CISRA’s Synergy Health Newsletter

Issue 4. Pre Fibromyalgia: A Possible Explanation for Many Common, Idiopathic, Functional and Pain Disorders (1999)

by J. C. Waterhouse, Ph.D.

Summary

The usual definition of fibromyalgia syndrome (FMS) requires the identification, during physical examination of tenderness in at least 11 of 18 predetermined tender areas. In contrast, the “mapping” technique of R. Paul St. Amand, M.D., identifies lesions wherever they may occur, regardless of the patient’s pain sensitivity, through palpation of the hard, swollen, fibrous areas or “bumps”, found in muscle or connective tissue. Certain patients, often relatives of fibromyalgia patients, are found who have local concentrations of lesions or a pattern of lesions that do not add up to the 11 of 18 tender points in the definition of fibromyalgia. Yet their symptoms and lesions disappear with the same guaifenesin treatment that Dr. St. Amand uses for fibromyalgia. Based on Dr. St. Amand’s success in treating fibromyalgia patient’s relatives with a variety of unexplained disorders, it is suggested that at least a portion of these idiopathic, functional and pain disorders may actually be pre fibromyalgia or fibromyalgia (e.g., irritable bowel syndrome, chronic fatigue syndrome, certain chronic sports injuries, vulvodynia, migraine and tension headaches, irritable bladder syndrome, see p. 5 for complete list). Although other cofactors and triggers may be involved in these illnesses, the tendency to pre fibromyalgia may explain why the triggers cause illness in one person and do not in another. This article discusses Dr. St. Amand’s theory and treatment approach for fibromyalgia and related disorders, followed by some examples of undiagnosed fibromyalgia and pre fibromyalgia from the author’s experience. The manner in which patients may reduce or adapt to their early symptoms using exercise, caffeine, workaholism and diet, are then discussed. These adaptive behaviors, along with naturally higher levels of certain neurotransmitters when still young, are proposed to explain why some with pre fibromyalgia may lead a relatively normal life, sometimes with minimal symptoms or symptoms affecting only one particular function or region of the body. Later, a trigger, like a trauma or infection may occur that may initiate a change in the central nervous system mechanisms (e.g., an increase in substance P or a decrease in serotonin), decreasing the ability to inhibit pain signals. At this point, the lesions may become increasingly painful, while local irritation or injury may favor even greater lesion formation. Reasons for the common occurrence of fibromyalgia and pre fibromyalgia are discussed in terms of differences between our environment, diet and lifestyle as compared to previous centuries and pre-agricultural times. Although genetic predisposition is clearly very important, it is proposed here that environmental and dietary changes may be responsible for the widespread and increasing prevalence of these disorders in modern society. Finally, the close connections between the concept of fibromyalgia and pre fibromyalgia proposed here and ideas from the new field of Darwinian medicine are discussed.

Introduction

Fibromyalgia syndrome (FMS) has been increasingly recognized as a disease which causes a great deal of suffering and disability. It would be hoped that earlier detection of the disease might result in earlier treatment and a greater potential for rapid recovery. One possible way for this early detection has arisen from the experience of R. Paul St. Amand, M.D. (Assistant Clinical Professor of Medicine at Harbor/UCLA Medical School, an internist/endocrinologist and fibromyalgia expert). He has developed a technique for detecting and “mapping” tender area lesions wherever they occur, rather than only noting them at the 18 predetermined tender areas identified by the American College of Rheumatology (St. Amand et al 1997). These “lesions” are detected as swollen, hard or fibrous areas in muscle and connective tissues that can be “mapped” during physical examination by a physician trained in the mapping technique (see Waterhouse, 1999, p. 13, this issue). After diagnosis, the patient is then treated with guaifenesin according to Dr. St. Amand’s protocol (for important details on how to use this approach, further technical information, and lists of sources of “hidden” salicylates and lists of salicylate-free products, see Reference section, below and Waterhouse 1999, p. 6-10, this issue ). Often, relatives of Dr. St. Amand’s fibromyalgia patients also become his patients when they realize that they had been experiencing one or more symptoms of fibromyalgia most of their lives. These patients may not meet the current criteria for fibromyalgia, yet they have lesions in areas that correspond to their symptoms, and both symptoms and lesions disappear with the same guaifenesin treatment used for fibromyalgia. It is for these patients that the term pre fibromyalgia (PF) is proposed. After a brief explanation of St. Amand’s theory, the nature, diagnosis and treatment of pre fibromyalgia will be described. The interplay of genetics and environment from an evolutionary perspective will also be discussed as a possible explanation for the high prevalence of fibromyalgia and pre fibromyalgia.

Excess Phosphate and Reduced Energy (ATP) Production as a Possible Cause of Fibromyalgia and Pre Fibromyalgia

According to Dr. St. Amand’s theory, fibromyalgia is associated with an inherited tendency to phosphate retention. The excess phosphate is then stored within cells in various body tissues and leads to increased intracellular calcium. Although the theory involves a harder to detect, intracellular process, it is useful to consider more well known examples of other problems arising from calcium and phosphate excess. It is well known that when the product of calcium and phosphate levels are too high, there is a tendency to deposit calcium and phosphate in soft tissues. Dr. Hans Selye, the noted expert on stress described calciphylaxis as occurring in response to stress. Calcium phosphate is found to be associated with pain in tendonitis and is associated with two common types of arthritis. Excessive intracellular calcium is also associated with neuronal and other cell damage in certain illnesses. In the case of fibromyalgia, according to Dr. St. Amand’s theory, susceptible people have a tendency to inadequately excrete phosphate via the kidney. The combination of increased phosphate retention and various types of stressors to particular muscles, tendons and joints, or to the body as a whole, appears to provide the conditions for calcium and phosphate accumulation within cells of many tissue types. St. Amand et al (1997) proposes that low cellular energy production (ATP), due to increased phosphate in the mitochondria of lesions, prevents the cells from removing excess calcium in the cytosol of the cell (see Wilson et al 1988, on correlation between intracellular phosphate and muscle fatigue). The excess intracellular calcium and phosphate are thought to account for the individualistic pattern of diverse and varying symptoms, and the palpable lesions (due to constant muscle contraction and excess intracellular fluid) mapped in fibromyalgia and pre fibromyalgia. The different patterns of lesion location makes it possible for diverse symptoms to have a similar underlying mechanism, making it harder to link the diverse forms of pre fibromyalgia. Since calcium, phosphate and ATP are essential to so many processes in the body, there is a potential for effects at fundamental levels of function. For instance, entry of calcium into the cell cytosol causes muscle contraction and calcium is an important secondary messenger molecule involved in hormonal production, MAST cell degranulation, and nerve function. Since the phosphate and calcium accumulation occurs within cells and mitochondria, the changes are not detectable with many current laboratory tests (see Waterhouse 1999, p. 8-9, this issue for exceptions to this).

The similarities and differences between gout and fibromyalgia are also interesting (for more on this, see Waterhouse, 1999, p. 10-11, this issue). The excess phosphate theory proposes that they are similar in that both are retention diseases, i.e., the kidneys cause too much of a substance to be retained, rather than excreted. In both cases, medication is able to enhance excretion by the kidney of the substance, but its effects can be blocked by salicylates. In both cases, a pronounced increase in symptoms occurs when the medication dose is adequate to begin reversing the disease. In the case of gout, it is those prone to uric acid retention and elevation in the blood, mostly men, who are most at risk for this painful disorder where uric acid crystals are deposited in joints. In fibromyalgia, what is believed to be retained in excess is phosphate. Serum phosphate levels are generally higher in the serum in children and post menopausal women. This is compatible with the observed incidence of fibromyalgia, which is found in children as well as adults, in more women than men, and begins to increase among women in perimenopause and menopause. The tendency of some children to have fibromyalgia when quite young (sometimes only noted as “growing pains”) and then sometimes to have symptoms decrease when they have their growth spurt (when calcium and phosphate use in growing bones is increased), is also explained by this theory. Fibromyalgia is much less obvious than gout, because the accumulation is intracellular, and the over activation of diverse tissues (due to elevated calcium and low ATP) results in an ability to mimic many illnesses and even make one prone to develop additional illnesses (e.g., chronic infections, hypoglycemia). It is interesting that Charles Darwin, thought to have a disease resembling CFS or FM, was told by one doctor that he suffered from “suppressed gout”. This doctor’s idea may turn out to have some crude resemblance to the truth, in that Darwin may have had a retention disease, analogous to, but distinct from gout, but the substance retained (phosphate) was “hidden” within cells and thus, in a sense, “suppressed.”

It should be remembered, however, that what Dr. St. Amand is most certain of, is that guaifenesin (when not blocked by salicylates) works to reverse fibromyalgia and related disorders. The theory to explain how it works is still speculative and is, in a sense, less important. The theory that the kidneys tend to retain too much phosphate in fibromyalgia is simply the explanation that most closely fits a variety of observations collected over the years, including a 60% increase in phosphate in the urine observed after treatment under a controlled dietary phosphate regime (St. Amand, 1998). I presented the theory in some detail to show that there is a reasonable theoretical basis that could explain the efficacy of this approach, but if the theory turns out to be wrong, that will not affect the many years of observation of the treatment’s effectiveness in patients.

Pre Fibromyalgia (PF): Description, Development and Treatment

Pre fibromyalgia is a term for those who have only slight fibromyalgia symptoms, or who have only one or two symptoms or conditions that are seemingly unconnected to fibromyalgia syndrome, yet occur frequently in fibromyalgia patients. Thus, the easiest way to describe pre fibromyalgia is to refer to a list of the many varied symptoms of fibromyalgia. Increased levels of pain, stiffness, fatigue, depression, irritability and problems with memory and concentration head the list. Other symptoms and conditions occurring in some patients include irritable bowel syndrome, dizziness, headaches, numbness and tingling, unexplained anxiety, sugar craving, blurring of vision, eye irritation, nasal congestion, ringing in the ears, constipation, irritable bladder syndrome, interstitial cystitis, vaginal irritation, restless legs and cramps.

As mentioned previously, fibromyalgia or pre fibromyalgia cases are frequently missed when standard diagnostic methods are used. This was the case with both my mother and my father. My mother was diagnosed with osteoarthritis, however her pain, fatigue and other symptoms were probably sufficient for a diagnosis of full-fledged fibromyalgia, though it had not been recognized before Dr. St. Amand mapped her. My father’s case was mild enough that it can provide a good example of pre fibromyalgia (PF). Symptomology exhibited before the triggering events, in patients like myself, can also provide examples of the characteristics of PF. In many cases, the accumulation of calcium and phosphate appears to begin in childhood, however the symptoms may be so mild as to not even be noticed. And what is more, how is a child to know what to compare their experiences with? Many fibromyalgics report that they just thought everyone felt the same pains, stiffness, and problems with attention and memory, or whatever symptoms first appeared. For instance, in my father’s case, he found he had a great deal of trouble concentrating in school, possibly a reflection of effects on brain function. In my case, the only early signs I can identify in my childhood were a recurring cramp in my foot and a tendency to muscle tension, which I often relieved by stretching exercises.

The first sign of PF might be any one of the list of fibromyalgia symptoms, like the recurring pain at the site of a sports injury, constipation, dizziness, headaches, vulvodynia, or irritable bowel syndrome. The first symptoms might be viewed as the breakage that occurs at the weakest link, or as the tip of an iceberg that slowly becomes more visible as the years ebb. In my father’s case, it was his knee that was the biggest problem. He also had pain in the shoulder he used for his tennis serve, as well as pain in his upper back, between his shoulder blades. For myself, my most noticeable early PF symptom was probably occasional migraine headaches (see Waterhouse, 1998, for more detailed information on the development of chronic fatigue syndrome, multiple chemical sensitivity and fibromyalgia, which ensued). It seems quite possible that many of the myriad idiopathic conditions that doctors often have little ability to cure, may turn out to be aspects of the fibromyalgia process in PF patients. In the absence of large triggering factors to exacerbate the condition, many cases of PF are relatively mild and only become debilitating in old age. This implies hope for our aging population, in that many of our aches and pains and other symptoms of old age, may actually turn out to be treatable as pre fibromyalgia or fibromyalgia.

According to Dr. St. Amand’s experience, for many pre fibromyalgics, the process can be easily reversed with relatively little discomfort. These are the fortunate patients who have the chance to start treatment early. All they have to do is to obtain an adequate dose of guaifenesin (for 90%, 600-1800 mg. per day is sufficient, while 10% require more) and avoid salicylates (both obvious and hidden), which block the treatment. In my father’s case, when he began guaifenesin, I kept warning him that his pain would get worse before it got better, due to the guaifenesin reversal process. However, as not uncommonly occurs in milder cases, he seems to be just getting better, with little or none of the initial increase in symptoms that many fibromyalgics must go through. It may not be a pain-free reversal for all PFs, and it may have helped my father to have gone on the hypoglycemic diet first. However, even if there is reversal pain and other symptoms, they are not likely to last long, and it is certainly better than letting the PF worsen and potentially develop into fibromyalgia, often accompanied by arthritic damage to joints.

Why So Common?: Possible Role of Changing Environment and Diet

This rather broad and inclusive description of the illness may make it seem like I am claiming that a very large proportion of people have fibromyalgia, or the preliminary phases of it. The fact is, the numbers may really be quite large, although more research is needed. A Norwegian study (Forseth et al 1992) found 1 in 10 women they examined between 25 and 50 years of age had fibromyalgia, and other estimates have also been fairly high (2-3% of the general U.S. population). It would be likely to be even more common if one were to use St. Amand’s mapping method and include more elderly and pre fibromyalgics. Dr. St. Amand rarely, if ever, finds a patient who suspects they have FMS or CFS and then has no lesions upon examination. Among the many relatives of fibromyalgia patients that Dr. St. Amand sees, most have only been diagnosed with one of the many fibromyalgia-related complaints (e.g., irritable bowel syndrome, headaches, osteoarthritis, sports injury, carpal tunnel syndrome). He almost always finds they have obvious fibromyalgia lesions and they respond to guaifenesin and the hypoglycemic diet (necessary in 40-60% of patients). Their primary complaint improves, as well as other problems that they may not have recognized as medical problems (e.g., fatigue, attention problems). To make it clear that these lesions do actually reflect the existence of fibromyalgia (or PF), it should be mentioned that Dr. St. Amand does not find these lesions in all patients he examines. For years he has examined non-fibromyalgia patients coming in for routine physical examinations and in these patients he only occasionally finds lesions. These basically asymptomatic patients probably are early in the PF phase. If Dr. St. Amand is correct, and fibromyalgia is actually a part of the same illness that leads to osteoarthritis (via calcium and phosphate accumulation in joints), then judging by the high frequency of osteoarthritis in the aging population, pre fibromyalgia and fibromyalgia are indeed very common.

One might wonder, if all this is true, why fibromyalgia and PF are this common. I believe that it may be that fibromyalgia is analogous to an illness like arteriosclerosis. In other words, we all have the possibility of developing it to a certain extent. With arteriosclerosis, we know there are genetic and environmental factors that contribute over many years to hardening of the arteries and then to actual cardiovascular symptoms. Known environmental factors include homocysteine levels, dietary fat and cholesterol and exposures to toxic chemicals, like from tobacco smoke. Stressors of all kinds, including traumas, surgery and infections, as well as psychological factors may be important as well. In a similar way, fibromyalgia probably involves several genes and a variety of environmental factors. Investigation into the environmental factors that may contribute to fibromyalgia reveals a number of factors that promote excess phosphate and/or stress the tissues through injury, surgery, allergy/sensitivity, infection, nutrient depletion or toxicity. Genetic factors are clearly relevant as well, thus leading to a complex pattern of genetic predispositions and environmental triggering factors.

Further investigation reveals that many of the environmental factors that may trigger fibromyalgia are phenomena that our bodies were not adapted to during our evolutionary history. For instance, our bodies are exposed to a wide variety of chemicals, including pesticides, antibiotics, food additives, cleaning products and fragrances many of which are toxic substances or known carcinogens, and others that our detoxification systems are not always well adapted to handle. In fact, recent research on Gulf War Syndrome points to genetic differences in detoxification enzyme levels as an explanation of individual differences in reactions to toxins (Haley et al 1999). Other substances may not be generally toxic, but they may initiate hypersensitivity reactions or may cross react with normal tissue and cause production of antibodies against the body’s tissues.

Our diets have also changed a great deal since the days of our prehistoric ancestors. Agriculture and domestication of animals in the last 10,000 years has led to consumption of large amounts of grains and dairy products. Human milk has a much lower level of phosphate relative to calcium than cow’s milk. Presumably, the lower phosphate in human milk is what evolution has arrived at as optimal, yet many cultures, since the domestication of cattle, have relied heavily on high phosphate dairy products. In more modern times, sodas, sports drinks and processed foods add even more phosphate to our diet. Recent evidence suggests that some people are less well-adapted to consumption of certain grains (e.g. gluten-containing grains, like wheat and rye) or to dairy products (particularly those containing lactose), as well as other foods that make up increasingly large parts of our diets. A version of this theory was recently presented by Dr. Peter D’Adamo (1997). D’Adamo identifies foods containing lectins, which are specifically harmful to people with certain blood types, which he argues are connected to our evolutionary past. However, regardless of the truth of this evolutionary connection between foods and blood types, it is becoming increasingly recognized that grain, dairy, and other food allergies or intolerances are fairly common. In a recent controlled study using the ELISA/ACT test for “hidden” immune sensitivities (Types II, III, and IV), all 32 fibromyalgia patients tested had between 15 and 32 immune sensitivities (Jaffe, 1996). The ELISA/ACT treatment program used in the study resulted in a 30-50% reduction in fibromyalgia symptoms. The most common reactive items included MSG, Candida albicans, caffeine, chocolate, food coloring, cola beverages, shrimp and dairy products. Soy, peanuts, cheese, wheat, citrus, tomato, eggs, aspartame, and corn are other frequent offenders (Randolph & Moss, 1989).

We are also exposed to large amounts of refined carbohydrates, unlike our ancient ancestors. Large amounts of sugar are known to be a problem for many people and may lead to the development of Type II diabetes (the levels of adult onset diabetes are astonishingly high in certain populations, such as Pacific Islanders and Native Americans). Excessive sugar or carbohydrates are also a source of elevated triglycerides, which contributes to heart disease. It is increasingly clear that refined carbohydrates can lead to excessive levels of insulin. This is particularly relevant to fibromyalgia, since insulin not only increases phosphate retention, but also tends to help drive phosphate into cells, which could be another contributing factor to this disease process. Dr. St. Amand (1998) discusses how high carbohydrate consumption in many fibromyalgics prone to reactive hypoglycemia, lead to increased stress levels, weight gain, dizziness, anxiety, and headaches as a result of the large fluctuations in insulin and blood sugar levels (also, see Heller et al 1995; Waterhouse, 1999, p. 9-10, this issue). Increased stress levels, with the associated increase in stress hormones like cortisol, can lead to poor sleep, osteoporosis, poor digestion, depletion of nutrients, immune dysregulation etc…, all further contributing to the environmental component in a vicious cycle. As the body becomes more and more debilitated, immune problems may result in increased susceptibility to infections, further straining the body’s resources. People with genetic predispositions to other illnesses (e.g. autoimmune illnesses) may find them expressed as well. Increased acidity, arising from immune reactions and other sources, also act to increase phosphate retention. In addition, certain important nutrients may be depleted by various stressors or may be less abundant in refined foods (e.g., magnesium, B vitamins, essential fatty acids and certain amino acids), which may promote even more phosphate retention and immune dysregulation, and further reduce the metabolic efficiency of energy production.

Thus, although genetic factors are clearly very important, it may be that the essence of the problem is a mismatch between our current environment/lifestyle and our genetic makeup. Those with fibromyalgia just happen to have a genetic makeup that is not as well adapted to the “unnatural” environment we have created for ourselves. It may be that guaifenesin is able to compensate or fine tune the existing phosphate excretion to help equalize the playing field for those whose genes make them less well adapted to this new environment. A lower carbohydrate diet is also necessary for many, while others may need to avoid certain foods and chemicals or treat an infection, or make other compensatory changes. Taking guaifenesin alone may be enough for some, but it would seem wise to take heed of this warning about how environmental changes have their price, for this and many other illnesses. Conversely, just changing our diet and environment, although it may help a great deal for some, may not be enough by itself, particularly when the genetic factor is strong, or the illness has been prolonged. According to St. Amand’s theory, for many with fibromyalgia and pre fibromyalgia, the reversal of the calcium and phosphate accumulation within cells will need guaifenesin, as well.

Possible Illnesses That May be Pre Fibromyalgia or Fibromyalgia in at Least Some Portion of the Cases

Irritable bowel syndrome, certain chronic sports injuries, temporal mandibular joint disorder, migraine and tension headaches, costochondritis (rib pain), irritable bladder syndrome, repeated bladder infections, interstitial cystitis, vulvodynia, chronic yeast infections, carpal tunnel syndrome, restless leg syndrome, Raynaud’s phenomenon, tinnitus, Meniere’s Disease, neurally mediated hypotension, chronic constipation, chronic diarrhea, osteoarthritis, chronic myofascial pain syndrome, sciatica, and other chronic back pain, tennis elbow, attention deficit disorder, some cases of anxiety or panic disorders, premenstrual syndrome, dysmenorrhea, undiagnosed pelvic pain disorders, unexplained rashes, unexplained dental pain, chronic fatigue syndrome (CFS, a.k.a. CFIDS or myalgic encephalomyelitis, for more on how chronic fatigue syndrome may relate to fibromyalgia, see Waterhouse, 1999, p. 8 this issue). Anxiety or panic disorders may be more closely related to hypoglycemia, while many of the others may be pre fibromyalgia or fibromyalgia with or without hypoglycemia. Clearly, other factors are often involved in the development of these conditions, however the tendency to pre fibromyalgia may explain why, for example, one factory worker develops carpal tunnel syndrome, while a worker standing next to him does not.

 
A Postscript: Darwinian Medicine

Since originally writing this article, I have read a fascinating book called, Why We Get Sick: The New Science of Darwinian Medicine, written by a physician and an evolutionary biologist (Nesse and Williams, 1994). In this book, they refer to a wide range of research that supports the value of looking at evolutionary causes, as well as the proximate or mechanistic causes of illness. They identify 6 evolutionary explanations for diseases or characteristics, including two that are quite relevant to the concepts of fibromyalgia and pre fibromyalgia presented above: 1. a novel environment, and 2. genes, including what they call genetic “quirks”. They stress the evidence for the powerful ability of natural selection to keep the level of harmful mutations at a very low level. They contend that when a harmful genetic disease has much above a 0.01% level of prevalence, this often indicates that the gene has some compensatory benefit or at least lacks the harmful effects, in a different environment or for the heterozygote (e.g., sickle cell anemia, in which the heterozygous individual, who has only one copy of the gene, is more resistant to malaria). For instance, the genes that predispose to heart disease were probably not much of a problem when our ancient ancestors lived in an environment in which a much lower fat diet was consumed. Thus these genes may qualify as genetic quirks, rather than defects, in that they arise from the mismatch of our current environment and the genes. This might provide a good analogy with the proposed phosphate retention explanation of fibromyalgia, in that those who tend to retain phosphate would probably not have a problem in a low phosphate environment, in fact they might even have an advantage. Although, I can not go into too much detail here, their discussion of toxins, allergies and diabetes also have some similarities to the arguments made in the this article and many of their speculative evolutionary explanations involve a similar mismatch between certain genetic “quirks” and our current novel environment.

Editorial Note (2008): For an update on my current views on fibromyalgia and related conditions and on what I now believe is a more effective approach to treatment, see the transcript of a talk I gave before a Support Group in 2005. I give an overview of what has helped me most, with an emphasis on a new approach, called the Marshall Protocol (MP) that is designed to eliminate the underlying cause: chronic infection with cell wall deficient (L-form) bacteria (also see http://AutoimmunityResearch.org and http://cureMyTh1.org, along with other recent articles on this web site, www.synergyhn.com.  I now think there is strong evidence for bacteria as the underlying cause of the disturbances in phosphate retention, energy metabolism, hypoglycemia and food sensitivities.  Environmental changes, such as vitamin D supplementation and the types of antibiotics used (beta lactam antibiotics that target cell walls) may have increased the levels of these hard-to-detect bacterial pathogens (see: http://bacteriality.com). In addition, I should note that evolutionary ideas about disease also recognizes the importance of infectious causes. The pathogens are evolving along with their human hosts and in fact, are in a sort of “arms race” with the organisms they infect, making them a very important challenge to our immune systems and maintenance of health. An interesting book on the role of infectious causes is evolutionary biologist, Paul Ewald’s Plague Time.

References

1. D’Adamo, Peter, N.D. 1996. Eat Right for Your Blood Type. Putnam. NY, NY.
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4. Haley R.W., S. Billecke and B.N. La Du. 1999. Association of low PON1 type Q (Type A) arylesterase activity with neurologic symptom complexes in Gulf War veterans. Toxicol. Appl. Pharmacol. Vol. 157(3):227-223.
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7. MacDonald, K.L. et al. 1996. A case control study to assess possible triggers and cofactors in chronic fatigue syndrome. Am. J. Med. 100(5):548-54.
8. Nesse, Randolph M., M.D. and George Williams, Ph.D. 1994. Why We Get Sick: The New Science of Darwinian Medicine. Random House, NY.
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14. St. Amand, R. Paul, M.D. 1999. Papers on “Fibromyalgia: For Patients,” “Fibromyalgia: For Physicians,” and “Hypoglycemia,” and Salicylate-Free product list, available on the web, at http://guaidoc.com and  http://www.csusm.edu/public/guests/nancym/fibromt.htm
15. Waterhouse, J.C., Ph.D. 1998. A case history of FMS/CFIDS/MCS and the roles of guaifenesin, a low carbohydrate diet and environmental medicine in recovery. CISRA’s Synergy Health Newsletter Vol. 1(2), CISRA, Pasadena, CA.
16. Waterhouse, J.C., Ph.D. 1999. How to “map” fibromyalgia: review of video and comments. CISRA’s Synergy Health Newsletter, Vol. 2(1), CISRA, Pasadena, CA.
17. Waterhouse, J.C., Ph.D. 1999. Guaifenesin and a hypoglycemic diet in fibromyalgia: common errors and misconceptions. CISRA’s Synergy Health Newsletter, Vol. 2(1), CISRA, Pasadena, CA.
18. Wilson, J.R. et al. 1988. Relationship of muscular fatigue to pH and diprotonated Pi in humans: a P-31 NMR study. J. Appl. Physiol. 64(6):2333-2339.

 
Disclaimer: All articles provided on the SynergyHN website are for information only and are not intended as medical advice. An effort is made to be accurate, however readers are advised to verify what is presented here and check with their own doctors. No guarantee of accuracy is expressed or implied. Neither CISRA nor the author receives any funding or income from any organization or manufacturer connected with the topics discussed.

Written by synergyhn

October 30, 1999 at 9:06 pm

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