduction in the REM latency (ie, reaching REM sleep earlier in the night), further suggesting that ameliorating GERD symptoms can have a positive impact on REM sleep. Future research exploring the physiological basis behind possible suppression of REM sleep by GERD would be beneficial, particularly due to the large increase in REM latency we observe in our GERD sample.

Growing evidence has suggested a link between GERD and obstructive sleep apnea; however, the mechanism behind this link remains controversial. While studies have reported an association between the presence of GERD and increasing OSA severity,^56,57 others have found no such relationship.^9,58–60 Furthermore, a recent meta-analysis of the effect of PPIs on OSA identified no significant effect on the apnea or hypopnea index.⁶¹ Finally, studies suggesting an epidemiological link between GERD and OSA did not control for obesity as a confounder.^62,63 While the relationship between GERD and OSA was not explored in the present study, there was no significant difference in median AHI between the GERD and non-GERD groups in our univariate analyses.

To examine the role of sleep position on the associations between GERD and sleep quality, we stratified patients by their percentage of time spent in right-sided and left-sided sleep. We then studied the interaction between the presence of GERD and sleeping for > 50% of the night on either the right or left side. We show that having both GERD and sleeping for > 50% of the night on the right side was associated with even greater decreases in sleep efficiency, total sleep time, and %REM sleep, as well as a greater increase in wake after sleep onset and %N3 sleep, compared to the total GERD sample. This suggests that there are more severe effects of GERD on sleep in patients who sleep primarily on their right-side. Conversely, in those who both had GERD and slept > 50% of the night on the left-side, detrimental associations with most sleep parameters were ameliorated, with the exception of a greater increase in sleep onset latency compared to the total GERD sample. Overall, this suggests that left-sided sleep may ameliorate most of the negative effects of GERD on sleep quality. These findings confirm the detrimental effects of right-sided sleep on reflux frequency and acid contact time in patients with GERD,^22–25 and further reinforce suggestions for left-sided sleep to prevent adverse sleep outcomes.

New therapies aimed at reducing nocturnal reflux events have focused on maintaining left-sided sleep. A recent trial using a novel sleep positional device that promotes left-sided sleep showed improvements in patient’s nocturnal GERD symptoms.⁶⁴ Our findings reinforce the potential beneficial effects of these innovative therapies on objective sleep quality.

This study has several limitations. First, the presence of GERD was based on self-report on a medical comorbidity questionnaire, which may be subject to recall bias, rather than on objective esophageal pH measurements or endoscopic evaluation. However, GERD is defined and diagnosed clinically based on patient-identified symptoms.^2,4 We further mitigated against false-positive self-reporting by classifying as patients with GERD only those patients who concomitantly reported use of physician-prescribed reflux medications (PPI and/or H2-antagonist). Of note, the nature of this approach does not permit analysis of correlations between objective sleep quality and the severity of GERD; as such, further studies are recommended to determine whether GERD severity based on objective measurements has a differential effect on sleep quality. Secondly, data on medication dosage, duration of use, and frequency of use were not available. Furthermore, we have no data on use of over-the-counter therapies by those who reported GERD without prescribed medication. As such, this study cannot assess treated vs untreated GERD, and this was not an objective of this study. Rather, the use of prescribed medication acts as a metric of clinically significant GERD. Finally, all patient polysomnography reports used in this study were collected from a single site, which may limit generalizability. The strengths of this study include the ability to objectively assess several sleep parameters using polysomnography and the relatively large sample size.

In summary, to our knowledge, this is the largest study to show an association between GERD and objective sleep parameters. We show that the presence of GERD is associated with a decrease in sleep efficiency, wake after sleep onset, total sleep time, and REM sleep, as well as an increase in both REM latency and N3 sleep using objective polysomnography data. We also show that these associations were more prominent during right-sided sleep and were mostly alleviated during left-sided sleep. The results of this study support past research showing the detrimental effects of GERD on self-reported sleep quality.

Based on our prior work on normal polysomnography values in healthy adults,³³ a 3.0% decrease in sleep efficiency corresponds with a change that would be expected after about 15 years of aging, while a 13.4-minute reduction in total sleep time would correspond to approximately 13 years of aging; superimposed on other sleep disorders, the changes we have reported in association with GERD may be significant. Therefore, we recommend that sleep quality be reviewed in all patients diagnosed with GERD. Furthermore, we recommend that further randomized controlled trials be conducted to evaluate the current evidence behind sleep position and nocturnal reflux events, which will help inform future clinical practice guidelines.

It is vitally important to identify and treat sleep problems in patients with GERD. Sleep disruption is directly linked to several detrimental cognitive, neurological, emotional, behavioral, metabolic, cardiovascular, and gastrointestinal consequences.⁶⁵ The presence of nocturnal GERD symptoms also reduces work productivity^18,19 and negatively impacts quality of life.^20,21 These findings reinforce the need for physicians to recognize the potential for poor sleep quality in patients with GERD and take steps to identify and mitigate poor sleep outcomes.

ABBREVIATIONS

AHI

apnea-hypopnea index

BMI

body mass index

CI

confidence interval

GERD

gastroesophageal reflux disease

OSA

obstructive sleep apnea

PPI

proton-pump inhibitor

REM

rapid eye movement

DISCLOSURE STATEMENT

All authors have read and approved the final manuscript. Dr. Mark Boulos’ research program received support from the Mahaffy Family Research Fund. Patrick Gurges was supported by funding from a Branch Out Neurological Foundation summer student award. The authors report no conflicts of interest.