The study was published online October 31 in Gut.
The researchers point out, however, that this was an observational study, which can’t prove cause and effect.
A strength of the study is its use of data from a large population-based database with complete information on subsequent diagnoses and drug prescriptions, which minimizes selection, information, and recall biases, the researchers say. Use of strict exclusion criteria as well as propensity score adjustment to control for potential confounders and restricting the sample to patients with successful H pylori eradication are other strengths.
In terms of study weaknesses, the researchers lacked information on some risk factors, such as diet, family history, and socioeconomic status. And despite the large sample of more than 63,000 H pylori–infected patients, the small number of gastric cancer cases did not allow for any “meaningful evaluation of the dosage effect and role of different PPIs,” the researchers say.
For a copy of the study go to:
I am so screwed.
The report also reaffirms the clear link between alcohol consumption and liver cancer, and for the first time quantifies the amount at which risk for liver cancer rises. “We now have a little more precision on the alcohol-liver cancer link,” said Hursting. “Getting above three drinks a day seems to dramatically impact the tumorigenic process and increase risk.”
More coffee! Less beer!
Urinary concentration of the benzene metabolite S-phenylmercapturic acid (SPMA) was more than four times greater in hookah smokers and two times greater in people exposed to secondhand hookah smoke, when compared with people who had no exposure. The findings put a damper on enthusiasm for hookah as a safer alternative to cigarettes, as reported online in Cancer Epidemiology, Biomarkers and Prevention.