Digestive DisordersLife Extension Suggestions
Dietary Approaches To Improve Digestive Disorders
Phosphatidylcholine. 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).
As noted earlier, the basic cause of many ulcers is the spiral-shaped bacterium H. pylori (Axon 1993). To investigate the effect of H. pylori infection on the gastric musocal 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). These findings suggest that H. pylori infection results in changes in the gastric mucosal phospholipid contents and their fatty acid composition, causing the gastric mucosa to be weakened. Attempts to increase the worthiness of the gastric mucosa appears indicated, particularly in individuals with a history of gastric ulcers or those on medicinal protocols known to impact the reliability of the mucosa.
Beyond the functions of gastric protection, polyunsaturated PPC assists in the digestion of fat. The presence of luminal PPC is important for normal lymphatic transport of absorbed digestion products of triglyceride, the major dietary fat (Tso 1981; Richmond 2001). Assisting in the metabolism and transport of fat may explain why some individuals find value in using lecithin in conditions of hypercholesterolemia.
PPC stimulates collagen breakdown in experimental models of liver cirrhosis. As important as this finding is relative to liver health, it also has pertinent implications regarding the integrity and maintenance of the GI tract. Bowel strictures (abnormal, temporary or permanent narrowing of the bowel) are characterized by excess deposition of collagen in the intestinal wall. A study was conducted to determine the effect of PPC in the prevention of bowel strictures. Three groups of rats were assessed: a control group, a confirmed colitis group, and a group of rats diagnosed with colitis, but receiving PPC. In conjunction with the study, collagen deposition and collagenase activity in colonic tissue were measured in all of the groups. None of the control rats, but 12 of 16 rats with colitis, developed colonic strictures.
In contrast, only 2 of 15 PPC-fed rats with colitis developed strictures. Collagen content was much higher in the rats with colitis than the PPC-fed rats with colitis and the control rats. Collagenase activity in colonic tissue was also much higher in the PPC-fed rats (Mourelle 1996). PPC appears to enhance collagen catabolism, restricting collagen buildup in inflamed intestinal tissue and the resulting stricture formation.
Individuals wishing to enhance the integrity of their GI tract or gain assistance in fat metabolism may wish to consider the use of unsaturated PPC. Unsaturated PPC is deemed well-tolerated and without major risk factors.
Zinc-Carnosine. Zinc is a micronutrient mineral that has multiple functions in human biology, chiefly acting as a coenzyme in many enzyme systems that defend against free radical damage (Gotz 1996; Gotz 1997; Langmead 2001; Noguchi 2002). Recognizing that H. pylori infection causes increased oxidative stress, a group of Ecuadorian scientists investigated whether zinc deficiency might cause increased inflammation in the stomachs of people infected with the organism (Sempertegui 2007). They studied 352 patients with dyspepsia (stomach pain and dysfunction) who had biopsy samples taken during endoscopy. Patients with H. pylori infections had significantly lower zinc concentrations in their tissue samples than uninfected patients. Indeed, the more severe the inflammation, the lower the zinc levels in the infected subjects (Sempertegui 2007). These results and others have led some researchers to consider zinc to be a “gastric cytoprotective” (cell-saving) nutrient (D’Souza 1991).
Zinc also has direct anti-inflammatory effects, helping to stabilize the membranes of mast cells. Mast cells release bursts of inflammatory cytokines when stimulated by injury or allergy (Cho 1991; Cho 1992). Further, zinc is an immune modulator that can reduce the recurrence rate of certain inflammation-sensitive cancers (Barrera 2000).
Another essential nutrient called carnosine can boost those effects even further. Japanese scientists have led the way in developing this zinc-carnosine compound. Until quite recently, gastric cancer (the result of gastritis and ulcer disease) was the top killer cancer in Japan; the dramatic decline in gastric cancer has been attributed in large part to dietary education of the Japanese people (Matsuzaka 2007). In fact, the zinc-carnosine compound, sold as polaprezinc, is a regulated prescription anti-ulcer drug in Japan (Matsukura 2000) Fortunately, this simple nutrient compound is available in the US as a non-prescription supplement that is safe for long-term use.
Zinc-carnosine also speeds the eradication of infection with H. pylori itself, as shown by another Japanese team in 1999 (Kashimura 1999). The group enrolled 66 patients with known H. pylori infections and symptoms, randomly assigning them to zinc-carnosine or placebo. All patients also received a cocktail of two potent antibiotics (aimed at curbing the infections) plus a proton pump inhibitor (aimed at promoting gastric healing). Only 86% of the antibiotic-proton pump inhibitor group achieved complete cure (eradication of detectable organisms), while 100% of those receiving zinc-carnosine were cured.
In early 2007, Western scientists began to examine zinc-carnosine’s mode of action and effectiveness. A British team, using a laboratory model of gut injury and repair, also conducted a clinical trial (Mahmood 2007). In the first study, they examined the effects of zinc-carnosine on cells lining animal digestive tracts after exposure to indomethacin (a potent NSAID notorious for its gastritis-producing tendencies) or stress. The nutrient combination reduced stomach injury by 75% and small intestinal injury by 50%. It also stimulated migration and growth of cells in and near the sites of injury, hastening the healing process nearly threefold. In the clinical trial, 10 healthy volunteers took indomethacin (50 mg) three times daily with either placebo or zinc-carnosine. Indomethacin increased gut permeability (impaired barrier function of the gut’s lining that allows inflammation to get its start) by a factor of three in the placebo group, whereas there was no increase in permeability in the supplemented group. The researchers concluded that zinc-carnosine stabilized the mucosal lining cells of the stomach and small intestine.
Cranberries. There is mounting clinical evidence of how effective cranberries and their extracts can be in mitigating H. pylori and other stomach ailments. Chinese researchers gave cranberry juice or a placebo drink (about two cups per day) to 189 adults with H. pylori infection (Zhang 2005). They checked for chemical evidence of continued infection at days 35 and 90 of treatment. More than 14% of the juice-supplemented group versus 5% of the placebo group showed complete eradication of the organism.
A large systematic review by nutritional experts has now concluded that regular intake of cranberry juice and other dietary products “might constitute a low-cost, large-scale alternative solution applicable for populations at risk for H. pylori colonization” (Gotteland 2006). It seems clear that cranberries and their extracts can take their place alongside zinc-carnosine as important components of an effective stomach health regimen.
Licorice. Long recognized for their multiple health benefits (Langmead 2001; Olukoga 2000), licorice extracts (with the potentially blood pressure-elevating glycyrrhizin molecule removed) provide yet another nutritional weapon in fighting H. pylori infection (Petry 2001). Various laboratory studies have shown that these extracts have potent anti-inflammatory activities, reducing cytokine production while increasing production of protective stomach mucus (Khayyal 2006; Kim 2006). Licorice extracts can also kill H. pylori in stomach tissue (O’Mahony 2005), even antibiotic-resistant strains of the organism (Fukai 2002; Krausse 2004). Indeed, in one laboratory head-to-head comparison, licorice extracts were as effective as famotidine in preventing ulcers (Aly 2005), and animal studies have shown a potent effect on speeding the healing of existing ulcers (Baker 1994). These characteristics of licorice neatly complement those of zinc-carnosine and cranberry extracts.
Picrorhiza. News about another natural remedy called picrorhiza (Picrorhiza kurroa) is now generating intense excitement in the medical community (Anon 2001; Govindarajan 2003). Well-known to practitioners of Ayurvedic medicine, picrorhiza is a perennial herb found high in the Himalayas. Its extracts are now being found to have potent antioxidant (Chander 1992; Chander 1998; Sun 2007), immune-stimulating (Vaidya 1996; Gupta 2006; Puri 1992; Sharma 1994; Smit 2000), and anti-inflammatory (Barbieri 2004; Thomas 2007; Zhang 2004) properties—activities that clearly have a role in gastric protection. Since picrorhiza so dramatically combats the very changes caused by H. pylori (i.e., infection, inflammation, oxidant stress, and tissue injury), it is no wonder that this ancient herb is now at the forefront of research on stomach health.
Already used to speed healing in other infectious gastrointestinal conditions such as hepatitis A (Vaidya 1996; Luper 1998), picrorhiza extracts also demonstrate unique wound-healing properties, stimulating tissue growth, nerve cell recovery, and blood vessel formation that may promote recovery from tissue damage (Gaddipati 1999; Li 2000; Singh 2007). In a dramatic illustration of the extract’s ability to combat stomach ulcers, Indian scientists administered it to rats with ulcers induced by the potent NSAID indomethacin (Ray 2002). Compared with an untreated group of animals, the supplemented group had much faster rates of ulcer healing, accompanied by a profound drop in levels of oxidized tissue components. And while antioxidant enzyme activity was decreased in the untreated animals, those treated with picrorhiza had elevated antioxidant activity.