The gastrointestinal (GI) system is a complex system for processing food, extracting nutrients, and eliminating wastes. Intricate processes exist for the regulation of digestion and absorption, which include autonomic, nervous, and hormonal mechanisms. In addition, digestive glands act to provide moisture, lubrication, emulsification, and enzymes for digestion of proteins, carbohydrates, and fats.
The digestive and immunologic functions of the digestive tract are inseparable. The normal gastrointestinal tract is protected by a number of host defenses, both immunologic and non-immunologic. The gastrointestinal tract's first introduction to mucosal immunity comes in the form of colostrum, the first mammary secretion provided for newborns in the first 24 to 72 hours before the onset of lactation. (2) Colostrum contains immunoglobulin fractions that are responsible for passive immunity to infections. The colostmm consists of four forms of immunoglobulins: IgG, IgA, IGM, and IgE. IgG confers specific immunity in response to foreign organisms. IgA, IgM, and IgE contribute to mucosal immunity by surveying the gut for pathogens, as well as binding antigenic substances in order to be cleared from the body. Mucosal membranes separate the tissues of the body from the onslaught of dietary material. This membrane provides a defense by means of humoral immunity (immunoglobulin production), cell-mediated immunity (activated lymphocyte production), and mast cell production. A defense is mounted by the digestive tract in response to substances known as antigens, proteins, or large polysaccharides. The digestive tract and the mucosal immune system associated with it are remarkably flexible and have a tremendous capacity for adapting to an enormous variety of foods. Despite the continuous bombardment of food antigens and commensal bacteria that provoke a low-grade immune response, the digestive tract allows the passage of nutrients and tolerates the presence of useful microorganisms.
The average individual will process an estimated 100 tons or more of food during a lifetime. Therefore, food represents the largest antigenic load that the human immune system must confront. Food allergens (the food fragments responsible for an allergic reaction) are proteins within the food that usually are not broken down by the heat of cooking or by stomach acids or enzymes that digest food. (3) As a result, they survive to cross the gastrointestinal lining, enter the bloodstream, and go to target organs, causing allergic reactions throughout the body. In general, food allergens have unique properties. They are predominately water-soluble, heat- and acid-stable glycoproteins. One such protein found abundantly in foods is lectin. Lectins in foods can interfere with the proper functioning of the digestive, metabolic, and immune systems. (4-6) Lectins have an affinity for binding to glycosylated cells. The small intestinal wall is abundant in glycosolated cells and therefore, contains many sites for lectin binding. Lectins can provoke the production of antibodies against themselves, inhibit enzymes that break down proteins, increase gut permeability, damage absorptive cells in the small intestine, and impair absorption of glucose and the use of dietary proteins. (7-10)
An allergic reaction involves two features of the human immune response. (11-13) One is the production of immunoglobulins, a type of protein called an antibody that circulates through the blood. There are five major classes of immunoglobulins: IgA, IgE, IgM, IgG, and IgD. IgE has a major role in immediate hypersensitivity reactions to food antigens. Of the remaining antibodies, IgG is the most abundant in less immediate antigenic responses. The other is the mast cell, a specific cell that occurs in all body tissues but is especially common in areas of the body that are typical sites of allergic reactions, including the nose and throat, lungs, skin, and gastrointestinal tract. Abnormal immune reactions in the gastrointestinal tract alter its structure and function and thereby cause or contribute to disease processes. The activation of intestinal mast cells by food antigens can result in increased permeability of the gut membrane, mucosal inflammation, and increased antigen and macromolecule uptake.
Before an allergic reaction can occur, a person who is predisposed to form IgE to foods first has to be exposed to the food. (14,15) The ability of a given individual to form IgE against something as benign as food is an inherited predisposition. Generally, such people come from families in which allergies are common, not necessarily food allergies but perhaps hay fever, asthma, or hives. Someone with two allergic parents is more likely to develop food allergies than someone with one allergic parent.
As this food is digested, it triggers certain cells to produce specific IgE in large amounts. The IgE is then released and attaches to the surface of mast cells. The next time the person ingests that food, it interacts with specific IgE on the surface of the mast cells and triggers the cells to release chemicals, such as histamine. Depending upon the tissue in which they are released, these chemicals will cause a person to have various symptoms of food allergy. If the mast cells release chemicals in the ears, nose, and throat, a person may feel an itching in the mouth and may have trouble breathing or swallowing. If the affected mast cells are in the gastrointestinal tract, the person may have abdominal pain or diarrhea. The chemicals released by skin mast cells, in contrast, can prompt hives.
The complex process of digestion affects the timing and the location of a reaction. (11-13) If an individual is allergic to a particular food, for example, they may first experience itching in the mouth as they start to eat the food. After the food is digested in the stomach, abdominal symptoms, such as vomiting, diarrhea, or pain may start. When the food allergens enter and travel through the bloodstream, they can cause a drop in blood pressure. As the allergens reach the skin, they can induce hives or eczema, or when they reach the lungs, they may cause asthma. They also may result in headaches, loss of memory, and inability to concentrate. All of this takes place within a few minutes to an hour.
Abnormal immune reactions in response to food antigens have been classified into four types. (11-13)
Type I--Immediate Hypersensitivity Reactions: These are IgE-mediated immediate reactions to food occurring within less than two hours after ingestion or inhalation of the food antigen. The interaction of the IgE on the mast cell surface with the food extract causes the release of chemical mediators, such as histamines, prostaglandins, leukotrienes and cytokines. These cell mediators may also contribute to IgE-mediated late phase response. In addition, there is increased intestinal mucosal permeability after mast cell activation. This then allows for the entry and distribution of food antigens to other target organs.
Type II--Cytotoxic Reactions: Preformed IgG or IgM antibodies against food constituents bind to epithelial cells. Cytotoxic cells recognize and attack the epithelial cell, or the antigen-antibody complex activates the complement cascade, which leads to local damage.
Type III--Immune Complex Mediated Reactions: Activation of intestinal damage occurs through mucosal deposition of immune complexes. The immune complexes contain IgE, IgG, and IgA antibodies. In response to the immune complexes, there is a recruitment of neutrophils and other cells that release mediators. These chemical mediators cause inflammation, tissue destruction, and mucosal ulceration. This may result in a delayed allergic reaction to foods, occurring hours or days after exposure.
Type IV--T-cell Dependent Reactions: This type of reaction is most often seen in gluten-sensitive individuals (celiac disease). The reaction is mediated by T-lymphocytes that then release cytokines which damage the mucosal membrane.
Common Symptoms and Most Likely Culprits
Allergic reactions can occur immediately, or they can be delayed and take days to surface. A delayed allergic reaction can make it more difficult to pinpoint the allergen. Common symptoms of an allergic reaction are respiratory congestion, eye inflammation, swelling, itching, hives, and stomachache and vomiting. Food allergies can contribute to chronic health problems, such as acne, asthma, bedwetting, diarrhea, ear infections, eczema, fatigue, hay fever, headache, irritability, chronic runny nose, and even difficulty maintaining concentration (attention deficit disorder or hyperactivity). (12) Food allergies can also cause intestinal irritation and swelling that interferes with the absorption of vitamins and minerals. Even if you are consuming a wholesome, nutritious diet, if you are consuming foods to which you are allergic, you may not be able to absorb food properly and therefore may not be deriving the full benefits of all the foods you are eating.
Food allergy patterns in adults differ somewhat from those in children. The most common foods to cause allergies in adults are shrimp, lobster, crab, and other shellfish; peanuts (one of the chief foods responsible for severe anaphylaxis); walnuts and other tree nuts; fish; and eggs. (11) In children, eggs, milk, peanuts, soy, and wheat are the main culprits.
Some of the most common warning signs of food allergy are: (11)
* Dark circles under the eyes (allergic "shiners")
* Puffiness under the eyes
* Horizontal creases in the lower eyelids
* Fluid retention and bloating (not the premenstrual kind)
* Chronic swollen glands (under the jaw, armpits, groin)
Symptoms and diseases associated with food allergies are: (11)
* Gastrointestinal: Canker sores, celiac disease (an extreme intolerance to a fraction of wheat called gliadin which produces crippling diarrhea and weight loss), stomach ulcer, gas, irritable colon, malabsorption, ulcerative colitis (may often produce blood in the stool and a constant hungry feeling).
* Genitourinary: Bed-wetting (eneuresis), chronic bladder infections (cystitis), kidney disease
* Immune: Chronic infections, including ear infections
* Mental/Emotional: Anxiety, depression, hyperactivity, inability to concentrate, insomnia, irritability, mental confusion, personality change, seizures
* Musculoskeletal: Bursitis, joint pain, low back pain
* Respiratory: Asthma, (16) chronic bronchitis, wheezing
* Skin: Acne, eczema (dry or weeping, itchy, thickened, reddened patches of skin usually on the face, wrists, and inside elbows and knees), hives, itching, skin rash
* Other: Irregular heart rate, edema (fluid swelling), fainting spells, fatigue, headache, hyperlglycemia, itchy nose or throat, migraines, sinusitis
There is a substantial body of scientific evidence that links assaults on the gastrointestinal tract to allergic disorders. Crohn's disease is a serious condition that can cause a wide range of symptoms, including severe cramping, diarrhea, and irreversible damage to the gastrointestinal tract. One scientific study revealed that 69% of patients with Crohn's disease were allergic to wheat products and 48% were allergic to dairy. (17) Another study showed that eliminating foods to which Crohn's sufferers were allergic was at least as effective as steroids in producing remission. (18)
A recent article in the journal Allergy discusses the current epidemic of allergic disorders in children. (19) The prevalence of asthma in children and young adults has tripled or quadrupled over the past two decades. Evidence was found that excessive use of antibiotics, which are a major stressor on the gastrointestinal mucosal system, was a contributing factor.
Another disease that is associated with food allergies is eczema. A recent double-blind study found that food additives, such as tartrazine, benzoate, nitrite, and food colors, could aggravate eczema. (20) A Finnish study found a positive correlation between MMR vaccines and allergies. (21) Early exposure to infections in life seems to prime the immune system and prevent the development of allergies later in life. Both antibiotics and vaccines limit this exposure. Repeated or long-term use of antibiotics disrupts the normal balance of bacterial flora in the intestinal tract. This bacterial flora aids us in digesting our food, absorbing nutrients, and balancing the immune system, thus preventing the onset of allergies.
Type I allergic reactions are conveniently diagnosed by assaying IgE antibodies. (22,23) IgE antibodies have a half-life of one to two days when circulating freely and a half-life on the mast cell of 14 days, making them an ideal candidate for assessing immediate hypersensitivity reactions. Moreover, because IgG antibodies and complexes are involved in 80% of food allergy reactions, IgG serves as a useful marker in diagnosing Type II and III allergic reactions. (24,25) IgG antibodies have a half-life of 21 days when circulating freely and can survive on mast cells for up to three months. Therefore, IgG is critical for diagnosing delayed hypersensitivity reactions.
Oral challenge testing for immediate food hypersensitivities is accurate but can be time consuming. (23) Under ideal conditions, the individual should be symptom free during the elimination diet. A baseline is established by beginning with an elimination diet to observe whether reported symptoms resolve with the removal of one or more foods from the diet. Then symptoms are recorded after food challenges take place. Conventional skin testing and radioallergosorbant test (RAST) measure IgE-mediated reactions but cannot evaluate delayed hypersensitivity reactions (IgG). (11,14,26) A skin test involves the introduction of minute amounts of antigen intradermally. Generally, the extent of the skin test reaction observed within 30 minutes correlates with the degree of sensitivity. However, skin testing is not always 100% accurate due to the fact that individuals possess IgE-specific antibodies to foods to which they do not react to when they are ingested. IgE may be necessary but not sufficient to produce an immediate allergic reaction to food. (27) It has been shown that patients who exhibit delayed allergic reactions fail to show evidence of positive skin test or RAST results to a specific antigen. RAST is a more quantitative assay that correlates with clinical symptoms. It involves the linking of an allergen to a paper disk to which the serum of the patient is added. The amount of specific IgE bound to the allergen is measured by the quantity of radioactivity. Lastly, the Enzyme Linked Immunosorbent Assay (ELISA) identifies antibodies associated with both immediate and delayed type hypersensitivity reactions and is therefore more comprehensive than skin testing or the RAST method. ELISA will identify both IgE and IgG specific antibodies to food substances.
Managing Food Allergies With Nutritional Supplements
Aside from managing food intolerance with rotation and elimination diets, the strategic use of specific nutritional supplementation is generally beneficial in both alleviating the symptoms and improving the health of the digestive tract. Healing the functional lining of the gastrointestinal system and protecting the tissues from further degeneration are primary therapeutic goals. Supplements that may be useful in achieving these ends include N-acetyl glucosamine, N-acetyl neuraminic acid (sialic acid), D-mannose, L-glutamine, L-glutamic acid HC1, inulin, quercitin, methylsulfonylmethane (MSM), Manapol[R], and digestive enzyme formulations, with, or without, hydrochloric acid. (28, 29) GI ReNu[R] is an example of a nutritional supplement which provides these important immune modulating nutrients. By ingesting appropriate nutrients 15-30 minutes before meals, the stomach and intestines may be preconditioned and abnormal responses to foods lessened or eliminated. We will now briefly discuss how these nutrients may interact with the digestive system.
N-acetyl glucosamine, an amino-saccharide, is produced under the influence of an enzyme called glucosamine synthetase acting upon glucosamine-6-phosophate, from which n-acetyl glucosamine is formed. Pathology of the intestinal mucosa has been associated with decreased intracellular concentrations of this sugar. (30) This fact is coupled with a concurrent reduction in levels of glucosamine synthetase found when there is general atrophy of the functional epithelium. During recovery from acute phases of ulcerative colitis, this enzyme was found to rise to levels well above normal, while no similar elevation was noted in patients who did not experience a recovery phase. (31) Increases in this enzyme's presence could be linked to renewed synthesis of gastrointestinal mucus, immunoglobulin and secretory components of IgA, all of which contain large amounts of N-acetyl glucosamine. Supportive data has been evidenced in studies measuring the N-acetylation of glucosamine in patients with inflammatory bowel disease, and it has been proposed that such impairment may be linked to decreased production of the glycoprotein which protects the intestinal mucosa from damage by bowel contents? N-acetyl glucosamine has also demonstrated an ability to reduce gluten-based reactions within the small intestine by blocking macrophage activation. This sugar also modulated insulin resistance in a positive way and reduces undesirable effects of wheat germ agglutinating lectin. (32) It has been utilized as an effective adjunct in the management of non-tropical sprue.
N-acetyl neuraminic acid is an important immunomodulating carbohydrate that plays a very important role in the proper development of the lining of the small intestine from the standpoint of both its digestive and immune functions. (33) It is a potent anti-inflammatory agent, modulating tumor necrosis factor, several interleukins, and histamine release and metabolism. It is useful as a nutritional supplement for the management of inflammatory bowel disease and IgA- and IgE-mediated reactions in the gut and respiratory systems. It is a major component of mucin, a critical component in the management of healthy mucus membranes.
D-Mannose is an important monosaccharide that aids in the elimination of undesirable bacteria from the gastrointestinal, urinary, and respiratory systems. It also modulates immune responses to yeasts, such as candida species. It appears to play a constructive role, especially when acetylated, in the control of mucus membrane healing.
L-Glutamine is an amino acid whose deprivation has been shown to produce apoptosis in the enterocytes of animal models. Exclusion of glutamine for only 24 hours has been associated with induced apoptosis and overall reduction of epithelia in the human gut. Glutamine is also necessary to support nitrogen-stimulated proliferation in intestinal epithelial cells. It is curious to note that while glutamine is the most abundant amino acid in the blood, capacity to convert this compound from its most common precursors (glutamic acid, argentine, and proline) is apparently insufficient to fill the nominal requirements of intestinal epithelial cells. Glutamine has also shown promise when administered in liberal quantities to human patients receiving cytotoxic therapies, with associated increases in dosage tolerance being observed. (34) Oral glutamine has been associated with elevated levels of circulating growth hormone, increased bicarbonate reserves, and gut glutathione production. (35,36) During radiochemotherapy for esophageal cancer, glutamine supplementation protected lymphocytes and attenuated gut permeability in treated patients. (37) Immune system enhancement has also been noted in tests on mice. (38) Oral glutamine-supplemented animals demonstrated a marked increase in interleukin-2 concentration and a modest increase in intestinal T-cell counts.
L-Glutamic acid HC1, also an amino acid, is a fundamental component of glycosaminoglycan structure. It is a precursor to glutamate. Recent studies have also linked it with chemical signaling systems directed at osteoblastic and osteoclastic regulation. (39) It is complexed with aspartic acid within macromolecular motifs associated with glycosaminoglycans that bind calcium to linked acidic phosphoproteins, structures essential to healthy bone.
Sulfur plays an indispensable role in human nutrition, participating in detoxification, as well as antioxidant, enzymatic, and synthetic pathways of human metabolism. Methylsulfonylmethane (MSM) (40) is a naturally occurring derivative of DMSO and is suitable for dietary utilization. Studies have indicated that MSM can enhance stress responses and reduce gastrointestinal upset, inflammation of mucus membranes, allergic responses to ingested antigens, and some types of pain. It appears to be non-allergenic, non-toxic, and able to inhibit cross-linking of collagen and other proteins. This serves to enhance tissue flexibility and resilience.
Inulin is a mixture of linear fructose-polymers (-2,1) with different chain-length and one glucose at each C2-end. It is a soluble dietary fiber that typically undergoes bacterial fermentation in the intestine to short-chain fatty acids which are reabsorbed in the colon. As a result, inulin tends to increase fecal volume, while decreasing transit time, as well as intraluminal pH levels. Associated increases in bifidus population promote improved intestinal flora generally. (41) Alleviation of constipation, decreased blood pressure and blood sugar levels, and increased levels of colonic butyrate have been reported.
Manapol[R] (42) is a proprietary blend of stabilized polysaccharides derived from aloe vera and is used for its anti-inflammatory effects and its ability to support cellular repair and tissue healing by enhancing amounts of elastin, collagen, and ground substance present in the early stage of healing. It is also a valuable source of metabolically important carbohydrates that serve to support the immune system, as well as trans-cellular and intracellular communication. It has been used for years in formulations designed to support dermal healing after radiation induced injury and is a basic ingredient in several compounds which promote immune regulation. (Manapol[R] is a registered trademark of Caraloe, Inc., of Carrington Laboratories.)
Digestive enzymes are important in digesting carbohydrates of various molecular weights and configurations. Complete hydrolysis of polyglucans frees important saccharides and reduces the propensity for excessive disaccharide and polysaccharide concentrations in the intestine. Consequently, the intraluminal environment of the intestine may be improved with concurrent reduction of pro-inflammatory effects and improved absorption characteristics. Recent studies have linked poor digestion of certain sugars with chronic inflammatory conditions, both in the bowel and elsewhere. Phytase NSP Blend specifically inactivates phytates, thereby reducing mineral binding.
(1) D'Adamo J. "Digestive Integrity" in Live Right for Your Type. New York: C.P. Putnam's Sons, 2001; 46-52.
(2) Bricker DS. "Colostrum: Implications for accelerated recovery in damaged muscle and cartilage, prevention of some pathogenic disease." The American Chiropractor.
(3) Buckley RH and Metcalfe D. "Food Allergy." JAMA, 1982; 248:2627-31.
(4) Pusztai A. "Dietary lectins are metabolic signals for the gut and modulate immune and hormone functions." Eur J Clin Nutr, October 1993; 47(10):691-99.
(5) Falth-Magnusson K, et al. "Elevated levels of serum antibodies to the lectin wheat germ agglutinin in celiac children lend support to the gluten-lectin theory of celiac disease." Pediatr Allergy Immunol May 1995; 6(2):98-102.
(6) Brady PG, et al. "Identification of the dietary lectin wheat germ agglutinin, in human intestinal contents." Gastroenterology, August 1978; 75(2):236-39.
(7) Hollander DC, et al. "Increased intestinal permeability in patients with Crohn's disease and their relatives. A possible etiologic factor." Ann Intern Med, December 1986; 105(6):883-85.
(8) Jordinson M and Playford Calam RJ. "Effects of a panel of dietary lectins on cholecystokinin release in rats." Am J Physiol, October 1997; 273(4 Pt I):G946-50.
(9) Jordinson M, et al. "Soybean lectin stimulates pancreatic exocrine secretion via CCK- A receptors in rats." Am J Physiol, April 1996; 270(4 Pt I):G653-59.
(10) Weinman MD, et al. "Repair of microvilli in he rat small intestine after damage with lectins contained in red kidney bean." Gastroenterology, November 1989; 97(5):1193-204.
(11) Metcalfe DD, Sampson HA, Simon RA, editors. Food Allergy: Adverse Reactions to Food and Food Additives. Cambridge: Blackwell Science, 1997.
(12) Lessof MH, editor. Clinical Reactions to Food. New York: John Wiley and Sons, 1983.
(13) "Adverse Reactions to Foods" American Academy of Allergy and Immunology, Committee on Adverse Reactions to Foods, National Institute of Allergy and Infectious Disease, U.S. Department of Health and Human Services, July 1984.
(14) Kaczmarski M, et al. "IgE in children with adverse reactions to food." Pneumonologia I Alergologia Polska 1992; 60(Suppl 1):9-15.
(15) Edwards AM. "Food allergic disease." Clin Exp Allergy, 1995; 25(Suppl 1):16-19.
(16) Businco L et al. "Food allergy and asthma." Pediatric Pulmonology, 1995; 11(Suppl):59-60.
(17) Shoda R, Matsueda K, Yamato S, and Umeda N. "Epidemiologic analysis of Crohn disease in Japan: increased dietary intake of n-6 polyunsaturated fatty acids and animal protein relates to the increased incidence of Crohn disease in Japan." American Journal of Clinical Nutrition, 1996 May; 63(5):741-5.
(18) Zoli G, Care M, Parazza M, et al. "A randomized controlled study comparing elemental diet and steroid treatment in Crohn's disease." Alimentary Pharmacology & Therapeutics, 1997 Aug; 11 (4):735-40.
(19) Strannegard O and Strannegard IL. "The causes of the increasing prevalence of allergy: is atopy a microbial deprivation disorder?" Allergy. 2001 Feb; 56(2):91-102.
(20) Worm M, Vieth W, Ehlers I, et al. "Increased leukotriene production by food additives in patients with atopic dermatitis and proven food intolerance." Clinical & Experimental Allergy, 2001 Feb; 31(2):265-73.
(21) Patja A, Makinen-Kiljunen S, Davidkin I, et al. "Allergic reactions to measles-mumps-rubella vaccination." Pediatrics, 2001 Feb; 107(2):E27.
(22) Shakib F, et al. "Elevated serum IgE and IgG4 in patients with atopic dermatitis." Br J Dermatol, 1977; 97:59-63.
(23) El Rafei A, Peters SM, Harris N, and Bellanti JA. "Diagnostic value of IgG4 measurement in patients with food allergy." Ann Allergy, 1989; 62:94-99.
(24) Van Arsdel PP and Larson EB. "Diagnostic tests for patients with suspected allergic disease." Ann Intern Med, 1989; 110 (4):304-12.
(25) Gwynn CM and Ingram J. "Bronchial provocation tests in atopic patients with allergen specific IgG4 antibodies." Lancet, 1982; 1:254-56.
(26) Paganelli F, et al. "Detection of specific antigen within circulating immune complexes." Lancet, 1979; 1:1270.
(27) Perlmutter L. "Non-IgE mediated atopic disease." Ann All, 1984; 52:640.
(28) Birch GG. "Metabolic effects of rare food sugars." Lancet. 1971; 2:1419-1420.
(29) Harper's Biochemistry, 24th edition (1996); published by Appleton & Lange; Chapters 4, 15, 55, 56,57.
(30) Burton AF and Anderson FH. "Decreased incorporation of 14C-glucosamine relative to 3H-N-acetyl glucosamine in the intestinal mucosa of patients with inflammatory bowel disease." Am J Gastroenterol, 1983;78:19-22.
(31) Goodman MJ, Kent PW, and Truelove SC. "Glucosamine synthetase activity of the colonic mucosa in ulcerative colitis and Crohn's disease." Gut, 1977; 18:219-228.
(32) Auricchio AS, DeRitis G, DeVincenzi M, et al. "Mannan and oligomers of N-acetyl glucosamine protect intestinal mucosa of celiac patients with active disease from in vitro toxicity of gliadin peptides." Gastroenterology, 1990; 99:973-978.
(33) Kai H, Murata Y, Ishii T, et al. "Anti-allergic effect of n-acetylneuraminic acid in guinea pigs." J Pharm Pharmacol, 1990; 42:773-777.
(34) Klinberg VS and Souba WW. "The importance of intestinal glutamine metabolism in maintaining healthy gastrointestinal tract and supporting the body's response to injury and illness." Surg Annu, 1995; 22:61-67.
(35) Welborne TC. "Increased plasma bicarbonate and growth hormone after an oral glutamate load." Am J Clin Nutr, 1995; 61 (5):1058-1061.
(36) Cao Y, Feng Z, Hoos A, and Klimberg VS. "Glutamine enhances gut glutathione production." JPEN J Parenter Enteral Nutr, 1998; 22(4):224-227.
(37) Yoshida S, Matsui M, Shirouzu Y, et al. "Effects of glutamine supplements and radiochemotherapy on systemic immune and gut barrier function in patients with advanced esophageal cancer." Ann Surg, 1998; 227(4):485-491.
(38) Alverdy JC. "Effects of glutamine-supplemented diets on immunology of the gut." J Parenter Enteral Nutr, 1990; 14:109S-113S.
(39) Modrowski D, Lomri A, and Marie PJ. "Glycosaminoglycans bind granulocyte-macrophage colony-stimulating factor and modulate its mitogenic activity and signaling in human osteoblastic cells." Cell Physiol, October 1998; 177(1):187-195.
(40) Herschler RJ. "Methylsulfonylmethane and methods of use." United States Patent 4,296,130; October 20, 1981.
(41) Gibson GR, Beatty ER, Wang X, and Cummings JH. "Selective stimulation of bifidobacteria in the human colon by oligofructose and inulin." Gastroenterology, 1995; 108:975-982.
Raymond Dent, ND, is a member of the first graduating class of the John Bastyr College of Naturopathic Medicine (now Bastyr University), at Seattle, Washington. He was awarded his doctorate in Naturopathic Medicine four years after the institution's founding in 1978.
Dr. Dent has practiced privately, as well as in association with several holistically oriented clinics and laboratories over the last 20 years. He has served on the Board of Directors of the Washington Association of Naturopathic Physicians and has taught diagnostic ultrasound and clinical urology at Bastyr University. He has authored and co-authored numerous articles related to alternative health care and has appeared on several television and radio broadcasts over the years. Dr. Dent's practice is broad in scope and utilizes therapeutic nutrition, homeopathy, and botanical medicine. He is the only naturopathic physician in Washington offering in-office cosmetic radiosurgical procedures for the removal of facial veins (telangiectasia), spider veins and skin tags. He also provides specialized non-surgical therapy for those troubled by hemorrhoids. Dr. Dent is able to combine advanced medical therapies with traditional naturopathy, thereby optimizing patient satisfaction and health.
|Printer friendly Cite/link Email Feedback|
|Author:||Alonso, Larisa; Dent, Raymond Smith|
|Date:||Jun 1, 2003|
|Previous Article:||Effects of fraction SX of maitake mushroom on insulin resistance.|
|Next Article:||The legacy continues.|