BOSTON—It seems that Helicobacter pylori enjoys a rich meal as much as most humans do, and a low fat-diet may be one way to help control this key peptic ulcer pathogen.
Dr. Duane T. Smoot, of the division of gastroenterology, Howard University, Washington, DC, has found that polyunsaturated fats like linoleic acid inhibit the growth of H. pylori, in a “dose-response fashion.” Saturated fats, on the other hand, seem to suit the organism just fine, showing no bacteriostatic effect.
Dr. Smoot reported his observations in a poster presentation at the annual meeting of the American College of Gastroenterology.
It appears, then, that when it comes to dietary fat, what’s good for the heart may also be good for the gizzard, a message worth passing on to patients who have detectable H. pylori infections. “Diets rich in polyunsaturated fatty acids may have a beneficial effect in preventing gastric cancers and reducing ulcer recurrence by limiting growth of H. pylori.“
Dr. Smoot and his colleagues studied the effects of a range of commonly used dietary oils on the growth of H. pylori in culture.
They first grew the organism in tripticase soy agar, with 5% sheep’s blood for 48 hours, then dispersed the cultures into saline at a concentration of 5 × 106 bacteria per ml. They then exposed the bugs to linoleic acid at concentrations of 0%, 10%, 20%, 40% and 80% for one hour.
Other common dietary fats—olive oil, sunflower oil, fish oil, stearic acid, coconut oil, and palm oil—in varying concentrations, were similarly applied to the H. pylori cultures.
After oil exposure, the investigators plated the organisms onto blood agar and incubated the plates for 48 hours, then evaluated bacterial growth using a spectrophotometer.
Cultures exposed to linoleic acid had a hard time. Those exposed to the 10% concentration showed growth that was only 38.4% of that seen in the unexposed controls. In the 20%, 40% and 80% linoleic acid concentrations, H. pylori‘s growth was 34.3%, 5.8%, and 4.2% of the control values.
The other poly- or monounsaturated fats—the olive, fish, and sunflower oils—also showed bacteriostatic effects, but only at concentrations exceeding 30%. Saturated fats (stearic acid, coconut oil and palm oil), however, had no inhibitory effect on H. pylori.
While it is not possible to make definitive dietary recommendations based on this in vitro experiment, the findings clearly show that this pathogen behaves very differently in the presence of different fats. Dr. Smoot noted that previously published studies show polyunsaturated fats can inhibit the growth of Escherichia coli.
The World Health Organization attributes roughly 60% of the risk for gastric cancer world-wide to H. pylori infection.
Dr. Smoot believes diet may play a role in determining whether a person infected with H. pylori will remain disease-free, or will develop ulcers, carcinoma, or other disorders associated with the organism. If further study bears out this hypothesis, then the logical conclusion is that a diet rich in polyunsaturates but low in saturated fat could markedly reduce the public health burden of stomach disease.
THE REDUX: Linoleic acid and other poly-unsaturated fatty acids markedly inhibit growth of H. pylori in culture, while saturated fats do not. This suggests a diet high in poly-unsaturates but low in saturated fat may be beneficial in combating this peptic ulcer pathogen.
