CISRA’s Synergy Health Newsletter

Issue 4. Guaifenesin and A Hypoglycemic Diet in Fibromyalgia: Common Errors and Misconceptions (1999)

by J. C. Waterhouse, Ph.D.


Fibromyalgia is an illness in which patients suffer from generalized pain, fatigue, insomnia, non-restorative sleep and a variety of other symptoms, which may include irritable bowel syndrome, headaches and impaired memory and cognition. Dr. R. Paul St. Amand’s approach using guaifenesin to reverse the painful lesions and a low carbohydrate diet for those with hypoglycemia has been gaining wider recognition over its many years of use. Unfortunately, many people hear of the treatment without hearing all the details on how to use it successfully, resulting in a reputation of only mixed or partial success. A brief summary of the 5 common errors that may prevent success with guaifenesin treatment of fibromyalgia follows.
1. Inadequate dose. Individuals differ in the dose they require, from 600 mg to 4800 mg per day, with the majority needing 1200 mg or less. An inadequate dose will result in no improvement.
2. Giving up too soon. Though many show improvement in the first 2-6 months, some require a year or more to be certain they have improved.
3. Hidden salicylates in herbal and other plant extracts, over-the-counter drugs, lotions and cosmetics. Patients must substitute salicylate-free products for many of the usual things they use and keep up-to-date with new information on salicylate additions.
4. Unwilling to try or stay with treatment due to fear of exacerbations. Many do not know that an increase in symptoms initially is actually a sign that guaifenesin is working, or they are unaware that the hypoglycemic diet may help them through this initial increase in symptoms.
5. Don’t want to give up the benefits of salicylate-containing herbal medications. There are many mineral, vitamin and other supplements, pharmaceuticals, and other alternative treatment methods, which in most cases, work as well or better than herbal medications and do not contain salicylates.

The next section of this article attempts to clarify some theoretical and technical aspects of guaifenesin use. A brief summary of the main points:
1. St. Amand’s theory and treatment approach are consistent with other theories and with sudden onset in some fibromyalgia cases. Other treatments may work by either treating triggering or perpetuating factors, or by affecting phosphate absorption and retention.
2. Other mechanisms proposed, including the placebo effect, can not account for Dr. St. Amand’s and other doctor’s successes in treating thousands of patients with guaifenesin.
3. Although many common laboratory tests are unable to provide evidence to support St. Amand’s theory that excess phosphate and calcium in cells causes fibromyalgia, other more sophisticated tests do support his theory.
4. Guaifenesin has been used safely for many years and there is no evidence that it causes osteoporosis.
5. Significant levels of salicylates are found in many products even when the manufacturer is unaware of their presence, since virtually all plants produce salicylates, which may be concentrated in extracts.

The article then clarifies some issues regarding the low carbohydrate diet for hypoglycemia, as presented by Dr. St. Amand. The effects of low blood sugar on the autonomic nervous system is able to account for many symptoms, and the effects of the low blood sugar itself accounts for others. We describe how these effects go beyond what is accomplished through frequent small meals, environmental medicine and anti fungal medication, and may benefit patients regardless of their weight. Many find weight loss much easier using a lower carbohydrate diet, and research is cited to support this. Research is also cited that shows the cardiovascular and other benefits of a lower carbohydrate diet for those prone to excessive insulin.

The plausibility of Dr. St. Amand’s theory and treatment approach is evidenced by the willingness of Dr. Robert Bennett, a fibromyalgia researcher at Oregon Health Sciences University, to carry out a double blind study of guaifenesin in 1995. Unfortunately, there were a number of flaws in the study that led to a failure to find a significant difference between the treatment and control groups. The primary mistakes were hidden salicylates, inadequate dose and probable inclusion of untreated hypoglycemics. Much information on sources of hidden salicylates was lacking at the beginning of the study. In fact, the year in which the study was conducted was just the period in which salicylates and salicylate-containing herbal ingredients were being extensively added to products. It is unfortunate that although Dr. St. Amand was the technical advisor for the study and the most experienced with the treatment, his critique of the study has not received the attention it deserves among fibromyalgia researchers. The article concludes with recommendations for a future study, which is now in the planning stages. Several researchers at prestigious institutions (e.g., New York University and Scripps Institute) have been impressed with results from guaifenesin and have shown interest in collaborating on future research.

Part A. Common Errors in Using Dr. R. Paul St. Amand’s Guaifenesin Treatment Approach in Fibromyalgia

Fibromyalgia is an illness in which patients suffer from generalized pain, fatigue, insomnia, non-restorative sleep and a variety of other symptoms, which may include irritable bowel syndrome, headaches and impaired memory and cognition. Dr. R. Paul St. Amand’s approach using guaifenesin to reverse fibromyalgia and related diseases, such as chronic fatigue syndrome, has been gaining wider recognition in recent years. Guaifenesin, a safe, inexpensive, non patentable medication that is most frequently used for coughs and certain respiratory conditions, has been found by Dr. St. Amand to reverse fibromyalgia lesions. The theory that he feels best explains his observations involves the ability of guaifenesin to enhance excretion of excess phosphate by the kidney. He believes that excess phosphate is stored within cells and reduces ATP production and is accompanied by increased intracellular calcium, which leads to excessive muscle contraction in local areas of accumulation (St. Amand and Malek, 1997 and 1999; also, see below, Part B for more on theory or Part D for more on the history of this treatment). Unfortunately, there are a number of errors that people frequently make in using this treatment, thus resulting in a reputation of only mixed or partial success in treating fibromyalgia. The purpose of this section is to specify these errors and explain how they can be avoided.

1. Inadequate Dose. Some people do not achieve success because they do not use a high enough dose of guaifenesin. The appropriate dose varies among individuals, from 600 mg/day to 4800 mg/ day. There appears to be a threshold dose, below which no benefit will be achieved. A definite increase of symptoms is usually a sign that one has achieved an adequate dose. However, the mapping of decreased lesion size by a trained physician or therapist is the most accurate way to determine whether the dose has been adequate (see Waterhouse, 1999, p. 13, this issue). If mapping is unavailable, one may start with 300 mg twice a day for 1-2 weeks and then raise to 600 mg twice daily for 2 weeks (70% find 1200 mg or less adequate). The dose at which a noticeable exacerbation occurs, which signals lesion reversal has begun, is the dose usually considered adequate. If there is still no symptom exacerbation, one can raise the dose in 300 mg increments every 2 weeks, until either a change in the lesions or an exacerbation is observed. Some patients find that after 6-12 months on their initial dose, their progress begins to slow somewhat and raising the dose by an additional 300-600 mg results in faster progress. However, if you choose faster progress with higher doses, the reversal process may be more intense, less cyclic and result in fewer “good” days, which often appear between cycles. The fewer “good” days along the way with this approach is the primary reason that Dr. St. Amand does not usually recommend the higher doses. Also, beyond a certain point, which probably varies among individuals, increased doses will not increase the pace of the reversal process further. (Note: Specify plain prescription guaifenesin tablets. Do not use over-the-counter syrups or pills containing other drugs. If you feel you must resort to non prescription guaifenesin, it may be ordered in a form free from other drugs from a mail order pharmacy: Dave Ributsky, R. Ph. 800-846-5525. In countries where guaifenesin is unavailable, mail order prescription guaifenesin may be obtained from: College Pharmacy 800-888-9358, FAX: 800-556-5893).

2. Giving up too soon. There are several reasons some will conclude guaifenesin isn’t effectively reversing their fibromyalgia and quit too soon. They may not know that although some improve quickly, for others it may take 6 months or even as long as a year or more to be certain of improvement. Sometimes it is concluded that if their symptoms don’t reverse in a cyclic manner as usually occurs, then it isn’t really working. However, there are varied patterns of response and not everyone experiences cycles. Some may even have few noticeable reversal symptoms. Some may be rapid responders and experience a lot of reversal symptoms at a low dose, and progress much more rapidly, without cycles. Unfortunately, some are unaware that reversal symptoms are to be expected and are a good sign, and they mistakenly conclude that guaifenesin is making them worse and therefore quit. It is also better to judge improvement by the “good” days, which occur more frequently and more noticeably over time, rather than judge by the more symptomatic periods during cycles in which the guaifenesin is intensively reversing lesions. It should be emphasized that return of lesions can be quite rapid if guaifenesin is discontinued. We speculate that this is because the bones may have built up a relatively high amount of phosphate relative to calcium (R. Van Konynenburg, Ph.D., personal communication), which could help make lesion formation more rapid than would be expected based on current phosphate intake.

3. Hidden salicylates in herbal and other plant extracts, over-the-counter drugs, lotions and cosmetics block guaifenesin’s effect. Sometimes patients are not aware of, or are not consistent in their avoidance of hidden salicylates. Supplements, like echinacea, and over-the-counter medicines (e.g. Alka Selzer, Ben Gay or other salicylate-containing ointments) must be carefully and continually examined. Cosmetics and other personal care items are frequent offenders. Deodorants containing castor oil and lipsticks containing castor oil, camphor oil, or aloe, are frequently overlooked, and cause problems. Changes in formulas for various products do often occur and sometimes Dr. St. Amand becomes aware of a new source of salicylates. For instance, the most recent sources of salicylates that have been identified are a number of toothpastes, mouthwashes and mint flavored gums and breath mints, as well as plant saps that get on the skin of gardeners. On numerous occasions, Dr. St. Amand and his patients have observed reappearance of lesions due to salicylate blockage and then their disappearance once again when the salicylate is eliminated and the guaifenesin is once again effective (For more complete information on the many items that may block guaifenesin, as well as salicylate-free alternatives, consult web sites, St. Amand’s papers, CISRA’s Salicylate Alerts, or Waterhouse, 1998, ref. #24).

4. Unwilling to try or continue due to fear of exacerbations. The patient has to be prepared to undergo an increase in symptoms for some months before improvement occurs. Taking extra measures to take it easier, like spending more time relaxing with books-on-tape, decreasing stress, treating symptoms with salicylate-free supplements or medications should help with the temporary symptom increase. Going on St. Amand’s low carbohydrate diet is often of great benefit to those who have hypoglycemia or crave carbohydrates. If one knows enough about the process, the exacerbation may even be viewed as something positive, since it is confirmation that guaifenesin works, and one can really look forward to being well. One thing I have observed in myself and a few others that is encouraging to the chemically sensitive, is that the intensification of symptoms due to the guaifenesin reversal process so far, does not seem to be as bad as severe chemical and food reactions (Waterhouse, 1998, ref. #23). So, for most MCS patients, if one initiates or continues one’s avoidance or treatment of reactive foods and chemicals, the reversal process itself will probably be quite tolerable. Preliminary evidence suggests that lesion location is correlated with the locus of MCS symptoms and may account in part for the exaggerated degree of reaction to foods and chemicals in at least some of these patients. It is also interesting that the guaifenesin reversal process seems to intensify during the withdrawal phase of food reactions as evidenced by both symptoms and alterations in urine appearance (bubbles and other urine changes frequently correlate with reversal but should not be relied on too much).

5. Don’t want to give up the benefits of salicylate-containing herbal medications. There are many alternatives to salicylate-containing herbal medications that may have similar or sometimes superior levels of benefit. Many vitamins, minerals and other non-herbal supplements can be used with guaifenesin, if so desired, as well as all non aspirin-containing pharmaceuticals. In many cases, pharmaceuticals are not any more of a “drug” than the active ingredients in the herbs. In fact, many drugs are simply the pure active ingredients that were originally derived and purified from an herbal extract and now the identical molecules are synthesized. In fact, guaifenesin is one such plant derivative originally obtained from a tree bark. An extensive list of supplements commonly suggested for different body systems or ailments, divided into salicylate-containing and salicylate-free approaches, is available (Waterhouse, 1998, ref. #24). Although Dr. St. Amand does not use supplements in his approach to fibromyalgia, there are a few vitamins that he believes are worth taking under certain circumstances, for example, to help prevent heart disease (see, Addendum to Waterhouse, 1998, ref. #24 and SynergyHN web site).

Part B. Clarification of Some Theoretical and Technical Aspects of Guaifenesin Use

This section has been written in response to a number of questions from physicians, researchers and patients regarding more theoretical and technical aspects of guaifenesin treatment of fibromyalgia and the relationship with other theories and treatments.

1. St. Amand’s theory and treatment approach is consistent with most other theories and treatments, including those involving sudden onset due to various types of stressors and traumas. Based on St. Amand’s theory, a sudden onset occurs when a trigger (trauma, infection, chemical exposure etc…) makes a demand on the body for ATP such that a threshold is passed and the shortfall in ATP causes symptoms. In this view, most other treatments work by either treating a trigger and thus reducing ATP demand, thus pushing the patient back over the threshold to a state of pre fibromyalgia (see Waterhouse, 1999, p. 1, this issue), or affecting the retention or absorption of phosphate (e.g., calcium and magnesium supplements help bind excess phosphate). The tendency to excess phosphate plays the role of an inherited underlying factor tending to create lesions and reduce ATP and thus causing disproportionate and longer lasting response to triggering events than would occur in those not predisposed to phosphate retention.

The triggers combined with the low ATP and constant muscle contraction can initiate a vicious cycle in which stress and/or pain lead to poor sleep, which leads to immune dysfunction and lower growth hormone, which could lead to reduced tissue rest and repair, reactivation of viruses, allergies, hypoglycemia, more stress and pain and so on. Or environmental toxins, an infection, or a physical or emotional trauma can initiate the immune dysfunction, with or without the sleep problems, and lead to the downward cycle. There are many perpetuating factors and feedback loops that may contribute to the vicious cycle and their relative importance is likely to vary from person to person. The genetic characteristic leading to the calcium and phosphate accumulation means that the fibromyalgic just doesn’t have the ATP production available to a healthy person, who might find the above stressors only cause a self-limiting and brief illness. In addition, research indicates that many of these stress-related changes also may increase phosphate absorption, decrease phosphate excretion and increase phosphate and calcium release through osteoporosis (i.e., see Ilyia, 1996 for some of the effects of stress). Chronic stress can also raise insulin levels, which increases phosphate retention and even helps drive phosphate into cells. This all adds up to more excess phosphate that the body must store in the tissue, thus accelerating the fibromyalgia process and the downward spiral.

The many characteristics shared by fibromyalgia and chronic fatigue syndrome (CFS) lead many researchers to believe that they may be variations of the same illness. This fits with Dr. St. Amand’s observations, since he finds lesions in virtually all patients with CFS he has examined and he finds them similar in their response to guaifenesin. He finds that CFS patients are less pain sensitive, which agrees with reports of lower substance P levels. It may be that greater fatigue in some patients results from a greater effect of excess phosphate on the brain, or perhaps relates to differences in blood flow to the brain and/or blood pressure regulation. There may be many factors that contribute to individual differences in the patterns of symptoms experienced.

2. Other mechanisms can’t account adequately for guaifenesin response. Some doctors have proposed alternative mechanisms for St. Amand’s success with guaifenesin that differ from the enhanced excretion of phosphate by the kidneys. Although it is possible that guaifenesin has some additional effects, there are several lines of evidence that support his theory and argue against these alternatives (e.g., immune system, anti fungal, antibacterial, antihistaminic, serotonergic, GABAergic, or placebo effects). First of all, St. Amand has used other medications with uricosuric and presumably phosphouric effects successfully for many years (e.g., probenecid, a gout medication). Second, an initial exacerbation of several months duration, involving cyclic exacerbations of pain and other symptoms is more compatible with St. Amand’s theory. Third, the ability of salicylates to block the action of guaifenesin (analogously to salicylate-blockage of probenecid in gout), and cause progress to halt or reverse, as evidenced by both symptoms and mapping of the lesions provides further support for the kidney-level mechanism. When the salicylate is stopped, progress begins again. The latter two arguments also refute the idea of a placebo effect being responsible for the improvement. Placebo effects are usually short-lived, and do not typically cause such long-term and dramatic effects in fibromyalgia. Nor can success be attributed to the low carbohydrate diet alone. Approximately 30-50% of his patients never use the low carbohydrate diet because they are not judged to be hypoglycemic and recover with guaifenesin treatment alone. Neither can salicylate avoidance explain the level of success. Although this might have some relevance in a few patients who might have an allergy/sensitivity to salicylate, it should be pointed out that patients do not avoid salicylates entirely, since there are no restrictions that forbid salicylate-containing foods. Also, patients generally continue to consume foods with food additives and food colorings that contain salicylates, unlike diets such as the Feingold diet. It appears from St. Amand’s work that the symptoms result from the reduced intracellular ATP and the excessive contraction of muscles and over activation of various other cell types due to the increased intracellular calcium and phosphate in affected areas. Presumably, calcium and phosphate are mobilized from storage areas within the cell during the reversal process and this causes the temporary increase of muscle contractions, spasms, tenderness and other symptoms. For those who suspect financial motives for promoting guaifenesin, it should be noted that guaifenesin is a very inexpensive, non patentable drug, originally derived from a tree bark until it was replaced by a synthetic form. Over more than 30 years, Dr. St. Amand and his patients have, at their own expense, spread the word about this treatment approach, recently greatly aided by the availability of the Internet.

3. A few highly sophisticated laboratory tests support St. Amand’s theory, whereas most commonly used tests are inadequate for this purpose. Some have suggested that one should find signs of elevated phosphate in serum or elevated intracellular calcium and phosphate in red blood cells or buccal cells before treating. Elevated phosphate levels in fibromyalgics from these tests has not been found to be a necessary condition for success with guaifenesin. The supposed reason for this is that the heterogeneity of lesion locations is such that no one particular type of cell or location will have an accumulation of calcium and phosphate in all patients. This heterogeneity is also likely to account for different results in studies that look at muscles in different locations, which may be unaffected. Other tests looking for calcium phosphate crystals, such as x-rays, would generally not be helpful, because the accumulations are thought to be in solution within the cell and even within the mitochondria. Even more refined techniques, such as NMR spectroscopy would not detect the accumulation of phosphate within the mitochondria. There is some possibility that an increased ratio of serum phosphate to calcium may be lower after an overnight fast in fibromyalgics. This has not yet been verified, though, and may not be true in all patients who might potentially benefit from guaifenesin. If there is abnormally low serum phosphate (actually the labs only measure phosphoric acid), it might be useful to do further testing of kidney function to determine if phosphate diabetes is present. A recent study found 10% of 87 CFS patients actually appeared to have phosphate diabetes (De Lorenzo et al 1999). However, there is still uncertainty how to interpret this study, since Dr. St. Amand has measured low serum phosphate and fairly high phosphate clearance rates in some patients who still responded well to guaifenesin. More study of phosphate dynamics in fibromyalgia and chronic fatigue syndrome is clearly needed.

Some highly sophisticated tests using labeled phosphate (P-31) in research studies have shown evidence of problems with muscle metabolism and continually contracting areas of muscle, called myogeloses (see Park et al 1998; Olsen et al 1998; also see Waterhouse, 1999, p. 13, this issue, for discussion). Other research has shown glycolysis abnormalities (Eisinger et al 1994), continually contracted areas of muscle observed with surface EMG (Thorsen, 1998), and low ATP in muscle lesions (Bengtsson et al 1989). These and other research findings are consistent with St. Amand’s view that the peripheral muscle mechanisms are the primary factors, while breakdowns in the central pain control mechanisms and the increases in substance P are secondary factors and not specific to fibromyalgia. Since excess phosphate may affect brain function, this provides another means by which central nervous system signs and symptoms may be secondary to phosphate retention.

4. Osteoporosis has not been a problem with patients treated with St. Amand’s approach. St. Amand has been using guaifenesin and other “uricosuric” drugs for over 30 years and has not observed a problem with an increased incidence of osteoporosis in his treated fibromyalgia patients.

5. Restriction of dietary phosphate is not necessary. Avoidance of phosphate in sodas, sports drinks and additives may be useful for some, however, it is not really necessary in St. Amand’s approach. Nor is it necessary for those on guaifenesin to try to avoid significant phosphate intake in food. Consuming a low phosphate diet by avoiding high phosphate foods may be difficult and in the case of hypoglycemics, even counter productive, since many of the good animal-derived protein sources are high in phosphate. Also, many have restrictions due to food sensitivities or oxalate avoidance that make it hard enough to find an adequate diet. For most, however, it is preferable to avoid calcium supplements that have additional phosphate (e.g., in the form of hydroxyapatite).

6. Hidden salicylates are found in many products, including herbal medications and lotions, even though many manufacturers are not aware of their presence. Herbal medicines, plant extracts, and cosmetics have been a problem in blocking guaifenesin and have caused the reversal of progress in numerous patients as evidenced by both symptoms and mapping. It turns out that virtually all plants produce salicylates and the medicinal parts of plants generally contain the highest concentrations. Ointments and cosmetics have also been a particular problem. Even relatively small amounts are apparently effective in blocking the guaifenesin when they are applied to the skin (see the list of brand name cosmetics that St. Amand compiled for his patients for salicylate-free alternatives). Absorption through the skin is known to be good, and through this route the salicylates are able to avoid the metabolic actions of the liver that can alter much of the salicylate that is ingested (Brubacher, 1996). For this reason, particular care must be taken that skin products are salicylate-free.

Part C. Some Clarifications of St. Amand’s Low Carbohydrate Diet for Hypoglycemia (a.k.a. low blood sugar or pseudohypoglycemia)

St. Amand finds that the majority of his fibromyalgia patients have hypoglycemia or carbohydrate cravings and greatly benefit from a low carbohydrate diet. In his suggested diet, he recommends that patients limit their consumption of high carbohydrate foods to a piece of bread or fruit for every 4 hour period. The diet also requires the complete elimination of sugars, fruit juices and other highly concentrated carbohydrates and caffeine (see St. Amand, 1998). Meats and other proteins, dairy, nuts, oils and vegetables are not limited (except for a few starchy vegetables, like corn, potatoes or baked beans).

1. The primary effect in most patients of using the low carbohydrate diet is through the reduction of autonomic nervous system blood sugar regulation mechanisms. Candida reduction alone, as proposed by some, is not an adequate alternative explanation for success with low carbohydrate diet among St. Amand’s fibromyalgia patients. Many doctors practicing nutritional and environmental medicine have recommend low carbohydrate diets for their patients because it is thought to reduce overgrowth of the yeast, Candida. These doctors attribute the benefits of the diet to yeast reduction rather than treating hypoglycemia. Although patients with yeast hypersensitivity might possibly benefit from carbohydrate reduction partly for that reason, other evidence supports an important role for its effect on reactive hypoglycemia. For instance, some patients who already had extensive anti fungal medication, still had a dramatic response to Dr. St. Amand’s “hypoglycemic” diet beyond what they achieved with anti fungals. This diet dramatically reduced symptoms of epinephrine release that occur as a counter-regulatory response to drops in blood sugar. The epinephrine release produces symptoms ranging from anxiety and tachycardia, to irritability and night sweats. Studies have shown that these symptoms can occur even though the blood sugar does not drop as low as the levels usually regarded as hypoglycemic (Genter et al 1994). The diet also relieves central nervous system symptoms such as dizziness, headaches and confusion associated with low blood sugar. The term pseudohypoglycemia has recently been applied to this condition (Fauci et al 1997, p. 2082 & 2086). In these patients, the blood sugar levels do not generally drop any lower than in control patients, yet the patients experience increased effects of epinephrine release. According to the above standard medical text, a low carbohydrate, high protein diet or beta blockers are the recommended treatments. St. Amand disagrees with the use of beta blockers, since they block the nervous system response of increasing epinephrine that is designed to respond to low blood sugar levels and return them to the preferred range. Instead, the low carbohydrate diet has the natural effect of better blood sugar regulation and thus the epinephrine response becomes unnecessary.

2. Strict carbohydrate reduction works better than frequent small meals, particularly by reducing sleep disruptions due to epinephrine release occurring when blood sugar levels drop during the night. An alternative approach to hypoglycemia is often proposed that does not limit overall carbohydrates but instead involves frequent small meals that always include at least some animal protein. This approach frequently moderates the hypoglycemic symptoms and can make a big difference for some people. However, Dr. St. Amand and his patients have found that much more benefit is generally received by limiting the total carbohydrate and the types of carbohydrates in the manner proposed in St. Amand’s protocol, particularly for those with more severe hypoglycemia. By following this protocol for two months, the patient can experience the full extent of improvement possible from a hypoglycemic diet and can then more accurately judge the success of lesser degrees of carbohydrate reduction and other approaches. St. Amand’s low carbohydrate diet also tends to, as he puts it, “build up one’s bank account”, presumably of hormones, like glucagon, that help regulate blood sugar. This may eventually allow one to relax the restrictions on carbohydrates to varying degrees, depending on the patient.

3. St. Amand’s protocol forbids some foods that are less glycemic than others he allows, because he bases his list on over 30 years of experience with patient symptoms and compliance, combined with the average serving size of foods that are typically eaten. Sometimes, foods are prohibited because they are typically eaten in amounts that easily exceed the carbohydrate limitations. For instance, baked beans or lentils are not allowed, because the serving size is usually enough to give a fairly large amount of carbohydrate. For patients with very restricted diets due to food sensitivities, some deviations might need to be made. For example, someone with extensive grain allergies might use an amount of rice with the equivalent amount of carbohydrate grams instead of bread (a slice of bread with 10 grams of carbohydrate would be equivalent to about ¼ cup cooked rice).

4. Carbohydrate reduction may be helpful even if food and chemical reactions have been treated and regardless of patient’s weight. Environmental medicine and nutritional doctors have observed hypoglycemic reactions to foods due to food allergies and sensitivities. Although removal of these reactive items has been observed to reduce symptoms dramatically, some patients have achieved additional benefit from reducing carbohydrates in accordance with St. Amand’s recommendations. Allergy/sensitivity reduction may eventually allow an easing of the carbohydrate restrictions for some patients, depending on the susceptibility of each patient.

5. Recent research shows that a low carbohydrate diet can be healthy for your heart and actually reduce cardiovascular risk factors and the risk of adult-onset (Type II) diabetes. Excess carbohydrates, especially in the presence of high insulin, are converted into triglycerides and low density lipoproteins (LDL), the “bad” cholesterol (Reaven, 1991). Reaven (1997) shows that a lower carbohydrate, higher fat diet resulted in more favorable lipid profiles in a study of postmenopausal women. A high carbohydrate diet also may lead to diabetes in those who have a predisposition, since the excessive carbohydrates lead to chronically high insulin and then insulin resistance. The book, Healthy For Life (1995), also reviews some of the research in this area.

6. Contrary to the commonly held view, there is evidence that weight loss depends on the amount of carbohydrate consumed, rather than simply the total calories consumed vs. calories expended. The low carbohydrate diet affects the levels of hormones, like insulin, which affect metabolism and fat storage (Rabast et al 1981; Young, 1971; Kekwick & Pawan 1964; and 12 more references cited in Atkins 1992) and thus can lead to weight loss with relatively high total calories consumed. These studies show the weight loss can not be attributed to loss of water alone. However, regardless of the validity of the above argument, the low carbohydrate diet has two other advantages for weight loss. If blood sugar can be stabilized in a hypoglycemic with a low carbohydrate diet, the person is much more likely to be able to overcome the carbohydrate cravings and control their food intake. The person also feels better, is more energetic and is able to be more active, which also helps them lose weight. Although some may feel able to be more active, exercise is not required to lose weight on this diet. This is a significant advantage to those who are chronically ill and capable of little exercise.
(Editor’s Note: Dr. St. Amand does not use anti fungal, nutritional or environmental medicine therapies for his fibromyalgia patients. For more on his thoughts on alternative and symptomatic therapies, refer to Waterhouse, 1998, ref. #24).

Part D. The Oregon Guaifenesin Study: Responses to Misconceptions

A number of misunderstandings have arisen regarding Dr. R. Paul St. Amand’s use of guaifenesin for fibromyalgia and the study done by Dr. Robert Bennett on guaifenesin in 1995 at the Oregon Health Sciences University (Thorsen, 1998). Dr. Bennett concluded, based on this double blind, placebo controlled study, that guaifenesin was no better than a placebo. Dr. St. Amand is convinced that several major flaws in the study caused this failure to show guaifenesin’s effectiveness (St. Amand and Malek, 1997 and 1999; St. Amand 1998). It is hoped that the following point by point discussion will help clear up the misconceptions. Part of the problem seems to arise from Dr. St. Amand’s inclusion of a historical account of how he came to believe uricosuric drugs could be helpful in fibromyalgia. In this historical account, certain observations are made that illustrate the process of his discovery, but are not really directly relevant to his current theory to explain the success of these drugs based on over 30 years of experience in successfully treating fibromyalgia patients.

1. Misconception: It has been said that Dr. St. Amand says that large crystalline calcium phosphate deposits in muscles are the cause of fibromyalgia. Since researchers do not generally find these crystals, then Dr. St. Amand’s theory must be wrong.

Response: It is excess calcium and phosphate inside cells that Dr. St. Amand theorizes are the cause of fibromyalgia. The misunderstanding arose because Dr. St. Amand began his account by describing how a patient found that when using uricosuric medication for gout, the patient was able to scrape tartar (composed of calcium and phosphate) from his teeth with his fingernail. This observation was the clue that led Dr. St. Amand to try uricosuric drugs on fibromyalgia patients. He reasoned that there might be a similarity between calcium phosphate deposits, and some process occurring in tender areas related to excess calcium and phosphate in the saliva and serum. This phenomenon of the tartar effect is not found regularly in his FMS patients; it was simply the clue that led him to initiate his trial of uricosuric drugs in FMS. His later experience and study led him to conclude that most of the calcium and phosphate storage in tender areas was due to excess phosphate (due to inadequate kidney excretion) entering the cell and being followed by calcium to balance the charge. This excess intracellular calcium and phosphate results in lowered ATP and continual cell contraction, occurring by well-known biochemical processes. Both the lowered ATP and the muscle contractions have been observed in FMS. It may be that in some unusual cases crystals may be found as well. Calcium phosphate crystals in joints are also a well-known feature of osteoarthritis. Dr. St. Amand thinks there is a close connection between FMS and osteoarthritis based on his observation of the pattern of illness within families he has observed. However, calcium phosphate in the form of crystals in muscle tissue in FMS appear to be the exception and not the rule, thus explaining why many researchers have not observed them. The excess calcium and phosphate are primarily inside the cells where they cause lowered ATP and continual muscle contraction.

2. Misconception: Salicylates were eliminated in the study, so the treatment should have worked. If there were hidden sources of salicylates that Dr. St. Amand only recently discovered, then how was the treatment working all this time for Dr. St. Amand.

Response: Not all sources of salicylates were eliminated in the study because many were not known about until the study was over. There was a great increase in the use of salicylates in cosmetics, lotions and other products around the time of the study. One reason is that the public’s recent concern about skin cancer has led products to add sunscreen protection to all sorts of products. Previously UVA protection was added to some things, but recent addition of a UVB protectant, almost always a salicylate, has greatly increased. Also, the addition of herbal extracts, like aloe, has become very common. One now has to make a special effort to find products without salicylates. Speculations by dermatologists as to how much cosmetic would be needed to provide an amount of salicylate able to block the treatment would not be likely to be reliable since they would be unlikely to have any firsthand experience of the use of guaifenisen in treating FMS. There is no question that absorption of many compounds through the skin is often more effective than when taken orally and this effect is being used with a number of drugs, including aspirin (salicylic acid). Of course, there is clearly much that is not known. Even Dr. St. Amand does not know why some people are more sensitive to the effects of salicylates than others. In some cases, where there may have been some hidden salicylates in Dr. St. Amand’s patients, it appears that dosage increases were enough to overcome it. In some patients he has had to use as many as 3 or 4, or even as many as 6 or 8 guaifenisen tablets per day. The study, however, used a uniform two pills per day (1200 mg) which generally is enough for only 70% of Dr. St. Amand’s patients, even when salicylates are avoided. So with unknown amounts of hidden salicylates, the percentage of response would be considerably lower.

3. Misconception: Since phosphate excretion was not observed in the study, then Dr. St. Amand’s theory is wrong.

Response: Since the guaifenisen effect was apparently blocked in most patients, then one would not expect changes in phosphate excretion in any case. However, even if the guaifenisen had not been blocked, Dr. St. Amand finds that phosphates in the urine are quite variable because their excretion depends on so many factors, like diet and deposition in bone and teeth (where most phosphate in the body is found), and the cycles of the guaifenesin reversal process. Dr. St. Amand did observe, however a 60% increase in phosphate excretion, and a smaller increase in calcium and oxalate in the urine in a small study using one of the uricosuric drugs he had used previously, when he carefully had the patients keep their diet constant (St. Amand, 1998). That was one of the reasons he originally theorized that phosphate excretion was the key to why the uricosuric drugs worked in fibromyalgia.

4. Misconception: Cycling of symptoms was not found in the study, thus Dr. St. Amand’s theory must be wrong. Changes in tender points did not indicate that guaifenisen was effective either.

Response: Since the guaifenisen was apparently blocked, the cycling and changes in tender areas would not be expected.

5. Misconception: Uric acid level changes in the urine or blood should have revealed whether patients were getting any hidden salicylates. These changes were not observed, and therefore the patients were not exposed to any salicylates.

Response: Since Dr. St. Amand believes that the effect of guaifenisen has no relationship to uric acid, then this is not relevant to the action of guaifenesin in enhancing phosphate excretion. The uricosuric effect (i.e., causing an increase in uric acid in the urine) was only relevant in that it led him to focus on a process occurring at the level of the kidney. In other words, the uricosuric effect was just a clue pointing to a kidney level process being involved in FMS. Clearly, if urates had a direct relevance to fibromyalgia, then the more strongly uricosuric drugs he had used previously would have worked better on fibromyalgia than guaifenisen, which is only weakly uricosuric. Dr. St. Amand and his patients have witnessed the rapid reversal of progress that has been clearly traced to changing to a brand of cosmetics that has added salicylates. This apparently occurs because guaifenisen is affected by salicylates in a way that is analogous to the way salicylates affect uricosuric gout medication. This is because they apparently both involve somewhat similar renal excretion mechanisms with one affecting mainly urates and the other affecting primarily phosphates.

6. Misconception: The placebo effect accounts for the recovery of Dr. St. Amand’s patients and occurred in the study as well.

Response: The placebo effect generally only occurs for about 3 months and then patients typically return to their previous state or worse. Dr. St. Amand’s patients and many other patients who go to different doctors that use guaifenesin for fibromyalgia (Dr. St. Amand has a list of over 130 doctors who have used it) continue to improve over the long term and regain greater health than patients using conventional treatment, to the point where they are eventually symptom-free. I have postulated that one explanation for the mild improvement in both treatment and control groups reported in the Oregon study may relate to hypoglycemia, another important component in about half of Dr. St. Amand’s patients. I wonder how many of the study subjects in both the treatment and control groups had read Dr. St. Amand’s paper and had cut back partially on sugar and other concentrated carbohydrates during the study period. This might possibly have resulted in the mild improvement in both study and control groups on average. I know I would have had a tendency to cut back on glycemic foods if I had hypoglycemia and were in the study (perhaps even subconsciously), if I were aware of the dietary recommendations.

7. Misconception: One must go through excruciating pain for a long time with guaifenesin, and patients will be forsaking other more beneficial treatments.

Response: First of all, one does not need to give up any other treatment methods, unless they involve herbs. Other pain medications can be substituted for aspirin and are probably safer for long-term use in any case. Some treatments, like cortisone injections, even become more feasible, since one will not need to continue them indefinitely as guaifenisen leads to improvement. The initial exacerbation of symptoms is primarily during the first few months after an effective dose is achieved and is generally tolerable, especially if one is prepared for it. It was helpful to me to have taken magnesium glycinate and taurine and to have had my food sensitivities treated before starting guaifenesin. Many hypoglycemics and those who crave carbohydrates find that going on the low carbohydrate diet before or during guaifenesin treatment is also very helpful. Guaifenesin may not be an instantaneous cure, but most people find that the initial exacerbation in the first few months is really not that bad, especially when you know it is the process of healing. The lesions took a long time to develop and thus take some time to reverse.

Despite my own and many other’s positive experiences with guaifenesin (Waterhouse, 1998, ref. # 23), I agree that further research will be needed to prove the effectiveness of guaifenesin to the medical community. In the meantime, Dr. St. Amand has been and will continue to assist any physician who contacts him. He feels he has a moral obligation to try to educate others so that they will be freed from this trap of pain, which he and his family suffered from at one time, and provides information free of charge to those who request it (send an SASE with 2 stamps to him with your request: 4560 Admiralty Way, Suite 355, Marina Del Rey, CA 90292).

Dr. St. Amand takes responsibility for the shortcomings in the Oregon study, for which he was technical advisor. Since he was the only person experienced with this treatment involved in the study, it seems fair to expect that his point of view on the study results should be given precedence. The study should be regarded as a “pilot” study in which valuable lessons can be learned. Another study should be done in which a higher dose should be used, the hypoglycemics should be either removed or treated beforehand with the low carbohydrate diet, and the increased knowledge of hidden salicylates should be utilized. Dr. St. Amand should personally do the tender area mapping on patients, without knowing who is receiving guaifenisen and who is in the control group. Younger patients should be used because they will respond more quickly to treatment and thus it will be easier to see the effects of guaifenesin in a one year study (Editor’s Note: I have been informed that a study along these lines is now in the planning stages).


1. Atkins, R.C. 1992. Dr. Atkin’s New Diet Revolution, Evans & Company, NY.
2. Bengtsson, A. and Hendriksson, K. G. 1989. The muscle in fibromyalgia: a review of Swedish studies. The J. of Rheumatology, Vol. 16:(19):144-149.
3. Brubacher, J.R. and R.S. Hoffman. 1996. Salicylism from topicals salicylates: review of the literature. J. of Toxicology, 34 (4): 431-436.
4. Delaney, T.P. et al. 1994. A central role of salicylic acid in plant disease resistance. Science, Vol. 266.
5. De Lorenzo et al. 1998. Phosphate diabetes in patients with chronic fatigue syndrome. Postgrad Med J., 74(870): 229-32.
6. Eisinger, J. et al. 1994. Glycolysis abnormalities in fibromyalgia. J. of the Amer. College of Nutr. 13(2):144-148.
7. Fauci, Anthony S., M.D., and others, editors. 1997. Harrison’s Principles of Internal Medicine. McGraw Hill
8. Genter, P. and E. Ipp. 1994. Plasma glucose thresholds for counterregulation after an oral glucose load. Metabolism, Vol. 43(1):98-103.
9. Heller, Richard F., Ph.D., and Rachael F. Heller. 1995. Healthy For Life. Penguin Books, NY.
10. Ilyia, E. 1996. Stress dynamics: its objective evaluation and pertinent clinical correlates in health and illness. American Academy of Environmental Medicine Annual Meeting. Boston, MA.
11. Jeppesen J., et al. 1997. Effects of low-fat, high-carbohydrate diets on risk factors for ischemic heart disease in postmenopausal women. Am. J. Clin. Nutr., 65(4):1027-1033.
12. Kekwick, A. and Pawan, G.L.S. 1964. The effect of high fat and high carbohydrate diets on rates of weight loss in mice. Metabolism, 13(1):87-97.
13. Olsen, N.J. and J.H. Park. 1998. Skeletal muscle abnormalities in patients with fibromyalgia. Am. J. of Med. Sci., Vol. 315(6):351-358.
14. Park, J.H. et al. 1998. Use of P-31 magnetic resonance spectroscopy to detect metabolic abnormalities in muscles of patients with fibromyalgia. Arthritis Rheum., Vol. 41(3):406-413.
15. Rabast, U. et al. 1981. Loss of weight, sodium, and water in obese persons consuming a high or low carbohydrate diet. Annals of Nutr. Metabol. 26(6):341-349.
16. Reaven, G.M. 1991. Insulin resistance and compensatory hyperinsulinemia: role in hypertension, dyslipidemia, and coronary heart disease. Am. Heart J., 121(4 Pt 2):1283-8.
17. Reaven, G.M. 1997. Do high carbohydrate diets prevent the development or attenuate the manifestations (or both) of syndrome X? A viewpoint strongly against. Curr. Opin. Lipidol., 20 Suppl 8(1):23-7.
18. St. Amand, R. Paul, M.D., and Claudia Potter, MA., 1997. The use of uricosuric agents in fibromyalgia: theory, practice, and a rebuttal to the Oregon study of guaifenesin treatment, Clin. Bull. of Myofascial Therapy, Vol. 2(4):5-12, The Haworth Press.
19. St. Amand, R. Paul, M.D., 1998. A description of fibromyalgia and hypoglycemia: their combined morbidity and therapy with guaifenesin and diet. American Academy of Environmental Medicine Annual Meeting. Baltimore, MD.
20. St. Amand, R. Paul, M.D., 1999. Papers on “Fibromyalgia: For Patients,” “Fibromyalgia: For Physicians,” and “Hypoglycemia,” and Salicylate-Free Product list, all available on the web at, further information available at
21. St. Amand, R. Paul, M.D. ,and Claudia Marek, M.A. 1999 (in press, available in December). What Your Doctor May Not Tell You About Fibromyalgia: The Revolutionary Treatment that Can Reverse the Disease. Warner Books, New York, NY.
22. Strobel, et al. 1997. Tissue oxygen measurement and P-31 magnetic resonance spectroscopy in patients with muscle tension and fibromyalgia. Rheumatol. Int. 16: 175-180.
23. Waterhouse, J.C. 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, Issue 2. Vol. 1(2), CISRA.
24. Waterhouse, J.C. 1998. Natural therapies with and without salicylates”, CISRA’s Synergy Health Newsletter, Issue 3. Vol. 1(3), CISRA.
25. Waterhouse, J.C. 1999. Pre fibromyalgia: a possible explanation for many common idiopathic, functional, and pain disorders, CISRA’s Synergy Health Newsletter, Issue 4. Vol. 2(1), CISRA.
26. Waterhouse, J.C. 1999. How to “map” fibromyalgia: review of video and comments, CISRA’s Synergy Health Newsletter, Issue 4. Vol. 2(1), CISRA.
27. Web sites with guaifenesin and salicylate information:  early issues of this newsletter; and
28. 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.
29. Thorsen, K. 1998. Are your muscles functioning correctly?: dynamic surface-electromyograph (sEMG) can pinpoint your problems. Fibromyalgia Network. April 1998 Issue 41. Tucson, AZ.
30. Thorsen, K. 1998. American College of Rheumatology Speech: is one placebo better than another, Fibromyalgia Network, January 1998 Issue 36. Tucson, AZ.
31. Young, C.M. et al. 1971. Effect on body composition and other parameters in young men of carbohydrate level of reduction diet, Am. J. of Clin. Nutr., 24: 290-296.

Editorial Note (2008): I was helped by guaifenesin, but stopped progressing and am now using the Marshall Protocol (see and recent issues of this newsletter).

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 2:09 am

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