Shorts

briefed by Jule Klotter

Gallstones

The gallbladder has two functions: to store liver-produced bile and release it into the small intestine. Without bile, the body cannot break down dietary fats and absorb fat-soluble vitamins. Signs of insufficient bile include indigestion, belching, bloating, cravings for fatty or fried foods, and pain or tension below the ribs on the right side. Gallstones (usually composed of bile components, calcium salts, and cholesterol) can obstruct ducts, limiting the amount of bile released. In some cases, gallstones produce sudden, severe pain after eating. Gallbladder removal (cholecystectomy) is the usual conventional treatment for symptomatic gallstones; but less invasive treatments are available.

Michael Gerber, MD, HMD, lists several treatments for addressing gallbladder stress and insufficient bile including bile salts, herbs, neural therapy, homeopathy, acupuncture, and liver/gallbladder flush. Mild symptoms may respond to a liver/gallbladder flush, according to patient reports. A liver/gallbladder flush is a folk remedy that involves ingesting olive oil and a citrus juice. Protocols vary. Gerber uses a combination of olive oil, pink grapefruit juice, and Epsom salts. He does not recommend a flush for people in severe gallbladder pain.

For severe pain, Gerber has found castor oil packs, applied over the painful area for 30 to 60 minutes, and massage of the thoracic paraspinal muscles and Bladder 18-19 acupuncture points (at the bottom edge of the scapulae) particularly helpful. He also uses intradermal neural therapy injections (1% procaine) on these and other gallbladder and liver points.

Alan R. Gaby, MD offers several suggestions for preventing gallstones in a 2009 article for Alternative Medicine Review. The first is to identify food allergies and remove offending/reactive foods from the diet. Food allergy/intolerance may contribute to delayed gallbladder emptying, which is known to contribute to gallstone formation, according to a 1985 study. Gaby cites a study in which gallbladder symptoms were eliminated in “100 percent of 69 patients with gallstones or postcholecystectomy syndrome” after 1 week on an elimination diet. Other dietary changes, such as increasing polyunsaturated or monounsaturated fat, fiber, and vegetable and fruit intake and decreasing refined sugars, have also been linked to fewer gallbladder problems.

Gaby also discusses supplements, such as vitamin C, and a product called Rowachol. Both help prevent gallstone formation. Vitamin C is used by the enzyme that converts cholesterol to bile salts. Rowachol contains six plant monoterpenes that stimulate bile production and inhibit cholesterol crystal formation in bile. It has been marketed for over 50 years and has no reported serious side effects.

Gaby AR. Nutritional approaches to prevention and treatment of gallstones. Alt Med Rev. 2009;14(3):258–266. Available at http://www.altmedrev.com/publications/14/3/258.pdf. Accessed November 22, 2014.

Gerber M. Gallbladder Rescue. Townsend Lett. July 2011;40–41. Available at www.townsendletter.com/July2011/momiracles0711.html. Accessed December 4, 2014.

Tweed V. Gallstones – healing foods & remedies. Better Nutrition. March 2014;53–56.

Helicobacter Pylori and Crohn’s disease

Because the bacterium Helicobacter pylori can cause peptic ulcers, some researchers hypothesized that it may also contribute to Crohn’s and inflammatory bowel disease. In support of this hypothesis, animal models indicate that H. pylori can produce bowel inflammation; and a 2006 study found more H. pylori in the intestinal mucosa of patients with ulcerative colitis than in the mucosa of healthy controls. However, recent case reports and studies indicate that H. pylori may actually protect against Crohn’s disease. Antonio Tursi, MD, reported on two patients who developed Crohn’s disease three-to-four months after receiving triple antibiotic therapy (esomeprazole, amoxicillin, and clarithromycin) to eradicate H. pylori. A 2010 meta-analysis, involving 23 studies and 5903 participants, found that H. pylori infection was less – not more – prevalent in patients with inflammatory bowel disease (27.1%) compared with controls (40.9%). Most recently, a 2013 retrospective case control study, led by Zun Xiang, reported an inverse correlation between the presence and severity of Crohn’s disease and presence of H. pylori.

The 2013 study, involving 477 Chinese patients with GI symptoms, used endoscopy and biopsy to diagnose Crohn’s disease (CD) in 229 of the patients. The remaining 248 with normal endoscopy and biopsy results acted as controls. All participants were checked for H. pylori by using biopsy sample culture or the C-urea breath test (C-UBT), both of which have higher sensitivity and specificity than the serum H. pylori-IgG test, according to the authors. Only 27.1% of the CD patients tested positive for H. pylori infection compared with 47.9% in the control group. Zun Xiang and colleagues also divided the CD group into three subgroups: remission (n = 32), moderate CD (n = 88), severe CD (n = 109). H. pylori infection rate was highest in patients with the least severe disease; 34.3% of the remission subgroup were H. pylori positive compared with 30.7% of the moderate CD group and 22% of the severe CD group.

Zun Xiang et al. point out that H. pylori triggers Th1-mediated cell defense, which could account (at least partially) for the protective effect. Although other types of Helicobacter may cause inflammatory bowel disease, H. pylori appears to be protective. “In conclusion, our results provide evidence for the involvement of H. pylori in CD prevalence,” the authors write. “These findings should serve as an important reminder to clinicians when considering H. pylori eradication in CD patients.”

Luther J, Dave M, Higgins PD, Kao JY. Association between Helicobacter pylori infection and inflammatory bowel disease: a meta-analysis and systematic review of the literature [abstract]. Inflamm Bowel Disease. June 2010:16(6):1077–1084. Available at http://www.ncbi.nlm.nih.gov/pubmed/19760778. Accessed April 3, 2015.

Oliveira AG, Rocha GA, Rocha AM, et al. Isolation of Helicobacter pylori from the intestinal mucosa of patients with Crohn’s disease [abstract]. Helicobacter. February 2006;11(1):2–9. Available at http://www.ncbi.nlm.nih.gov/pubmed/16423084. Accessed April 3, 2015.

Tursi A. Onset of Crohn’s disease after Helicobacter pylori eradication. Inflamm Bowel Dis. October 2006;12(10):1008. Available at http://onlinelibrary.wiley.com. Accessed March 25, 2015.

Zun Xiang, Yi-Peng Chen, Yue-Fang Ye, et al. Helicobacter pylori and Crohn’s disease: A retrospective single-center study from China. World J Gastroenterol. July 28, 2013;19(28):4576–4581. Available at www.ncbi.nlm.nih.gov/pmc/articles/PMC3725384. Accessed March 25, 2015.

Helminths and Inflammation

Helminths (parasitic worms that have evolved to live in the intestines or other locations of their animal hosts) can cause disease; but, like commensal bacteria, they may also provide health benefits. In the 1990s, Joel V. Weinstock, MD, and David E. Elliot, MD, first suggested that helminths may be one of the environmental factors that protect against inflammatory bowel disease (IBD) and other immune-mediated illnesses. They noted that people living in industrialized societies, which have less exposure to intestinal helminths, have a higher incidence of IBD. In a 2009 article, Weinstock and Elliot cite epidemiological evidence that helminths may protect against allergies and other immunological diseases. For example, case-control studies in Ethiopia and Vietnam found a lower incidence of asthma in people infected with hookworm. Also, Gabonese children who received antihelminth therapy to eradicate flukes that cause urinary disease (Schistosoma hematobium) showed increased risk of house dust mite allergy compared to a control group.

Over eons, helminths have developed methods for subduing their hosts’ inflammatory and immune responses in order to promote their own survival and colonization. Intestinal worms call forth regulatory T cells that make IL10 and TGFβ, cytokines that limit immune reactivity. In addition, parasites release compounds that modify lymphocyte, mast cell, NK cell, and macrophage functions, thereby reducing inflammation. Trichuris suis (pig whipworm), for example, suppresses TLR4-induced inflammatory responses in human macrophages, according to M. K. Ottow and colleagues.

Weinstock and Elliot hypothesize that helminths’ ability to calm the body’s immune response may be useful in treating inflammatory bowel disease and other immune-mediated illnesses. As an example, parasite-infected patients with multiple sclerosis in a 2007 study had fewer disease exacerbations and fewer new brain lesions compared with uninfected patients. Although some parasites can incite disease, particularly in immune-compromised people, many worms “hold little pathogenic potential,” say Weinstock and Elliot. Several pharmaceutical companies are investigating the use of “pharmaceutical-grade” helminths and testing helminth-derived compounds as possible treatments for inflammatory conditions.

Correale J, Farez M. Association between parasite infection and immune responses in multiple sclerosis. Ann Neurol. 2007;61:97–108. Available at http://www.coronadobiosciences.com/pdfs/Correale%20and%20FarezAnn_MS.American%20Neurological%20Association.2007%2061%2097-108.pdf.

Accessed April 15, 2015.

Ottow MK, Klaver EJ, van der Pouw Kraan TCTM, et al. The helminth Trichuris suis suppresses TLR4-induced inflammatory responses in human macrophages [abstract]. Genes Immun. October/November 2014;15:477–486. Available at http://www.nature.com/gene/journal/v15/n7/full/gene201438a.html. Accessed March 25, 2015.

Winstock JV, Elliott DE. Helminths and the IBD hygiene hypothesis. Inflamm Bowel Dis. January 2009;15(1):128–133. Available at http://opensourcehelminththerapy.org/mediawiki2/images/0/05/Helminths_and_the_IBD_Hygiene_Hypothesis.pdf. Accessed April 15, 2015.

Histamine Intolerance

“Histamine intolerance is based on an imbalance between the build up and breakdown of histamine,” say Laura Maintz and German colleagues in a 2006 review article. Histamine is produced in mast cells, basophils, platelets, and some neurons. It stimulates nociceptive (pain sensitive) nerve fibers, vasodilation, gastric acid secretion, smooth muscle contraction, mucus secretion, endothelial permeability, and tachycardia/arrhythmia. Consequently, a buildup of histamine can produce a puzzling diversity of symptoms. Some symptoms – such as sneezing, wheezing, hives, and itching – are characteristic of allergies. But too much histamine can also produce dizziness, nausea, hypotension, abdominal cramps, diarrhea, meteorism (accumulation of intestinal/abdominal gas), and even cyclical headaches and dysmenorrhea in women. High histamine levels have been associated with Crohn’s disease, ulcerative colitis, allergic enteropathy, food allergies, colorectal polyps, and carcinomas.

Excessive histamine results from the consumption of too many histamine-rich foods and/or insufficient amounts of the enzyme diamine oxidase (DAO). Normally, DAO breaks down excessive histamine; but, if DAO is not available, headache, rhinitis, flushing, diarrhea, tachycardias or arrhythmias and other symptoms associated with histamine intolerance arise. Several medications inhibit DAO or stimulate the release of histamine. “All medications, in particular long term treatments, should therefore be taken into account when interpreting histamine intolerance symptoms, as well as the DAO level, where appropriate,” advise the review’s authors.

When allergy tests are negative for IgE-mediated immune response, Maintz and colleagues suggest that histamine buildup be considered. They recommend using a placebo-controlled histamine provocation test to confirm diagnosis in people who have at least two typical symptoms, a reduced DAO level and/or raised histamine level, and show improvement on a histamine-free diet. Many patients find that maintaining a diary to keep track of symptoms and consumed foods is very helpful.

A histamine-reduced diet is the primary treatment for histamine intolerance. Histamine-rich foods include aged/matured foods such as wine, aged cheese, cured meats, yeast, and sauerkraut. In addition, some low-histamine foods such as citrus fruit, strawberries, pineapple, tomato, spinach, chocolate, egg white, and shellfish can promote the release of stored histamine, thereby producing symptoms,

People with low DAO activity may benefit from vitamin B6 and C supplementation. DAO activity depends on the supply of these vitamins and copper, all of which are cofactors. Vitamin C has the additional benefit of contributing to histamine’s breakdown.

Maintz L, Bieber T, Novak N. Histamine intolerance in clinical practice [translation]. Dtsch Arztebl. 2006;103(51–52):A3477–A3483. Available at http://www.aerzteblatt.de/pdf/103/51/a3477e.pdf. Accessed March 24, 2015.

Laryngopharyngeal Reflux and Pepsin

Stomach acid is not the only component of gastric fluid that damages epithelial tissue and mucosa during reflux. In the past decade, attention has turned to pepsin (a protein-digesting enzyme produced in the stomach), which can injure laryngeal/esophageal epithelium and produce inflammatory disorders and neoplastic disease. Pepsin remains active even in weak acid environments (up to pH 6.5). Moreover, pepsin is stable for at least 24 hours at pH 7.0 at body temperature and can reactivate in the presence of acid, according to laboratory studies. It becomes totally inactive at pH 8.0. “This is of clinical importance because pepsin, which can be detected in laryngeal epithelia after a reflux event, could be inactive because the mean pH of the laryngopharynx is 6.8,” say Nikki Johnston, PhD, and colleagues. “However … it would potentially remain stable and thus could be reactivated after a subsequent acidic reflux event or once taken up by laryngeal epithelial cells into acidic intracellular compartments.”

The most common method for diagnosing laryngopharyngeal reflux (LPR) is simultaneous esophageal and pharyngeal pH monitoring with ambulatory 24-hour double-probe, an expensive procedure with 50% to 80% sensitivity. Researchers have developed a simple pepsin immunoassay to screen for LPR in patients who fail to respond to anti-acid treatment and continue to experience symptoms (e.g., throat burning, bad taste in the mouth, sensation of lump in the throat, heartburn, cough, regurgitation, or eructation). “Gastroesophageal reflux always contains pepsin, but not all reflux occurs below pH 4.0,” write John Knight, PhD and colleagues in a 2005 study. The study compared the assay to pH monitoring in 23 patients with clinical LPR. The participants were asked to cough, clear the sputum from the back of their throat, and spit into a tube containing citric acid (0.1 mol/L; pH 2.5) whenever they experienced LPR symptoms. Using pH monitoring as the control, the pepsin assay was 100% sensitive (“ … when the sputum contained measurable pepsin, the patient always experienced LPR by pH monitoring criteria”) and 89% specific (“ … when a pharyngeal reflux event occurred, measurable pepsin was found 89% of the time”). This “spit-in-a-cup” pepsin assay is less expensive than pH monitoring and noninvasive, making it a useful screening test. The test is in its final stage of development, according to laryngologist Jamie Koufman.

Johnston N, Dettmar PW, Bishwokarma B, Lively MO, Koufman JA. Activity/stability of human pepsin: implications for reflux attributed laryngeal disease. Laryngoscope. June 2007;117:1036–1039. Available at www.researchgate.net. Accessed March 23, 2015.

Knight J, Lively MO, Johnston N, Dettmar PW, Koufman JA. Sensitive pepsin immunoassay for detection of laryngopharyngeal reflux. Laryngoscope. August 2005; 115:1473–1478. Available at www.researchgate.net. Accessed March 23, 2015.

Koufman J. The Chronic Cough Enigma. New York: Katalitix Media; 2014:5.

Vegan Diet and Inflammation

A vegan diet may protect against metabolic illnesses and inflammatory conditions to a greater degree than vegetarian diets, according to a 2014 review article conducted by Marian Glick-Bauer and Ming-Chin Yeh (CUNY School of Public Health, Hunter College, City University of New York). A strict vegan diet consists of whole grains, legumes, vegetables, and fruit. No animal-derived foods – fish, meat, dairy, eggs, or honey – are eaten. Several studies have shown that a vegetarian diet (devoid of meat and poultry) improves cardiometabolic risk factors and lowers the risk of cardiovascular diseases and some cancers when compared to an omnivore diet. The vegan diet appears to have even more health benefits.

Although studies involving vegans are still rare, an increasing number of people are choosing to follow a vegan diet for ethical and/or health reasons. A 2014 study involving Seventh-day Adventists (practitioners of a religion that advocates vegetarianism) found that people who followed a vegan diet had lower incidence of obesity, hypertension, type 2 diabetes, and cardiovascular mortality than those on a lacto-ovo-vegetarian diet (Le and Sabaté 2014). Other studies indicate that a vegan diet reduces inflammation in rheumatoid arthritis and lowers the risk of hypothyroid disease.

In their review, Glink-Bauer and Yeh suggest that the anti-inflammatory benefits of a vegan diet may stem, at least partially, from the resulting gut microbiota. Several studies have found a difference in gut flora when comparing meat-eaters, vegetarians, and vegans. In one study, for example, Slovenian vegans had a higher ratio of the bacterium Faecalibacterium prausnitzii in their guts (Matijašić et al. 2014). F. prausnitzii, an abundant butyrate producer, has anti-inflammatory effects. Glink-Bauer and Yeh comment that the gut bacteria which thrive on the abundant fiber content of plant-based diets produce more short-chain fatty acids (acetate, propionate, butyrate). These fatty acids act as signaling molecules that modulate inflammatory response. In addition to the effect on gut microbiota, a vegan diet contains more phytonutrients and antioxidants, avoids some common food allergens/intolerances (such as dairy and eggs), and contains fewer calories.

Despite the abundance of nutrients in plants, a long-term strict vegan diet can result in deficiencies of nutrients found primarily in animal-derived foods such as vitamin B12. Access to vitamin D, calcium, iron, zinc, and long-chain omega-3 fatty acids may also be limited, according to Winston J. Craig. A long-term vegetarian diet has produced hyperhomocysteinemia, protein deficiency, anemia, decreased creatinine content in muscles, and menstrual disruption in physically active women, according to a 2013 Polish review article. Weston A. Price, DDS, found no traditional diet that consisted solely of plant foods in his world travels to compare the health effects of eating traditional whole foods to processed foods. He did, however, come upon groups that advocated vegetarian diets for ethical reasons: “In every instance where the groups involved had been long under this teaching, I found evidence of degeneration in the form of dental caries, and in the new generation in the form of abnormal dental arches to an extent very much higher than in the primitive groups who were not under this influence.” Price viewed oral health and structure as a window into the skeletal structure and overall health.

The health benefits of vegan and vegetarian diets may have more to do with their emphasis on nutrient-rich, whole-plant food and avoidance of refined starches, added sugar, and processed foods than on their avoidance of animal-derived foods. As Glick-Bauer and Yeh point out, the Mediterranean diet also improves metabolic conditions such as type 2 diabetes. They conclude, “Thus a patient’s personal taste and cultural traditions may need to dictate whether a vegan diet is the ideal choice for medical nutrition therapy.”

Craig WJ. Health effects of vegan diets. Am J Clin Nutr. 2009;89(suppl):16275–16335. Available at http://ajcn.nutrition.org/content/89/5/1627S.full.pdf+html. Accessed March 25, 2015.

Glick-Bauer M, Yeh M-C. The Health Advantage of a Vegan Diet: Exploring the Gut Microbiota Connection. Nutrients. 2014:6(11):4822–4838. Available at www.mdpi.com/2072-6643/6/11/4822/htm. Accessed March 25, 2015.

Le LT, Sabaté J. Beyond meatless, the health effects of vegan diets: findings from the Adventist cohorts. Nutrients. 2014;6(6):2131–2147. Available at http://www.mdpi.com/2072-6643/6/6/2131/htm. Accessed April 3, 2015.

Matijašić BB et al. Association of dietary type with fecal microbiota in vegetarians and omnivores in Slovenia. Eur J Nutr. 2014;53:1051–1064.

Pilis W, Stec K, Zych M, Pilis, A. Health benefits and risk associated with adopting a vegetarian diet [abstract]. J Sci Food Agric. 2013;93:2362–2371. Available at http://www.ncbi.nlm.nih.gov/pubmed/24964573 . Accessed April 3, 2015.

Price WA. Nutrition and Physical Degeneration. 6th ed. La Mesa, CA: Price-Pottenger Nutrition Foundation; 1997:279.