H pylori infection plus deficient vitamin D levels double metabolic syndrome risk

Tuesday, June 7, 2016

The May 2016 issue of the journal Medicine reports the finding of a two times greater risk of metabolic syndrome among vitamin D deficient men and women who tested positive for the ulcer-causing bacterium Helicobacter pylori (H pylori) compared to those with neither condition.

The study included 792 men and 1,321 women over the age of 30 who resided in northeastern Taiwan. Participants were considered to have metabolic syndrome if they exhibited three or more of five traits (increased waist circumference, blood pressure, triglycerides and glucose, and low serum high-density lipoprotein (HDL) cholesterol levels) that increase the risk of type 2 diabetes and cardiovascular disease. Urea breath tests were administered to detect H pylori infection. Blood samples collected upon enrollment were analyzed for serum 25-hydroxyvitamin D, inflammatory cytokines, adipokines, and other factors.

Metabolic syndrome was found in 26.3% of the participants, infection with H pylori was detected in 53.3% and vitamin D deficiency, defined as serum 25-hydroxyvitamin D levels of less than 20 nanograms per milliliter (ng/mL), was revealed in 19.8%. Those who were infected with H. pylori had a 50% higher adjusted risk of metabolic syndrome compared with uninfected participants. For subjects with vitamin D deficiency, the risk of metabolic syndrome was 42% higher than those with sufficient levels of over 30 ng/mL. Study participants with both vitamin D deficiency and H pylori infection had more than double the risk of metabolic syndrome compared to uninfected subjects with sufficient vitamin D. This group also was found to have low levels of protective HDL cholesterol.

"The correlation analysis revealed that vitamin D deficiency was associated with decreased adiponectin level but also with increased leptin level, a combination that has been linked to HDL cholesterol abnormality," Li-Wei Chen, MD and colleagues note. "However, H pylori infection was not correlated with adiponectin, leptin, or HS-CRP [high-sensitivity C-reactive protein] level. We surmise that the link between H pylori infection and metabolic syndrome status may involve other adipokines or inflammatory cytokines."

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Higher vitamin C levels associated with lower risk of stomach cancer
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The November 2013 issue of the American Journal of Clinical Nutrition reports a protective effect for higher plasma vitamin C levels against gastric adenocarcinoma in Chinese men and women.

The current study involved follow-up participants in the Linxian General Population Nutrition Intervention Trial, which concluded in 1991. Blood samples collected between 1999 and 2000 were analyzed for plasma vitamin C levels. Four hundred sixty-seven men and women diagnosed with gastric adenocarcinoma and 618 subjects with esophageal squamous cell carcinoma were compared with 948 subjects who did not have the diseases.

A lower risk of gastric cancer was observed in association with higher plasma vitamin C levels. Participants with normal vitamin C levels, defined as greater than 28 micromoles per liter, had a 27% lower risk of gastric cancer in comparison with those whose levels were low at 28 micromoles per liter or less. A meta-analysis that included the current study and two other cohort studies resulted in similar findings. No association for vitamin C levels with esophageal squamous cell carcinoma was determined.

Authors Tram Kim Lam and colleagues remark that vitamin C may help protect the cells from oxidative DNA damage and other adverse effects of H. pylori infection, which is a common cause of gastric cancer. They note that H. pylori is not believed to increase the risk of esophageal squamous cell cancer, which could explain the lack of protective effect for vitamin C against this type of cancer that was observed in this study.

"This study was the largest prospective cohort study on the association between circulating vitamin C and gastric adenocarcinoma risk to date and the first prospective evaluation of the relation with esophageal squamous cell carcinoma," they announce. "Results based on our meta-analysis of prospective cohort studies suggest that plasma vitamin C is inversely associated with gastric adenocarcinoma incidence."

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Life Extension Magazine® June 2016 Issue Now Online

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On the cover

How to reverse markers of prostate cancer, by William Faloon


Oral sunscreen reduces skin cancer risk, by Kathy Ramirez

Unique magnesium compound reverses brain aging, by Jamie Rivington

Major advance in screening and treating prostate cancer, by Jules Chesterfield

Solutions for common prostate problems, by Michael Tewson

Topical vitamin C for skin rejuvenation, by Robert Goldfaden and Gary Goldfaden, MD

Immune-modulating cancer drugs finally get some respect, by Chancellor Faloon

The insulin/cancer connection, by Miles Mueller


In the News

Journal abstracts: Prostate cancer, magnesium and vitamin C topical

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Health Concern

Digestive disorders

The medical community has discovered that H. pylori bacteria cause most stomach ulcers. Blood tests can reveal the presence of the H. pylori antibody. Special antibiotic combinations can be used to eliminate H. pylori bacteria from the stomach within a matter of weeks. Those who fail to eradicate H. pylori are at a far greater risk for contracting stomach cancer.

Extracellular phospholipids, synthesized on gastric mucosa, assist in the hydrophobic (non-wettable) characteristics of the epithelium, yielding protection from stomach acid and injurious materials. The non-wettable status of the epithelium is extremely important to the health of the GI tract. This valuable protection is, however, vulnerable and can be transformed by aspirin or NSAIDs from a non-wettable (resistant to harmful substances) to a wettable (mucosa is susceptible to injury from caustic substances) state.

Once the gastric mucosa has been disturbed, ulcers loom as an ongoing threat. Polyunsaturated phosphatidylcholine (PPC) has been shown to reduce the incidence of gastric ulcers, even after aggressive experimental ulcer inducement. Individuals at high risk for gastric ulcers, such as those taking high doses of either aspirin or NSAIDs, have lessened the injurious nature of the drugs when phospholipids are bound to the anti-inflammatory drugs (Leyck 1985).

To investigate the effect of H. pylori infection on the gastric mucosal barrier, phospholipid and fatty acid composition of the gastric mucosa were analyzed in healthy volunteers with and without H. pylori infection. The gastric PPC content of H. pylori-positive healthy volunteers was less than that of H. pylori-negative healthy volunteers (p < 0.05) (Wakabayashi 1998).

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