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BMJ No 7121 Volume 315 Editorial Saturday 6 December 1997
Helicobacter pylori and its interaction with risk factors for chronic diseaseWe are not quite ready to recommend green tea and saki to the exclusion of coffeeSee Paper (abstract only) p 1489In this issue Brenner and colleagues document the effects of lifestyle on Helicobacter pylori infection in 447 patients in a German rural practice (p 1489).(1) They found that the H pylori infection rate appeared to be reduced by alcohol consumption (100 g and over per week), increased by coffee drinking (3 cups and over per day), and non-significantly increased by smoking. In the past, when idiopathic gastric hyperacidity was considered to be the chief cause of dyspeptic symptoms, smoking, coffee, and alcohol were often implicated as exacerbating the condition and advice given to eliminate these habits. Increasingly since 1984, however, when Warren and Marshall hypothesised that campylobacter-like organisms were the cause of peptic ulcer disease,(2) there has been a need to re-evaluate the role of these traditional risk factors. This need has been addressed by Brenner et al with some seemingly unexpected results. There are reasons why alcohol, coffee, and smoking might have little effect on, or even increase, the hostility of the gastric environment to H pylori. The acid gastric pH prevents most organisms from thriving or even surviving in the stomach. H pylori, however, has an electropositive internal milieu; twice the number of basic amino acids, argenine and lysine, as Haemophilus influenzae and Escherichia coli; and powerful urease activity, with the ability to produce both ammonia and factors that inhibit parietal cell acid production.(3) All these attributes make survival of H pylori in the stomach less influenced by the reduction in pH which may accompany coffee, smoking, and alcohol consumption.(4-6) Alcohol and smoking tend to increase the rate of gastric emptying.(4)(7) However, H pylori has at least five different adhesins to attach itself to gastric epithelial cells. These, together with the fact that the surface lipopolysaccharide of H pylori is several orders of magnitude less immunoganic than other enteric bacteria, may allow it to adhere to the gastric mucosal surface and create a quasi "stagnant loop syndrome" despite adequate luminal flow. These functions have been highlighted by the recent complete sequencing of the H pylori gene.(3) One of the remaining questions is why alcohol is effective in the face of this powerful bacterial genetic machinery. Is it the time honoured antiseptic effect of alcohol, to which H pylori has developed no defence? H pylori infection is the most common human chronic bacterial infection, affecting half the population and associated with duodenal and gastric ulceration, chronic active and atrophic gastritis, gastric carcinoma, and mucosa associated lymphoid tissue lymphoma.(8) As well as the risk of cancer, Brenner et al draw attention to the role of H pylori in cardiovascular disease in a fashion similar to Chlamydia pneumoniae.(9) They speculate that the beneficial effect of low alcohol consumption on coronary heart disease may relate to its ability to reduce H pylori infection. A corollary might be that smoking and coffee consumption contribute to the risk of coronary heart disease by increasing susceptibility to H pylori infection. Furthermore, since coffee raises serum cholesterol concentrations unless it is filtered to remove the offending diterpenes,(10) will filtered coffee lacking deterpenes still promote H pylori infection? Should we screen patients at high risk of coronary heart disease for H pylori? If so, can we use the more generally available IgG test requiring simply a serum sample or should a 13C urea breath test be the standard? Finally, will alcohol consumption be advised to help eliminate H pylori? Brenner et al outline the possible positive effect of alcohol and the negative effect of coffee on the elimination of H pylori. H pylori is important because of its association with a broad range of diseases. However, in view of its high prevalence, other factors, including genes and environment, are likely to be pivotal in the pathogenesis of disease. The high prevalence of this bacteria also raises the question of routine screening and, if so, which test to use. In addition, should changes in lifestyle to reduce H pylori infection be encouraged - for example, green tea and saki rather than coffee in Japan? Certainly, these data are the closest we have had to support St Paul's injunction to "take a little wine for thy belly's sake." The emphasis, however, may be on "little" - that is, 1-2 drinks daily. Above this level, despite the continued lower risk of coronary heart disease, the risk of cancer, stroke, and all cause mortality rises.(11,12) Finally, recent publications from the health professionals study of 47,806 men found no increased risk of duodenal ulcer associated with coffee, smoking, or alcohol(13) but a negative association with dietary fibre and vitamin A.(14) We require more studies before we are confident in giving advice on this important and complex topic. David J A Jenkins
Professor of nutritional sciences and
medicine
References
1 Brenner H, Rothenbacher D, Bode G, Adler G.
Relation of smoking and alcohol and coffee consumption to active
Helicobacter pylori infection: cross sectional study.
BMJ 1997;315:1489-2.
2 Warren J R, Marshall B. Unidentified curved bacilli in the
stomach of patients with gastritis and peptic ulceration.
Lancet 1984;i:1311-5.
3 Tomb J-F, White O, Kerlavage A R, Clayton R A, Sutton G G,
Fleischmann R D, et al. The complete genome sequence of the gastric
pathogen Helicobacter pylori. Nature 1997;388:539-47.
4 Endoh K, Leung F W. Effects of smoking and nicotine on the
gastric mucosa: A review of clinical and experimental evidence.
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5 Singer M V, Leffmann C, Eysselein V E, Calden H, Goebell H.
Action of ethanol and some alcoholic beverages on gastric acid
secretion and release of gastrin in humans.
Gastroenterol 1987;93:1247-54.
6 van Deventer G, Kamemoto E, Kuznicki J T, Heckert D C, Schulte
M C. Lower esophageal sphincter pressure, acid secretion, and blood
gastrin after coffee consumption. Dig Dis Sci
1992;37:558-69.
7 Jian R, Cortot A, Ducrot F, Jobin G, Chayvialle J A, Modigliani
R. Effect of ethanol ingestion on postprandial gastric emptying and
secretion, bilipancreatic secretions and duodenal absorption in man.
Dig Dis Sci 1986;31:604-14.
8 Cover T L, Blaser M J. Helicobacter pylori infection, a paradigm
for
9 Patel P, Mendall M A, Carrington D, Strachan D P, Leatham E,
Molineaux N, et al. Association of Helicobacter pylori and Chlamydia
pneumoniae infections with coronary heart disease and cardiovascular
risk factors. BMJ 1995;311:711-4.
10 Urgert R, Meyboom S, Kuilman M, Rexwinkel H, Vissers N M, Klerk
M, et al. Comparison of the effect of cafetiere and filtered coffee on
serum concentration of liver amino transferases and lipids: six month
randomized controlled trial. BMJ 1996;313:1362-6.
11 Boffetta P, Garfinker L. Alcohol drinking and mortality among
men enrolled in an American Cancer Society prospective study.
Epidemiology 1990;1:342-8.
12 Marrot M, Brunner E. Alcohol and cardiovascular disease: the
status of the U shaped curve. BMJ 1991;303:565-8.
13 Aldoori W H, Giovannucci E L, Stampfer M J, Rimm E B, Wing A L,
Willett W C. A prospective study of alcohol, smoking, caffeine, and the
risk of duodenal ulcer in men. Epidemiology
1997;8:420-4.
14 Aldoori W H, Giovannucci E L, Stampfer M J, Rimm E B, Wing A L,
Willett W C. A prospective study of diet and the risk of duodenal ulcer
in men. Am J Epidemiol 1997;145:42-50.
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