| Forces International | SMOKING DOES NOT CAUSE ULCERS OR STOMACH CANCER |
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| Forces International | SMOKING DOES NOT CAUSE ULCERS OR STOMACH CANCER |
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. In a meta-analysis of 753 other published gastric ulcer cases, 64% were HP+. 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" 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%" 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 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 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" 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 ..." Courtesy of Carol Thompson
08/23/93 |
