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  • Roy Jamron
    Roy Jamron

    Unraveling Fibromyalgia

    Reviewed and edited by a celiac disease expert.

    Journal of Gluten Sensitivity Winter 2006 Issue. NOTE: This article is from a back issue of our popular subscription-only paper newsletter. Some content may be outdated.

    Unraveling Fibromyalgia - University of Kentucky. Image: CC PDM 1.0--NIH-NCATS
    Caption: University of Kentucky. Image: CC PDM 1.0--NIH-NCATS

    Celiac.com 12/07/2021 - Fibromyalgia frequently occurs among those with celiac disease, but no published study to date provides prevalence data. However, one survey found that in cases of celiac disease that were initially misdiagnosed by physicians, 9% were initially diagnosed as having fibromyalgia(1,2,3).

    Fibromyalgia is defined as a chronic widespread pain lasting more than three months in all four body quadrants with pain present in at least 11 of 18 specific tender point sites. Fibromyalgia does not cause joint pain or swelling, as arthritis does, but produces pain in soft tissues around joints, in skin, and in organs throughout the body. A large variety of symptoms and syndromes are usually associated with fibromyalgia. These include fatigue, stiffness (especially upon awakening), disturbed sleep, dry mouth, dry eyes, dry skin, headaches, frequent urination, cold sensitivity, mental fog, dizziness, irritable bowl syndrome, restless legs syndrome, and more. Pain location and severity, as well as the severity of symptoms and syndromes, can vary in an individual from day to day. The characteristics of fibromyalgia differ widely from individual to individual. The condition can be long-term and extremely debilitating, affecting quality of life and limiting one’s employment options. People with chronic fatigue syndrome suffer many of the same symptoms of fibromyalgia suggesting a possible relationship(4,5).

    Celiac.com Sponsor (A12):
    There is no laboratory test for fibromyalgia. Diagnosis is a process of ruling out other possible conditions through medical history and exam, and, finally, evaluating the 18 tender points. The number of tender points is found by a skilled examiner applying pressure to the tender points and the patient identifying whether pain is present upon pressure. As the number of tender points can vary from day to day, and the test relies on the skill of the examiner and the patient’s pain perceptions, rheumatologists are recognizing the shortcoming of this type of diagnosis. In fact, the number of tender points does not even correlate to the severity of the pain experienced by fibromyalgia patients. There is a view developing that those meeting the 11 out of 18 tender point criteria simply fall on one end of a spectrum of fibromyalgia-like chronic widespread pain.

    Some 80% of those diagnosed with fibromyalgia are women. Across different countries, the prevalence rate of fibromyalgia is 0.5% to 5%. Chronic widespread pain, where the criteria of having at least 11 tender points may not be met, affects 7.3% to 12.9% of the general population6 . This means there are many more people who suffer fibromyalgia-like pain and symptoms without technically being diagnosed as having fibromyalgia. This discussion is meant to include those people, as well, so when fibromyalgia is mentioned here, it will refer to the pain suffered by all with fibromyalgia-like symptoms regardless of the number of tender points.

    Medical science is still grappling over the issue of just what is the cause and nature of fibromyalgia. First thought to be an inflammation of the muscles and soft tissue, studies have found no inflammation and normal muscle response in patients(7,8). Now most researchers suspect that abnormalities of the brain and central nervous system are responsible for the disorder. Initiation or triggering of fibromyalgia has been attributed to injuries, stress, infections, or toxins, and frequently accompanies a number of autoimmune diseases. Treatment of fibromyalgia in the world of conventional medicine is limited to over-the-counter and prescription pain relievers including analgesics, anti-inflammatory medications, narcotics, and pain patches. Anti-depressants, muscle relaxants, anti-spasm and anti-convulsive medications, sleep medications and sedatives, and some newer neurological drugs are additionally prescribed. Therapies also include physical rehabilitation and nutrition. The effectiveness of these treatments varies widely among individuals, and none offers any potential of a cure. Many people turn to alternative medicine for remedy when conventional medicine fails to provide relief. Magazine and newspaper ads and Internet Web sites target the desperate, and sufferers may be more likely to be relieved of their money than their pain.

    My Symptoms

    I don’t know how many tender points I have had or may have had and never cared, but I have fibromyalgia-like chronic widespread pain and symptoms that became so bad I had to quit my job a few months ago. I am a self-diagnosed celiac, gluten-free for over six years. Over a year ago I developed a pain in my left shoulder which eventually shifted to the right shoulder. Then the pain moved into my legs, especially the right leg. I was fatigued. My mouth and throat were dry at night. I had to urinate frequently. I felt colder than normal. My right leg ached when lying in bed. I was extremely stiff in the morning. Bowel discomfort was already present from celiac disease, but fibromyalgia may have made it worse. There was often swelling in my ankles and feet. It became painful to walk or put on a shirt or a coat. And the symptoms continued to worsen, affecting both arms and shoulders, both legs and the right hip. Any small chore or physical activity became a challenge. Turning the steering wheel of my truck hurt. Grocery shopping was an absolute dread.

    I suspect my condition may have been triggered by years of exposure to chemicals and cleaning solvents present in the environment at my job in the automotive industry— chemicals I did not use—but they were used in quantity adjacent to my work area. This would not be the first time chemicals or toxins caused fibromyalgia-like pain. Seven years ago I underwent surgical repair of a right inguinal hernia (a tear in the tissue near the groin allowing the intestine to protrude beneath the skin), followed six months later by a repair of a left inguinal hernia. In each case, I was given an intravenous antibiotic, local anesthetic and sedation. After the first surgery, I experienced a sharp pain in the right leg that made it too painful to even move the leg or bend the knee. The pain died down after a day, but it took over a month to fully regain movement in the right leg without pain. After the second surgery, I did not experience any leg pain, but I did experience a strange dry, metallic cotton-like sensation in my mouth lasting more than a day. These two sensations would later come back to haunt me when I engaged in a self-experiment.

    After diagnosing myself with celiac disease, I wondered if an overabundance of bacteria could be responsible for continuing bowel discomfort. I wanted to try an antibiotic to see if it could provide relief. On the internet, I found that over-the-counter Pepto-Bismol tablets (bismuth subsalicylate) have antibiotic properties. It has been used to treat microscopic colitis and, in combination with other antibiotics, helicobacter pylori infection. Label instructions state that up to eight doses of Pepto-Bismol may be taken in a 24 hour period (for adults, a dose is two tablets.) The treatment for microscopic colitis is eight tablets a day for eight weeks, and I decided to try this treatment. It seemed safe enough. No warnings, no adverse reactions were indicated. Millions of people use Pepto-Bismol without any problems. From the beginning, Pepto-Bismol made me uncomfortable. I could only tolerate six tablets a day, instead of eight. After one week, I began to experience stiffness in my legs in the morning. At the end of two weeks I felt so bad that I decided to end the experiment—but it was too late. Even after stopping, the stiffness in the legs continued to worsen. A few days later, I experienced both the exact same intense pain in my right leg plus the strange, dry metallic cotton-like mouth sensation I had experienced after the hernia surgeries, only much worse. I was bed-ridden and unable to walk or go to work for three days. The pain was at first localized to my right leg, my right wrist, and a finger which had received stitches for a cut when I was seven years old, but after a few days the pain began to spread out. Eventually the pain spread to both shoulders and both legs and looked very much like fibromyalgia. The pain finally remained primarily in the right leg. Other symptoms were frequent urination, night chills, and night sweats that left my sheets soaked. After four months, the pain and symptoms finally went away, and I resumed “normal” activities hoping never to experience such pain again.

    In the case of the surgery and of the Pepto-Bismol, the trigger of the pain was clear and certain. Two weeks of Pepto-Bismol exposure resulted in four months of pain. I can only speculate on if and what chemical exposure may have caused my current condition, how long I may have been exposed to the chemicals, and have no idea how long the current symptoms may last. The question is why am I overly sensitive to these chemicals and drugs, and exactly what is the mechanism that causes fibromyalgia pain? Medical science offers no answers at this time. Therefore, it falls on me to try to come up with a reasonable hypothesis to explain fibromyalgia, and, perhaps, even find a treatment. What follows is a hypothesis which I believe successfully does just that.

    There are some assumptions I have to make. I have to assume that the nature of the chronic widespread pain I feel is similar to the pain experienced by other fibromyalgia sufferers. I can only relate to my own pain. I cannot get into the heads of others. I am also assuming that whatever mechanism is causing my own pain is the same mechanism that causes pain in most, if not all, fibromyalgia victims.

    Fibromyalgia: Neuropathy or Inflammation?

    Medical science believes abnormal brain and central nervous system response is behind fibromyalgia pain. I do not. My pain exists at specific body locations and intensifies with certain stretching and extension movements of the limbs. Intuitively, it feels to me like multiple local inflammations. If the central nervous system or brain is generating abnormal pain signals, then why is the pain not coming from points everywhere in my body instead of from specific locations and specific limb movements? Additionally, why would I have swelling in my ankles and feet? Finally, at times, I hear and feel “squishing” at the sites of pain when I move my limbs. The brain is certainly not creating this “squishing”. All signs point to a physical abnormality, and if inflammation is not present in the muscle tissue, then it must be somewhere else.

    In a review of medical publications, I first became intrigued by a reference to two Spanish sisters with alpha1- antitrypsin (AAT) deficiency and fibromyalgia. The liver produces alpha1-antitrypsin, an important anti-inflammatory and proteinase inhibitor that circulates in serum impregnating most body tissues. A study found in vitro that a low level of alpha1-antitrypsin induces human monocytes (white blood cells) to release pro-inflammatory substances. In those with AAT deficiency, a genetic flaw prevents liver cells from secreting alpha1-antitrypsin, and it builds up within the liver instead of being circulated. The risk of liver and lung disorders is increased in AAT deficient patients The two Spanish sisters underwent AAT replacement therapy, and, strikingly, their fibromyalgia symptoms vanished. During a worldwide commercial shortage of AAT replacement therapy, their therapy was halted for 4-6 months a year during each of 5 years of treatment. Each time therapy was halted and resumed, their fibromyalgia symptoms reappeared and vanished. This led their doctors to propose a hypothesis that fibromyalgia may be related to an imbalance between inflammatory and anti-inflammatory substances(9,10,11).

    A review of AAT deficiency websites and discussion sites did not provide any prevalence data for fibromyalgia among AAT deficient patients nor was fibromyalgia a significant topic of discussion, suggesting fibromyalgia requires more than just AAT deficiency. Low levels of AAT are found in patients testing positive for human immunodeficiency virus (HIV). Studies have found rates of fibromyalgia, based on tender points, in HIV positive patients at 11% and 29%(12,13,14,15). Interestingly, low levels of AAT were found in a significant percentage of a group of children from an industrial air pollution area compared to children from an unpolluted area. AAT levels were restored to normal in most of the children after a year and a half16. This suggests that chemicals in the environment may have an adverse affect on liver function, in turn, reducing AAT production, in turn, increasing the risk of developing fibromyalgia symptoms.

    At this point, my attention turned to liver function. Could abnormal liver function be a factor contributing to fibromyalgia? Liver dysfunction of any type in celiac disease at time of diagnosis has been reported in up to 42% of adults and 54% of children. The most common irregularity is a raised level of liver transaminase enzymes (released by damaged liver cells) which usually normalizes on a gluten-free diet. Chronic hepatitis, fibrosis, cirrhosis, fatty liver, primary biliary cirrhosis, primary sclerosing cholangitis, and autoimmune hepatitis have all been found present in celiac disease patients, usually achieving remission with treatment and a gluten-free diet. Increased intestinal permeability and gluten toxicity have both been proposed as mechanisms leading to liver dysfunction(17,18,19).

    The liver plays a number of crucial roles in maintaining the body. It regulates serum levels of substances such as glucose and cholesterol which it also synthesizes. It synthesizes and secretes numerous blood proteins. Bile, necessary for the digestion of fats, is also synthesized and secreted by the liver. The liver stores glucose, minerals such as copper and iron, fat soluble vitamins (vitamins A, D, E, and K), vitamin B12, folate, and other substances. Through processes of purification, transformation and clearance, the liver removes harmful substances from the blood (such as ammonia and toxins), breaking them down or transforming them into less harmful compounds. Most hormones and ingested drugs are metabolized by the liver into either more active or less active products. Many toxins or chemicals inhaled, digested, or absorbed through the skin are fat soluble, and it is the liver that can transform fat soluble toxins into water soluble products allowing them to be eliminated by the kidneys. The liver also filters out dead cells, various debris, and microorganisms including bacteria, viruses, fungi, and parasites. Pre-existing liver disease or dysfunction can compromise liver function causing hormonal imbalances, blood protein deficiencies, and inhibiting the liver’s ability to remove or transform toxins. The very same chemicals and toxins the liver is attempting to remove may cause liver dysfunction or damage creating a vicious cycle where the liver is unable to fight back allowing the chemicals and toxins to further accumulate and do still more harm.

    It is interesting that fibromyalgia researchers to date have not published anything on the relationship between liver function and fibromyalgia. Yet there is strong reason to suspect such a relationship. A relationship to alpha1-antitrypsin, synthesized and secreted by the liver, has already been discussed. Growth hormone deficiency has been linked to at least a subset of fibromyalgia patients. Some 30% of fibromyalgia patients have a low level of insulin-like growth factor-1 (IGF-1) (20). As it happens, IGF-1 is produced by the liver. Glutathione depletion has been suggested as factor in chronic fatigue syndrome, and by implication, therefore, a possible factor in fibromyalgia(21). Glutathione is most concentrated in the liver where it is both produced and stored. Thyroid hormone disorders have also been linked to fibromyalgia. In addition to the thyroid gland, the liver plays an important role in the regulation and circulation of thyroid hormones. And, of course, the liver removes chemicals and toxins, a suspected trigger of fibromyalgia.

    Thyroid hormones are a key to stimulating the body’s many metabolic activities. They increase protein synthesis in virtually every body tissue and increase oxygen consumption, and they are essential for normal growth, development, and the regulation of cellular energy metabolism. Neuromuscular complaints are extremely common in patients with thyroid dysfunction(22). There is a high prevalence of thyroid disorder among celiac disease patients(23). Thyroid function was tested in a small group of fibromyalgia patients. While basal thyroid hormone levels were in the normal range, when injected with thyrotropin-releasing hormone (TRH), the fibromyalgia patients responded with a significantly lower secretion of thyrotropin and thyroid hormones24. One chiropractic doctor, Dr. John C. Lowe, has been studying the thyroid status in fibromyalgia patients, coming to the conclusion that some form of thyroid disease may be present in up to 89% of fibromyalgia patients. He has been administering therapeutic dosages of T3 to his fibromyalgia patients who test normal for thyroid status with up to 75% showing improvement in fibromyalgia symptoms and theorizes these normal thyroid fibromyalgia patients may have “thyroid hormone resistance(25,26).”

    The thyroid gland secretes the hormones thyroxine (T4) and tri-idothyronine (T3) with T3 secreted in very small quantities compared to T4. T3, however, is the more active hormone, with ten times more T4 needed to produce the same physiological effect. Since T4 is the inactive hormone and the major product of the thyroid gland, it needs to be converted into the active T3 hormone. The liver accounts for a large percentage of T4 to T3 activation. Conversion of T4 to rT3 and T3 to T2, both inactive metabolites, also takes place in the liver. T3 and T4 are not water soluble, and, in order to circulate in the blood, must bind with plasma proteins. These binding proteins consist of thyroxin-binding globulin, thyroxin-binding prealbumin, and albumin, all of which are produced in the liver. The binding proteins also serve to protect T3 and T4 permitting a storage pool of hormones which can last for many days. More than 99% of the thyroid hormones are bound to these proteins, and it is the small free unbound hormone fraction that accounts for the biological activities of the hormones. Plasma concentrations of free T3 and T4 are held at a steady state, exposing tissues to the same concentrations of free hormone. Normal thyroid function is dependent on both a normally functioning thyroid and liver. Dysfunction in the liver can affect thyroid function, and vice versa(27,28).

    Glutathione is a tripeptide composed of the amino acids glutamate, cystine, and glycine and participates in numerous cellular reactions. It functions in many roles. As an antioxidant, it scavenges free radicals and other reactive species, removes hydrogen and lipid peroxides, and prevents oxidation of biomolecules. It acts in many metabolic activities, including storage and transport of cysteine. And it serves in the regulation of signal transduction and gene expression, DNA and protein synthesis, proteolysis, cell proliferation and apoptosis, cytokine production and immune response, mitochondrial function, and more. Glutathione, most highly concentrated in the liver, is a key to the liver’s ability to remove toxic substances where it is required in the process of converting fat-soluble substances into excretable water-soluble products. Liver disease can both cause and result from a glutathione deficiency. Intravenous infusions of glutathione are being used in therapy for chronic fatigue syndrome and fibromyalgia(29,30).

    Liver dysfunction and toxic substances appear to be involved in fibromyalgia, but what causes fibromyalgia pain and where is the pain centered? An answer to this question was inspired by a worsening of my own fibromyalgia pain symptoms. After quitting my job, my symptoms seemed to slowly improve. However, suddenly everything went downhill. The pain in my right leg and hip was especially bad. Lying in bed only intensified the pain, and it was impossible to find a comfortable position for my right leg. After keeping the right leg straight in one position for any length of time, the slightest motion would cause the hip joint to pop accompanied by a brief, sharp, excruciating pain at the hip joint. I saw this new pain and discomfort as a valuable opportunity and clue for solving the mystery of fibromyalgia pain. I realized that whatever was causing this sharp hip pain had to be related to the source of fibromyalgia pain.

    It’s Not the Muscle, It’s the Fat

    Up until the sharp hip pain, I felt my pain was centered in the muscles. But now, here was a pain specifically located in the hip joint. Joint popping results from the rubbing motion of uneven surfaces in the joint. Now if lying in bed for a time caused a slight gap between hip joint surfaces to open, inflamed and sensitive tissue in the immediate area could work its way into the gap. Then a slight leg movement would pop the joint, close the gap, and pinch the inflamed tissue causing the brief sharp pain. The question then becomes, just what is this inflamed tissue? That sent me to internet to find info on joint anatomy and joint pain. I came across a key paper published in December 2004 that seemed to provide the answers to all questions, “Adipose tissue at entheses: the rheumatological implications of its distribution. A potential site of pain and stress dissipation?”(31)

    Adipose tissue is fat tissue, composed of fat cells or adipocytes and is often mixed with fibrous tissue. Entheses are the attachment points on either side of a joint where muscle tendons and ligaments connect to the bone. Entheses exist everywhere joints exist, from the neck and shoulders down to the toes. The December 2004 paper is an anatomical study of entheses which found, “Adipose tissue was present at several different sites at numerous entheses. Many tendons/ligaments lay on a bed of well vascularised, highly innervated, “insertional angle fat.” Fat filled, meniscoid folds often protruded into joint cavities, immediately adjacent to attachment sites. The adipose tissue was not simply a collection of fat cells alone but it also contained nerves and blood vessels—with the proportions varying according to site. Thus ‘‘insertional angle fat’’ was generally more richly innervated than endotenon fat and some regions of fat may be more susceptible to inflammation than others by virtue of their greater blood supply.” (Insertional angle fat is found in the angle between tendon or ligament attachments to the bone.)

    The discovery of this paper was a moment of great enlightenment. Inflamed, highly innervated fat tissue protruding into and being pinched by a gap in the hip joint surely caused that sharp pain I experienced. Inflamed, highly innervated fat tissue at entheses fits in well as being the site and cause of all fibromyalgia pain. Indeed, the locations of all my fibromyalgia pain sites centered and radiated from the vicinity of either side of the joint, exactly where entheses are located. Any motion tugging on the tendons and ligaments at those sites could irritate sensitive nerves of inflamed adipose tissue producing pain. Thus fibromyalgia is not an abnormality of the brain or central nervous system. It is not an inflammation of muscle tissue. Fibromyalgia is fully explainable as an inflammation of innervated adipose tissue. And what could cause this inflammation? Fat soluble toxic substances, possibly in the presence of an abnormally low liver production level of anti-inflammatory proteins.

    Numerous potentially harmful chemicals and toxins are fat soluble and end up accumulating in adipose tissue where they can persist for many years or even a lifetime. Toxic fat soluble chemicals may be inhaled, ingested, or absorbed through the skin. Such chemicals include dioxins, PCBs, pesticides, petroleum distillates, hydrocarbons, metals, chemicals used in cleaning solvents and plastics, drugs, and even personal care products. Recent research has revealed that adipose tissue functions much more than just as a storage depository for fat. Fat cells or adipocytes are now considered part of one big adipose tissue endocrine organ secreting hormones and a wide range of proteins involved in inflammation and the immune system which have been collectively named “adipokines”. Taken together with the fact that nerves and blood vessels run through adipose tissue, it should not be unexpected that toxic substances accumulating in adipose tissue could give rise to an inflammatory response in adipocytes(32,33,34).

    With a dysfunctional or damaged liver, as might be present in celiac disease, the inability of the liver to remove harmful fat soluble substances increases the risk of accumulating toxic substances making one more susceptible to inflammation of adipose tissue and fibromyalgia. Increased intestinal permeability or leaky gut provides an additional pathway for harmful substances, undigested food proteins, and toxins to reach and accumulate in adipose tissue. Irritable bowl syndrome (IBS) caused by bacterial overgrowth is common in fibromyalgia, and bacterial overgrowth is a cause of leaky gut(35). Leaky gut is also present in celiac disease. It is now clear why celiac disease may leave one at higher risk for developing fibromyalgia.

    Women make up 80% of fibromyalgia patients. Why? The answer may lie in a relationship between estrogen, adipose tissue, and xenobiotic estrogens. Adipocytes express receptors that bind to estrogen. There are six known forms of estrogen receptors classified as ER-alpha and five forms of ER-beta1 thru ER-beta5. Fat deposition in females differs from fat deposition in males. Research has found that the type and number of estrogen receptors expressed in adipose tissue differs at different body locations. The concentration of estrogen in conjunction with adipocyte receptor type and number seems to control where fat is deposited in the body. Estrogen treatment in males can alter male fat distribution into female fat distribution. In addition, females express a significantly greater number of adipocyte estrogen receptors than males(36,37).

    Many of the same fat soluble toxic chemicals mentioned above have properties that mimic estrogens and are called xenobiotic estrogens or xenoestrogens. These xenoestrogens can bind to estrogen receptors and wreck havoc in the body. Exposure to xenoestrogens is believed to cause some breast cancers. Because females have a much greater number of adipocyte estrogen receptors than males, there is much more opportunity for these xenoestrogens to bind with adipocytes in females than in males. Binding with xenoestrogens may cause an inflammatory response in adipocytes. Additionally, fibromyalgia is more likely to occur in women after menopause, when estrogen levels drop. The lower estrogen levels mean there are more free adipocyte estrogen receptors available and less competition for them between estrogen and xenoestrogen, increasing the likelihood of adipose tissue inflammation and fibromyalgia in women after menopause. Thus it is the increased number of adipocyte estrogen receptors which may account for the higher incidence of fibromyalgia in women. Also, any condition which lowers estrogen levels in women (or men) might increase the risk of fibromyalgia(38,39,40,41).

    Preventing, treating, or curing fibromyalgia would seem to first require the elimination of exposure to whatever toxic or harmful substances may be causing inflammation of the adipose tissue. This may be very difficult to achieve if one has little or no knowledge of which substances one is exposed to or may be contributing to the problem. Is the substance in the air, water, at work—at home? Are they emitted by a factory or could the be chemicals used on the job or for a hobby? Is it a cleaning product or solvent, adhesive, a garden product or pesticide, a personal care product, a drug or medication, or a food? Could it come from a plastic product? Did a bacterial or viral infection seem to trigger the fibromyalgia? Was it inhaled, ingested, or absorbed through the skin? Everything must be considered. One study found that a reduced use of cosmetics in a group of women with fibromyalgia significantly improved their symptoms over a two year period(42).

    Olestra to the Rescue?

    Even if one successfully eliminates exposure to the harmful substance(s), those substances have already accumulated in the adipose tissue and could, depending on their properties, potentially reside there for many years causing inflammation until eventually being eliminated by the liver and body. I already mentioned that it took me four months to recover from a two week exposure to Pepto-Bismol. If the liver is damaged or dysfunctional, that time could increase even further. This explains why fibromyalgia often persists in individuals for months and years. Is there some way to “detoxify”? Is there a way to accelerate the elimination of these fat soluble substances?

    There are numerous Web sites promoting controversial methods of detoxification, including large doses of B vitamins, saunas, diet, herbal remedies, and chelation. Saunas, for instance, are used for “sweat” therapy. But sweating can only eliminate water soluble products and has no effect on eliminating fat soluble substances. However, there is one valid, medically proven treatment which can accelerate the removal of a number of fat soluble toxic substances. Oddly enough, this can be achieved by eating potato chips purchased directly off the shelves of local grocery stores.

    Olestra, the non-absorbable fat substitute from Procter & Gamble, has been successfully used to treat patients with high accumulations of dioxin and PCB. In one case, two Austrian women with record high levels of dioxin intoxication and suffering from chloracne were administered Olestra, both in pure form and as Olestra contained in fat-free potato chips, increasing fecal excretion of dioxin by eight to ten fold and reducing the normal elimination half-life of dioxin from seven years to one to two years. In another case, a Western Australian man suffering from PCB toxicity was treated with two once ounce servings of Pringles fat-free potato chips daily for two years. His PCB level dropped dramatically, and his chloracne vanished(43,44,45,46).

    The effects of diet restriction and Olestra on the tissue distribution of a chlorinated hydrocarbon were studied in one experiment. Mice were administered hexachlorobenzene labeled with radioactive carbon-14. When diet was restricted, carbon-14 increased by 3-fold in the brain and the total amount in adipose tissue did not change. On a restricted diet combined with Olestra, there was a 30-fold increase in the rate of carbon-14 excreted in stool compared to a diet without Olestra. Dietary Olestra also reduced the increase of carbon-14 into the brain resulting from a restricted diet by 50%(47).

    My fibromyalgia was quite likely caused by exposure to chemicals inhaled daily at work for years. Since I quit my job, I was no longer exposed to those chemicals. For my fibromyalgia symptoms to end, I needed to eliminate those chemicals which accumulated in my adipose tissue. If I did nothing but wait for the chemicals to be excreted over time, there was no way of knowing how long my fibromyalgia symptoms would last. There was a good chance that the chemicals I was exposed to are the type Olestra can help remove, but I could not be certain. If I decided to treat myself with Olestra, there was no way to know how long it would take for me to begin to see any improvement in fibromyalgia symptoms. But there was nothing to lose by trying.

    I had a choice of fat-free Pringles or Lays Light or Ruffles Light potato chips, all made with Olestra. Pringles contain cornstarch, and I have corn sensitivity. So my choice was two one ounce daily servings of either Lays Light Original or Ruffles Light Original potato chips. I saw no reason to alter my diet otherwise. I am already quite lean and trim, and do not need to lose weight. I would give it at least two months of treatment to see any improvement in symptoms, but I hoped to see at least some small improvement in as little as two weeks. After all, it had previously taken less than two weeks for Pepto-Bismol to cause pain symptoms.

    When I began Olestra treatment, my fibromyalgia symptoms were at their peak. My arms and shoulders ached. Reaching for anything was a dread. Walking any distance was nearly unbearable. My right leg and hip just plain hurt, and the pain was even worse lying in bed. I was still experiencing that sharp hip pain when my hip joint popped. I was greatly fatigued. I could do almost no exercise or stretching. Lifting grocery bags was a trial.

    After just two weeks of Olestra treatment, I was not disappointed. There was a small, but very definite improvement in my symptoms. The sharp hip joint pain and popping were going away. There was just enough overall decrease in pain to begin to do some limited stretching exercises. With the ability to do some daily stretching exercise, I could now monitor how well my symptoms were improving on the basis of an increased range of limb motion and flexibility as well as how well I could walk. Almost daily, there were unquestionable signs of improvement. The range of limb motion during exercise steadily increased in small, but definite increments. Pain levels decreased. Leg pain in bed became tolerable. I was able to add daily walks to my exercise regimen. Fatigue was decreasing. Into the11th week of treatment all seemed to be going great. I had recovered much flexibility in my legs. My arms no longer ached and I could reach all the way across my car seat to reach the latch to unlock the passenger door without pain. I was able to do some pushups, regained some arm strength, and was able to handle grocery bags. It looked as though a full recovery might be possible in just a few more weeks—but then came a setback.

    My left leg had been the least affected limb during my fibromyalgia. The left leg had always retained a degree of flexibility. But by the end of the 11th week of treatment, my left leg began to stiffen in pain. Fatigue increased. I had to curtail my exercise. On the plus side, however, despite this setback, flexibility and pain levels in my arms, shoulders, and right leg remained relatively unchanged. Overall, my condition was still vastly improved over what it was before starting Olestra treatment. I have no idea why my left leg suddenly became so affected. For a few days at that time, I was not feeling so great. Perhaps it was some minor bacterial or viral infection as I also experienced an increase in bowel discomfort at that time. All I could do was let the symptoms in the left leg run their course, and begin my exercise regimen once again just as soon as my left leg loosened up.

    As I write this, I am now into of my 15th week of Olestra treatment. My left leg is just beginning to loosen up. Symptoms in my other limbs remain in a stable improved condition. In a few days, I will begin to concentrate on my exercise and stretching routine, hoping to quickly restore flexibility in my left leg. Hopefully, I can make it to full recovery this time without any more setbacks. I am pretty well convinced that Olestra has played a significant role in dramatically improving my fibromyalgia symptoms.

    Loose Ends

    Before concluding, there are a few loose ends about fibromyalgia to consider. The increased discomfort in my legs experienced when lying in bed can readily be explained as a result of lateral displacement of the joints due to gravity. The lateral displacement pulls on the tendons and ligaments at the entheses, tugging on and aggravating the sensitized nerves within the inflamed adipose tissue at the attachment sites. This may also explain the cause of “restless legs syndrome” so common in fibromyalgia. Just the weight of the bed covers on my feet increases the tension in the leg tendons and ligaments adding to the discomfort. Bed “cradles” which can lift the bed covers above the feet and legs are available from health care product stores.

    I have noted, in addition to being very stiff in the mornings, my fibromyalgia pain seems to let up somewhat and be at its lowest level late in the evenings. The pain cycle seems to be on a 24-hour circadian clock and corresponds to levels of cortisol secreted by the adrenal glands. Cortisol, among many functions, is an anti-inflammatory. In the 24- hour cycle, cortisol secretion is at its lowest around 7:00 am, just about the time most of us need to get up in the morning. Cortisol secretion then picks up and peaks shortly after breakfast, gradually dropping off into the evening. Cortisol has the opportunity to infuse into the inflamed adipose tissue throughout the day, lowering the inflammation and providing pain relief. By late evening, the accumulation of cortisol in adipose tissue is apparently at its maximum. With little cortisol being secreted overnight the cortisol level drops off and the inflammation in the adipose tissue increases resulting in morning stiffness and pain. The relationship between cortisol secretion and fibromyalgia symptoms has been studied(48).

    Exercise and stretching have been a part of my therapy. While exercise works primarily on the muscles and not adipose tissue, I have found it beneficial if not overdone. Keeping up muscle tone, strength, and flexibility improves mobility and also seems to lower the level of fibromyalgia pain. Pain, however, can severely limit one’s ability to perform exercise. I usually take advantage of the reduced pain in the evening and perform my exercises then. I push myself to the threshold of pain tolerance when stretching my limbs. Exercise has been found to have important effects on the immune system. Anti-inflammatory cytokines, such as IL-6, are released by muscle tissue during exercise(49,50,51). Adipose tissue has also been found to secrete IL-6 during exercise under the influence of a release of epinephrine (better known as adrenaline)(52,53). As I perform my exercise, the pain level subsides, and my range of motion increases. It seems clear that anti-inflammatories released by muscle and adipose tissue during exercise actually make it possible to do more exercise with less pain. This pain relief is temporary and short-lived, however. Not long after I complete my exercise, I begin to stiffen up.

    Since liver dysfunction seems a part of fibromyalgia pathogenesis, can liver tests be useful? There are a number of liver function tests which can be performed which measure the blood serum levels of proteins and enzymes produced by the liver. However, these tests primarily assess liver injury rather than liver function. Abnormal test results often, but not always, indicate a liver problem and offer clues as to the nature of the problem. Normal liver function tests do not always mean the liver is normal(54). Physicians seeing patients for fibromyalgia should consider ordering liver function lab tests, but should not rule out liver dysfunction even if test results come back normal. Studies of the prevalence of liver abnormalities in celiac disease rely on the results of liver function tests. Since normal test results do not rule out the possibility of liver dysfunction, the incidence of liver abnormalities in celiac disease could be much higher than reported.

    Conclusion

    The current medically prevalent view that sees fibromyalgia as a condition involving brain and central nervous system abnormalities does not adequately explain the symptoms manifested during my own experience with fibromyalgia. An inflammation of highly innervated and vascularised adipose tissue in the vicinity of entheses readily offers a full explanation of the source of fibromyalgia pain. The inflammation of adipose tissue can be attributed to an accumulation of fat soluble toxic substances within the tissue. The accumulation of fat soluble toxic substances and susceptibility to fibromyalgia likely involves liver dysfunction as well as exposure to toxic substances. Liver dysfunction decreases the liver’s ability to remove fat Unraveling Fibromyalgia, continued soluble substances. Liver dysfunction may also reduce the level of anti-inflammatory proteins produced and secreted by the liver, and this, too, may be a factor in the initiation of inflammation in adipose tissue. Conditions such as celiac disease have a high prevalence of liver abnormalities and a high prevalence of fibromyalgia. Increased intestinal permeability, common with bacterial overgrowth and celiac disease, provides an additional pathway for toxins, undigested proteins, and other harmful substances to overload the liver and accumulate in adipose tissue. Olestra, a non-absorbable fat substitute readily available as an additive in fat-free potato chips, holds great promise as a treatment to accelerate the removal of fat soluble toxic substances from inflamed adipose tissue offering a potential fibromyalgia cure.

    References:

    1. Frissora CL, Koch KL. Symptom overlap and comorbidity of irritable bowel syndrome with other conditions. Curr Gastroenterol Rep. 2005 Aug;7(4):264-71.
    2. Wallace DJ, Hallegua DS. Fibromyalgia: the gastrointestinal link. Curr Pain Headache Rep. 2004 Oct;8(5):364-8.
    3. Zipser RD, Patel S, Yahya KZ, Baisch DW, Monarch E. Presentations of adult celiac disease in a nationwide patient support group. Dig Dis Sci. 2003 Apr;48(4):761-4.
    4. FM Monograph - Fibromyalgia: symptoms, diagnosis, treatment & research. National Fibromyalgia Partnership, Inc. 2004.
    5. Bennet RM. Chronic widespread pain and the fibromyalgia construct. Oregon Health Sciences University, Portland, Oregon.
    6. Neumann L, Buskila D. Epidemiology of fibromyalgia. Curr Pain Headache Rep. 2003 Oct;7(5):362-8.
    7. Simms RW. Fibromyalgia is not a muscle disorder. Am J Med Sci. 1998 Jun;315(6):346-50.
    8. Simms RW. Is there muscle pathology in fibromyalgia syndrome? Rheum Dis Clin North Am. 1996 May;22(2):245-66.
    9. Blanco LE, de Serres FJ, Fernandez-Bustillo E, Kassam DA, Arbesu D, Rodriguez C, Torre JC. Alpha1-antitrypsin and fibromyalgia: new data in favour of the inflammatory hypothesis of fibromyalgia. Med Hypotheses. 2005;64(4):759-69.
    10. Blanco I, Canto H, de Serres FJ, Fernandez-Bustillo E, Rodriguez MC. Alpha1-antitrypsin replacement therapy controls fibromyalgia symptoms in 2 patients with PI ZZ alpha1-antitrypsin deficiency. J Rheumatol. 2004 Oct;31(10):2082-5.
    11. Aldonyte R, Jansson L, Janciauskiene S. Concentration-dependent effects of native and polymerised alpha1-antitrypsin on primary human monocytes, in vitro. BMC Cell Biol. 2004 Mar 29;5:11.
    12. Bristow CL, Patel H, Arnold RR. Self antigen prognostic for human immunodeficiency virus disease progression. Clin Diagn Lab Immunol. 2001 Sep;8(5):937-42.
    13. Shapiro L, Pott GB, Ralston AH. Alpha-1-antitrypsin inhibits human immunodeficiency virus type 1. FASEB J. 2001 Jan;15(1):115-122.
    14. Simms RW, Zerbini CA, Ferrante N, Anthony J, Felson DT, Craven DE. Fibromyalgia syndrome in patients infected with human immunodeficiency virus. The Boston City Hospital Clinical AIDS Team. Am J Med. 1992 Apr;92(4):368-74.
    15. Buskila D, Gladman DD, Langevitz P, Urowitz S, Smythe HA. Fibromyalgia in human immunodeficiency virus infection. J Rheumatol. 1990 Sep;17(9):1202-6.
    16. Wagnerova M, Wagner V, Kriz J, Wokounova D, Madlo Z, Slesingerova B. The morbidity of children with decreased serum levels of alpha 1-antitrypsin in an air pollution area. Czech Med. 1980;3(4):280-8.
    17. Davison S. Coeliac disease and liver dysfunction. Arch Dis Child. 2002 Oct;87(4):293-6.
    18. Duggan JM, Duggan AE. Systematic review: the liver in coeliac disease. Aliment Pharmacol Ther. 2005 Mar 1;21(5):515-8.
    19. Abdo A, Meddings J, Swain M. Liver abnormalities in celiac disease. Clin Gastroenterol Hepatol. 2004 Feb;2(2):107-12.
    20. Bennett RM. Adult growth hormone deficiency in patients with fibromyalgia. Curr Rheumatol Rep. 2002 Aug;4(4):306-12.
    21. Van Konynenburg RA. Is Glutathione depletion an important part of the pathogenesis of Chronic Fatigue Syndrome. Paper presented at the AACFS Seventh International Conference, Madison, Wisconsin, October 8-10, 2004
    22. Duyff RF, Van den Bosch J, Laman DM, van Loon BJ, Linssen WH. Neuromuscular findings in thyroid dysfunction: a prospective clinical and electrodiagnostic study. J Neurol Neurosurg Psychiatry. 2000 Jun;68(6):750-5.
    23. Sategna-Guidetti C, Volta U, Ciacci C, Usai P, Carlino A, De Franceschi L, Camera A, Pelli A, Brossa C. Prevalence of thyroid disorders in untreated adult celiac disease patients and effect of gluten withdrawal: an Italian multicenter study. Am J Gastroenterol. 2001 Mar;96(3):751-7.
    24. Neeck G, Riedel W. Thyroid function in patients with fibromyalgia syndrome. J Rheumatol. 1992 Jul;19(7):1120-2.
    25. Lowe JC, Reichman AJ, Honeyman GS, Yellin J. Thyroid status of fibromyalgia patients. Clinical Bulletin of Myofascial Therapy, 3(1):47-53, 1998.
    26. Lowe JC, Honeyman-Lowe GS. Thyroid disease and fibromyalgia syndrome. Lyon Méditerranée Médical: Médecine du Sud-Est., 36(1):15-17, 2000.
    27. Malik R, Hodgson H. The relationship between the thyroid gland and the liver. QJM. 2002 Sep;95(9):559-69.
    28. Kelly GS. Peripheral metabolism of thyroid hormones: a review. Altern Med Rev. 2000 Aug;5(4):306-33.
    29. Wu G, Fang YZ, Yang S, Lupton JR, Turner ND. Glutathione metabolism and its implications for health. J Nutr. 2004 Mar;134(3):489-92.
    30. Kidd PM. Glutathione: systemic protectant against oxidative and free radical damage. Altern Med Rev 1997;1:155-176.
    31. Benjamin M, Redman S, Milz S, Buttner A, Amin A, Moriggl B, Brenner E, Emery P, McGonagle D, Bydder G. Adipose tissue at entheses: the rheumatological implications of its distribution. A potential site of pain and stress dissipation? Ann Rheum Dis. 2004 Dec;63(12):1549-55.
    32. Rajala MW, Scherer PE. Minireview: The adipocyte--at the crossroads of energy homeostasis, inflammation, and atherosclerosis. Endocrinology. 2003 Sep;144(9):3765-73.
    33. Trayhurn P, Wood IS. Adipokines: inflammation and the pleiotropic role of white adipose tissue. Br J Nutr. 2004 Sep;92(3):347-55.
    34. Fantuzzi G. Adipose tissue, adipokines, and inflammation. J Allergy Clin Immunol. 2005 May;115(5):911-9
    35. Riordan SM, McIver CJ, Thomas DH, Duncombe VM, Bolin TD, Thomas MC. Luminal bacteria and small-intestinal permeability. Scand J Gastroenterol. 1997 Jun;32(6):556-63.
    36. Pedersen SB, Kristensen K, Hermann PA, Katzenellenbogen JA, Richelsen B. Estrogen controls lipolysis by up-regulating alpha2A-adrenergic receptors directly in human adipose tissue through the estrogen receptor alpha. Implications for the female fat distribution. J Clin Endocrinol Metab. 2004 Apr;89(4):1869-78.
    37. Dieudonne MN, Leneveu MC, Giudicelli Y, Pecquery R. Evidence for functional estrogen receptors alpha and beta in human adipose cells: regional specificities and regulation by estrogens. Am J Physiol Cell Physiol. 2004 Mar;286(3):C655-61.
    38. Cassidy A, Milligan S. How significant are environmental estrogens to women? Climacteric. 1998 Sep;1(3):229-42.
    39. Starek A. Estrogens and organochlorine xenoestrogens and breast cancer risk. Int J Occup Med Environ Health. 2003;16(2):113-24.
    40. Daston GP, Gooch JW, Breslin WJ, Shuey DL, Nikiforov AI, Fico TA, Gorsuch JW. Environmental estrogens and reproductive health: a discussion of the human and environmental data. Reprod Toxicol. 1997 Jul-Aug;11(4):465-81.
    41. Waxman J, Zatzkis SM. Fibromyalgia and menopause. Examination of the relationship. Postgrad Med. 1986 Sep 15;80(4):165-7, 170-1.
    42. Sverdrup B. Use less cosmetics--suffer less from fibromyalgia? J Womens Health (Larchmt). 2004 Mar;13(2):187-94.
    43. Moser GA, McLachlan MS. A non-absorbable dietary fat substitute enhances elimination of persistent lipophilic contaminants in humans. Chemosphere. 1999 Oct;39(9):1513-21.
    44. Geusau A, Tschachler E, Meixner M, Sandermann S, Papke O, Wolf C, Valic E, Stingl G, McLachlan M. Olestra increases faecal excretion of 2,3,7,8-tetrachlorodibenzo-p-dioxin. Lancet. 1999 Oct 54(9186):1266-7.
    45. Geusau A, Abraham K, Geissler K, Sator MO, Stingl G, Tschachler E. Severe 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) intoxication: clinical and laboratory effects. Environ Health Perspect. 2001 Aug;109(8):865-9.
    46. Redgrave TG, Wallace P, Jandacek RJ, Tso P. Treatment with a dietary fat substitute decreased Arochlor 1254 contamination in an obese diabetic male. J Nutr Biochem. 2005 Jun;16(6):383-4.
    47. Jandacek RJ, Anderson N, Liu M, Zheng S, Yang Q, Tso P. Effects of yo-yo diet, caloric restriction, and olestra on tissue distribution of hexachlorobenzene. Am J Physiol Gastrointest Liver Physiol. 2005 Feb;288(2):G292-9.
    48. McLean SA, Williams DA, Harris RE, Kop WJ, Groner KH, Ambrose K, Lyden AK, Gracely RH, Crofford LJ, Geisser ME, Sen A, Biswas P, Clauw DJ. Momentary relationship between cortisol secretion and symptoms in patients with fibromyalgia. Arthritis Rheum. 2005 Nov;52(11):3660-9.
    49. Petersen AM, Pedersen BK. The anti-inflammatory effect of exercise. J Appl Physiol. 2005 Apr;98(4):1154-62.
    50. Pedersen BK, Hoffman-Goetz L. Exercise and the immune system: regulation, integration, and adaptation. Physiol Rev. 2000 Jul;80(3):1055-81.
    51. Steensberg A, Fischer CP, Keller C, Moller K, Pedersen BK. IL-6 enhances plasma IL-1ra, IL-10, and cortisol in humans. Am J Physiol Endocrinol Metab. 2003 Aug;285(2):E433-7.
    52. Steensberg A, Toft AD, Schjerling P, Halkjaer-Kristensen J, Pedersen BK. Plasma interleukin-6 during strenuous exercise: role of epinephrine. Am J Physiol Cell Physiol. 2001 Sep;281(3):C1001-4.
    53. Keller P, Keller C, Robinson LE, Pedersen BK. Epinephrine infusion increases adipose interleukin-6 gene expression and systemic levels in humans. J Appl Physiol. 2004 Oct;97(4):1309-12.
    54. Johnston DE. Special considerations in interpreting liver function tests. Am Fam Physician. 1999 Apr 15;59(8):2223-30.


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    Roy Jamron

    Roy S. Jamron holds a B.S. in Physics from the University of Michigan and an M.S. in Engineering Applied Science from the University of California at Davis, and independently investigates the latest research on celiac disease and related disorders.


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