Gastro-oesophageal reflux disease and nutrition

Chapter 3.3
Gastro-oesophageal reflux disease and nutrition

Mark Fox^1,2 and Henriette Heinrich²

¹University Hospitals and University of Nottingham, Nottingham, UK

²University Hospital Zürich, Zürich, Switzerland

3.3.1 Factors involved in causation of reflux disease

Gastro-oesophageal reflux disease (GORD) is a common disorder affecting at least one in 10 of the population on a weekly basis, that is present when the return of gastric contents into the oesophagus causes symptoms or damages the mucosa [1]. Heartburn and acid regurgitation are typical presenting complaints but GORD can be associated with a variety of other problems, including chest pain, chronic cough and lung diseases. The underlying cause of this condition is most often disruption of the ‘reflux barrier’ at the gastro-oesophageal junction. The risk of reflux increases as this disruption becomes more severe, particularly in the presence of a hiatus hernia [2]. Additionally, patients with severe GORD clear the oesophagus less efficiently, leading to prolonged acid exposure and complications such as reflux oesophagitis, peptic stricture and Barrett’s metaplasia (a premalignant condition). Twin studies have shown that inherited factors are responsible for 20–40% of GORD and acquired factors, such as Helicobacter pylori infection, may play a role; however, recent reviews emphasise the importance of lifestyle and dietary factors as a cause of disease [3]. Smokers, workers engaged in strenuous physical activity and individuals with a high body mass reported higher rates of reflux symptoms in epidemiology studies [4,5]. Indeed, the ‘epidemic’ of obesity may be responsible also for the perceived increase in GORD and its complications [6]. However, this is a complex issue because overweight and obese people also tend to eat larger meals and make food choices that increase the risk of reflux.

It is a common belief among patients and doctors that reflux symptoms may be induced or worsened by certain foods and beverages and published guidelines recommend avoiding ‘reflux-inducing foods’ as part of the first-line management of GORD [7,8]. Despite this broad-based agreement, the effects of diet on GI function are hotly debated and the efficacy of dietary management for GORD has not been established.

Meal volume and consistency

Physiology studies have shown that distension of the stomach after meals triggers transient lower oesophageal sphincter relaxations (TLOSRs) that open the reflux barrier to release air swallowed with the meal (belching) [2]. A key difference between patients and healthy individuals is that TLOSRs in GORD patients frequently allow ‘reflux’ not only of air but also gastric acid and semi-digested food, leading to heartburn and regurgitation [9]. Large amounts of food cause more gastric distension and also take a long time to empty from the stomach. Thus larger meal volumes trigger more TLOSRs and lead to more reflux events. On this basis, GORD patients can be advised to avoid large meals and to eat ‘little and often’; however, the clinical benefits of this pragmatic approach have never been tested.

Limited data exist on the impact of meal consistency on GORD. Studies that assessed the effect of meal viscosity or compared the effects of liquid and solid meals have shown no change in the frequency of reflux events or acid exposure in the distal oesophagus [10,11]. However, increasing meal viscosity does appear to suppress ‘volume regurgitation’ and the use of alginate preparations (e.g. Gaviscon) that produce a viscous layer above the meal also reduces reflux and symptoms [12,13]. These effects are useful in clinical practice as regurgitation and also laryngopharyngeal symptoms often persist despite standard acid suppression [2].

Meal composition

In principle, any meal component that delays gastric emptying, stimulates acid secretion, impairs oesophageal function or increases sensitivity of the oesophagus to reflux will worsen the severity of reflux and/or reflux related symptoms [14]. Foods such as chocolate, fried and spicy foods are often mentioned by patients as causing reflux symptoms; however, well-controlled studies reveal little impact of these specific items on objective measurements of acid exposure [15,16]. Further, none of the individual dietary items evaluated was associated with the risk of reflux symptoms in a recent twin study [5]. Thus it seems likely that the effects of food and drink on GORD are most often related to general nutrient composition and not individual ingredients.

The initial findings of a large, cross-sectional study in 951 volunteers suggest that a high-fat diet is an important risk factor for both reflux symptoms and erosive eosophagitis [4]. However, it is difficult to distinguish the effects of fat intake and total energy (i.e. calorie) intake in this work. This was highlighted by the interaction between diet, obesity and reflux such that the effects of fat intake on GORD symptoms became non-significant when adjusted for Body Mass Index [4]. This finding is consistent with other epidemiology and physiology studies that found no consistent effect of fat on TLOSR frequency or acid reflux after a meal when total energy intake is controlled [16–19].

The clinical effects of macronutrient composition and energy intake in GORD were clarified by a study that monitored acid reflux events and symptoms following intake of high-caloric, high-fat (1000 kcal, 50% fat), high-caloric, low-fat (1000 kcal, 25% fat) and low-caloric, low-fat (500 kcal, 25% fat) meals on consecutive days in randomised order [10]. Prolonged, wireless pH monitoring demonstrated that the frequency of reflux events and oesophageal acid exposure was directly related to total energy intake but not to fat content. In contrast, the number of reflux symptoms was 40% higher in the high-fat than the low-fat study day [10]. Thus, similar to its effects on gastric function (see Chapter 1.3), fat does not appear to affect motility but does increase visceral sensitivity to reflux events and so the number and severity of symptoms reported [20,21].

In contrast to fat, there is no evidence that varying the amount of carbohydrate or whole protein in a meal will alter the risk of acid reflux or symptoms. However, it should be noted that aromatic amino acids (e.g. phenylalanine, tryptophan) as well as calcium stimulate gastrin secretion and gastric acid production [22]. Consistent with these data, ingestion of food supplements and test meals containing high concentrations of these micronutrients can cause reflux symptoms even in healthy volunteers [23]. Reflux symptoms are more common also among those who regularly use extra table salt compared with those who never do so, possibly because gastric emptying time increases with osmolality of the meal. Nitrates in the diet mainly derived from the increased use of nitrogenous fertilizers have also been implicated in the aetiology of GORD [4,24]. When saliva, with its high nitrite content derived from the enterosalivary recirculation of dietary nitrate, meets acidic gastric juice, the nitrite is converted to nitrous acid, nitrosative species and nitric oxide. This has been shown to decrease lower oesophageal sphincter (LOS) pressure and increase TLOSR frequency. Moreover, the ‘chemical warfare’ at the reflux barrier produces chemicals that could be carcinogenic [24,25].

Dietary fibre has been linked to a reduced risk of reflux [4,5]. The mechanism of action is not certain but may include increasing the viscosity of gastric contents and slowing the release of nutrients that exacerbate reflux. However, it is still possible that high fibre intake is simply a marker of a relatively low-fat, low-calorie diet that has not been fully accounted for in the analysis. Indeed, not all effects of fibre are beneficial; one study reported increased TLOSR activity after a high-fibre meal triggered by colonic fermentation and distension [26].

Beverages

Citrus fruit juices, carbonated drinks and other acidic beverages are often avoided by GORD patients as they can aggravate reflux symptoms [27]. This may be due to direct stimulation of acid receptors in the oesophageal mucosa; however, repeated exposure to mildly acidic fluid or other irritants may also impair mucosal integrity, producing wide intracellular spaces that are observed in non-erosive reflux disease and may be responsible for an increase in acid sensitivity [28]. For carbonated drinks these effects are compounded by gross distension of the proximal stomach that reduces LOS pressure and causes repeated TLOSRs that can be accompanied by reflux [29].

Coffee causes reflux symptoms in many GORD patients [30] and direct infusion into the oesophagus can cause heartburn [31]; however, the clinical relevance of these observations has not been confirmed by epidemiology studies [32]. Similarly, although caffeine has several effects on gastric motility and secretory function, physiological studies do not show consistent effects of coffee or caffeine on oesophageal motility or reflux [33,34].

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