Helicobacter pylori and Inflammatory Bowel Disease

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Investigators conclude that H. pylori infection is inversely associated with IBD, whereas non–H. pylori chronic gastritis is positively associated with it.
Some preliminary studies have suggested that patients with Helicobacter pylori infection are less likely to have inflammatory bowel disease (IBD) than the general population.
To investigate this possibility further, investigators used a large national database of surgical pathology reports to examine biopsy results for patients who underwent both upper endoscopy and colonoscopy on the same day. The results from gastroscopy specimens were reviewed for the presence of esophagitis, gastritis, and H. pylori infection; those from colonoscopy specimens were evaluated for the presence of ulcerative colitis (UC), Crohn disease (CD), and indeterminate colitis.

IBD was identified in 1061 (1.6%) of 65,515 patients; the remaining patients were used as controls. The associations between H. pylori infection and IBD as well as between non–H. pylori gastritis and IBD were evaluated using multivariate logistic regression, with adjustment for potential confounders.
The presence of H. pylori infection was inversely associated with diagnosis of any IBD (adjusted odds ratio, 0.53; 95% confidence interval, 0.39–0.70), CD (AOR, 0.48; 95% CI, 0.27–0.79), UC (AOR, 0.59; 95% CI, 0.39–0.84), and indeterminate colitis (AOR, 0.43; 95% CI, 0.15–0.95). Conversely, the presence of non–H. pylori chronic gastritis was positively associated with these diagnoses: any IBD (AOR, 5.61; 95% CI, 4.35–7.14), CD (AOR, 11.06; 95% CI, 7.98–15.02, UC (AOR, 2.25; 95% CI, 1.31–3.60), and indeterminate colitis (AOR, 6.91; 95% CI, 3.50–12.30).

Comment: This well-designed study confirms suggestions that patients with H. pylori infection are at decreased risk for IBD. This finding, along with the positive association between non–H. pylori gastritis and IBD, raises questions about the mechanism underlying these associations. It should be noted that the prevalence of H. pylori infection was only 9% in the cohort overall, and even lower in the younger age groups. This might reflect the decreasing prevalence of the infection in the U.S. population or a potential selection bias. Less than 1% of the patients had no insurance, 3% were covered by Medicaid, and 69% had private insurance. Underrepresentation of patients from lower economic groups might have reduced the prevalence of H. pylori infection and introduced the possibility that the findings are due to factors associated with higher economic status.

Source:
Sonnenberg A and Genta RM. Low prevalence of Helicobacter pylori infection among patients with inflammatory bowel disease. Aliment Pharmacol Ther 2012 Feb; 35:469.

Metformin Associated with Lower Cancer Risk

Compared with sulfonylurea users, metformin users had a 10% lower incidence of cancer.
During the past decade, observational studies have suggested associations between cancer and type 2 diabetes (or insulin therapy). Although several plausible mechanisms exist (e.g., cancer cells express insulin receptors that when activated could promote cell proliferation in type 2 diabetic patients with hyperinsulinemia), the association remains controversial (CA Cancer J Clin 2010; 60:207). In some studies, metformin has been associated with decreased cancer risk.
In a population-based retrospective study, Dutch researchers recorded the incidence of cancer in 85,000 type 2 diabetic patients who initiated metformin or sulfonylurea monotherapy. During up to 10 years of follow-up, metformin users were less likely to receive cancer diagnoses than sulfonylurea users (hazard ratio, 0.9; 95% confidence interval, 0.88–0.91) after adjustment for age, sex, and several other variables. This 10% reduction was modest in relative terms but highly statistically significant. Metformin-associated lower risks were noted for cancers of the esophagus, stomach, colon, liver, pancreas, lung, breast, and prostate.
Comment: If hyperinsulinemia really does promote cancer, metformin theoretically could lower cancer risk in type 2 diabetic patients because it lowers circulating glucose and insulin levels in patients with insulin resistance and hyperinsulinemia. Unrecognized confounders could have affected the results of this study, but its intriguing results reinforce metformin as first-line therapy for type 2 diabetes.
Daniel’s Comment: If Metformin can achieve these results are there not botanical treatments, which can manage blood sugar?
Source:
Ruiter R et al. Lower risk of cancer in patients on metformin in comparison with those on sulfonylurea derivatives: Results from a large population-based follow-up study. Diabetes Care 2012 Jan; 35:119. (http://dx.doi.org/10.2337/dc11-0857)

Benefits of Physical Activity After Cancer Treatment

Exercise improved physical function, psychological outcomes, and quality of life in cancer survivors.
Can physical activity mitigate some of the debilitating effects of cancer treatment? To find out, investigators conducted a meta-analysis of 34 randomized, controlled trials in which patients were assigned to physical-activity interventions after their cancer treatment or did not engage in posttreatment exercise regimens. Twenty-two of the trials (65%) included only breast cancer patients; most of the others included patients with various types of cancer. Physical-activity interventions (median duration, 13 weeks) included aerobic exercise and resistance strength training. Exercise intensity, specified in only 13 trials, was usually moderate.
Compared with physical inactivity, exercise interventions were associated with significant improvements in body weight, body-mass index, peak oxygen consumption, peak power output, 6-minute walking distance, bench- and leg-press weight capacity, handgrip strength, fatigue, depression, and some quality-of-life measures.
Comment: This meta-analysis showed that exercise improved the physical function, psychological outcomes, and quality of life in patients who had been treated for cancer. Although most of the trials involved only breast cancer patients and none assessed the effects of physical activity on cancer recurrence or mortality, the findings nevertheless make a compelling case for advising cancer survivors to be physically active.
Source:
Fong DYT et al. Physical activity for cancer survivors: Meta-analysis of randomised controlled trials. BMJ 2012 Jan 31; 344:e70. (http://dx.doi.org/10.1136/bmj.e70)

Will mandatory folic acid fortification prevent or promote cancer?

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An overwhelming body of evidence for a protective effect of periconceptional folic acid supplementation against neural tube defects (NTDs) led to mandatory folic acid fortification in the United States. The effectiveness of folic acid fortification in improving folate status has already been shown to be quite striking, with a dramatic increase in blood measurements of folate in the United States. Preliminary reports also suggest a significant reduction (≈15–50%) in NTDs in the United States. The success of folic acid fortification in improving folate status and in reducing NTD rates is truly a public health triumph and provides a paradigm of collaboration between science and public health policy. Although folic acid is generally regarded as safe, there continues to be concern that folic acid fortification may have adverse effects in subpopulation groups not originally targeted for fortification. In this regard, an emerging body of evidence suggests that folic acid supplementation may enhance the development and progression of already existing, undiagnosed premalignant and malignant lesions. Over the past few years, the US population has been exposed to a significant increase in folate intake, for which essentially no data on safety exist. The potential cancer-promoting effect of folic acid supplementation needs to be considered in carefully monitoring the long-term effect of folic acid fortification on the vast majority of the US population, who are not at risk of NTDs.
Kim Y-I. Am J Clin Nutr November 2004 vol. 80 no. 5 1123-1128

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