Open Access
Open Peer Review

This article has Open Peer Review reports available.

How does Open Peer Review work?

Dietary guideline adherence for gastroesophageal reflux disease

  • Ai Kubo1,
  • Gladys Block2,
  • Charles P QuesenberryJr1,
  • Patricia Buffler2 and
  • Douglas A Corley1Email author
BMC Gastroenterology201414:144

DOI: 10.1186/1471-230X-14-144

Received: 13 May 2013

Accepted: 4 August 2014

Published: 14 August 2014

Abstract

Background

Gastroesophageal reflux disease (GERD) is the most common gastrointestinal disease, and the cost of health care and lost productivity due to GERD is extremely high. Recently described side effects of long-term acid suppression have increased the interest in nonpharmacologic methods for alleviating GERD symptoms. We aimed to examine whether GERD patients follow recommended dietary guidelines, and if adherence is associated with the severity and frequency of reflux symptoms.

Methods

We conducted a population-based cross-sectional study within the Kaiser Permanente Northern California population, comparing 317 GERD patients to 182 asymptomatic population controls. All analyses adjusted for smoking and education.

Results

GERD patients, even those with moderate to severe symptoms or frequent symptoms, were as likely to consume tomato products and large portion meals as GERD-free controls and were even more likely to consume soft drinks and tea [odds ratio (OR) = 2.01 95% confidence interval (CI) 1.12-3.61; OR = 2.63 95% CI 1.24-5.59, respectively] and eat fried foods and high fat diet. The only reflux-triggering foods GERD patients were less likely to consume were citrus and alcohol [OR = 0.59; 95% CI: 0.35-0.97 for citrus; OR = 0.41 95% CI 0.19-0.87 for 1 + drink/day of alcohol]. The associations were similar when we excluded users of proton pump inhibitors.

Conclusions

GERD patients consume many putative GERD causing foods as frequently or even more frequently than asymptomatic patients despite reporting symptoms. These findings suggest that, if dietary modification is effective in reducing GERD, substantial opportunities for nonpharmacologic interventions exist for many GERD patients.

Keywords

Gastroesophageal reflux Heartburn Diet

Background

Gastroesophageal reflux disease (GERD) is one of the most common illnesses in the United States. The prevalence of diagnosed GERD cases is estimated to be 13-19% worldwide [1] and about 25% of the Western population suffers from heartburn or acid regurgitation at least once per month; 12% have symptoms at least weekly and 5% experience heartburn daily [2]. Symptoms associated with GERD include heartburn, acid regurgitation, dysphagia (difficulty in swallowing), and chest pain, as well as extraesophageal manifestations such as nausea, chronic cough, asthma, and hoarseness [3, 4].

The financial burden of disease from GERD is high; much of this is for anti-acid medications. The cost of health care and lost productivity due to GERD is estimated at over $24 billion annually in the US alone [57], 60% of which is used for medication [8]. The annual average medical costs and services for patients with GERD may be twice that of the non-GERD population due to additional outpatient visits, hospitalizations, emergency department utilization, and pharmacy costs [5]. In addition, the quality of life in GERD patients is also compromised: the impact of GERD on quality of life measures is similar to that of other chronic diseases such as diabetes, heart failure, or ischemic heart disease [9].

Newly recognized potential adverse effects of acid suppression have heightened the interest in nonpharmacologic approaches for GERD treatment in persons with nonerosive GERD. Although results conflict somewhat between studies, acid suppression has been recently associated with decreased absorption of dietary calcium and calcium supplements [10, 11], an increased risk of hip fractures [1214], food borne infections, and an increased risk of clostridium difficile infection [15, 16]. These findings led to a recent modification in the labeling of proton pump inhibitors to include concerns about an increased risk of hip fracture and a search for methods to decrease GERD patients’ reliance on pharmacologic methods of acid suppression.

Dietary modification is a proposed first-line therapy for patients with GERD. The National Institutes of Health and the American College of Gastroenterology recommend that patients with GERD reduce their intakes of total fat, chocolate, alcohol, citrus and tomato products, coffee, tea, and large meals, and implement other lifestyle changes such as stopping smoking and weight reduction [17, 18]. However, no previous population-based study has evaluated what proportions of GERD patients actually follow these dietary guidelines. Therefore, we evaluated, within a large community-based population, the associations between a GERD diagnosis, reflux symptoms and dietary intake. We hypothesized that patients with more severe or frequent symptoms were less likely to adhere to the dietary modification recommendations.

Methods

Study population

We performed an analysis of a case–control study of Barrett’s esophagus; the study recruited members of the Kaiser Permanente, Northern California (KPNC) population, an integrated health services delivery organization, between 2002 and 2005. The KPNC membership contains approximately 3.3 million persons whose demographics closely approximate the underlying census population of Northern California [17, 18]. The study included Barrett’s esophagus patients as cases and two sex and age-matched control groups: GERD patients and population controls. The details of this original study were described previously in detail [19]. The present analysis contrasts the GERD and population control groups. The study and analyses were approved by the KPNC institutional review board and were performed in accordance with the Declaration of Helsinki. Informed consent was obtained.

GERD patients

GERD patients consisted of 317 eligible KPNC members who were selected from among all individuals with a physician-assigned GERD diagnosis (e.g. ICD-9 codes 530.11 reflux esophagitis and 530.81 gastroesophageal reflux) who also had a prescription for at least 90 days supply of anti-secretory medications and no diagnosis of Barrett’s esophagus (any visible columnar metaplasia) from an esophagogastroduodenoscopy close to the index date. Endoscopy and pathology reports were manually reviewed. The validity of identifying GERD patients using encounter and pharmacy databases was previously evaluated in a 100,000 member managed care organization [20]. All patients in the current study also ultimately received questionnaires regarding GERD symptoms and actual medication use.

Exposure to anti-secretory medications utilized a pharmacy database with information on prescription type, frequency of dispensing, and number of pills dispensed. We defined anti-secretory medications (e.g., histamine-2 receptor antagonists (H2 blocker) or proton pump inhibitors (PPI)) using data from the year prior to control selection (the reference dates).

Population controls

Population controls were randomly selected from among members of the entire KPNC membership at the time the Barrett’s esophagus cases were identified. Individuals with Barrett's esophagus were excluded. For the current study, we also excluded population controls who, upon interview, reported heartburn or acid regurgitation once a month or more.

Measurements of dietary intake

All study subjects completed: an in-person interview (most commonly at the subject’s home) of GERD symptoms, medication use, medical history, diet, tobacco use and alcohol use; phlebotomy; and anthropometric measurements.

We assessed dietary intake using a validated 110-item food frequency questionnaire (FFQ) [2124]. This questionnaire estimates average daily nutrient intake based on questions about frequency and portion size of a given food and usual eating habits for the year before the index date [25]. Dietary data were translated to daily intakes of specific nutrients using NutritionQuest (Berkeley, CA), and the raw data were used to estimate weekly consumption of particular food items. We excluded subjects with over 20 missing food items or with extremely high (>6000 kcal/day) or low (<400 kcal/day) total daily energy intakes.

We evaluated the associations between consumption of commonly discussed “reflux-triggering” dietary factors based on recommendations from the American College of Gastroenterology [17], National Institute of Health [18], and food items that have been studied in previous clinical research of GERD [26, 27]. Among those food items, data were available in our questionnaire for: coffee, tea, soft drinks, alcohol (total, wine, beer, and liquor), citrus, tomato products, total fat, fried foods, and large portion meals. “Soft drink” consumption was used as the proxy for “carbonated drinks” in the data; the questionnaire did not include diet sodas. Coffee and tea consumption did not distinguish between caffeinated or decaffeinated types, but excluded herbal tea. The food items and nutrients included total fat; fried foods (e.g., French fries, fried chicken, fish, and doughnuts); tomato products (e.g., fresh tomatoes, canned tomatoes, and tomato juice); and citrus (fruits and juice). The measurement units were mostly “servings per week”, except for fat (grams/day), coffee and tea (cups/day) and alcohol (drinks/day). The term ‘drink’ for alcohol was defined as: wine (7-8 oz), beer (12 ounces), liquor (one shot). Portion size reporting was facilitated by pictures depicting small (1/4 cup), medium (1/2 cup), large (1 cup), and extra-large (2 cups) servings. In this study, each person was scored on the proportion of foods that were reported as large or extra large. For instance, if a person indicated that half of what he/she consumed was in large or extra-large portions (1–2 cups), the person was considered to consume 50% of the meal in large portion. On the other hand, if a person always consumed small or medium portion meals (1/4-1/2cup), the person was categorized to consume 0% of the meal in large portion.

We constructed tertile categories for items with a normal distribution, such as fat intake and portion size. For most other food items, the distributions were skewed with large number of subjects consuming none of the item. For those items, intakes were categorized as follows: zero intake (referent), low intake, and high intake. Tertile cutoff points were chosen a priori (prior to analysis) to create relatively even distributions of population controls.

Measurements of GERD symptoms

GERD symptoms were defined as either heartburn (a burning pain or discomfort behind the breastbone) or acid regurgitation (a bitter or sour-tasting fluid coming up into the throat or mouth) using a validated questionnaire [28]. Symptom severity was recorded as either mild (could be ignored), moderate (could not be ignored, but didn’t affect lifestyle), severe (could not be ignored and did affect lifestyle), or very severe (markedly affected lifestyle). Symptom frequency was coded as: less than once a month, less than once a week (but more than once a month), once or more a week, or daily. For the analysis of severity, we compared individuals who had moderate to severe symptoms (with at least monthly frequency) to asymptomatic population controls, and excluded individuals with mild severity (N = 75). For frequency analysis, we compared two categories (GERD symptoms greater than several times a week; more than once a month to once a week) to asymptomatic population controls.

Statistical analysis

We evaluated whether GERD was associated with the intake of certain beverages, nutrients, or food items using unconditional logistic regression to calculate odds ratios (ORs) as an estimate of the relative risk with GERD status as an independent variable and dietary factors as the dependent variable [29]. We evaluated the following additional variables as potential confounders: race/ethnicity (classified as white vs. non-white due to small sample sizes in the race/ethnic subgroups), smoking (ever vs. never and current vs. never), body mass index (BMI, kg/m2), medical center, recent alcohol use (number of drinks per week), aspirin or nonsteroidal anti-inflammatory drug (NSAID) use, a comorbidity index (the DxCg score) [30, 31], education, income, serum Helicobacter Pylori (H. Pylori) antibody status, and energy consumption (kcal/day). Confounders were included in the final model if their inclusion altered the odds ratio by >10% [29]. We evaluated for interaction by gender, race, long-term (2 + years) vitamin supplement use, NSAIDs use, H. pylori, or regular use (at least once a week) of GERD medication (antacid, H2 blocker, or PPI) using cross product terms in the logistic regression model and stratified analysis. All analyses were performed using STATA statistical software (College Station, TX).

Results

Study population

Of the 316 GERD patients and 317 population controls from the original study, dietary data were available for 622 subjects (98% of interviewed subjects). Exclusion of six subjects with extreme values of caloric intake or ≥6 missing values on the food questionnaire and 126 population controls who reported acid regurgitation or heartburn more than once per month provided 308 GERD patients and 182 GERD-free population controls (Tables 1 and 2). The proportions of smokers and individuals who consumed large or extra-large portion sizes were similar between the groups.
Table 1

Characteristics of study groups

 

GERD Group (physician-assigned)

Population controls without GERD1

 

Number or Mean (% or standard deviation)

Number or Mean (% or standard deviation)

Number of subjects

308

182

Age (years)

  

 20-39

11 (4)

9 (5)

 40-59

111 (36)

63 (35)

 60-79

186 (60)

110 (60)

Race/Ethnicity

  

 White

247 (80)

154 (84)

 Black

20 (6)

10 (5)

 Hispanic

20 (6)

7 (4)

 Asian

8 (3)

5 (3)

 Others/Missing/Unknown

13 (4)

6 (3)

 Male

211 (69)

123 (68)

GERD symptoms

  

Severity2

  

 Severe & very severe

124 (40)

--

 Moderate

109 (35)

--

 Mild

75 (25)

--

Frequency

  

 Daily

78 (25)

--

 Several times a week

89 (29)

--

 Once month – once a week

91 (30)

--

 Less than once a month

50 (16)

--

 BMI

28.9 (5.2)

28.3 (5.5)

Smoking

  

 Current smoker

30 (10)

19 (10)

 Portion size

  

 % extra large or large

27.9 (16.3)

28.8 (17.2)

1Self-reported heartburn or acid reflux <1/month.

2Severity with at least monthly or less than once a month frequency.

Table 2

Mean intake between physician-assigned GERD patients and population controls with no or little reported symptoms

 

GERD Group (physician-assigned)

Population controls without GERD1

 

Number or Mean (% or standard deviation)

Number or Mean (% or standard deviation)

Number of subjects

308

182

Beverages

Soft drinks (servings/week)

3.2 (6.7)

2.1 (5.4)

Coffee (cups/day)

8.7 (10.4)

9.9 (9.9)

Tea (cups/day)

4.1 (7.4)

2.9 (5.2)

Alcohol (drinks/day)

  

 Non drinker

109 (35)

41 (23)

 <=1/day

128 (42)

91 (50)

 >1 & <2/day

29 (9)

31 (17)

 > = 2/day

42 (14)

19 (10)

Nutrients/food items

Calories (kcal/day)

1828 (770)

1797 (776)

Total fat (g/day)

77.9 (37.9)

77.5 (39.6)

Fried foods (fried potatoes, chickens, fish, doughnuts-servings/week)

0.7 (1.5)

0.6 (1.1)

Tomato products (servings/week)

1.5 (2.8)

1.5 (2.3)

Citrus (citrus fruits + juice- servings/week)

2.3 (3.8)

2.8 (3.5)

1Self-reported heartburn or acid reflux <1/month.

Beverage choice and gastroesophageal reflux symptoms

Patients with moderate to severe GERD symptoms were over twice as likely as GERD-free controls to consume soft drinks, adjusting for smoking and education [OR = 2.11, 95% CI:1.16-3.84] (Table 3); there was no association with GERD frequency (Table 4).
Table 3

Association between moderate to severe GERD symptoms and intake of certain food items, comparing patients with moderate to severe symptoms to GERD-free population controls

Severity

Moderate to severe GERD symptoms

 

N

OR1

95% CI

 

Case

Control

   

Softdrinks2

     

 None

70

86

1.0 (ref)

  

 >1/week

84

57

1.86

1.16

2.97

Coffee3

     

 None

92

55

1.0 (ref)

  

 2+/day

72

44

0.89

0.52

1.51

Tea4

     

 None

44

61

1.0 (ref)

  

 1+/day

51

41

1.86

1.02

3.40

Alcohol5

     

 None

116

57

1.0 (ref)

  

 <1 drink/day

74

70

0.56

0.35

0.90

 1+ drink/day

48

70

0.83

0.46

1.48

Wine

     

 None

72

86

1.0 (ref)

  

 1 + glass/day

49

94

0.74

0.45

1.23

Beer

     

 None

53

99

1.0 (ref)

  

 1 + drink/day

29

101

0.54

0.31

0.96

Liquor

     

 None

31

126

1.0 (ref)

  

 1 + shot/day

36

99

1.50

0.85

2.66

Citrus

     

 <2servings/week

106

125

1.0 (ref)

  

 2+/week

59

133

0.62

0.41

0.94

Tomatoes

     

 None

55

176

1.0 (ref)

  

 1+/week

48

144

1.10

0.70

1.75

Fried foods

     

 <1serving/week

42

189

1.0 (ref)

  

 1+

49

143

1.52

0.94

2.45

Total fat

     

 1st Tertile (<57 g/day)

67

88

1.0 (ref)

  

 2nd Tertile

50

76

1.67

1.03

2.71

 3rd T >90 g/day

66

52

1.77

1.07

2.93

Portion size

     

 <20% large portion

58

83

1.0 (ref)

  

 40 +%

55

56

1.30

0.78

2.19

1Models are adjusted for smoking and education.

2Not including diet soda.

3Includes both caffeinated and decaffeinated types.

4Excludes herbal tea.

5Excludes individuals who are occasional drinkers (more than once a year but less than one drink/week).

Table 4

Association between the frequency of GERD symptoms and intake of certain food items (GERD patients vs. no-GERD population controls)

Frequency

> = Several times/week

Once a month to once a week

 

N

OR1

95% CI

N

OR1

95% CI

 

Case

Control

   

Case

Control

   

Softdrinks2

          

 None

46

50

1.0 (ref)

  

46

50

1.0 (ref)

  

 >1/week

97

70

1.54

0.93

2.58

31

47

0.75

0.41

1.39

Coffee3

          

 None

56

37

1.0 (ref)

  

56

37

1.0 (ref)

  

 2+/day

83

53

0.98

0.56

1.72

47

27

1.25

0.65

2.39

Tea4

          

 None

29

36

1.0 (ref)

  

29

36

1.0 (ref)

  

 1+/day

57

50

1.54

0.81

2.93

20

37

0.70

0.34

1.47

Alcohol5

          

 None

72

31

1.0 (ref)

  

72

31

1.0 (ref)

  

 <1 drink/day

91

82

0.51

0.30

0.85

56

36

0.69

0.38

1.26

 1+ drink/day

53

82

0.68

0.35

1.30

30

37

0.88

0.42

1.85

Wine

          

 None

48

51

   

48

51

1.0 (ref)

  

 1 + glass/day

56

111

0.64

0.37

1.10

36

47

1.02

0.54

1.91

Beer

          

 None

31

57

1.0 (ref)

  

31

57

1.0 (ref)

  

 1 + drink/day

35

120

0.52

0.28

0.96

28

59

0.89

0.46

1.71

Liquor

          

 None

19

74

1.0 (ref)

  

19

74

1.0 (ref)

  

 1 + shot/day

43

120

1.44

0.77

2.70

17

70

1.07

0.51

2.26

Citrus

          

 <2servings/week

63

78

1.0 (ref)

  

63

78

1.0 (ref)

  

 2+/week

69

118

0.62

0.40

0.98

55

132

1.03

0.62

1.69

Tomatoes

          

 None

28

113

1.0 (ref)

  

28

113

1.0 (ref)

  

 1+/week

55

171

1.35

0.80

2.28

31

91

1.44

0.80

2.59

Fried foods

          

 <1serving/week

20

121

   

20

121

1.0 (ref)

  

 1+

59

167

2.10

1.19

3.70

29

93

1.87

1.00

3.52

Total fat

          

 1st Tertile (<57 g/day)

48

57

1.0 (ref)

  

48

57

1.0 (ref)

  

 2nd Tertile

88

67

1.57

0.94

2.62

40

38

1.27

0.70

2.31

 3rd T >90 g/day

71

70

1.69

0.98

2.91

44

40

1.89

1.03

3.47

Portion size

          

 <20% large portion

33

52

1.0 (ref)

  

33

52

1.0 (ref)

  

 40 +%

61

71

1.23

0.75

2.02

33

43

1.01

0.57

1.77

1Models are adjusted for smoking and education.

2Not including diet soda.

3Includes both caffeinated and decaffeinated types.

4Excludes herbal tea.

5Excludes individuals who are occasional drinkers (more than once a year but less than one drink/week).

Patients with moderate to severe GERD symptoms were also more likely to consume one or more cups of regular tea a day compared to asymptomatic controls [OR = 1.86; 95% CI:1.16-2.97 for severe GERD]. There was no association between GERD symptom severity or frequency and coffee consumption.

GERD patients with severe or frequent symptoms were less likely to consume beer, and there was also an inverse association between GERD symptom severity and general alcohol drinking, especially light drinking. For instance, patients with moderate to severe symptoms were almost half as likely to drink beer as those without GERD [OR = 0.54 95% CI 0.31-0.96]. Similarly, patients with frequent GERD symptoms (>1/week) were half as likely to drink beer [OR = 0.52 95% CI: 0.28-0.96]. There were non-significant, though positive association between GERD symptom severity and frequency and liquor drinking: individuals with severe GERD symptoms were 50% more likely to drink liquor compared to those without GERD [OR = 1.50 95% CI: 0.85-2.66].

Food, total fat, portion size and gastroesophageal reflux symptoms

Patients with severe or frequent GERD symptoms were less likely to consume citrus fruits compared to asymptomatic controls [OR = 0.62; 95% CI: 0.41-0.94; OR = 0.62; 95% CI: 0.40-0.98, respectively]. On the other hand, there was no association between the severity or frequency of GERD symptoms and consumption of tomato products, another acidic food which GERD patients are recommended to avoid (Tables 3 and 4).

Individuals with severe symptoms had higher total fat consumptions than those without GERD [OR = 1.77 95% CI: 1.07-2.93 for highest tertile; OR = 1.67 95% CI: 1.03-2.71 for second tertile]. Similar associations were observed for frequency of GERD symptoms and total fat. In addition, individuals with frequent symptoms were twice as likely to consume fried foods [OR = 2.10; 95% CI: 1.19-3.70 for most frequent; OR = 1.87 95% CI: 1.00-3.52 for monthly-weekly frequency]. There was no association between the severity or frequency of GERD symptoms and large portion sizes.

Supplementary analyses

Composite severity and frequency GERD and diet

To evaluate the dietary habits of individuals with severe and frequent GERD symptoms, we created a composite variable including those with moderate to severe symptoms with at least weekly frequency and compared with asymptomatic controls. Most of the individuals who were in the moderate to severe category overlapped with this composite category (120/124 = 97%), and the results were similar to those presented in Table 3, though the associations strengthened slightly. For instance, individuals with severe and frequent symptoms were twice as likely as controls to consume soft drinks or tea [OR = 1.98 95% CI: 1.18-3.31; OR = 2.16 95% CI: 1.15-4.03, respectively].

Effect modification

The association between soft drink consumption and GERD severity was stronger among women [OR = 5.71 95% CI 1.75-18.66] than among men [OR = 1.55 95% CI: 0.75-3.23].

Analysis of potential confounding

There was no evidence of strong confounding by age, gender, ethnicity, BMI, NSAIDS, alcohol use, income, total energy, facility of diagnosis, income, co-morbidity score, long-term vitamin supplement use, or serum H. pylori antibody status. A fully adjusted model for citrus intake vs. moderate to severe GERD symptoms (containing all these factors plus education and smoking), for example, produced effect estimates [OR = 0.56; 95% CI: 0.29-0.77] similar to a model that contained only education and smoking [OR = 0.62; 95% CI: 0.41-0.94]. The results were similar for other dietary variables.

Discussion

The current study, to our knowledge, is the first population or community-based study to assess whether patients with GERD adhere to dietary guidelines that are often recommended as a part of non-pharmacological, lifestyle modification to reduce their symptoms [17, 18]. Patients with severe or frequent GERD symptoms were less likely to consume citrus and beer and more likely to consume tea, soft drinks, total fat, and possibly liquor. There was no association between portion size, tomato products, coffee and GERD severity or frequency.

Our study extends the existing knowledge regarding the relationship between GERD symptoms and dietary intake. First, our data demonstrate that patients with more severe or frequent reflux symptoms are less likely to consume citrus. Citrus and other acidic foods such as tomatoes are often considered reflux-triggering. A previous clinical study reported that acid-sensitive patients were sensitive to intraesophageal infusion of orange or tomato juice, even when the pH of juice was adjusted to neutral [32], suggesting that some other component in citrus or tomato beside acidity may affect the symptoms. We cannot assess from our data whether the patients in our study avoided citrus (but not tomato products) because they actually worsened their symptoms or because of perceived stronger recommendations to avoid citrus than tomato products.

Our results suggest that individuals with severe GERD symptoms are less likely to drink beer but more likely to drink liquor. Alcohol ingestion is thought to induce GERD by reducing lower esophageal sphincter pressure, increasing acid secretion through gastrin stimulation, decreasing esophageal motility and impairing gastric emptying [3336]. Multiple differences exist between beverage types including alcohol content (lower in beer), volume (higher per serving for beer), and carbonation (present in beer but not liquor). These differences may partially explain the alcohol choices found in GERD patients, although we cannot exclude confounding by other factors, since liquor drinkers may differ from beer drinkers in many ways.

Patients with moderate to severe GERD symptoms were more likely to drink soft drinks than controls. Soft drinks, often carbonated, may result in a very short decline in intra-esophageal pH and transient reduction in lower esophageal sphincter basal pressure [37]. A recent small clinical experiment demonstrated that in healthy individuals, ingestion of carbonated water, caffeinated cola, or caffeine-free cola reduced lower esophageal sphincter pressure compared with tap water ingestion [38]. A multicenter, longitudinal, cohort study of the cardiovascular consequences of sleep-disordered breathing reported that carbonated soft drink consumption was a major predictor of nocturnal heartburn [39]. Our data suggests that, despite the recommendation to avoid soda, GERD patients do not avoid its consumption.

This study has potential limitations. First, cross-sectional studies cannot establish cause and effect [29]. The inverse associations, such as the avoidance of citrus among GERD subjects, could be because such foods cause GERD symptoms (so the subject avoids them), because patients adhere to the dietary guidelines even if avoidance is not completely ineffective, or even conceivably because the absence of such foods causes GERD (and the reason the person has GERD is because they don’t consume them), although the latter possibility seems less likely for the foods studied. In contrast, the positive association between soda consumption and GERD symptoms, for example, could be either from soft drinks causing the greater GERD symptoms or, alternatively, patients actually drinking soda to relieve their GERD symptoms, despite the reported adverse mechanistic associations. However, if the association is true (GERD patients drink more soft drinks than controls and soft drinks worsen symptoms), then it may indicate that GERD patients may benefit from enhanced dietary modification. Second, the GERD patients evaluated, by study definition, had a physician-assigned diagnosis of GERD and had previously received anti-secretory medications. This population may represent patients with more severe GERD symptoms than a general population sample; however, it also represents patients who, if medications have potential for harm, may benefit most from nonpharmacologic treatments (if they are effective). Third, some of the dietary information obtained for this study was not complete. For instance, we did not have information on types of coffee (decaffeinated or regular).

Strengths of the present study include its community-based design, random sampling of patients from the population base (rather than convenience sampling of clinic-based patients), use of a validated food frequency questionnaire and a validated GERD questionnaires for symptom frequency and intensity, in person interviews for GERD symptoms, the availability of high quality interview and laboratory data for multiple confounders, and the review of pertinent medical records. In addition, we used a well characterized population of GERD patients confirmed by both self-report and a physician diagnosis. The combination of these features provides a high quality evaluation of the associations within the limits of an observational study. Subjects came from a diverse KPNC membership base that closely approximates the region’s census demographics, and the results can likely be generalized to similar large populations.

Conclusions

In summary, to our knowledge, this is the first large, community-based U.S. population to evaluate whether GERD patients adhere to the dietary guidelines commonly recommended for GERD patients. We found that while GERD patients, consistent with dietary recommendations, are less likely to consume citrus and certain types of alcohol, they were more likely to consume soft drinks, tea, and fatty foods than asymptomatic controls. The results suggest that GERD patients do avoid some, but not all, of the foods commonly thought to worsen GERD symptoms. Given the prevalence of GERD symptoms and the emergence of possible adverse effects of long-term gastric acid inhibition, more studies, particularly randomized clinical trials on the effectiveness of dietary modification, are needed to better understand the role of nonpharmacologic approaches, such as dietary modification, in the treatment of GERD.

Declarations

Funding

Supported by National Institutes of Health grants R01 DK63616 and K08 DK02697.

Authors’ Affiliations

(1)
Kaiser Permanente Division of Research, University of California, San Francisco, 2000 Broadway
(2)
University of California, Berkeley; School of Public Health

References

  1. Dent J, El-Serag HB, Wallander MA, Johansson S: Epidemiology of gastro-oesophageal reflux disease: a systematic review. Gut. 2005, 54 (5): 710-717.View ArticlePubMedPubMed CentralGoogle Scholar
  2. Moayyedi P, Axon AT: Review article: gastro-oesophageal reflux disease–the extent of the problem. Aliment Pharmacol Ther. 2005, 22 (Suppl 1): 11-19.View ArticlePubMedGoogle Scholar
  3. Lippmann QK, Crockett SD, Dellon ES, Shaheen NJ: Quality of life in GERD and Barrett’s esophagus is related to gender and manifestation of disease. Am J Gastroenterol. 2009, 104 (11): 2695-2703.View ArticlePubMedPubMed CentralGoogle Scholar
  4. Fennerty MB, Castell D, Fendrick AM, Halpern M, Johnson D, Kahrilas PJ, Leiberman D, Richter JE, Sampliner RE: The diagnosis and treatment of gastroesophageal reflux disease in a managed care environment, Suggested disease management guidelines. Arch Intern Med. 1996, 156 (5): 477-484.View ArticlePubMedGoogle Scholar
  5. Brook RA, Wahlqvist P, Kleinman NL, Wallander MA, Campbell SM, Smeeding JE: Cost of gastro-oesophageal reflux disease to the employer: a perspective from the United States. Aliment Pharmacol Ther. 2007, 26 (6): 889-898.View ArticlePubMedGoogle Scholar
  6. Sandler RS, Everhart JE, Donowitz M, Adams E, Cronin K, Goodman C, Gemmen E, Shah S, Avdic A, Rubin R: The burden of selected digestive diseases in the United States. Gastroenterology. 2002, 122 (5): 1500-1511.View ArticlePubMedGoogle Scholar
  7. The Burden of Gastrointestinal Diseases. Edited by: Association AG. 2001, Bethesda, MD: American Gastroenterological Association
  8. Richter JE: Gastrooesophageal reflux disease. Best Pract Res Clin Gastroenterol. 2007, 21 (4): 609-631.View ArticlePubMedGoogle Scholar
  9. Sjoland H, Wiklund I, Caidahl K, Haglid M, Westberg S, Herlitz J: Improvement in quality of life and exercise capacity after coronary bypass surgery. Arch Intern Med. 1996, 156 (3): 265-271.View ArticlePubMedGoogle Scholar
  10. O’Connell MB, Madden DM, Murray AM, Heaney RP, Kerzner LJ: Effects of proton pump inhibitors on calcium carbonate absorption in women: a randomized crossover trial. Am J Med. 2005, 118 (7): 778-781.View ArticlePubMedGoogle Scholar
  11. Graziani G, Como G, Badalamenti S, Finazzi S, Malesci A, Gallieni M, Brancaccio D, Ponticelli C: Effect of gastric acid secretion on intestinal phosphate and calcium absorption in normal subjects. Nephrol Dial Transplant. 1995, 10 (8): 1376-1380.PubMedGoogle Scholar
  12. Corley D, Kubo A, Zhao W, Quesenberry C: Proton pump inhibitors and histamine-2 receptor antagonists are associated with hip fractures among at-risk patients. Gastroenterology. 2010, Epub ahead of printGoogle Scholar
  13. Yang YX, Lewis JD, Epstein S, Metz DC: Long-term proton pump inhibitor therapy and risk of hip fracture. JAMA. 2006, 296 (24): 2947-2953.View ArticlePubMedGoogle Scholar
  14. Targownik LE, Lix LM, Metge CJ, Prior HJ, Leung S, Leslie WD: Use of proton pump inhibitors and risk of osteoporosis-related fractures. CMAJ. 2008, 179 (4): 319-326.View ArticlePubMedPubMed CentralGoogle Scholar
  15. Aseeri M, Schroeder T, Kramer J, Zackula R: Gastric acid suppression by proton pump inhibitors as a risk factor for clostridium difficile-associated diarrhea in hospitalized patients. Am J Gastroenterol. 2008, 103 (9): 2308-2313.View ArticlePubMedGoogle Scholar
  16. Dial S, Alrasadi K, Manoukian C, Huang A, Menzies D: Risk of Clostridium difficile diarrhea among hospital inpatients prescribed proton pump inhibitors: cohort and case–control studies. CMAJ. 2004, 171 (1): 33-38.View ArticlePubMedPubMed CentralGoogle Scholar
  17. DeVault KR, Castell DO: Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Am J Gastroenterol. 2005, 100 (1): 190-200.View ArticlePubMedGoogle Scholar
  18. Heartburn, Gastroesophageal Reflux (GER), and Gastroesophageal Reflux Disease (GERD). http://digestive.niddk.nih.gov/ddiseases/pubs/gerd/,
  19. Corley DA, Kubo A, Levin TR, Block G, Habel L, Zhao W, Leighton P, Quesenberry C, Rumore GJ, Buffler PA: Abdominal obesity and body mass index as risk factors for Barrett’s esophagus. Gastroenterology. 2007, 133 (1): 34-41. quiz 311View ArticlePubMedGoogle Scholar
  20. Ofman JJ, Ryu S, Borenstein J, Kania S, Lee J, Grogg A, Farup C, Weingarten S: Identifying patients with gastroesophageal reflux disease in a managed care organization. Am J Health Syst Pharm. 2001, 58 (17): 1607-1613.PubMedGoogle Scholar
  21. Block G, Hartman AM: Issues in reproducibility and validity of dietary studies. Am J Clin Nutr. 1989, 50 (5 Suppl): 1133-1138. discussion 1231–1135PubMedGoogle Scholar
  22. Block G, Hartman AM, Dresser CM, Carroll MD, Gannon J, Gardner L: A data-based approach to diet questionnaire design and testing. Am J Epidemiol. 1986, 124 (3): 453-469.PubMedGoogle Scholar
  23. Block G, Thompson FE, Hartman AM, Larkin FA, Guire KE: Comparison of two dietary questionnaires validated against multiple dietary records collected during a 1-year period. J Am Diet Assoc. 1992, 92 (6): 686-693.PubMedGoogle Scholar
  24. Block G, Woods M, Potosky A, Clifford C: Validation of a self-administered diet history questionnaire using multiple diet records. J Clin Epidemiol. 1990, 43 (12): 1327-1335.View ArticlePubMedGoogle Scholar
  25. Sobell J, Block G, Koslowe P, Tobin J, Andres R: Validation of a retrospective questionnaire assessing diet 10–15 years ago. Am J Epidemiol. 1989, 130 (1): 173-187.PubMedGoogle Scholar
  26. Festi D, Scaioli E, Baldi F, Vestito A, Pasqui F, Di Biase AR, Colecchia A: Body weight, lifestyle, dietary habits and gastroesophageal reflux disease. World J Gastroenterol. 2009, 15 (14): 1690-1701.View ArticlePubMedPubMed CentralGoogle Scholar
  27. Kaltenbach T, Crockett S, Gerson LB: Are lifestyle measures effective in patients with gastroesophageal reflux disease? an evidence-based approach. Arch Intern Med. 2006, 166 (9): 965-971.View ArticlePubMedGoogle Scholar
  28. Locke GR, Talley NJ, Weaver AL, Zinsmeister AR: A new questionnaire for gastroesophageal reflux disease. Mayo Clin Proc. 1994, 69 (6): 539-547.View ArticlePubMedGoogle Scholar
  29. Rothman K, Greenland S: Modern Epidemiology. 1998, Philadelphia, PA: Lippincott Williams & Wilkins, 2Google Scholar
  30. Zhao Y, Ash A, Ellis R, Ayanian J, Pope GC, Bowen B, Weyuker L: Predicting pharmacy costs and other medical costs using diagnoses and drug claims. Med Care. 2005, 43 (1): 34-43.PubMedGoogle Scholar
  31. Zhao Y, Ash A, Haughton J, McMillan B: Identifying future high cost cases: through predictive modeling. Dis Manage Health Outcomes. 2003, 11 (6): 389-397.View ArticleGoogle Scholar
  32. Price SF, Smithson KW, Castell DO: Food sensitivity in reflux esophagitis. Gastroenterology. 1978, 75 (2): 240-243.PubMedGoogle Scholar
  33. Keshavarzian A, Rizk G, Urban G, Willson C: Ethanol-induced esophageal motor disorder: development of an animal model. Alcohol Clin Exp Res. 1990, 14 (1): 76-81.View ArticlePubMedGoogle Scholar
  34. Bujanda L: The effects of alcohol consumption upon the gastrointestinal tract. Am J Gastroenterol. 2000, 95 (12): 3374-3382.View ArticlePubMedGoogle Scholar
  35. Boekema PJ, Samsom M, van Berge Henegouwen GP, Smout AJ: Coffee and gastrointestinal function: facts and fiction. a review. Scand J Gastroenterol Suppl. 1999, 230: 35-39.PubMedGoogle Scholar
  36. Cohen S: Pathogenesis of coffee-induced gastrointestinal symptoms. N Engl J Med. 1980, 303 (3): 122-124.View ArticlePubMedGoogle Scholar
  37. Johnson T, Gerson L, Hershcovici T, Stave C, Fass R: Systematic review: the effects of carbonated beverages on gastro-oesophageal reflux disease. Aliment Pharmacol Ther. 2010, 31 (6): 607-614.View ArticlePubMedGoogle Scholar
  38. Hamoui N, Lord RV, Hagen JA, Theisen J, Demeester TR, Crookes PF: Response of the lower esophageal sphincter to gastric distention by carbonated beverages. J Gastrointest Surg. 2006, 10 (6): 870-877.View ArticlePubMedGoogle Scholar
  39. Fass R, Quan SF, O’Connor GT, Ervin A, Iber C: Predictors of heartburn during sleep in a large prospective cohort study. Chest. 2005, 127 (5): 1658-1666.View ArticlePubMedGoogle Scholar
  40. Pre-publication history

    1. The pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1471-230X/14/144/prepub

Copyright

© Kubo et al.; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited.

Advertisement