Padding the Death Toll From Stomach Cancer

Relationship between Tobacco, cagA and vacA i1 Virulence Factors and Bacterial Load in Patients Infected by Helicobacter pylori.
Santibáñez M, Aguirre E, Belda S, Aragones N, Saez J, Rodríguez JC, Galiana A, Sola-Vera J, Ruiz-García M, Paz-Zulueta M, Sarabia-Lavín R, Brotons A, López-Girona E, Pérez E, Sillero C, Royo G.
PLoS One 2015 Mar 20;10(3):e0120444.

The academic editor of this paper evidently lacked expertise on the socioeconomics of H. pylori infection, because this group put one over on her.

In 155 patients, mostly with ulcers, they claim that “There was a statistically significant association between cagA positive status and active smoking at endoscope (ORadjusted 4.52; 95%CI 1.28–15.98). Table 2 shows the associations between vacA i1 region status and active smoking at endoscope. vacA i1 positivity is associated with smoking, though this association does not attain statistical significance (crude OR 2.69; 95% CI 0.92–7.92).”

This disgraceful effort attempts to overcome the inconvenient fact that the vast majority of people infected by H pylori were infected when they were young children, before they even began smoking. This makes it difficult to blame smoking, but anti-smokers are undaunted. They proceed by ignoring the fact that H. pylori infection is also more common among the less wealthy classes, who are also more likely to become smokers later on, along with the implication that they are presumably more frequently exposed to more strains H. pylori, and more often.

Upon this foundation of evasion they erected an edifice of speculation: “The higher bile salt reflux and gastric bile salt and the lower concentrations of vitamin C in gastric juices [12,13] in smokers in comparison with non-smokers support a biological plausibility on the relationship between smoking and a higher prevalence of new more virulent strains with higher bacterial loads.”

Their speculation isn’t supported by their citations. [12, Sobala 1993] said nothing about smokers. [13, Jarosz 2000] claimed that Vitamin C plays a role in the”inhibition of the formation of N-nitroso compounds, which have a strong carcinogenic activity,” about which Sobala 1993 stated “we have previously failed to find raised nitrosocompound concentrations in association with intestinal metaplasia or bile reflux.”

They continue: “If this hypothesised synergistic effect is firmly established, smoking cessation would be associated with a lower risk of high virulence strains infection, so the combined effect of smoking and H. Pylori trends on past and future gastric cancer incidence, could be higher than estimated by microsimulation models [37].”

[37] happens to be a specious estimate of supposed smoking related gastric cancer, whose academic editor was no less than the archvillain of scientific fraud himself, Jonathan M. Samet! He and his ilk happily embrace anything that helps spread lies about smoking dangers, and whether it’s “firmly established” among legitimate scientists is irrelevant to them. Samet even lied under oath at the Minnesota tobacco trial that smoking causes ulcers, notwithstanding that the National Institutes of Health had issued its directive on Helicobacter pylori four years previously.

Contribution of H. pylori and smoking trends to US incidence of intestinal-type noncardia gastric adenocarcinoma: a microsimulation model.
Yeh JM, Hur C, Schrag D, Kuntz KM, Ezzati M, Stout N, Ward Z, Goldie SJ.
PLoS Med 2013 May; 10(5): e1001451.

Six of the eight authors have ties to Harvard or Massachusetts General Hospital, the other two to the University of Minnesota and to Imperial College, London. It was funded by the National Cancer Institute. To the mass media propaganda organs, these affiliations are “prestigeous,” so anthing they say must be true because they so.

This one claims that “With no tobacco control, incidence would have declined only 56%, suggesting that lower smoking initiation and higher cessation rates observed after the 1960s accelerated the relative decline in cancer incidence by 7% (range = 0%–21%).”

The graphs are conspicuous for the one they didn’t show, namely that death rates from gastric cancer have declined steadily since the 1930s, and the increased rates of smoking between then and the 1964 Surgeon General report showed no influence on the trend. Viewed from the longer perspective, the decline began to level off in the 1970s, exactly the opposite of the acceleration they pretend occurred!

They also ignore the role of Epstein-Barr virus, which is the leading known cause of gastric carcinoma after H. pylori, and by which smokers are also more likely to have been infected for socioeconomic reasons.

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