H. pylori on the hook for diabetes risk

H. pylori on the hook for diabetes risk


October 26, 2011

BY NEIL OSTERWEIL
BOSTON – Already convicted for its role in causing peptic ulcers, Helicobacter pylori is also being indicted as a possible co-conspirator in the development of diabetes, investigators from two separate studies said at the annual meeting of the Infectious Diseases Society of America.

In a study of nearly 1,800 older Latinos in California, H. pylori infection was associated with a more than twofold greater risk for diabetes, reported Dr. Christine Y. Jeon of the Columbia University School of Nursing, New York.

In addition, a separate study of National Health and Nutrition Examination Survey (NHANES) data found that, after excluding for diabetes and controlling for other risk factors, H. pylori seropositivity was positively associated with hemoglobin A1c (HbA1c) levels – suggesting that the bacterium may play a role in impaired glucose tolerance, said Dr. Yu Chen of New York University Langone Medical Center, New York.

Dr. Jeon noted that, although the mechanism for the association between H. pylori infection and diabetes is unknown, it does not appear to be mediated by either the inflammatory pathway or insulin resistance.

“This highlights the need for future studies on how the timing and severity of H. pylori infection affect glucose control in younger individuals, and how H. pylori alters gut microbiota and subsequent host gene expression and energy uptake,” she said.

Dr. Jeon and her colleagues conducted a study to examine whether risk of diabetes changes with various common chronic infections, including herpes simplex virus 1, varicella virus, cytomegalovirus, Toxoplasma gondii, and H. pylori.

The study and its focus on H. pylori in particular were motivated in part by observation of a racial gradient in both diabetes prevalence and H. pylori infection in the United States, with Mexican Americans having a higher prevalence of both than either whites or non-Hispanic blacks.

In addition, studies have found evidence of association between periodontal bacteria and increased diabetes risk, as well as links between decreased insulin sensitivity and higher antibody titers to herpes simplex virus 2 and Chlamydia pneumoniae.

Other studies, however, have not shown an association between common infections and insulin resistance or diabetes.

The study investigators analyzed data on 1,789 men and women older than 60 years who were enrolled in the Sacramento Area Latino Study on Aging (SALSA). Of that group, 782 people did not have diabetes and had available baseline pathogen data.

During the 10-year study, 144 of those 782 people developed diabetes (18% incidence rate), with diabetes defined as self-report of a physician’s diagnosis of diabetes or of taking hypoglycemic medication, including insulin, at semiannual interviews; fasting glucose of at least 126 mg/dL at four follow-up visits; or death certificate inclusion of diabetes as a cause of death.

In bivariate analysis adjusted for gender and education, none of the pathogens reached statistical significance for an association with diabetes.

In multivariate analysis, however, the only significant association seen with diabetes was H. pylori (hazard ratio, 2.69). The association was stronger than that for either vascular disease (HR, 1.78) or being a former smoker (HR of 1.34 in bivariate analysis).

Possible explanations for the association include H. pylori–induced alterations in gut microbiota, changes in nutrient metabolism in the gut, increased energy harvesting, or altered host gene expression, Dr. Jeon said.

In the second study, Dr. Chen and her colleague Dr. Martin Blaser looked at data from NHANES III (1988-1994) and IV (1999-2004).

In NHANES III, they found a positive association between H. pylori and HbA1c in the overall cohort and in people with body mass indices (BMI) both below 25 and 25 and higher (P for interaction for each comparison less than .01).

They also saw a synergistic interaction between H. pylori and higher levels of BMI in both NHANES III and IV (P for interaction less than .01), suggesting that H. pylori exacerbated the rise in HbA1c often seen with weight increase.

In addition, in NHANES III but not NHANES IV, the synergistic effect was seen among patients seropositive for the cagA strain of H. pylori, which has been associated with virulence.

The investigators did not, however, find an association between self-reported diabetes and H. pylori infection.

Dr. Jeon’s study was supported by grants from the National Institutes of Health. Dr. Chen did not disclose a funding source. Both investigators reported that they had no relevant financial disclosures.