Role of Dietary Factors in Gastroesophageal Reflux Disease İsmail Hakkı Kalkan, MD Kırıkkale University Faculty of Medicine Kırıkkale, Turkey Ülkü Dağli, MD Başkent University Faculty of Medicine Ankara, Turkey Various foods are thought to be associated with gastroesophageal reflux disease (GERD) or to aggravate its symptoms. In routine clinical practice, suspected food products are often restricted in the diet. GERD symptoms generally occur during the post-prandial period, indicating that diet is an important factor in the development of symptoms (1). However, there are controversial reports about the foods that aggravate GERD. Although Nebel et al. (2) showed that fried and spiced food products and alcohol precipitate pyrosis most, there was no control group in their study and amount consumed of these food products was not stated, raising questions about the generalizability of the study results. In their epidemiological study in a large population, Ruhr et al. investigated the role of fat-rich diet in erosive esophagitis but they did not find a meaningful relationship (3). On the other hand, Shapiro et al. reported that attacks of reflux were more frequent in individuals who were taking a fat-rich diet (4). Similarly, in their large scale, case-control study, El-Serag et al. documented the relation between the total amount of daily consumed fat and both non-erosive GERD and erosive esophagitis (5). Furthermore, Shapiro et al. showed that a diet rich in cholesterol and fatty acids and a high ratio of fat to daily calorie consumption led to an increased risk of episodes of GERD (4). In a Swedish monozygotic twin study, Zheng et al. found no relation between GERD and the consumption of vegetables, fruits, fish, red meat, rice, pasta, milk, sandwich, potato or grilled food (6). As for the effect of alcohol consumption, in their case control study with more than 40,000 individuals, Nilsson et al. found no association between alcohol intake and GERD symptoms (7). Similarly, in another population-based study, El-Serag et al. found no association between total amount of daily consumed alcohol and either non-erosive or erosive GERD development (5). Consistent with the findings of these large scale population studies, Shapiro et al. showed that alcohol consumption did not increase the risk of GERD episodes (OR:0.26, CI:0.05-1.3) (4). However, there are studies suggesting that smoking may play an aggravating role in GERD pathogenesis although the mechanism or mechanisms underlying this observation have not, yet, been clarified. Various studies have shown sudden decreases in lower esophageal sphincter pressure (LESP) during smoking but these studies, also, determined that LESP returned completely to normal, 5-8 minutes after cessation of smoking (8,9). Several large scale clinical studies have demonstrated the association between smoking and GERD. Nilsson et al. reported that smoking 6 or more cigarettes per day was an independent risk factor for GERD development. Furthermore, they demonstrated that the number of cigarettes smoked daily was directly proportional to the increased risk (7). In their study investigating the association between lifestyle related factors and GERD in monozygotic twins involving more than 25,000 participants, Zheng et al. found an increase in the risk of GERD development in active smokers, 37% in women and 53% in men; this increased risk was, also, shown to be dose-dependent (6). In different population based studies, smoking was detected as a risk factor for GERD development and it was, also, shown to cause more serious symptoms in patients who already have GERD (10,11). Schindlbeck et al. found more reflux episodes in smokers compared to non-smokers, but determined that neither having a history of smoking, nor being an active smoker had an effect on esophageal acid exposure time (12). Zheng et al. showed, as in the case of alcohol consumption, that there was no association between coffee consumption and development of GERD symptoms (6). Nilsson et al. determined that even consumption of more than 7 cups of coffee did not lead to an increased risk of developing GERD symptoms (7). In a case control study, it was documented that coffee consumption did not increase either the duration of post-prandial acid reflux or the number of reflux episodes. Furthermore, coffee consumption did not affect post-prandial LESP in the same study (13). The relation between salt consumption and reflux symptoms has been documented in various studies. Consumption of salted fish or meat twice a week and the addition of extra salt to meals were found to be risk factors for development of reflux symptoms (7). Increased consumption of dietary fiber has been claimed to reduce the risk of reflux-related esophageal adenocarcinoma development (14). Moreover, there is evidence suggesting that a fiber-rich diet is an important protective factor against the development of reflux. In the population based study by Nilsson et al., there was a reduced risk of reflux development in individuals whose dietary fiber intake exceeded 4% of their diet; this risk decreased further, as they increased their fiber consumption (7). Murphy et al., in 1988, reported that chocolate decreased basal LESP and they confirmed, by intra-esophageal pH monitoring, that esophageal acid reflux increased after chocolate consumption (15). However, to date, no clinical study has investigated the association between chocolate and GERD. Apart from chocolate, there are limited data from clinical studies to suggest an association of carbonated soft drinks with reflux symptoms although, in a multivariate analysis, Fass et al. reported that consumption of carbonated soft drinks increased nocturnal reflux symptoms (16). World Digestive Health Day WDHD May 29, 2015 WGO HANDBOOK HEARTBURN: A GLOBAL PERSPECTIVE 19
WDHD-2015-handbook-final
To see the actual publication please follow the link above