Search by Keyword
SYMPTOM SURVERY and DOCTOR'S CONSULTATION COST $50.00
Paid by sending a check to: Dr. Bernard Presser D.C.
2632 E. Larkspur Drive
Phoenix, AZ 85032
Password and Instructions are sent by e-mail once we have your name, phone number and e-mail address.
Results are sent to you by e-mail. Consultation is done over the phone by a licensed chiropractor.
Your $50.00 will be applied to your first order of supplements from us making your Symptom Survey and Doctor's Consultation FREE.
If you have any questions, please contact us at 602-882-0648.
For over 20 years a bacteria "peculiarly specific" to humans - Helicobacter pylori - has been associated with peptic ulcers, gastritis, and gastric cancer. Other problems attributed to H pylori include atrophic gastritis (chronic stomach inflammation with wasting of the mucous membrane lining and glands), gastroenteritis (inflammation of the stomach and intestinal tract), idiopathic thrombocytopenic purpura (leakage from capillaries due to inadequate platelet levels for blood clotting), rosacea (chronic facial skin condition), chronic urticaria (hives), atherosclerotic stroke, migraine headaches, hyperplastic gastric polyps (excessive tissue growths in the stomach), and heart attacks (as an "influence" rather than a cause). An H pylori subtype - cytotoxin-associated gene-A (CagA) strain - is thought to produce the potent toxins that attack tissues. i
Back in 1982, Dr. Barry Marshall and his colleagues found H pylori in the cultured material which was swabbed from ulcer craters taken from stomachs of patients suffering from gastric ulcers. H pylori always seemed to be present, though there were usually other microorganisms present too, including other bacteria and yeast-like organisms. Further research identified H pylori in cases of chronic gastritis. Dr. Marshall's research was overlooked for a while since, for many years, it was assumed that bacteria could not survive the acid environment of the human stomach. So Dr. Marshall swallowed some cultured H pylori himself and eventually developed severe stomach pain. This won attention to his work. Now it is medically "accepted" that H pylori causes stomach ulcers. Patients with ulcers ALMOST always have H pylori. Ulcers USUALLY go away once the bacterium is "eradicated with medication. ii
Almost half the population carries H pylori. It seems to be harmless for most, dangerous to some, and beneficial to others. The majority of people who test positive for it do not have ulcers or stomach cancer or any other conditions associated with it. Because H pylori infection is so prevalent, it is often present in people who have common gastrointestinal (GI) problems like indigestion, abdominal pain, and gastroesophageal reflux disease (GERD). Yet eliminating H pylori does not help these conditions. In fact, it may aggravate symptoms. Some studies suggest that the presence of the bacterium REDUCES the likelihood of developing GERD. One study found that the rate of infection was only half as high in people with reflux esophagitis (inflammation of the esophagus) as it was among healthy people - 34% vs. 76%. So H pylori appears to be beneficial in some areas.
Stomach ulcers have the biggest link to H pylori. The bacterium is thought to weaken the protective mucus coating of the stomach and duodenum (first part of the small intestine), allowing acid (hydrochloric acid, a digestive juice) to penetrate the sensitive lining beneath. The acid and bacterium irritate the lining and cause a sore or ulcer. Unfortunately, scientists do not yet know why H pylori causes ulcers in some people but not in most others. However, the "triple therapy" used to eradicate H pylori eliminates symptoms in 95% of cases with little recurrence. The two-week regimen usually consists of TWO ANTIBIOTICS (like tetracycline, amoxycillin, metronidazole) plus EITHER a PROTON-PUMP INHIBITOR (Prilosec, Nexium, etc.) which suppresses acid production OR BISMUTH (Pepto-Bismol). While this treatment seems successful 9 times out of 10, patients must take as many as 20 pills a day and the antibiotics commonly cause side effects such as nausea, vomiting, diarrhea, digestive upsets, yeast overgrowth, and a number of other problems. Beneficial bacteria, needed by the body for proper function, are drastically reduced, causing more troubles. ii
A study from Japan found that getting rid of H pylori triggers a marked increase in levels of a powerful appetite-boosting hormone called ghrelin. This may explain why weight gain is a big problem for many people taking medication to get rid of the bacterium.
A small percentage of people harboring H pylori (3%) will develop gastric cancer. Eradication of the bacterium - in conjunction with surgery, chemotherapy, or both - is thought to help. But, since family history is definitely a factor, there are more causes involved in developing this cancer.
Obviously, the H pylori story is complicated with many variables. In the US, infection is more common in older adults, African Americans, Hispanics, and persons of low socioeconomic circumstances. Why? And why do some people with H pylori become sick and others do not? Not known. ii Also, antibiotic resistance to H pylori "is a growing problem" so eradication therapy "may become complicated" with a need to first test for antibiotic susceptibility. iii There is no clear-cut, direct cause-and-effect process and cure for H pylori infection and gastric (or other) diseases. The "clinical outcome of H pylori infection is determined by a complex interaction of environmental influences and host and microbial virulence factors." It is not simple. iv
A peptic ulcer is an open sore or lesion of the mucous membrane lining, accompanied by sloughing of inflamed necrotic (dead) tissue, occurring in the lower end of the esophagus, in the stomach, or in the duodenum. The mucous membrane linings coat the digestive tract with a layer of mucus which normally protects the tissues from potent gastric juices (hydrochloric acid, pepsin, other enzymes). Prostaglandins keep the blood vessels of the digestive tract dilated, insuring sufficient blood flow to the mucosal tissue for mucus secretions. A rich nerve supply and immune system participation also play important roles. Irritation or injury to the GI lining, increased susceptibility (due to nutritional deficits, for example), stress, use of non-steroidal anti-inflammatory drugs (NSAIDs), use of steroids, food allergies or intolerances, excess alcohol or caffeine consumption, smoking, increased intake of highly refined or processed foods, and other factors have all been linked to ulcers and decreased integrity of the mucosal barrier. Yet many doctors consider H pylori as "the" cause of peptic ulcer. v
Because of its corkscrew shape, H pylori can penetrate the mucus coating and attach itself to the lining of the digestive tract. This bacterium can survive the acidic conditions of the stomach because it produces an enzyme, urease, which generates ammonia and bicarbonate to neutralize acid. Because the problem appears to be a "bug" and there are drugs to kill "bugs," the medical community has embraced the bacterial theory. However, there are bugs in the bug theory.
A study in Denmark found that a quarter of the ulcer patients treated for H pylori did not respond to the drug therapy. A study in Spain found that antibiotics often failed to eradicate the bacterium. "We now recognize that only about 50 percent of ulcers are linked to H pylori," said Guy Pugh, MD, medical director, Marino Center for Progressive Health, Cambridge, MA. Clearly, "most of us are infected with this bacterium but have no symptoms." Some scientists feel the bacterium may be able to coexist harmlessly with its host, or may even have beneficial effects. There is evidence that it has been in people "for at least 11,000 years, and possibly much longer." Thus, the question is being asked: "Does infection always cause disease or is it harmful under certain circumstances?" This type of question has been raised since the discovery of microorganisms - is the problem the bacteria or the terrain (host)? vi
ANYTHING that harms or disrupts the lining of the digestive tract and/or the cells (goblet cells) that secrete the mucus may cause problems. H pylori is thought to adhere to and weaken epithelial cells that line the stomach. Yet such "corrupt behavior" is "unlike that of other bacteria" and "runs counter to many medical beliefs." Infection with this bacterium can coexist with "mysterious abdominal pain, complete with negative x-rays." And this is the first time that a bacterium has been blamed for causing a cancer.
Although H pylori is accused of CAUSING problems, "gastric atrophy [damage and death of cells lining the digestive tract] and reduced hydrochloric acid secretion may be the initiating factors in Helicobacter pylori infection, along with reduced vitamin C secretion in the stomach..." (Emphasis added) Thus an unhealthy condition of the digestive tract, reduced stomach acid, and decreased vitamin C secretion may set up conditions for H pylori habitation. Tissues are ALREADY susceptible to irritation or injury and, in fact, may ALREADY be damaged. Many physicians believe that low stomach acid, for example - not excessive acid - is a significant cause of ulcers. So the question is whether H pylori nibbles away at HEALTHY gut cells or UNHEALTHY/DEAD gut cells. Is H pylori the CAUSE of GI woes or a RESULT of already deteriorating conditions?
Consider the common use of antacids and acid-reducing drugs. INDIGESTION becomes the much more serious problem of UNDIGESTION. Pain and discomfort may be eased, but foods and food supplements cannot be properly and completely digested. Nutrients are lost. As the mucosal lining becomes increasingly unhealthy or irritated, inflammation develops to attempt repair. Insufficient supplies of nutrients for repair, depressed secretion of digestive enzymes, and drug-induced low hydrochloric acid can all lead to increased tissue damage. Some researchers contend that bacteria are Nature's garbage collectors that engulf and break down dead substances. H pylori may be disassembling damaged tissues. Like little garbage bags, the bacteria harbor diseased, dead, and toxic substances. They themselves are not a problem, but the garbage they carry may be. vii
H pylori supposedly causes gastric cancer, but "20% - 30% of gastric mucosa-associated lymphoid tissue (MALT) lymphoma associated with Helicobacter pylori do not regress after antibiotic therapy." The bacterium is accused of causing ulcers, but its eradication does not always have a protective effect in patients with bleeding peptic ulcer. The simple presence of H pylori "is not an indication for eradication. Some disorders are improved by eradication, others are not." People who carry H pylori are at higher risk for developing peptic ulcer disease and gastric cancer than those who do not carry the organism, but "carriage is neither necessary nor sufficient to explain either disease..." Additionally, the very prevalence of H pylori in the population may be declining. This "may mean that an increasing proportion of cases of peptic ulcer disease will be H pylori negative." Evidently, ulcers will keep occurring without the presence of H pylori.
The frequency of H pylori infection varies from country to country. It is higher (70% to 90%) in most developing nations. In developed countries, less than 10% of children and about 50% of 60-year-olds carry the bacterium. Only a tiny fraction of those who are infected develop a disease. Since 1968, the number of people in the US infected with H pylori has dropped by 50% with similar trends in other developed countries. There have also been decreases in peptic-ulcer disease and lower-stomach cancers. However, maladies such as gastroesophageal reflux disease (GERD), Barrett's esophagus (an ulcer-like disease in the esophagus), and cancers of the lower esophagus and upper stomach "have been dramatically and progressively increasing." Could there be a connection? H pylori has beneficial effects. Infected people have stronger immune responses. Infection inhibits reflux esophagitis (inflammation of the esophagus). It "may be protective against gastroesophageal reflux disease." Patients who have had their H pylori colonies killed off have a higher risk of developing GERD and esophageal cancer. The presence of the bacterium is associated with a 50% to 80% reduction in risk of esophageal cancer.
Numerous "unsettling questions" remain to confound the assertion that H pylori causes cancer. "What is lacking is definite proof that H pylori eradication truly can prevent cancer." The incidence of stomach cancer in the general population is similar between people receiving H pylori eradication treatment and those receiving placebo. The increase in the rate of cancers near the gastro-esophageal junction and the upper stomach might be linked to the disappearance of H pylori. While one strain of H pylori "appears to be" a risk factor for both duodenal ulcers and gastric cancer, people with duodenal ulcers actually have a lower risk for gastric cancer than the general population. Colonization strains "may be protective against the formation of short- and long-segment Barrett's esophagus and its malignant complications." The bacterium is seen with two faces: "If you have it, it's bad news for your lower stomach. If you don't have it, it's bad news for your esophagus." viii
H pylori presence is associated with allergic reactions to foods along with increased epithelial permeability (‘leaky gut'). People's sensitivities can change and "this may be due to the status of their intestinal mucosa integrity." Whether the bacterium alters the lining of the digestive tract (allowing an increased uptake of inappropriate or partially digested compounds) OR an unhealthy mucous membrane lining necessitates the presence of the bacterium is not clear. Is the H pylori the problem or does the problem bring on the H pylori? ix
Although H pylori is considered "the" cause of ulcers, recent studies show that people who feel stressed are twice as likely as their counterparts to develop an ulcer. Moderate physical activity cuts in half the risk of ulcer compared to no physical activity. Alcohol irritates the stomach lining. Smoking increases the volume and concentration of acid secreted by the stomach. Obviously, ulcers "may turn out to have more than one ‘cause.'" Peptic ulcer is "an excellent example of the limitations of mono-causal thinking." Like most ailments, it has "a multifactorial origin." x
Non-steroidal, anti-inflammatory drugs (NSAIDs, such as aspirin, Advil, Motrin, Aleve, etc.) are a common cause of ulcers. People who use NSAIDs have four times the risk of developing peptic ulcers than non-users. The rate of ulcers associated with H pylori has FALLEN but the rate of ulcers related to NSAIDs has RISEN. Whether there is any interaction between H pylori, NSAIDS, and the risk of ulcer is a controversial issue. So far, findings indicate they are independent factors. For example, NSAIDs induce ulceration in the absence of H pylori and eradication of H pylori does not reduce the risk of ulcer in chronic NSAID users. xi An estimated 50 million Americans take low-dose aspirin daily ostensibly to prevent heart attack and stroke. How many of them know that aspirin carries the risk of upper GI bleeding at doses as small as 75 mg a day?
A meta-analysis found that 20% of patients had ulcer recurrence within only 6 months after eradication of H pylori. "The ideal treatment for H pylori has yet to be identified." But is it H pylori that NEEDS to be ‘treated'? Many questions remain. When Dr. Barry Marshall experimented on himself with H pylori, he developed some "acute changes" of gastritis, but he did not develop a peptic ulcer. After 14 days, all evidence of gastritis - along with the bacterium - had disappeared. Drinking the bacteria broth may have simply irritated his stomach lining.
Antibiotic therapy alone has not been clearly shown to heal peptic ulcers any better than placebo. Symptomatic success always includes either bismuth (Pepto-Bismol) or drugs that turn off acid secretion (Prilosec, Nexium, Prevacid, etc.) or histamine-2-receptor inhibitors (Pepcid, Tagamet, Zantac, etc.) - ALL of which have the ability to heal peptic ulcers by mechanisms unrelated to the elimination of H pylori. In fact, several studies reported on patients in whom peptic ulcers healed DESPITE persistence of H pylori in the stomach.
These and other findings have led some researchers to postulate that the association between H pylori and peptic ulcer is really an association between H pylori and "the background of mucosal inflammation in which the ulcer developed in the first place." In other words, H pylori resides on the surface of the mucous membrane lining of the stomach and/or duodenum "in any disease state in which there is a breach in the integrity of the mucosal barrier." By contrast, when there is NO BREACH in the integrity of the mucosal barrier, H pylori tends not to be found - such as in people with healthy stomachs or those with other problems that do not involve disruption of the mucosal lining. When "healthy" people DO have H pylori in their stomachs, "they also have histological gastritis present as a prerequisite." There is already evidence of irritation of the stomach lining. xii
Should a patient opt for conventional antibiotic treatment, the alternative clinician should probably wait before attempting more natural therapies (with the exception of suggesting probiotics). But if a patient decides to try food and herbal therapies, then a protocol that fits individual needs can be followed. Various deficiencies are associated with increased risk for ulcers or trigger symptoms. In particular, deficits of vitamin C complex (including its flavonoids) are common. B vitamins (especially B6, B12) and zinc are often low. Calcium, magnesium, iron, glutathione, vitamin A complex, vitamin E complex, and essential fatty acids as well as the vitamin C complex and B vitamins have all been shown to provide benefits.
When H pylori is present in the stomach, vitamin C complex concentrations of the gastric juice are lower than when the bacterium is not present. Vitamin C complex is a protection against gastric cancer. Gastritis associated with H pylori results in lowered secretion of vitamin C complex into the gastric juice. People with higher levels of ascorbic acid (as a marker for vitamin C complex) are less likely to become infected with H pylori. Vitamin C complex supports the health of epithelial cells (that line the digestive tract), the strength and integrity of blood vessels which nourish the digestive tract, and inflammation and repair functions. xiii Quercetin, rutin, and kaempferol - flavonoids and components of vitamin C complex - have been shown to inhibit gastric damage. Low intakes of vitamin A complex, B complex, potassium, and fiber greatly increase the risk of getting an ulcer. B vitamins are imperative to stomach and intestinal cells and their ability to maintain a proper acid/alkaline balance. H pylori is usually not found when stomach secretions are sufficiently acidic.
Both vitamin C complex and astaxanthin - a carotenoid-rich microalgae which can enhance immune response and ease gastric inflammation - appear to reduce (the need for) bacterial load. The rate of H pylori infection was less frequent among children who ate several servings of fruits and vegetables daily - foods rich in vitamin C complex, carotenoids, and other nutrients. Children whose daily vitamin C complex intake from fruits and vegetables was less than 40 mg had greatly increased odds of infection. There was also increase in risk if daily carotenoid intake was low.
Vitamin A complex is critical to the health and integrity of the GI mucosa. With deficiency, the mucous membranes become hardened and are more easily penetrated. Vitamin A complex is also needed for proper absorption of some minerals (such as zinc) and protein as well as playing a role in the inflammation and repair processes. The vitamin B complex is necessary for proper muscle tone, nerve function, stimulation of digestive secretions, fat metabolism and carbohydrate metabolism. Vitamin E complex contributes to proper muscle tone and mucous membrane health. Deficiency has been linked to digestive problems including peptic ulcers. Coenzyme Q10 (and other coenzyme Qs) is essential to muscle health and function as well as to provide intracellular energy to promote protective mucus secretion and, for healing, rapid cell growth.
Calcium is a key nutrient in inflammation and repair, and it also supports muscle and nerve function. Potassium is involved in the proper production of hydrochloric acid; in addition it supports muscle and nerve tissues. Zinc evidently speeds the healing of ulcers and reduces inflammation, including that caused by aspirin. It is depleted with injury, inflammation, and repair. Zinc strengthens and supports the health of the GI lining and stimulates mucus production to protect that lining. Zinc helps to break down hydrogen peroxide in the stomach, reducing the damage it may cause. Magnesium can help stop gut spasm. Chlorophyll is cleansing and healing to cells such as those lining the digestive tract; it appears with carotenoids, vitamin E complex, fatty acids (including the omega-3s), vitamin K, and magnesium, along with many other factors.
Protein is needed for mucous membrane soundness, resistance, mending, and maintenance. In particular, cysteine, methionine, carnosine, acetylcysteine, glutathione, and sulfhydryl compounds have been shown to be mucosal protectors or relapse preventers. Phosphatidylcholine is highly beneficial to the GI lining, preventing or healing lesions. Lecithin, egg yolks, and butter are good sources. The cells lining the GI tract are very rich in cholesterol; cholesterol-lowering treatments may adversely affect the digestive tract. xiv
Freeze-dried colostrum (milk taken from the cow immediately after the birth of a calf) has been shown to eliminate H pylori. Lactoferrin - a protein present in human and cow's milk - plus the medical "triple therapy" eradicated H pylori better than medication alone. Probiotics - such as Lactobacillus acidophilus, Bifidobacterium lactis, and other "good" bacteria (especially lactic-acid bacteria) or yeasts such as Saccharomyces - reduce urease activity and overgrowth of H pylori. Daily consumption of yogurt, for instance, can ‘down-regulate' H pylori presence and chronic gastritis. And probiotics stabilize the gut mucosal barrier. Use of probiotics has been proven effective in the treatment of many gastrointestinal conditions. Probiotic supplements or foods containing indigenous flora (such as UNpasteurized sauerkraut, miso, yogurt, etc.) inhibit H pylori growth and may result in eradication. An aggressive probiotic approach can sometimes reduce the symptoms of ulcer without the use of medication. And co-administration of probiotic therapy can markedly reduce the intestinal side effects resulting from antibiotic treatment. xv
Essential fatty acids are important for repairing damaged cells; deficits of omega-3s are especially common. Eicosapentaenoic acid (EPA, an omega-3 fatty acid), as found in fish oil for example, reduces acute gastric erosions and ulcers. Deficiency of polyunsaturated fatty acids (PUFAs) - especially gamma-linolenic acid, dihomo-gamma-linolenic acid, arachidonic acid, and EPA - may contribute to duodenal ulcer incidence. People with duodenal ulcers have low plasma levels of these PUFAs. In experimental animals and in humans, PUFAs can heal ulcers and protect the gastric mucosa from aspirin and steroid-induced damage. xvi
Natural, unprocessed honey (some varieties more than others, such as Manuka) is effective in eliminating H pylori and promoting healing of ulcers. xvii A number of herbs may be effective. Goldenseal, barberry, and Oregon grape root contain berberine which has "antimicrobial" properties. Barberry has been used for centuries as an effective treatment for stomach ulcers. Allicin, a component of garlic, may reduce bacterial load in some people; garlic itself may prove to be a "useful" therapy. A clinical trial on rhubarb showed an 89% success rate in treating H pylori. Marshmallow root, along with an equal part of yarrow, help to stop bleeding, and coats and soothes the lining of the digestive tract. (Yarrow should not be used by pregnant women.) An herb often used successfully in treating ulcers is licorice root. (People with high blood pressure should use only deglycyrrhizinized licorice root.) Licorice has a direct healing effect, soothes mucous membranes, and guards against ulcer recurrence. Chamomile exerts antispasmodic activity on the digestive tract, bathing inflamed tissue with relief. Gotu kola extract provided mucosal protection against gastric ulceration in animals. Ginger prevented chemically-induced gut damage and gastric ulcers. Capsicum (as in chili peppers) protected against mucosal injury from alcohol and aspirin. xviii
Poor diet - containing excessive refined, processed non-foods - as well as nutritional deficiencies and under- or mal-functioning digestive organs may all play a role in ulcer development. "A diet based on bad nutrition - junk food, sugar, and white flour - prevents the creation of energy necessary for healing at a cellular level," says John Foster, MD. Choosing the "right" foods can help health peptic ulcers. Fruits and vegetables appear to be especially protective against ulcer; refined sugars are a risk factor. Over a 5-year period, people on a highly refined diet experienced a relapse rate of 81% compared with a relapse rate of only 14% in people following a more unrefined diet.
Freshly made cabbage juice has a legendary reputation for healing ulcers. The "U factor" or "vitamin U" attributed to the power of cabbage is thought by some to be related to glutamine, an amino acid. Glutamine is important to a healthy mucus layer in the gastrointestinal tract and for healing the inflamed tissues lining it. Of course, the interaction of many nutrients and phytochemicals in cabbage is most likely the ‘secret'. Two cups of fresh cabbage juice a day is often recommended.
Cranberry juice prevents H pylori from adhering to gastric mucus - at least in the laboratory. A slice of raw white potato (or potato juice) sometimes provides almost instant relief from the misery of acid indigestion. Raw potato is very alkaline, rich in vitamin C complex, and a source of bioavailable protein. Treatments for gastric and duodenal ulcer with rhubarb extracts were "efficient in curing the upper digestive tract bleeding." Extracts of okra appear to prevent H pylori from sticking to the stomach wall. The mucilaginous, sticky ‘goo' in okra is rich in complex sugar compounds and glycoproteins that soothe the GI lining. When scientists tried to isolate and purify the okra preparation, it did not work as well.
The incidences of food and drug allergies occur in 25% and 30% (respectively) of patients with peptic ulcer. But about 70% manifest various "allergic" reactions, indicating more intolerances than true allergies (with elevations of IgE blood levels). Food elimination trials particularly point to refined foods (e.g., refined sugars, white flour products, milled grains, desserts, sweets), chocolate, colas, fried foods, alcohol, liqueurs, coffee and coffee with sugars as culprits. Avoidance of (pasteurized) milk products also appears to be beneficial. xix
This website has excellent nutritional protocols for ULSERS which are available in conjunction with the Symptom Survey. Take the Symptom Survey to discover specifically what nutrition you need for your individual health problems. I want to emphasize that the whole-food nutrition I recommend CANNOT be purchased in any retail store: so-called "health food" store, drug store, super market, etc. The whole-food nutrition I recommend will help rebuild your body and help restore your health. Those other products will only give you a pharmaceutical (drug) effect. They will attempt to deal with your symptoms, which is the ONLY thing any drug can do, while leaving the state of your health unchanged.
i M Aspholm et al, Science, 23 Jul 2004, 305 (5683): 519-22; Science News, 10 Aug 2002, 162(6): 94; A Pictroiusti, Circulation, 2002, 106: 580-84; N Sarraf-Zadegan et al, Coronary Health Care, 2001, 5: 202-7; Veg Times, Aug 2002, 300: 14.
ii E McDonagh, Acres USA, Nov 1999, 29(11): 38-9; S Bickston, Health News, Dec 2001, 7(12): 1-2; K Bone, Nutr & Healing, Mar 2005, 12(2): 7-8; Lancet, 16 Oct 1999, 354(9187): 1362; J Danesh et al, Lancet, 4 Mar 2000, 355(9206): 766-7; L Friedman, Health News, 1 Feb 1999, 5(2): 3; F Chan et al, Lancet, 21 Sept 2002, 360(9337): 933-4; Health News, Apr 2005, 11(4): 12.
iii M Guslandi, Lancet, 16 Jan 1999, 353(9148): 241-2; A van Zwet et al, Lancet, 14 Nov 1998, 352(9140): 1595.
iv M Hocker & P Hohenberger, Lancet, 11 Oct 2003, 362(9391): 1231-33.
v M Murray & J Pizzorno, Encyclopedia of Natural Medicine, Rocklin, CA(Prima Pub), 1991; M Werbach, Healing Through Nutrition, NY(Harper & Collins), 1993; A Guyton & J Hall, Textbook of Medical Physiology, Philadelphia(W B Saunders Co), 1995.
vi K Erickson, Herbs for Health, May/Jun 2001, 6(2): 60-3; I Das et al, Lancet, 5 Apr 1997, 349 (9057): 997-8; D Falush et al, Science, 7 Mar 2003, 299(5612): 1582-5; B Spratt, Science, 7 Mar 2003, 299(5612): 1528-9; D Bonn, Lancet Infect Dis, Jan 2003, 3(1): 6.
vii B Deplancke & H Gaskins, Am J Clin Nutr, Jun 2001, 73(6):1131-41S; M Amieva et al, Science, 30 May 2003, 300(5624):1338, 1430-4; S Rogers, Total Wellness, Apr 1999:1-4; P Reed, Int J Vitam Nutr Res, 1999, 69(3):220-7; K Bone, Nutr & Healing, Mar 2005, 12(2):7-8; K Hamilton, Clin Pearls News, Nov 1999, 9(11): 223.
viii H Liu et al, Lancet, 6 Jan 2001, 357(9249): 39-40; C Hawkey, Lancet, 19/26 Dec 1998, 352(9145): 2017; M Blaser, JAMA, 15 Dec 1999, 282(23): 2260-62; D Christensen, Sci News, 9 Oct 1999, 156(15): 234-5; I Bhattacharya, Lancet, 29 May 1999, 353(9167): 1859; J Infect Dis, 1999, 179(6):1523-30; Am J Gastroenterol, 2000, 95(9):2306-11; J Natl Cancer Inst, 2004, 96:388-96; J Parsonnet et al, JAMA, 14 Jan 2004, 291(2):244-5; B Wong et al, JAMA, 14 Jan 2004, 291(2):187-94; N Beckham, Mod Phytotherap, 2001, 6(2):11-18; C Marwick, JAMA, 23/30 Aug 2000, 284(8):948; S Spechler et al, JAMA, 8 Mar 2000, 283(10):1264-6; M Vaezi et al, Am J Gastroenter, 2000, 95:2206-11.
ix T Matysiak-Budnick & M Heyman, J Nutr Biochem, Dec 1998, 9(12): 668-74; K Hamilton, Clin Pearls News, Jun 1999, 9(6): 108-9.
x UC Berkeley Wellness Lttr, May 1999, 15(8): 8 & Feb 2001, 17(5): 1; S Rosenstock et al, Gut, 2003, 52: 186-93; R Anderson, Townsend Lttr D&P, Jun 2002, 227: 142; S Levenstein et al, JAMA, 6 Jan 1999, 181(1): 10-11; Y Cheng et al, WJM, Aug 2000, 173: 101-7; K Erickson, Herbs for Health, May/Jun 2001, 6(2): 60-3; JAMA, 24/31 Oct 2001, 286(16): 2052.
xi H Xia et al, Med J Australia, 2000, 173: 515-19; Health News, Mar 2004, 10(3): 11; Health Facts, Mar 2005, 30(3): 1; F Chan et al, Lancet, 21 Sept 2002, 360(9337): 933-41; J Huang, Lancet, 2002, 359: 14-22; R Pounder, Lancet, 5 Jan 2002, 358(9300): 3-4.
xii F Chan & W Leung, Lancet, 21 Sept 2002, 360(9337): 933-41; J Graham, Lancet, 29 Apr 1995, 345(8957): 1095-98; S Rogers, Total Wellness, Apr 1999: 1-4 & Oct 2004: 1-2; S Rogers, No More Heartburn, NY(Kensignton Pub), 2000: 92-104, 207-12.
xiii A Fraser & G Woollard, Gastroenterol Hepatol, 1999, 14: 1070-3; H Feiz, Nutr Rev, Jan 2002, 60(1): 34-6; J Simon et al, J Amer Coll Nutr, Aug 2003, 22(4): 283-9; Fitness, Dec 2003: 55; J Whitaker, Health & Healing, Mar 2004, 14(3): 5.
xiv V Akyon, Clin Microbiol Infect, 2002, 8:438-41; K Goodman et al, J Pediatr Gastroenterol Nutr, 1997, 25: 507-15; GP Sivam et al, Nutr Cancer, 1997, 27: 118-21; C Kockar et al, Acta Medica, 2001, 44: 970100; R Roundtree, Herbs for Health, Jul/Aug 1999, 4(3): 22-3; F DiMario et al, J Clin Gastroenterol, 2003, 36: 396-8; R Anderson, Nat Health, Jan/Feb 2001, 31(1): 48-9; S Cohen, Nat Health, Feb 2005, 35(2): 108; N Fuchs, Women's Hlth Lttr, Jan 2005, 11(1): 3-6; AG Plaza et al, Rev Esp Enferm Dig, Nov 1996, 88(11): 757-62; N Beckham, Mod Phytotherap, 2001, 6(2): 11-17; Clin Pearls News, Oct 2000, 10(10): 183-4; S Fallon & M Enig, Wise Traditions, Summer 2004, 5(2): 13-23; M Stipanuk, Biochemical & Physiological Aspects of Human Nutrition, Philadel (WB Saunders Co), 2000.
xv K Wang et al, Am J Clin Nutr, Sept 2004, 80(3): 737-41; P Marteau, Clin Rev Allergy Immunol, 2002, 22: 255-73; C Felley & P Mitchetti, Best Pract Res Clin Gastroenterol, 2003, 17(5): 785-91; J Udani & M Spar, Altern Med Alert, May 2002, 5(5): 57-61; M Alsahli & P Michetti, Nutrition, 2001, 17(3): 268-9; A Armuzzi et al Digestion, 2001, 63: 1-7.
xvi S Szabo & C Rogers, Lancet, 16 Jan 1988: 119; U Das, Prostaglandins, Leukot Essent Fatty Acids, 1998, 58(5): 377-80.
xvii D Williams, Alternatives, Jul 1996, 6(13): 102; W Douglass, Sec Opin, Jul 1998, 8(7): 2-3.
xviii K Bone, Nutr & Healing, Mar 2005, 12(2): 7-8; R Gladstar, Herbs for Health, Nov/Dec 2000, 5(5): 8-9; W Rees et al, Scand J Gastroenterol, 1979, 14: 605-7; R Rountree & D Gagnon, Herbs for Health, Jul/Aug 1999, 4(3): 22-4; K Erickson, Herbs for Health, May/Jun 2001, 6(12): 60-64; N Beckham, Modern Phytotherapist, 2001, 6(2): 11-17.
xix R Roundtree, Herbs for Hlth, Jul/Aug 1999, 4(3):22-3; K Erickson, Herbs for Hlth, May/Jun 2001, 6(2):60-3; Alternat, Apr 1991, 3 (22):4; G Misciagna et al, Digest Liv Dis, 2000, 32:468-72; G Cheney et al, Calif Med, Jan 1956, 84(1):39-42; H Zhou et al, Chung His I Chieh Ho Tsa Chih, Mar 1990, 10(3):150-1;131-2; J Agric Food Chem, 2004, 52(6):1495-1503; V Budagovskaia et al, Vopr Pitan, May/Jun 1984, 3:30-3; G Borok, CME: VMO, Feb 1989, 7(2):215-6; N Kumar et al, Brit Med J, 13 Sept 1986, 293:666; B Katschinski et al, Gut, 1990, 31:993-6.
Originally published as an issue of Nutrition News and Views, reproduced with permission by the author, Judith A. DeCava, CNC, LNC.