Fact Sheet 6
Author: Eurosciences Communication in co-operation with the Institute for Arteriosclerosis Research, University of Münster, Germany
From an increasing number of publications, it is becoming more and more evident, that the quality of dietary fat influences physiology and pathophysiology of the gastrointestinal tract. The main focus of these studies has been the effect of different dietary fatty acids on gastric acid secretion and gallstone formation. Diseases of the stomach and in particular gallstones are very common in western industrialised countries, e.g. the prevalence of gallstone disease is up to 38% in Europe and North America (4).
Gastric acid secretion
In 1886, in what was probably the first study to investigate the influence of dietary fat on gastric function, Ewald and Boas observed that the addition of olive oil to a test meal suppressed gastric acid secretion (6). Since then, numerous studies have confirmed, that the presence of fat in different segments of the intestinal tract inhibits gastric acid secretion. In most of these studies olive oil was used as a source of dietary fat. The intraduodenal presence of olive oil reduces gastric acid secretion in dogs (11), rats (20) and humans (18, 23). However, until recently it was unknown, whether this effect was also verifiable for other dietary fats, or if it was a specific feature of olive oil or monounsaturated fatty acids. In 1997, Serrano et al. compared the effects of diets rich in monounsaturated fatty acids (olive oil) with diets rich in polyunsaturated fatty acids (sunflower oil) on gastric acid secretion. They were able to show, that "a 30-day period of diets containing olive oil [ ...] resulted in attenuated gastric acid secretion in response to a liquid meal when compared with those containing sunflower oil" (22). Rhee et al. (20) also investigated the mechanical aspects of this suppressive action of oleic acid. They were able to show in rats, that the inhibitory effect of oleic acid on gastric acid secretion is mediated by a peptidic hormone released into the blood when the duodenal mucosa comes into contact with this fatty acid.
These findings consistently indicate that the consumption of olive oil reduces gastric acid secretion. This effect might be beneficial with regard to diseases such as gastric or duodenal ulcers, where the attenuation of gastric acid secretion is a key therapeutic goal.
There are numerous investigations into the relationship between diet and the formation of gallstones. Unfortunately, in some of these studies (9, 10, 15, 17, 19, 21, 25), the dietary fatty acid composition has not been determined, so these studies do not allow an evaluation of the relationship between gallstones and dietary fatty acids. Furthermore, wide variations in study design, methods of diet assessment or diagnosis of gallstone disease make a comparison of the studies on this topic rather difficult.
One of the first investigations describing a relationship between dietary fat and gallstone disease was a case-control study by Linos and colleagues in 1989. In their study they found that "from all the dietary factors the only one that showed a positive statistically significant (p<0.05) association was consumption of animal fat [ ...] . Interestingly high consumption of olive oil had a negative (i.e. protective) association with the disease" (12). Recently Misciagna and colleagues observed in a population-based case-control study that among other factors, saturated fats were a risk factor for gallstone formation while dietary monounsaturated fatty acids were inversely associated with this disease (14). In a prospective study, Gilat et al. observed a higher intake of energy, carbohydrates, fibre and unsaturated fatty acids in Arabs who had a low incidence of gallstones compared to Jews with a higher incidence of the disease (7). However, they concluded that "it cannot be determined which, if any, of these dietary differences is related to the lower frequency of gallstones". Further evidence of an association between the quality of dietary fat and gallstone formation is provided by a finding from the Nurses Health Study, where the authors observed an inverse association between the intake of vegetable fat and the incidence of gallstones (13). On the other hand, these authors did not observe a significant association between the disease and polyunsaturated or monounsaturated fatty acid intakes. Bravo and colleagues showed, that both dietary monounsaturated and polyunsaturated fatty acids increase the biliary excretion of cholesterol in rats (3). This was accompanied by an increased cholesterol saturation of the bile in the animals fed the polyunsaturated fatty acids, but not in those fed the monounsaturated fatty acids. The authors concluded, that this "may have implications for the risk of the development of cholesterol gallstone disease" (3).
These findings are in agreement with two studies conducted in hamsters, where saturated fatty acids were found to intensify gallstone formation while monounsaturated and polyunsaturated fatty acids caused a reduction (5, 8). Although in two other studies an association between dietary fat and gallstones could not be found (16, 24), and one of these even observed a higher intake of monounsaturated fatty acids in patients with gallstones (16), the general consensus from the studies conducted so far is that a high intake of saturated fatty acids appears to be a risk factor for gallstone formation, while the intake of monounsaturated fatty such as olive oil, and possibly also polyunsaturated fatty acids, might protect against gallstone formation. On the other hand there are still some open questions, e.g. why some investigators did not observe a protective effect of monounsaturated fatty acids while others did, and what the implications of dietary fatty acids in the aetiology of gallstone formation are. Thus, further investigation is needed to clarify these points.
From the existing studies on the relationship between dietary fat intake and physiology and pathophysiology of the gastrointestinal tract, there is evidence, that a high intake of monounsaturated fatty acids exerts beneficial effects on the gastrointestinal tract by reducing gastric acid secretion and preventing gallstone disease. The impact of the dietary fat composition on other gastrointestinal diseases, e.g. reflux oesophagitis or constipation, has not been evaluated thoroughly. There are, however, some studies, which suggest further favourable effects of diets rich in monounsaturated fatty acids. Barltrop and Oppe observed in infants, that olive oil is more quantitatively absorbed than butterfat (2). Ballesta and colleagues were able to show, that in dogs olive oil improves the digestibility and metabolic utilisation of dietary protein (1). Furthermore, initial studies on the effect of olive oil or oleic acid with regard to gastrointestinal motility and gastric emptying, show that oleic acid-rich meals delay gastric emptying compared with saturated fatty acid-rich meals, therefore supporting the reservoir function of the stomach (27). Spiller et al. (26) described an accelerated colonic transit when oleic acid was added to test meals. However, they did not compare oleic acid with other fatty acids, so it remains to be proven if this effect is true for fat in general or if it is a specific feature of monounsaturated fatty acids.
In conclusion, although many questions are still open, there is a body of evidence that the consumption of olive oil has beneficial effects on different metabolic functions of the gastrointestinal tract.
1. Ballesta MC, Martinez-Victoria E, Manas M, Mataix FJ, Seiquer I, Huertas JH: Protein digestibility in dog. Effect of the quantity and quality of dietary fat (virgin olive oil and sunflower oil). Nahrung 35: 161-167 (1991).
2. Barltrop D, Oppe TE: Absorption of fat and calcium by low birthweight infants from milks containing butterfat and olive oil. Arch Dis Child 48: 496-501 (1973).
3. Bravo E, Flora L, Cantafora A, De Luca V, Tripodi M, Avella M, Botham KM: The influence of dietary saturated and unsaturated fat on hepatic cholesterol metabolism and the biliary excretion of chylomicron cholesterol in the rat. Biochim Biophys Acta 1390: 134-148 (1998).
4. Brett M, Barker DJP: The World Distribution of Gallstones. Int J Epidemiol 5: 335-341 (1976).
5. Cohen BI, Mosbach EH, Ayyad N, Miki S, McSherry CK: Dietary fat and fatty acids modulate cholesterol cholelithiasis in the hamster. Lipids 27: 526-532 (1992).
6. Edwald CA, Boas J: Beiträge zur Physiologie und Pathologie der Verdauung. Virchows Arch Path Anat Physiol Klin Med 104: 271-305 (1886).
7. Gilat T, Horwitz C, Halpern Z, Bar Itzhak A, Feldman C: Gallstones and diet in Tel Aviv and Gaza. Am J Clin Nutr 41: 336-342 (1985).
8. Jonnalagadda SS, Trautwein EA, Hayes KC: Dietary fats rich in saturated fatty acids (12:0, 14:0, and 16:0) enhance gallstone formation relative to monounsaturated fat (18:1) in cholesterol-fed hamsters. Lipids 30: 415-424 (1995).
9. Jorgensen T, Jorgensen M: Gallstones and diet in a Danish population. Scand J Gastroenterol 24: 821-826 (1989).
10. Kato I, Nomura A, Stemmermann GN, Chyou PH: Prospective study of clinical gallbladder disease and its association with obesity, physical activity, and other factors. Dig Dis Sci 37: 784-790 (1992).
11. Kihl BO, Boden G, Landor JH: Bile-fat relationships in gastric secretory inhibition and bile flow stimulation. Surgery 81: 386-391 (1976).
12. Linos AD, Daras V, Linos DA, Kekis V, Tsoukas MM, Golematis V: Dietary and other risk factors in the aetiology of cholelithiasis: a case control study. HPB Surgery 1: 221-227 (1989).
13. Maclure KM, Hayes KC, Colditz GA, Stampfer MJ, Willet WC: Dietary predictors of symptom-associated gallstones in middle-aged women. Am J Clin Nutr 52: 16-22 (1990).
14. Misciagna G, Centonze S, Leoci C, Cisternino AM, Ceo R, Trevisan M: Diet, physical activity, and gallstones - a population-based, case-control study in southern italy. Am J Clin Nutr 69: 120-126 (1999).
15. Moermann CJ, Smeets FWM, Kromhout D: Dietary risk factors for clinically diagnosed gallstones in middle-aged men. Ann Epidemiol 4: 248-254 (1994).
16. Ortega RM, Fernandez-Azuela M, Encinas-Sotillos A, Andres P, Lopez-Sobaler AM: Differences in diet and food habits between patients with gallstones and controls. J Am Coll Nutr 16: 88-95 (1997).
17. Pastides H, Tzonou A, Trichopoulos D, Katsouyanni K, Trichopoulou A, Kefalogiannis N, Manousos O: A case-control study of the relationship between smoking, diet, and gallbladder disease. Arch Intern Med 150: 1409-1412 (1990).
18. Petersen F, Olsen O, Jepsen LV, Christiansen J: Fat and gastric acid secretion. Digestion 52: 43-46 (1992).
19. Pixley F, Mann J: Dietary factors in the aetiology of gall stones: a case-control study. Gut 29: 1511-1515 (1988).
20. Rhee JC, Chang TM, Lee KY, Jo YH, Chey WY: Mechanism of oleic acid-induced inhibition of gastric acid secretion in rats. Am J Physiol 260: G564-G570 (1991).
21. Sarles H, Gerolami A, Cros RC: Diet and cholesterol gallstones. Digestion 17: 121-127 (1978).
22. Serrano P, Yago MD, Manas M, Calpena R, Mataix J, Martinez-Victoria E: Influence of type of dietary fat (olive and sunflower oil) upon gastric acid secretion and release of gastrin, somatostatin, and peptide yy in man. Dig Dis Sci 42: 626-633 (1997).
23. Shiraori K, Watanabe SI, Takeuchi T: Intestinal fat digestion plays a significant role in fat-induced suppression of gastric acid secretion and gastrin release in the rat. Dig Dis Sci 38: 2267-2272 (1993).
24. Sichieri R, Everhart JE, Roth H: A prospective study of hospitalisation with gallstone disease among women: role of dietary factors, fasting period, and dieting. Am J Public Health 81: 880-884 (1991).
25. Smith DA, Gee MI: A dietary survey to determine the relationship between diet and cholelithiasis. Am J Clin Nutr 32: 1519-1526 (1979).
26. Spiller RC, Brown ML, Phillips SF: Decreased fluid tolerance, accelerated transit, and abnormal motility of the human colon induced by oleic acid. Gastroenterology 91: 100-107 (1986).
27. Thomsen C, Rasmussen O, Lousen T, Holst JH, Fenselau S, Schrezenmeir J, Hermansen K: Differential effects of saturated and monounsaturated fatty acids on postprandial lipemia and incretin responses in healthy subjects. Am J Clin Nutr 69: 1135-1143 (1999).