Bacterium linked to one cancer may deter another
BY MITZI BAKER
Research suggests a lack of H. pylori leads to a fivefold increase in risk of one type of esophagus cancer, almost twice the increased risk from smoking.
To kill the bug or not to kill the bug.
That is, with apologies to Shakespeare, the question surrounding whether the human body benefits from having the infection caused by the bacterium, Helicobacter pylori or H. pylori. On the one hand, the bug has been fingered as a culprit in causing stomach cancer and ulcers. On the other, there is mounting evidence that it may protect some people from cancer of the esophagus.
Add to the debate the latest study from medical school researchers that gives greater credibility to the argument that the bug has its virtues: the study, which is to be published in the March 1 issue of the Journal of Infectious Diseases, shows that people who are not infected have a greater risk of developing a type of cancer called esophageal adenocarcinoma than those who have the infection.
"It is truly a bad bug, but what we show is that it is not a bad bug in all people," said lead author Catherine de Martel, MD. "We will have to define better who should be treated for this infection and when."
De Martel is currently completing her doctoral studies in the lab of the study's senior author, Julie Parsonnet, MD, associate professor of medicine in the Division of Infectious Diseases and Geographic Medicine and the Division of Epidemiology.
While more than half of people throughout the world harbor H. pylori, the rate of H. pylori infection is steadily declining in so-called First World nations. What's so intriguing is that at the same time, the incidence of esophageal adenocarcinoma has been increasing dramatically in these developed countries.
Although previous studies have suggested a link between esophageal carcinoma and the absence of H. pylori infection, the relationship between these two phenomena remains controversial.
De Martel's study adds more credibility to the debate, as it is by far the largest and most rigorous. Her team took advantage of a Kaiser Permanente health check-up that collected health information and blood samples from nearly 129,000 Northern California members from 1964 through 1969. A total of 52 cases of esophageal adenocarcinoma had developed in this group by 2000.
The team looked at antibodies to H. pylori in the original blood samples for each case of cancer. For comparison, they identified three control samples from other check-up participants who were the same age, gender and race and had had their blood drawn in the same year and at the same Kaiser location.
In people less than 50 years old at the time of the original check-up, those without H. pylori infection were five times as likely as those who did carry the bacteria to develop esophageal adenocarcinoma during the follow-up period, which lasted from five to 35 years. The researchers found that the increased risk was independent of cigarette smoking or being overweight, two strong risk factors for the development of this type of cancer.
The findings do not prove a cause-and-effect relationship between the bacterium and this type of esophageal cancer, said de Martel, but this is the strongest evidence yet.
And there's a logical explanation for why such a causal connection would make sense: By decreasing gastric acid secretion in some people, H. pylori infection may prevent the acid reflux into the esophagus that can precede esophageal adenocarcinoma, de Martel said.
Although she is reluctant to speculate too much about the implications of her work, de Martel emphasized that it underscores the intricate balance we maintain with microbes.
"Humans have been living with this bug for hundreds of thousands of years, so it is probably not just a bad bug," she said. She postulates that, in addition to protection against esophageal cancers, it may do other good things as well. For example, she mentioned that in young children H. pylori has been associated with less diarrheal diseases.
But the fact that it causes ulcers and stomach cancer is not in doubt and has to be strongly considered, even though only a small proportion of individuals will suffer from these outcomes.
"We need to know more," she said, "to find the right balance of who should be treated for H. pylori infections and who should not."
Other Stanford researchers who contributed to this study are epidemiology graduate student Augusto Llosa, medical student Sara Farr and Gary Friedman, PhD, a consulting professor of health research and policy who also works at the research division of Kaiser Permanente Medical Care Program in Oakland.
The study was funded by the Baxter International Foundation.
