COFFEE AND GASTROINTESTINAL FUNCTION
The scientific evidence for effects of coffee consumption on the gastrointestinal system was last reviewed in 1999 (1). The authors of this review critically evaluated the evidence for effects of coffee on upper gastrointestinal symptoms such as dyspepsia and heartburn and aspects of gastrointestinal function such as gastric motor function, small intestinal secretion and transit, gallbladder contractility and colonic motor activity. They concluded that “Coffee promotes gastro-oesophageal reflux, but is not associated with dyspepsia. Coffee stimulates gallbladder contraction and colonic motor activity”.
The vast majority of cases of dyspepsia or indigestion have no obvious explanation and are referred to as non-ulcer (or functional) dyspepsia. A few cases of dyspepsia are caused by ulcers of the stomach or duodenum. In a study from the USA, there was no difference between the habitual consumption of coffee in duodenal ulcer patients, functional dyspepsia patients or controls (2). Surprisingly, dyspepsia symptoms were more prevalent in the 55 functional dyspepsia patients than in the 58 patients with duodenal ulcers. A cross-sectional study of 592 Australian blood donors which excluded peptic ulcer patients was unable to find any significant association between coffee consumption and dyspepsia (3). Similarly, a large cross-sectional study of 8,407 adults in the United Kingdom found no association between coffee consumption and dyspepsia (4). There are few data on the relationship between caffeine intake and dyspepsia although one study was unable to show any association between caffeine intake and indigestion in 4,558 Australians after adjusting for confounders (5). The anecdotal observation that conduction roasting by comparison with conventional roasting of coffee beans reduces dyspeptic symptoms in coffee sensitive individuals was not confirmed by a recent intervention trial (6). It can be concluded that coffee has no effects on dyspepsia in most individuals.
Gastro-oesophageal reflux (GOR) refers to the backward flow of acid from the stomach up into the oesophagus. People experience heartburn, also known as acid indigestion, when excessive amounts of acid reflux into the oesophagus. Gastro-oesophageal reflux disease (GORD) is the name given to this condition. In GORD patients oesophageal sensitivities to coffee, orange juice, and tomato drink are all significantly increased suggesting that the effects of these beverages are not specific to coffee (7). In 394 patients with heartburn, neither the acidity nor the osmotic strength of coffee was associated with reported heartburn (8). In 16 healthy subjects, ambulatory oesophageal pH-monitoring was used to show that coffee provokes more GOR than water (9). This effect was reduced but not eliminated by decaffeinated coffee suggesting that other components of coffee are involved. Improvement of GOR symptoms in 17 GORD patients by decaffeinated coffee was confirmed by a second study (10). A study of 20 subjects with coffee sensitivity looked at the effects of three different coffees on GOR and found that a European coffee provoked more GOR than a USA coffee (11). A more recent study compared the effects of coffee and water on GOR by ambulatory oesophageal pH-monitoring in 7 GORD patients and 8 healthy controls but no effects were found (12). The authors concluded that “The results of this study, therefore, do not support a general advice to patients with reflux symptoms to refrain from drinking coffee or to favour decaffeinated coffee”. Although this advice would seem to contradict the conclusions of the review (1) and the results of the above studies, it was pointed out that the effects of coffee on GOR observed were not large enough to be clinically significant.
There are several recent studies on effects of coffee on gastrointestinal function. The suggestion that changes in gastric motor and sensory function might mediate any effects of coffee on dyspepsia is not supported by the findings that coffee has no effects on the function of the proximal stomach (13) or gastric emptying (14). The belief that coffee promotes diarrhoea is not consistent with the observation that coffee has no effect on oro-caecal transit time (14). By contrast, the finding that regular or decaffeinated coffee increase cholecystokinin levels and decrease gallbladder volume may explain why gallstone patients claim that coffee provokes biliary pain (15).
Two studies on associations between coffee consumption and risk of peptic ulcer disease in the pre-Helicobacter pylori era failed to show any statistically significant associations (16, 17). A recent cohort study of 2,416 Danish adults showed that the major risk factors for peptic ulcer disease are tobacco smoking and Helicobacter pylori infection but coffee consumption was not a risk factor (18). A large USA cohort study of 47,806 men identified 138 new cases of duodenal ulcer in six years (19). There were no significant associations between duodenal ulcer risk and consumption of caffeine, caffeine- containing beverages or decaffeinated coffee.
Hence, there is no evidence that coffee consumption increases the risk of developing peptic (gastric plus duodenal) ulcer or duodenal ulcer alone.
The debate into whether coffee has any significant impact on gastroesophageal reflux disease continues. In 2006 a review paper was published that evaluated several lifestyle factors, including diet, to provide more clarity on this subject (20) . With regard to coffee and caffeine consumption, the authors still found the reported data to be conflicting with the relationship between caffeine or coffee and gastroesophageal reflux disease remaining unclear. However, they do state that 'There is insufficient evidence to support the routine recommendation that patients with gastroesophageal reflux disease avoid such beverages.
References:
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12. Boekema, P.J. et al. European Journal of Gastroenterology, 11, 1271-1276, 1999.
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14. Boekema, P.J. et al. European Journal of Clinical Investigation, 30, 129-134, 2000.
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16. Friedman, G.D. et al. New England Journal, 290, 469-473, 1974.
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19. Aldoori, W.H. et al. Epidemiology, 8, 420-424, 1997.20. Kaltenbach,T. et al, Archives of Internal Medicine, 166, 2006.
