Walker Berkley and Dr. Frost Steele, Nutrition, Dietetics, and Food Science
In 2005 Dr. Marshall, along with co-discoverer Dr, J Robin Warren, shared the Nobel Prize in Physiology or Medicine for their linking the bacteria H. pylori to gastric ulcers and instituting regiments of antibiotic treatments that culminated in the first long term cure for this dehabilitating stomach condition.
Since this discovery, H. pylori has been found and associated with a myriad of other health problems. In first world countries H. pylori infection has been associated with gastric atrophy, gastric cancer and mucosa-associated lymphoid tissue lymphoma in the stomach. In developing nations infection is tied to an increased risk of malnutrition, diarrhea, and stunted growth. It has been noted that the eradication rates for the standard triple treatment have fallen due to antibiotic resistance and a new quadruple therapy is being explored. New treatments of H. pylori are needed to combat further resistance escalation.
Many studies have shown the curative properties of honey against H. pylori. There are three mechanisms suggested to explain honey’s antimicrobial action against H. pylori. One model is that there is a special enzyme in the honey that kills bacteria or inhibits its growth. Another thought is that honey has so much sugar, which loves to bond with water, that the moisture in the bacteria is sucked out of the bacterium leaving the unfortunate H. pylori dried out like a prune. The third suggested model is a combination of the two. My research attempted to determine which view is correct.
Previous studies have suggested that the “osmotic pressure” or water migration view is the predominate effecter of microbial death. Osato et al. compared the antimicrobial effects of honey against H. pylori with a sugar solution that had a similar osmotic pressure, or ability to extract water form something like a bacteria. His experiments were conducted over a three day period and found no difference between growth inhibition caused by honey and that caused by the sugar solution. This suggests that it is simply the sugar in the honey and not a special enzyme or agent that is responsible for the antimicrobial properties of honey.
One question that remains after such an experiment is whether or not the antimicrobial action of honey over the three days as tested in the experiment is the same as the antimicrobial action of honey over the few minutes it is in the stomach. Enzymatic activity could prove to be the antimicrobial agent in the short term, but its effects would be indiscernible over the three day treatment as the osmotic pressure would overshadow any evidence of its effect. My researched focused on looking at the action of honey against H. pylori on the short term, within two hours, that better represents the length of time honey would be in the stomach of a patient treated by such a method.
To test and measure the antimicrobial effect of honey over a shorter period of time a protocol usually used to test disinfectants was modified. A culture of the bacteria was added to either honey, or a solution with a similar sugar constitution of honey. A baseline level of bacteria was measured when the culture was first added to either the honey or the sugar, then samples were taken out at thirty minute intervals and measured. The two sets of data were then plotted on a graph to be compared to each other. If the honey showed a much greater decrease in H. pylori than the sugar solution did, then we would have evidence that there might be something more to honey’s antimicrobial action than just its sugar composition.
Previous to the experiment we tested to see if we could replicate the work of Osato. 9 We observed compete growth inhibition after only one day of H. pylori being treated with honey.
The experiment was then performed three times. The first time was performed to test the protocol. It was done with E. coli and Campylobacter jejuni. The data showed little bacterial death at honey concentrations of fifty percent, so we decided to use honey at a ninety percent concentration to increase its action. The experiment was then repeated two times using H. pylori. The first experiment with H. pylori yielded contradictory results. The second experiment demonstrated no bacterial death over the two hour treatment time.
The data so far is decidedly inconclusive. Future experiments will need to be done with a lower initial concentration of bacteria to determine if that will result in a more measurable death curve. The data could also suggest that in vivo it is the repeated application of honey that results in the observed antimicrobial action, not simply a one time application. Indeed many of the in vivo studies used protocol outlining many honey treatments and not just one. 8 Future research should focus on generating consistent, replicatible data.
I presented my research as of November 23rd a meeting in Pullman Washington to the chief scientists and employees of Decagon Devices as part of a job interview. They were impressed with the initial findings and have since offered me a job following graduation. I know that such opportunities would not have come quite so readily if I had not the experience of an ORCA grant.
Thank yous are in order to Dr. Frost Steele for valuable advisement, ARUP labs, Salt Lake City, for donating the samples of H. pylori used in the study, and a grant from BYU’s Office of Research and Creative Activities.
References
Digestive Diseases and Sciences, 44 (3): 462-464