Detecting AllergensDoris J. Rapp, MD, has recently completed an 11-page booklet called Allergies: The Answers You Need Are Here. Rapp, one of the pioneers in identifying and treating environmental illness, is board certified in pediatrics and allergy and environmental medicine. This practical booklet explains how to recognize common and uncommon allergies and sensitivities. Most of us think that allergies manifest as itchy eyes and runny noses during pollen seasons, digestive and intestinal upsets when eating something that doesn't agree with us, or hives from a food. But allergies also cause many, many other symptoms. Young children can display hyperactivity, reluctance to keep clothes on, aversion to being touched, tics, twitches, seizures, and fatigue when exposed to allergens. Fatigue is also a symptom of allergy in older people. Other signs of allergen exposure in adults and older children include daily headaches, unexplained aggression or anxiety, sleep problems, fuzzy thinking, sudden mood changes, and sudden severe body odor (not eliminated by washing). Exposure to allergens (and toxic chemicals) can also produce a sudden difficulty with tasks that require motor coordination (writing, drawing, speaking, or walking). Most people do not realize the diverse and sometimes bizarre reactions that can arise when a sensitive person is exposed to an allergen or environmental trigger. As Rapp explains in her new booklet, the first step in tracking down triggers is to keep a record or log of foods, other exposures, symptoms, and locations where symptoms occur. In particular, she says to be on the lookout for the following sudden changes: abnormally red earlobes or cheeks; dark eye circles; bags under the eyes; a spaced out, frightening or "demonic" look to the eyes; wiggly legs; or sudden shifts in emotions, behavior, and/or movement. In addition, blood pressure can rise and the pulse rate increase to 100 at rest. Becoming aware of these changes and then continuously asking questions is the key to finding the environmental trigger: What is different? Where was I when my ability to breathe well decreased or increased? Why did this happen? What did I eat, touch or smell? Allergies: The Answers You Need Are Here offers ways to track down exposures that cause symptoms. It also explains how to identify problem foods by using a one-week multiple food allergy elimination diet. The booklet costs just $5 and is available at www.dorisrappmd.com.
Leaky Gut, Autoimmunity, and Celiac Disease
Though it is often undetected, an estimated 1 person in 133 in North America has celiac disease (CD). This autoimmune disease is characterized by inherited hypersensitivity to gluten, a difficult-to-digest protein found in grains. Bacteria living in the gastrointestinal appear to influence genetic expression. Dr. Alessio Fasano says in an article for Scientific American, "… a person whose immune system has managed to tolerate gluten for many years might suddenly lose tolerance if the microbiome [gut flora] changes in a way that causes formerly quiet susceptibility genes to become active." Stress and other factors may also turn on the susceptibility genes.
At this time, celiac disease is the only autoimmune disease whose environmental trigger (gluten) has been identified. In people with celiac disease, gluten protein fragments (peptides) stimulate the immune system to attack the gut, producing chronic inflammation and damaging the villi. (The villi in the small intestine transport nutrients across the gut wall to the bloodstream.) Impaired nutrient absorption produces a numerous and often unrecognized effects. "By robbing the body of particular nutrients," Fasano explains, "CD can thus produce such symptoms as osteoporosis, joint pain, [anemia, neurological problems,] chronic fatigue, short stature, skin lesions, epilepsy, dementia, schizophrenia, and seizure." Diarrhea, pain, and persistent indigestion are the most recognized symptoms. Staying on a gluten-free diet is the treatment for celiac disease and lets the small intestine heal.
In addition to a heightened immune response, people with acute or active celiac disease have elevated levels of the protein zonulin. Zonulin regulates permeability, which allows fluids and the substances that they carry to move from the gut to the bloodstream and from the blood into the brain. Increased gut permeability, also called leaky gut, characterizes many autoimmune diseases including celiac disease, type 1 diabetes, multiple sclerosis, and rheumatoid arthritis. Fasano, whose team discovered zonulin, helped set up Alba Therapeutics to investigate the therapeutic possibilities of a zonulin inhibitor called Larazotide. Larazotide has decreased permeability, inflammation, and gastrointestinal symptoms in celiac patients in two placebo-controlled studies as of 2009. The US Food and Drug Administration has approved studies that explore Larazotide's use in type 1 diabetes and Crohn's disease.
Fasano A. Celiac disease insights: clues to solving autoimmunity. Sci Am. July 27, 2009. Available at: www.scientificamerican.com/article.cfm?id=celiac-disease-insights. Accessed March 16, 2011.
Levin EB. Researchers find increased zonulin levels among celiac disease patients [online press release]. University of Maryland Medical Center. March 21, 2008.www.umm.edu/news/releases/zonulin.htm. Accessed March 24, 2011.
Heavy Metals, Mercury Amalgams, and AutoimmunityHeavy metals are among the environmental factors that trigger autoimmune disease in genetically susceptible people. While nickel, colloidal gold, and metals used occupationally have been linked to autoimmune disease, most research has focused on mercury, particularly mercury amalgams. Air pollution and contaminated seafood are other common sources of mercury exposure. Mercury, whose toxicity particularly affects nerves and kidneys, tends to accumulate in the body with chronic exposure. As with other autoimmune triggers (such as gluten), the severity of an individual's reaction depends on inherited sensitivity and the body's ability to deal with toxins. Several clinical studies have linked mercury amalgam fillings to autoimmune diseases. In 1994, R. L. Siblerud and E. Kienholz compared blood tests from multiple sclerosis (MS) patients who had amalgams with texts from those who had had their amalgam fillings removed. Those with amalgam fillings had significantly lower levels of red blood cells, hemoglobin, hematocrit, thyroxine, total T-cells, and CD8+ suppressor cells. In addition, MS patients with amalgams had 33.7% more exacerbations during the previous 12 months than the group without amalgams. Patients who show sensitivity to mercury, using MELISA lymphocyte stimulation tests, tend to improve when amalgams are removed, according to Czech research. In a 2004 study, 25 out of 35 autoimmune patients who had amalgams removed reported improved health and significantly decreased lymphocyte reactivity to inorganic mercury, silver, organic mercury, and lead with MELISA testing. Those who improved tended to show high reactivity to mercury at baseline. Amalgam removal also improved health in about 70% of patients with autoimmune thyroiditis in a 2010 Czech study. Mercury-specific lymphocyte responses in vitro and antithyroid autoantibodies normalized as well. As in the 2004 study, the patients who improved were those who initially showed lymphocyte reactivity to mercury. Apparently, individual sensitivity plays a greater role than does exposure. In a metal-sensitive person, even a small exposure causes systemic reactions. Studies that have sought to connect the number and size of amalgams to the severity of symptoms have usually found no correlation. In addition to genetic predisposition, nutrition, stress, and pathogens can increase a person's sensitivity to environmental triggers like heavy metals. "Considering the complexity of the immune system and its interaction with the nervous and endocrine systems," Stejskal and Stejskal write, "it is obvious that a combination of mechanisms is responsible for the induction of auto-immunity." Aminzadeh KK, Etminan M. Dental amalgam and multiple sclerosis: a systematic review and meta-analysis [abstract]. J Public Health Dent. Winter 2007;67(1):64–66. Available at: www.ncbi.nlm.nih.gov/pubmed/17436982. Accessed March 24, 2011. Hybenova M, Hrda P, Procházková J, Stejskal V, Sterzl I. The role of environmental factors in autoimmune thyroiditis [abstract]. Neuro Endocrinol Lett. 2010;31(3): 283–289. Available at: www.ncbi.nlm.nih.gov/pubmed/20588228. Accessed March 21, 2011. Procházková J, Sterzl I, Kucerova H, Bartova J, Stejskal VD. The beneficial effect of amalgam replacement on health in patients with autoimmunity [abstract]. Neuro Endocrinol Lett. June 2004; 25(3):211–218. Available at: www.ncbi.nlm.nih.gov/pubmed. Accessed March 24, 2011. Schiraldi M, Monestier M. How can a chemical element elicit complex immunopathology? Lessons from mercury-induced autoimmunity. Trends Immunol.2009. Available at www.toxcenter.de/artikel/Quecksilber-crasht-Autoimmunitaet.pdf. Accessed March 18, 2011. Siblerud RL, Kienholz E. Evidence that mercury from silver dental filings may be an etiological factor in multiple sclerosis [abstract]. Sci Total Environ. March 15, 1994;142(3):191–205. Available at www.ncbi.nlm.nih.gov/pubmed/8191275. Accessed April 12, 2011. Stejskal J, Stejskal VDM. The role of metals in autoimmunity and the link to neuroendocrinology. Neuroendocrinol Lett. 1999:20;351–364. Available at: www.i-gap.info/app/dokumente/Autoimmunity%20and%20metals.pdf. Accessed March 17, 2011.
Methanol and Multiple SclerosisWhat do canned fruits and vegetables, cigarette smoke, and aspartame have in common? All are sources of methanol (wood alcohol), a known toxin that produces symptoms identical to those of multiple sclerosis (MS). In an heavily referenced 2007 article, retired food science professor Woodrow C. Monte, PhD, presents a convincing argument that links methanol consumption to the growing rate of multiple sclerosis worldwide. "The symptoms of multiple sclerosis, chronic and acute methanol poisoning, and Aspartame toxicity are in all ways identical," Monte writes. Headaches, memory loss, nervousness, depression, tingling sensations, pain in the extremities, optic neuritis, bright lights in the visual field, seizures, and inability to urinate or to keep from urinating characterize all three conditions. French neurologist Jean-Martin Charcot presented the first documented case of multiple sclerosis during a lecture in 1868. Although the disease was rare, Monte says that incidence rose as access to canned fruits and vegetables increased. The first food cannery, devoted primarily to canning meats at first, opened in England around 1813. Gradually, the canning industry grew and began to process fruits and vegetables as well. As canned foods became more common, prices declined; and more people began using them. Monte says, "… when the fruits and vegetables and their naturally occurring pectin is placed in a sealed container (as in canning) that is then sterilized, heated or even just stored at room temperature for months, the normally unavailable, chemically bound methanol is released from the pectin. The methanol slowly builds up, trapped in the container, to hundreds of times more than when fresh. Very simply it is canned fruits and vegetables that were (before aspartame) the major source of free methanol in the human diet." Canned and bottled fruit juices and also tomatoes (fresh and canned) have high methanol levels. Fresh juice, made and consumed within minutes, has little or no free methanol. Depending upon the fruit, methanol levels in fresh juice rise within 30 minutes of storage. Tobacco leaves also have pectin-bound methanol. Fermentation of tobacco leaves, part of the manufacturing process, separates the plant's methanol from its pectin. Cigarette smoking is known to trigger MS relapses. In addition to pectin, unprocessed fruits and vegetables have another safeguard against methanol's toxic effects: ethanol. Ethanol is a "natural outcome of digesting plant material in the gut," Monte explains. Both ethanol and methanol are broken down by alcohol dehydrogenase (ADH), an enzyme found throughout the body. ADH prefers to metabolize ethanol, which becomes acetylaldehyde and acetic acid. When ethanol isn't available or when the methanol level is 10 times greater than ethanol's, ADH turns its attention to methanol. Here is the source of methanol's toxicity. ADH breaks methanol down into formaldehyde and then into formal hydrate (formic acid). Formaldehyde causes cancer and birth defects. Formal hydrate, an extremely acidic and powerful esterifying agent, readily reacts with proteins, including the proteins in myelin, the insulation that protects nerve fibers in the central nervous system. Monte says: "… the location of ADH in our bodily tissue seems to vary with our genetic makeup. ADH might, for reasons not fully understood, be found in the liver, gut, brain, eye, skin and sinew. These hereditary differences are most likely responsible for the varied manifestations of autoimmunity. Higher enzyme representation in the brain might predispose the individual to develop MS while its presence in the skin would be required for the evolution of lupus." The chemical sweetener aspartame breaks down into two amino acids (phenylalanine and aspartic acid) and methanol (wood alcohol). Unlike plants, aspartame has neither pectin nor ethanol to mitigate the damage produced by methanol. For decades, MS has been more prevalent in cooler latitudes. While people in tropical climates are exposed to more sunshine (and vitamin D), they also have access to an abundance of fresh fruits and vegetables and lower consumption of canned foods. The exceptions have been Australia and New Zealand, where canned foods are inexpensive and common and MS rates have been high. In contrast, Japan, which lies at a cooler latitude, has had a low incidence of MS. The Japanese tend to eat fresh produce in season rather than rely on canned foods. In recent years, both Japan and countries with warmer climates are reporting higher MS rates and increased MS relapse rates during the summer – when aspartame-containing sodas, juices, and "thirst quenchers are most frequently consumed," Monte says. "Viewing methanol toxicity as the ethnologic cause of MS seems to answer all of the nagging questions and unexplained anomalies that have stalled the cure for this increasingly persistent disease," Monte states. What if methanol triggers multiple sclerosis just as gluten triggers celiac disease? Hou C-Y, Lin Y-S, Wang YT, Jiang C-M, Wu M-C. Effect of storage conditions on methanol content of fruit and vegetable juices [abstract] J Food Composit Anal. August 2008;21(5):410–415. Available at: www.sciencedirect.com. Accessed March 27, 2011. Monte WC. A Deadly Experiment. Fitness Life. December 2007;34:38–42. Available at: http://thetruthaboutstuff.com/review2.html. Accessed March 19, 2011. Monte WC. Methanol: Where is it found? How can it be avoided? [online article]. TheTruthAboutStuff.com. http://thetruthaboutstuff.com/published/Monte%20Diet.pdf. Accessed March 19, 2011. Monte WC. Aspartame: methanol and the public health. J Appl Nutr. 1984;36(1). .
Managing Autoimmune Disease
Conventional medicine tends to view autoimmune illness as the result of an overstimulated immune system that attacks organs and tissues as if they were foreign invaders. "Immune suppression, the mainstream medical treatment of choice for auto-immune disorders, completely overlooks the upstream cause, toxic overload, and the downstream detoxification deficiency that leads to the immune system's confusion in distinguishing self from invader," write Jodi Friedlander, MS, and Ed Bauman, MEd, PhD. Autoimmune diseases such as rheumatoid arthritis, type 1 diabetes, systemic lupus erythematosis (SLE), Addison's disease, and Crohn's disease affect 5% to 8% of the US population. It is the third most prevalent type of illness after heart disease and cancer. According to the molecular mimicry hypothesis, amino acid sequencing (peptides) in pathogens and some body tissues are similar enough so that lymphocytes (particularly Th-1 cells from the thymus) attack invader and self. Normally, the body has regulating mechanisms that keep Th-1 and Th-2, which produce an allergic response, in balance. In autoimmune diseases, Th-1 dominates. Th-1 cells emit cytokines that produce inflammation.
While molecular mimicry appears to have a role in disease progression, it does not explain why the immune response becomes so imbalanced in the first place. Genetic variations that affect detoxification processes, sensitivity to specific antigens (e.g., the protein gluten), and/or immune reactivity make some people more prone to autoimmune diseases than others. As with many other diseases, genetics alone does not determine the presence and/or severity of autoimmune disease.
Friedlander and Bauman state that when a body becomes overwhelmed and is unable to eliminate foreign molecules (antigens), the antigens "can form complexes with antibodies and becomes part of our joints, nerves, and endocrine tissue." Agricultural and household chemicals, heavy metals, petrochemicals, prescription drugs, organic solvents, and silica have triggered autoimmune disease in genetically susceptible people. Stress is another trigger. "High levels of [the stress hormone] cortisol suppress the immune system," Friedlander and Bauman explain, "by reducing the amount of secretory IgA, the main mucosal antibody responsible for eliminating pathogens from the intestinal tract and in other mucus membranes [e.g., lungs]." With prolonged stress, the adrenals eventually produce less cortisol. Without cortisol to keep IgA in check, IgA reactions will produce inflammation in the GI lining and the lungs. Over time, inflammation will damage the mucosa, producing leaky gut syndrome. This increased permeability allows more foreign antigens into the bloodstream, perpetuating the inflammation response. Increased gut permeability is a common factor in autoimmunity. Bacterial imbalance in the GI tract can also promote inflammation that contributes to autoimmune disease, according to research by Tlaskalová-Hogenová et al. (Immunology Letters. May 15, 2004;93[2–3]:97–108).
A multifaceted treatment approach that addresses the many contributors to autoimmune disease is more likely to reduce damage and symptoms than a conventional drug approach. Friedlander and Bauman offer supportive dietary and supplement suggestions in their article "Self Destructive Tendencies: Natural Strategies for Managing Autoimmunity." Avoiding refined carbohydrates and sugar (especially fructose and high-fructose corn syrup) is perhaps one of the best dietary measures a person can take to stem the inflammatory-autoimmunity cycle. Processed, sugary foods disturb gut bacteria balance and contribute to inflammation. Friedlander and Bauman suggest numerous supplements, herbs, and foods that have anti-inflammatory effects, including olive oil (extra virgin), sesame oil, green tea (epigallocatechin gallate), and spices and herbs (ginger, turmeric/curcumin, rosemary, oregano). Short fasts using fresh vegetable and fruit juices, vegetable broths, and herbal teas also calm inflammation. People with an autoimmune diagnosis should be supervised by a knowledgeable practitioner during fasting.
Friedlander J, Bauman E. Self destructive tendencies: natural strategies for managing autoimmunity. Bauman College. 2008. Available at:www.nanp.org/downloads/NANP_Newsletters/BCArticle.Autoimmunity.pdf. Accessed March 27, 2011.
Gastrointestinal Microbes and Rheumatoid ArthritisWhat effect do toxic bacteria in the gastrointestinal tract have on autoimmune disease? Laboratory rodent studies indicate that GI bacteria and their toxins (e.g., gram-negative bacteria cell wall components) contribute to the development of autoimmune diseases. Absorption of these toxins from the GI tract stimulates inflammatory and immune responses. J. Vaahtovuo et al.reported significant difference in the GI bacterial makeup in people with early rheumatoid arthritis (RA) compared with controls in their 2008 study ( J Rheumatol 2008;35:1500–1505). Is it possible to relieve the symptoms of rheumatoid arthritis by reducing toxic bacteria in the GI tract? Kou Katayama and Japanese colleagues recently performed a small study to investigate this question. Their 2011 study involved 20 people with RA who either did not respond or were unable to take conventional medicines used to control the illness. (Eighteen completed the study). Another 18 background-matched RA patients acted as controls. Recognizing that antibiotics would contribute to further imbalance between pathogenic and nonpathogenic GI bacteria, the researchers decided to test the effect of a proprietary whey protein product containing natural milk antibodies called Bonyuno Chikara (Asama Chemicals Inc.). This whey protein concentrate contains immunoglobulins that function as antibodies against "at least 33 strains of pathogenic bacteria," according to laboratory tests. Tests with elderly volunteers indicate that the product reduces pathogenic bacteria like E. coli and Clostridium perfringens in feces and increases Lactobacilli. Eight of the 18 receiving the whey product for three months experienced relief from GI problems and statistically significant reduction in RA symptoms. Two showed some improvement, and the remaining 8 did not respond. C-reactive protein levels and the erythrocyte sedimentation rate significantly decreased in those who responded and remained low one month after they stopped taking the product. Symptoms did eventually return, but those who had initially responded to the product improved again when it was reintroduced. When trying to determine why some patients responded and others did not, the researchers found that responders had higher serum anti-type II collagen antibody levels and higher serum IgG and IgA anti-lipopolysaccharides (from E. coli) antibody levels than the nonresponders. They suggest that these higher levels may indicate greater intestinal permeability. The researchers also found genetic differences between the two groups. Katayama K, Matsuno T, Waritani T, Terato K, Shionoya H. Supplemental treatment of rheumatoid arthritis with natural milk antibodies against enteromicrobes and their toxins: results of an open-labeled pilot study. Nutr J. 2011:10(2). Available at: www.nutritionj.com/content/10/1/2. Accessed March 24, 2011.
Petroleum Chemicals, Mercury, and SLESystemic lupus erythematosis (SLE, or lupus), like other autoimmune illnesses, occurs when genetically susceptible people are exposed to environmental toxins that disrupt the immune system. In the case of lupus, antibodies react with cell nuclear material, producing inflammation and damage in organs and joints. Lacking a definitive laboratory test, doctors rely on patient symptoms to diagnose lupus. The presence of 4 or more of the "11 criteria of lupus" indicates the disease, according to the American College of Rheumatology. (See www.rheumatology.org.) People living near industrial pollution or contamination sites have a higher incidence of lupus and other autoimmune diseases, but researchers are just beginning to track down specific contaminants that trigger or worsen these illnesses. Pristane, a component of crude oil, and mercury, which is released during oil drilling, have each caused SLE-like symptoms and autoimmunity in laboratory mice. Mercury is known to disrupt immune function in both animals and humans. While case reports and epidemiological studies indicate that mercury can trigger SLE, the evidence linking oil components to autoimmune disease is more limited. A 2007 study, initiated at residents' request, found an unusually high incidence of SLE in a six-square-block area in Hobbs, New Mexico. From 1927 until the late 1960s, the neighborhood had been the site of an active oil field. Some homes had been built over an oil field waste pit. Ninety adults who had lived in the neighborhood for at least two years enrolled in the study. The California research team used 129 volunteers from a similar Southwestern town without a history of chemical exposure as a control. Researchers collected indoor and outdoor dust samples and air samples from some exposed homes and controls. They looked for the oil components pristane and phytane in the dust samples and measured mercury (which is more volatile) in the air. Blood and urine samples were also taken from some volunteers in each group. "We found higher levels of air mercury and house dust pristine/phytane in the affected neighborhood compared to other areas of Hobbs and the control town," James Dahlgren and colleagues write. In addition, 5 of 20 volunteers living in the exposed area and 1 of 25 controls had detectable pristane, phytane, and/or pristanic acid in their blood. All 6 had a diagnosis of lupus or symptoms associated with immune dysfunction. In addition, lymphocyte population in all exposed volunteer blood samples was abnormal, with significantly lower natural killer cells and significantly higher B-lymphocytes compared with controls. The incidence of lupus was extremely high in the exposed neighborhood: 13 cases out of an estimated 1490 inhabitants, which translates to 872/100,000. Medical literature indicates that SLE incidence "varies from 14.6 to 50.8 cases/100,000." Volunteers living in the oil-exposed area were also 10 times more likely to have rheumatic disease. In addition to other signs of immune dysfunction (e.g., mouth sores, numbness, rash), exposed volunteers were more likely to report cardiovascular, respiratory, and/or gastrointestinal problems. This study is reportedly the first one to link crude oil components to autoimmune disease. Will oil components be linked to an increase in autoimmune disease among clean-up workers of the 2010 Deepwater Horizon oil spill? On February 28, 2011, the National Institute of Environmental Health Sciences announced a 10-year study involving oil spill clean-up workers. The NIH scientists hope to recruit 55,000 of the estimated 100,000 workers. The study is open to people aged at least 21 who did oil spill cleanup work for at least one day or who completed oil spill worker training. Only eight oil spills have been investigated for health effects on clean-up crews, and even fewer for long-term effects. This NIH study may help clarify the relationship between petroleum and autoimmune disease, particularly SLE. Dahlgren J, Takhar M, Anderson-Mahoney P, Kotlerman J, Tarr J, Warshaw R. Cluster of systemic lupus erythematosus (SLE) associated with an oil field waste site: a cross sectional study. Environ Health. 2007;6(15). Available at: www.ehjournal.net/content/6/1/8. Accessed March 21, 2011. National Institute of Environmental Health Sciences. NIH launches largest oil spill health study [press release]. February 28, 2011. Available at: www.niehs.nih.gov/news/releases/2011/gulfstudyfinal. Accessed March 24, 2011.
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