Forces
Smoking Does Not Cause Ulcers Or Stomach Cancer

Forces International

Back to The evidence

SMOKING DOES NOT CAUSE ULCERS OR STOMACH CANCER

 

Return to FORCES International main page

Back to main page

GASTRIC ULCER:  According to an editorial in the New England Journal of Medicine, "We now recognize three major causes of peptic ulcer disease: Helicobacter pylori infection, the use of nonsteroidal anti-inflammatory drugs (NSAIDs), and pathologic hypersecretory states such as the Zollinger-Ellison syndrome... H. pylori infection is the most common known cause of peptic ulcer and accounts for the majority of cases. NSAIDs are the second most common cause and are responsible for the majority of cases not caused by H. pylori infection."(DY Graham. Treatment of peptic ulcers caused by Helicobacter pylori. NEJM 1993;328(5):349-350).
 

Out of 115 consecutive gastric ulcer patients, 61% were HP positive, including 30% who also used NSAIDs. Of 44 HP negatives, 66% used NSAIDs, 5% had malignant GUs, and 30% were of unknown cause. Only 11% of total GUs were of unknown cause. (TJ Borody, S Brandl et al. Helicobacter pylori negative gastric ulcer. Am J Gastroenterol 1992;87(10):1403-1406).
 

In a meta-analysis of 753 other published gastric ulcer cases, 64% were HP+. (G Borsch. In: Otterjan R, Schmitt W, eds. Aktuelle Gastroenterologie, Campylobacter pylori. Berlin, Heidelberg, New York: Springer 1988:101-115).
 

HP infection can persist for decades, and causes continuous low-grade inflammation. But clinical trials "have consistently shown that ulcer disease due to H. pylori can be cured." The role of acid is mainly "that of a con- contributor to the consequences of H. pylori infection, and it is not usually a dominant factor" (Graham). 
 

"The evidence that H. pylori is a pathogen and not just a common commensurreal is by now overwhelming and includes data from experimental challenges, treatment studies, and animal studies." "H. pylori infection is present throughout the world. In developed countries such as the United States, few infections occur during childhood but the incidence of infection is about 0.5%-1.0% per year; ~50% of 60-year-old adults are infected. Among Afro-Americans, Hispanics, and native Americans in the United States, the incidence early in life appears to be substantially higher. Infection clusters in families and is associated with low socioeconomic status, independent of ethnicity. In developing countries, most persons are infected with H. pylori by the age of 10 years"(MJ Blaser. Helicobacter pylori: Its role in disease. Clin Infect Dis 1992;15:386-393).
 

Before HP, smokers' excess risks were attributed to smoking. Although smoking is known to be associated with lower socioeconomic status, they didn't admit this fact. But uninfected smokers are no more likely to have an ulcer than non-smokers, and "smokers who took NSAIDs were no more likely to have an ulcer than smokers who denied taking NSAIDs, 38% versus 43%"(DF Martin, E Montgomery et al. Campylobacter pylori, NSAIDs and smoking: Risk factors for peptic ulcer disease. Am J Gastroenterol 1989;84(10):1268-1272).
 

DUODENAL ULCER: "Longitudinal studies have shown that the presence of chronic superficial gastritis is associated with a 13-fold increase in the risk of duodenal ulceration over a ten-year period" (Blaser). About 95% of duodenal ulcers are caused by HP infection, an even higher percentage than gastric ulcers (TJ Borody, LL George et al. Smoking does not contribute to duodenal ulcer relapse. Am J Gastroenterol 1992;87(10):1390-1393). When the infection was completely eradicated, 197 patients had no recurrences in 1 to 6 years, regardless of smoking status. Only the most unreasonable anti-smoker could be unhappy with such dramatic success. 
 

STOMACH CANCER: "Another consequence of chronic superficial gastritis is that it may ultimately progress to chronic atrophic gastritis; there is evidence- dence that this process requires decades, on average. This is a significant observation because chronic atrophic gastritis is a well-recognized risk factor for adenocarcinoma of the stomach."
 

"This infection also has many epidemiological characteristics in common with gastric cancer, including association with low socioeconomic status: higher rates among Afro-Americans, Hispanics, and native Americans as well as in developing countries; and family clustering. Therefore, an association between H. pylori and gastric cancer is at least biologically plausible."
 

"In the past year, four studies, three of which were prospective in design (nested case-control studies), showed significant associations between H. pylori infection and adenocarcinoma of the stomach, with odds ratios ranging from 2.7 to 6.0....It may be hypothesized that the long-term decline in the incidence of gastric cancer that has been observed in the developed countries of North America and Europe may be due in part to a progressive delay in the acquisition of an important environmental initiator or promoter of this condition, H. pylori" (Blaser). 
 

International gastric cancer rates correlate with rates of HP seropositivity (Eurogast Study Group. Lancet 1993 May 29;341(8857):1359-1361). "Our findings are consistent with an approximately six-fold increased risk of gastric cancer in populations with 100% H pylori infection compared with populations that have no infection."
 

ESOPHAGITIS: In 24-hour ambulatory monitoring of 184 subjects, statistical analysis showed that "(c) cigarette smoking was not correlated with esophagi's but was significantly associated with increased lower esophageal sphincter pressure...and (d) smoking was also not associated with increased acid contact time or increased frequency of reflex episodes"(SG Sonata, TG School et al. The importance of hiatus hernia in reflex esophagi's compared with lower esophageal sphincter pressure or smoking. J Clin Gastroenterol 1991;13(16):628-643). This, of course, is contrary to antismoker propaganda-  , which even the principal author of this study once uncritically repeated in a 1984 article in NEJM. 
 

The claim of increased gastric acidity in smokers is also spurious. "We found that heavy smokers secreted significantly higher amounts of gastric bicarbonate than non-smokers...In fact, a strong linear correlation was found between gastric bicarbonate secretion and both basal and maximal acid output ..."(PL Dal Santo, F Vianello et al. (letter) Smoking habit on gastric bicarbonate secretion in patients with duodenal ulcer. J Clin Gastroenterol 1991;13 (5):590).
 

Courtesy of Carol Thompson 08/23/93
Smokers' Rights Action Group
P.O. Box 259575
Madison, WI 53725-9575
Phone: 608-249-4568


FORCES is supported solely by the efforts of the readers. Please become a member or donate what you can.



Contact Info
Forces Contacts
Media Contacts
Advertisers
Links To Archived Categories

The Evidence
Inside Forces
About Forces
Research
Writers
Book case