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Mastic Gum: Its applications Go Far
Beyond the Treatment of Ulcers
Interview with Leo Galland, M.D.
Introduction: Leo Galland, M.D. is Director of the Foundation for Integrated Medicine, and author most recently of The Fat Resistance Diet. He has written many articles on the gastrointestinal ecosystem and novel approaches to gastrointestinal disorders. Here he discusses the latest research on mastic gum, and his protocol for the use of mastic gum not only in ulcers, but in other GI tract disorders.
Focus: You began using mastic gum in your practice years ago for stomach ulcers and found it highly effective. Can you briefly review mastic gum for us here?
Galland: Mastic gum has a long history of traditional use in the Mediterranean for digestive disturbances. Because of this a study was done that found it was able to kill H. pylori, the causative agent of stomach ulcers, in vitro. Before capsules were available, I actually found chunks of mastic gum in a middle eastern store in Brooklyn, and had my patients suck on it or chew it. Once capsules became available I started treating patients.
Focus: What is your preferred treatment regimen?
Galland: First, I test patients for H. pylori antigen in the stool, and for H. pylori antibodies in the blood. These are both noninvasive and effective screening methods. If the patient is positive and symptomatic, with gastritis or ulcers, I prescribe 1000 milligrams of mastic twice a day for thirty days. Then I add in 10-14 days of a combination of antibiotics, along with acidophilus culture, and lactoferrin. I use 200 milligrams of lactoferrin twice a day, because it is immune stimulating and controlled studies have shown that it enhances the response to antibiotic therapy. After that, I continue with the probiotic alone.
Focus: How many patients improve on this regimen?
Galland: At least 75% recover, become antigen- and antibody-negative and their symptoms clear up. I see only about a 10% relapse rate. But I’ve begun to be fascinated by other uses of mastic gum for gastrointestinal disorders. I had a patient with inflammatory bowel disease—with both gastritis and ulcerative colitis—who was H. pylori positive. I put her on mastic gum and her colitis cleared up. It was quite dramatic. She was on the mastic gum for six months total, and her symptoms have not returned. That was pretty amazing. I wasn’t sure if this was a fluke, but there have been recent studies with mastic gum that show it is quite helpful in a number of different gastrointestinal disorders. A 2007 study from the University of Athens showed that mastic actually altered the function of certain immune cells in patients with active Crohn’s disease. Another 2007 study showed that in patients with active Crohn’s disease, mastic gum downregulated inflammatory markers like NF-Kappa B and interleukin-6, as well as C-reactive protein. Their Crohn’s symptoms also improved. Research last year even showed that mastic gum can inhibit salivary bacteria.
Focus: So what do you think is the future for mastic gum?
Galland: Since there are virtually no side effects, and it is used as a food throughout the Mediterranean, I’ve begun to incorporate mastic gum in my protocols for any patient of mine with a GI complaint, from gastritis to ulcers to inflammatory bowel disease. Wherever there is gut inflammation, mastic gum may be helpful. One study even showed that mastic has anti-proliferative activity in human colon cancer cells. I like mastic gum, and I use it a lot, and I believe its applications go far beyond the treatment of ulcers and H. pylori.
 Mastic gum is derived from Pistacia lentiscus, a member of the pistachio tree family.
-Abstracts-
Kaliora AC, Stathopoulou MG, Triantafillidis JK, Dedoussis GV, Andrikopoulos NK. Alterations in the function of circulating mononuclear cells derived from patients with Crohn's disease treated with mastic. World J Gastroenterol. 2007 Dec 7;13(45):6031-6.
AIM: To assess the effects of mastic administration on cytokine production of circulating mononuclear cells of patients with active Crohn's disease (CD). METHODS: The study was conducted in patients with established mildly to moderately active CD, attending the outpatient clinics of the hospital, and in healthy controls. Recruited to a 4 wk treatment with mastic caps (6 caps/d, 0.37 g/cap) were 10 patients and 8 controls, all of who successfully completed the protocol. Interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), monocyte chemotactic protein-1 (MCP-1), macrophage migration inhibitory factor (MIF) and intracellular antioxidant glutathione (GSH) were evaluated in peripheral blood mononuclear cells (PBMC) before and after treatment. RESULTS: Treating CD patients with mastic resulted in the reduction of TNF-alpha secretion (2.1 +/- 0.9 ng/mL vs 0.5 +/- 0.4 ng/mL, P = 0.028). MIF release was significantly increased (1.2 +/- 0.4 ng/mL vs 2.5 +/- 0.7 ng/mL, P = 0.026) meaning that random migration and chemotaxis of monocytes/macrophages was inhibited. No significant changes were observed in IL-6, MCP-1 and GSH concentrations. CONCLUSION: This study shows that mastic acts as an immunomodulator on PBMC, acting as a TNF-alpha inhibitor and a MIF stimulator. Although further double-blind, placebo-controlled studies in a large number of patients is required to clarify the role of this natural product, this finding provides strong evidence that mastic might be an important regulator of immunity in CD.
Kaliora AC, Stathopoulou MG, Triantafillidis JK, Dedoussis GV, Andrikopoulos NK Chios mastic treatment of patients with active Crohn's disease.World J Gastroenterol. 2007 Feb 7;13(5):748-753
AIM: To evaluate the effectiveness of mastic administration on the clinical course and plasma inflammatory mediators of patients with active Crohn's disease (CD). METHODS: This pilot study was conducted in patients with established mild to moderately active CD, attending the outpatient clinics of the hospital, and in healthy controls. Ten patients and 8 controls were recruited for a 4-wk treatment with mastic caps (6 caps/d, 0.37 g/cap). All patients successfully completed the protocol. CD Activity Index (CDAI), Nutritional Risk Index (NRI), C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), monocyte chemotactic protein-1 (MCP-1), and total antioxidant potential (TAP) were evaluated in the plasma at baseline and at the end of the treatment period. Results were expressed as mean values +/- SE and P < 0.05 was considered to indicate statistical significance. RESULTS: Patients exhibited significant reduction of CDAI (222.9 +/- 18.7 vs 136.3 +/- 12.3, P = 0.05) as compared to pretreament values. Plasma IL-6 was significantly decreased (21.2 +/- 9.3 pg/mL vs 7.2 +/- 2.8 pg/ mL, P = 0.027), and so did CRP (40.3 +/- 13.1 mg/mL vs 19.7 +/- 5.5, P = 0.028). TAP was significantly increased (0.15 +/- 0.09 vs 0.57 +/- 0.15 mmol/L uric acid, P = 0.036). No patient or control exhibited any kind of side effects. CONCLUSION: The results suggest that mastic significantly decreased the activity index and the plasma levels of IL-6 and CRP in patients with mildly to moderately active CD. Further double-blind, placebo-controlled studies in a larger number of patients are required to clarify the role of this natural product in the treatment of patients with CD.
Aksoy A, Duran N, Toroglu S, Koksal F. Short-term effect of mastic gum on salivary concentrations of cariogenic bacteria in orthodontic patients. Angle Orthod. 2007 Jan;77(1):124-8.
OBJECTIVE: To determine antibacterial activity of chewing mastic gum against the salivary levels of Streptococcus mutans, the total number of viable bacteria, and lactobacilli in patients undergoing therapy with fixed orthodontic appliances. MATERIALS AND METHODS: In this study, the levels of S mutans, lactobacilli, and total cultivated bacteria were measured before and after chewing mastic gum. The antibacterial effects of chewing mastic gum against these microorganisms in saliva were compared with a placebo gum. The counts for orthodontically treated patients were evaluated before chewing gum; just after chewing gum; and after 45, 75, 105, and 135 minutes. Saliva samples taken from the patients were inoculated onto trypticase-yeast-cystine-bacitracin agar for mutans streptococci and onto Rogosa agar for lactobacilli. The agar plates were incubated for 48 hours anaerobically at 37 degrees C. The total number of viable bacteria was then counted. RESULTS: Just after chewing the mastic gum for 15 minutes, a significant decrease of total bacteria and S mutans was observed (P < .001). The reduction in lactobacilli was not significant at later first stage (P > .05). However, at the end of 135 minutes, there were significantly fewer S mutans (P < .001), total viable bacteria (P < .001), and lactobacilli (P < .001) in the oral cavity after chewing mastic gum than after chewing paraffin (P < .001). The results show that chewing mastic gum decreased the total viable bacteria, S mutans, and lactobacilli in saliva in orthodontically treated patients with fixed appliances. CONCLUSION: Chewing mastic gum might be useful in preventing caries lesions.
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