Am having a hard time right now with the comments from the authors of this new paper showing a correlation between H. pylori presence and both type II diabetes and blood glucose levels. As far as I can tell, the paper does not show any causal connection. That is, they do not determine if H. pylori infection is a cause of blood sugar issues or a consequence of blood sugar issues.
Yet the authors of the paper, one of whom (Martin Blaser) is a very respected H. pylori expert are saying things like
“This study provides further evidence of late-in-life cost to having H. pylori,”
And they suggest that antibiotic treatment for the elderly may help prevent diabetes.
This to be seems to be a bit over the top. Yes, it makes sense that H. pylori could cause these issues. And they have a model for how it might. But they really should be more careful with their words until a causal connection is established. After all, we have many well known negative effects of antibiotic overuse, including some shown by Blaser. The last thing we need is people going out and dosing up on antibiotics in the hope that it will prevent type II diabetes. But I can guarantee that is what will happen if this story gets overplayed.
At least a few sources report on the lack of anything showing a causal connection (e.g. see US News and World Report):
An expert not involved with the study said that while it did not show a cause-and-effect relationship between the bacterium and diabetes, the findings suggest certain possibilities
But I am worried that that is not enough skepticism to counteract the claims of the authors here. The study is certainly interesting. And their model for a causal connection is fine. But they probably need to do a little bit of toning down of their claims here.
After some people asked me questions about this study at a few recent meetings I dug a little deeper. And I am a bit startled to find out what the basis is for Chen and Blaser to claim a causative association between H. pylori and type II diabetes/ glucose levels. Here is a summary of their logic:
Helicobacter pylori is acquired almost exclusively in childhood , and there is no clear mechanism for how glucose intolerance present only after the age of 18 would increase risk of H. pylori colonization. It also is unlikely that H. pylori positivity and high levels of HbA1c levels share a mutual antecedent cause because there is no diathesis to both acquire H. pylori and to cause glucose intolerance.
They go on to discuss other lines of indirect evidence for why they think their conclusion is correct. And some of this is very suggestive. But “likely” and “suggestive” is not proof. There are many possible issues with their conclusion. In particular I think it is easy to come up with a scenario whereby something about the host (either their genetics or their history of exposure or even their micro biome) could influence both whether or not they get colonized by H. pylori or even whether or not they get colonized by particular strains of HP. And the same factor could influence microbiome interactions later in life. I see no evidence to indicate that H. pylori is the causative agent here. And for them to then basically recommend prophylactic antibiotics for elderly with HP seems dangerous at best.
4 thoughts on “Diabetes & H.pylori – a correlation but no known causation despite authors claims”
Don't doctors treat pretty much everyone in whom H. pylori is detected? I don't see much possibility of antibiotic overuse due to this article, since those folks should be treated anyway to prevent ulcers and stomach cancer.
No – they do not treat everyone in who HP is detached. > 50% of the worlds population have it apparently … so without a doubt if Blaser wants to treat all with HP to prevent diabetes (without evidence that HP actually causes diabetes) this would be a MASSIVE overuse of antibiotics.
Are there any theories why more than half the world have this bacteria but only a small percentage of them have gastritis or ulcers? Didn't one of the guys who discovered the connection infect himself with H. pylori? If so, was he just “lucky” to have that result in gastritis and prove the connection? Did he know that the chances of proving the connection by infecting himself was small?
Are there any theories why more than half the world have this bacteria but only a small percentage of them have gastritis or ulcers? Didn't one of the guys who discovered the connection infect himself with H. pylori? If so, was he just “lucky” to have that result in gastritis and prove the connection? Did he know that the chances of proving the connection by infecting himself was thus small?