Nutrition Q&A with Dan Lukaczer

Q: Is it true that whey protein can eradicate the bacteria that cause ulcers?

A: You are probably referring to work being done on the protein lactoferrin and the effect it has on Helicobacter pylori, a spiral-shaped bacterium that lives in the stomach and duodenum (a section of intestine just below the stomach). I'm sorry to say that lactoferrin can't eradicate H. pylori, but it might help as part of the treatment.

Lactoferrin is specifically found in the whey-protein portion of both human's and cow's milk. While it is a relatively minor part of typical commercial whey products, there are techniques to concentrate it, and a number of commercial bovine lactoferrin supplements are available. Lactoferrin was once thought to only transport iron in the blood, but recent studies show it has other activities such as inhibiting certain microbes. This includes H. pylori, which is the main cause of gastritis, gastroduodenal ulcers and gastric cancer.

That said, the best-known approach to H. pylori treatment is called triple therapy, a strategy that combines either bismuth salts or proton-pump inhibitors with two antibiotics. However, approximately 20 percent of patients will not be able to successfully eradicate the bacteria using this treatment. Complicating matters, a second, more-prolonged treatment course can be difficult because of side effects.1^,2

A recent study evaluated the effect of adding bovine lactoferrin to the triple-therapy treatment regime. The researchers compared three groups of patients diagnosed with H. pylori. One group was given standard triple therapy, a second was given 200 mg lactoferrin twice a day before the triple-therapy treatment, and the third group was given 200 mg lactoferrin twice a day with the triple-therapy treatment. Researchers found that giving lactoferrin before the treatment was no better than the triple-therapy treatment itself, but when given with the triple therapy, the effectiveness of the treatment improved significantly—from the normal treatment success of 77 percent H. pylori eradication to 90 percent eradication. They concluded that lactoferrin is an effective adjuvant to seven-day triple therapy.3 So if you have been diagnosed with H. pylori, I would not suggest using lactoferrin alone, but it appears it may be a good addition to standard care.

Q: How do I know if I have a leaky gut?

A: I get asked this question quite a lot. First, what is a leaky gut? The cells that line the intestinal wall form a barrier that is one-cell thick. Each cell is in contact with the cell next to it to form tight junctions, or connections, between each other. These tight junctions constitute a barrier between what's within the gut and what's inside the body (or the systemic circulation). Under normal, healthy conditions, this barrier provides limited access for molecules in the gut to enter the systemic circulation unless the molecules are absorbed through a cell. Without a tight junction barrier, however, all types of molecules are able to go around the cells and enter the systemic circulation. When this happens, someone is said to have abnormal intestinal permeability—or a "leaky gut."

Many things, from alcohol to aspirin and from radiation to stress, can induce abnormal intestinal permeability. Many diseases and conditions have been shown, at least in part, to be caused by or result in increased permeability. These include migraine headaches, ulcerative colitis, eczema, rheumatoid arthritis and food allergies.4^,5 Poor nutrient intake or absorption may also cause a leaky gut because the cells that line the intestine may be more susceptible to leakiness if they are not well-nourished.

If you are worried you may have this condition, some laboratory tests can measure permeability of certain areas of the gut. While there is no foolproof way to assess for a leaky gut, the best way to see if your health issues are related is to work with a health-care provider who is well-acquainted with the condition and the testing.

Q: Is hoodia for real? Does it work?

A: There is likely something to hoodia (Hoodia gordonii), but it's a complicated issue. Hoodia is a plant that grows in the semi-arid regions of South Africa, where it was traditionally used as an appetite-suppressant. A particular component of that plant, named P57AS3 (called P57 for short), is thought to be the active constituent. There has been quite a lot of talk about hoodia's effects, but surprisingly little published research.

Animal studies suggest it may suppress appetite through an effect on one of the central-nervous-system mechanisms such as the hypothalamus, which may be involved with appetite responses.6 Although there are quite a few claims made about hoodia, no human trials have been published in the peer-reviewed literature to date.

The plant's active ingredient had been patented by South Africa's state research institute, called the Council for Scientific and Industrial Research, and licensed for further development to a British company named Phytopharm. In turn, this company sold additional licenses to the American pharmaceutical company Pfizer.⁷ However, Pfizer discontinued development in 2003. This does not necessarily mean there is no activity of the plant or component, but that researchers didn't see the commercial viability of the venture for them. Phytopharm continues to work with the herb.

There are quite a few issues around the plant, not least of which is quality control. It is likely that not all commercial hoodia products contain P57, or that they are even the correct genus and species.

Testing for it is a complicated process,8 so you might not be getting what's on the label. Another issue is safety. While it has been used traditionally for hundreds, if not thousands, of years, hoodia has had no controlled studies on safety and dosage. No one really knows what dose, if any, is effective, and what dose is safe. This is an herb with a lot of hype and some suggestive findings, but there is a lot we don't know. We clearly have a case of "caveat emptor"—let the buyer beware.

References
1. Calvet X. Helicobacter pylori infection: treatment options. Digestion; 2006;73 Suppl 1:119-28.
2. Di Mario F, Cavallaro LG, and Scarpignato C. 'Rescue' therapies for the management of Helicobacter pylori infection. Dig Dis, 2006;24(1-2):113-30.
3. Di Mario F, et al. Bovine lactoferrin for Helicobacter pylori eradication: an open, randomized, multicentre study. Aliment Pharmacol Ther, 2006;23(8):1235-40.
4. Farhadi A, et al. Intestinal barrier: an interface between health and disease. J Gastroenterol Hepatol, 2003;18(5):479-97.
5. Fasano A and Shea-Donohue T. Mechanisms of disease: the role of intestinal barrier function in the pathogenesis of gastrointestinal autoimmune diseases. Nat Clin Pract Gastroenterol Hepatol, 2005;2(9):416-22.
6. MacLean DB and Luo LG. Increased ATP content/production in the hypothalamus may be a signal for energy-sensing of satiety: studies of the anorectic mechanism of a plant steroidal glycoside. Brain Res, 2004;1020(1-2):1-11.
7. [no authors listed] Protecting traditional knowledge: the San and hoodia. Bull World Health Organ, 2006;84(5):345.
8. Avula B, et al., Determination of the appetite suppressant P57 in Hoodia gordonii plant extracts and dietary supplements by liquid chromatography/electrospray ionization mass spectrometry (LC-MSD-TOF) and LC-UV methods. J AOAC Int; 2006;89(3):606-11.

Natural Foods Merchandiser volume XXVIII/number 1/p. 62