Guai/fibro/and robaxin?

Discussion in 'Fibromyalgia Main Forum' started by lisjhn, Feb 23, 2003.

  1. lisjhn

    lisjhn New Member

    Wow, stumbled upon this one, it's VERY long but informative.


    The Truths and Myths of the use of Guaifenesin for Fibromyalgia
    An investigatory paper by Mark London
    Last modified 27-MAY-2002
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    In the early 1990s, I belonged to the first fibromyalgia discussion group on the internet, the FIBROM-L mailing list. We were probably the first people to hear about guaifenesin via the internet, given that at the time, this was the only such group. It was claimed by Dr. St. Amand that the drug guaifenesin could treat fibromyalgia symptoms by removing excess phosphate from the body, which he believes to be the cause of fibromyalgia., The removal of the phosphate would supposedly reverse all fibromyalgia symptoms, thus essentially being a cure. Given this claim, many people on the mailing list decided to try it. While some people found it to be of some benefit, it disappointingly did nothing for others, including myself, and it definitely was not a cure. This led to a continuous debate about it's effectiveness and the theory behind it.
    Dr. Robert Bennett, an expert in fibromyalgia, agreed to do a study on guaifenesin, with Dr. St. Amand being the technical advisor to the study. The results of this long term study showed that it had no effect on fibromyalgia. However, the debate did not end. Dr. St. Amand claimed that the patients in the study must have unknowingly been exposed to products that contained salicylates, which he believes can block the effects of guaifenesin. Dr. Robert Bennett countered, saying that if there were sufficient quantities of low levels of salicylates to block guaifenesin, then this should have caused a decrease in urinary uric acid. Low levels of salicylates are known to have this effect. But lab tests from the study did not show that this occurred. Thus, Dr. Bennett concluded that there was no such exposure to salicylates.

    Dr. Bennett went on to say that much of Dr. St. Amand's success with guaifenesin could be attributed to the placebo effect. The placebo effect could have been a factor here, since guaifenesin was essentially described as a cure, so that people would be more likely to want it to work. However, in my own opinion, it's unlikely that the placebo effect could explain all of the people who felt they benefitted from guaifenesin. However, neither Dr. Bennett, nor Dr. St. Amand, appear to have researched guaifenesin in the medical literature. If they had done so, they would have discovered that there are at least 2 other effects which could benefit people with fibromyalgia.

    In 1996, before the study was published, I was convinced that guaifenesin had some effect in some people, so I started researching guaifenesin in the medical literature, and found it haa a skeletal muscle relaxant property, a fact that people in the fibromyalgia community were not aware of. Surprisingly, anyone could have easily discovered this fact if they looked guaifenesin up in the Merck Index, a drug handbook, which lists guaifenesin as having this effect. Guaifenesin has effects on the nervous system that many people are not aware, because it's simply not been well studied. It presently is only used for this effect in veterinary medicine. However, guaifenesin is very closely related to mephenesin, a drug that has been studied and used in humans for these effects. And a slightly different form of guaifenesin, guaifenesin carbamate, is used as a muscle relaxant in humans, and is sold under the name Robaxin.

    At the time that I discovered this information, I believed that this was the reason why it helped some people, so I lost interest in researching it any further. However, in the summer of 2000, I became reinvolved in discussing fibromyalgia via the internet, and found that people were still discussing guaifenesin. I therefore decided to do a more in depth medical investigation of guaifenesin, as this appears never to have been done,.and have since found much more information about guaifenesin's effects. I have found that it's effect on the nervous system appears to be more than a simple muscle relaxant effect, but may also include an analgesic, or pain relieving capability. I also believe that another ability, the ability to inhibit platelet aggregation, and act as an anticoagulant, may also be significant, as all of the uricosuric drugs that Dr. St. Amand previously used for fibromyalgia, also have this ability.

    Guaifenesin was selected for treating fibromyalgia by Dr. St. Amand because it has a uricosuric effect. Uricosuric means that the drug has the ability to increase uric acid excretion in urine. He had previously believed that other uricosuric drugs, such as probenecid, had helped fibromyalgia. But these other drugs often required high doses to be useful, often leading to side effects. So he experimented with guaifenesin, and found it to work better than the previous drugs. Dr. St. Amand believes that it not the excretion of uric acid that helps fibromyalgia, but that it's due to the excretion of another substance. He hypothesizes it to be phosphate.

    However, no medical evidence has been presented by anyone, that shows that excess phosphate is the cause of fibromyalgia. Additionally, uricosuric drugs are not known to increase phosphate excretion, except in very rare circumstances. If Dr. St. Amand truly believes that phosphate excretion occurs, why has he not presented evidence of this, not just to the fibromyalgia community, but to the rest of the medical community also? Very few drugs are available that mainly increase phosphate excretion, without causing many side effects. The medical community would welcome a new option, so why has this never been done? And if he has done this, why has it been ignored? And why has he never properly researched the effects of guaifenesin? For example, he makes mention of the fact that guaifenesin increases urinary excretion of 5HIAA, a serotonin metabolite. While indeed guaifenesin does affect 5HIAA urine tests, it doesn't really increase 5HIAA. Instead, one of guaifenesin's own metabolites interferes with the test, creating a false positive. A more precise lab test, which is not usually done, is able to distinguish between the two different metabolites.

    Dr. St. Amand also appears to downplay any possible side effects from guaifenesin. From his web page, he says "Guaifenesin is distinctly more effective than our previous medications and has no listed side effects." Unfortunately, this is not true either, as many web pages list side effects, including headaches and dizziness. Coincidentally, headaches and dizziness are symptoms that some people on guaifenesin initially do experience, yet such symptoms are often abscribed to the cycling process of reversing fibromyalgia. That is to say, that Dr. St. Amand believes that guaifenesin is reversing fibromyalgia by removing phosphate deposits, and this causes cycles in which fibromyalgia symptoms intensify. However, these symptoms could simply be side effects from guaifenesin, and that people with fibromyalgia might be more sensitive to them than the average population. Guaifenesin actually hasn't been studied that well, and in fact it has never been tested in animals for carcinogenicity,tumorigenicity, or mutagenicity. And, of course, these so called cycling symptoms simply could be fibromyalgia symptoms that would have occurred anyway, regardless of the guaifenesin, as it's quite common for fibromyalgia symptoms to increase and decrease due to hormonal and other factors. Thus, some people on the guaifenesin protocol may be wrongly attributing their worsening fibromyalgia symptoms to a reversal process that doesn't exist, thereby needlessly suffering, believing instead that these symptoms represent a good thing.

    I will attempt to show, based on all available studies on guaifenesin, that it has several known effects which may be responsible for claims that it benefits people with fibromyalgia. I will also attempt to show that there is no proof that either phosphate excretion could be the cause of fibromyalgia, or that uricosuric drugs could increase phosphate excretion.

    Guaifenesin's Effects on the Nervous System
    Guaifenesin has a property which is not well known by many people (including doctors), but is well documented in the medical literature. It is capable of acting as a skeletal muscle relaxant. It does this by depressing transmission of nerve impulses in the central nervous system. The reason that this information is not well documented is because it was a grandfathered drug, so it was never subjected to thorough testing, as later drugs had to be. And it is not used for this property by traditional doctors, because other drugs were found to be more effective.
    In the mid to late 1940s, another old drug called mephenesin, a close relative of guaifenesin, was the subject of several studies. Given intravenously in tests on animals, it was found to have a strong effect, being able to induce skeletal muscle paralysis. Researchers continued to study mephenesin, but they also created and tested other chemically related compounds, and discovered that mephensin belongs to a class of chemicals known as propanediol derivatives, all of which exhibited the same muscle relaxant effect, to one degree or another. Mephensin is 1,2-Propanediol, 3-(2-methylphenoxy)-. One of other compounds created was 1,2-Propanediol, 3-(2-methoxyphenoxy)-, which is commonly known today as guaifenesin. At the time, it was known as guaiacol glyceryl ether. Unfortunately, the muscle relaxant effect only lasts a short time, due to the drugs being rapidly metabolized. That is to say, they are converted into other chemicals, and then these resulting "metabolites" are excreted in the urine. Thus, because of their short effective duration, the first propanediol drugs that were created had limited use for humans (the timed release version of guaifenesin was not created until decades later). However, they could be used in veterinary medicine, in intravenous anesthetic preparations for surgery. But another problem was that all of these drugs have a also hemolytic side effect, i.e. causing cellular destruction of red blood cells. Guaifenesin, however, has less hemolytic activity, and it also has greater water solubility, so it became the preferred drug to use.

    Researchers continued to study these drugs to find a longer lasting form. In the 1950s, such a form was created, known as a carbamate. The following paper documents a study comparing the effects of mephenesin, guaifenesin, mephensin carbamate, and guaifenesin carbamate:

    Journal of Pharm. Expt. Ther. 1958, 122;239 (Truitt and Little)

    This study shows that all these drugs exhibit a comparable muscle relaxant activity at similar doses. However, guaifenesin carbamate was effective over a much longer time, so it could be used effectively in humans as a muscle relaxant. It is now known as methocarbamol or robaxin, the latter being the brand name. For the National Library of Medicine entries on these drugs, see:



    It has been found that all of these propanediol derivatives act as central-acting skeletal muscle relaxants by selectively depressing transmission of nerve impulses at the internuncial neurons of the spinal cord, brainstem, and subcortical regions of the brain. At low doses they act to relax hypertonic muscles and to lower response to sensory stimuli, i.e. pain. Thus, they might be very useful for people with fibromyalgia. At high enough of a dose, they can cause temporary muscle paralysis. This is all explained on the following web page:


    To achieve muscle paralysis, the recommended dose for large animals is 50mg per pound. Assuming a similar dose rate for humans, for a person weighing 100 pounds, the recommended dose would be 5000mg. Of course, this amount is meant for extreme relaxation in order to allow surgery. A muscle relaxant effect would still be seen at much lower doses. Patients on guaifenesin for fibromyalgia take anywhere from 600 to 3600mg per day. Dr. St. Amand's own wife takes as much as 4800mg per day. So this effect would likely be significant in these people, especially when taking a timed release form that would avoid the quick metabolization problem.

    Additionally, since the previously mentioned study that compared Robaxin and guaifenesin found them to have comparable muscle relaxant effects at similar dose levels, and the maintenance dose for Robaxin is 1500mg, again we can see evidence that the dose level of guaifenesin being used by fibromyalgia patients might be seeing benefit from this effect.

    Other propanediol derivate drugs have also been created for their effects on the nervous system. The first anti-anxiety prescription drug was Meprobate, 2-Methyl-2-propyl-1,3-propanediol dicarbamate, also commonly known as Equanil and Miltown. It is no longer used, because the nervous system effect was not specific to anxiety, plus it was also very addictive. However, several other propanediols are still in use. Carisoprodol, or soma, is N-isopropyl-2-methyl-3-propyl-1,3-propanediol dicarbamate, and is a commonly prescribed muscle relaxant, and is sometimes prescribed for fibromyalgia. Another propanediol is Felbatol (felbamate), 2-phenyl-1,3-propanediol dicarbamate, an anticonvulsant. It should also be noted that some people have been found to experience allergic symptoms from propanediols, and the medical literature warns people not to use any propanediol drug if they have experienced side effects from any one of them. This might explain why some people experience immediate side effects from using guaifenesin, so people should be aware of this possibility.

    It should also be noted that guaifenesin's relaxant effect on the nervous system might be the reason for it's expectorant property. Guaifenesin was being used as an expectorant well before propanediols were discovered, as it can be derived from the bark of the guaiac tree. However, as shall be shown later, guaifenesin doesn't appear to have a direct effect on mucus. Instead, perhaps it's expectorant ability is due to it's muscle relaxant effect. Some types of expectorants are known to act due to a relaxant effect, as the effect helps to soothe spasms and allow mucous to flow easier. Two common herbal remedies that are known to act both as relaxants and expectorants are kava kava and peppermint oil. Some relaxants, like pepperment oil, are also useful for digestion problems such as Irritable Bowel Syndrome, so it's not surprising that some people have reported guaifenesin to be useful for IBS (although IBS is a multifaceted problem, so relaxants don't work for everyone.) In any event, this shows how a single effect can have widespread and diverse effects on the body.

    Guaifenesin's Analgesic Effect
    However, the effect on the nervous system is not simply limited to acting as a muscle relaxant. In the 1970s, mephenesin was found to increase levels of the amino acid glycine. A later study in the 1992 showed evidence that mephenesin may be an antagonist of excitatory amino acids. This could be releavant to fibromyalgia, since studies have shown that levels of excitatory amino acids are raised in fibromyalgia, and may be involved in the pain process of fibromyalgia. Another study in 1994 on mephenesin went on to hypothesize that this effect on amino acids may be the reason for mepehensin's ability to act as a muscle relaxant: "Mephenesin acts mainly by inhibitting the polysynaptic reflexes in the spinal cord, and these reflexes are mediated by the intersegmental network using EAAs as neurotransmitters." And a study on other EAA antagnoists have shown them have muscle relaxant effects. Thus, mephenesin, and therefore guaifenesin, may indeed have an ability to lower pain levels. While there are few studies regarding this effect, one study has shown that mephenesin does have an analgesic effect. Another study on guaifenesin also shows that it has an analgesic effect. (Plus, guaifenesin is known to have an additive effect on narcotics.) However, neither of these studies specifically studied the effect on fibromyalgia pain, and it's well known that many of the usual analgesics, such as aspirin, are not very effective for fibromyalgia. Thus, it's possible that this analgesic effect might even be more effective for fibromyalgia pain, rather than for other types of pain, given it's mode of action. This would therefore explain why the average person might not have noticed an analgesic effect when taking guaifenesin. Additionally, as mentioned in the fibromyalgia study on amino acids, there are many other factors which would influence the pain effect from amino acids, so that this analgesic action might not be felt by everyone. Thus, this might be the reason that the original study on guaifenesin did not show such an effect. The amino acid study showed that glycine was only relevant for people who had primary fibromyalgia, rather than secondary fibromyalgia to another disease. And it also showed that the significance of glycine was not very high when the data was looked at for females alone. Plus, the patients in the guaifenesin study might have already been taking analgesic medicine. Many people who take guaifenesin, often do so because they want to avoid having to take prescription medicine, such as muscle relaxants and pain killers. In other words, the guaifenesin study might have not accurately reflected the population who have found the most benefit from taking guaifenesin, or whom would find the most benefit from a reduction of amino acids.
    When I first became aware of the effects of guaifenesin on the nervous system, I believed it was the reason why guaifenesin was able to treat fibromyalgia. However, since other uricosuric drugs were also used by Dr. St. Amand in treating fibromyalgia, there must be a common urinary effect to explain why these drugs appeared to be effective. However, the other effects of guaifenesin would explain why it appears to work much better than those other drugs. And it also might explain why its effectiveness varies in different people.

    There appears to be evidence that the rate of metabolism of guaifenesin could vary greatly in different people. A study in MEDLINE shows that the half-life of guaifenesin in healthy subjects varied from 1.36 to 5.25 hours. This quoted maximum is much much higher than the average half-life which is usually reported for guaifenesin in the literature. It could be that some people with fibromyalgia have a slower metabolic rate. In fact, there is possible evidence to support this. The main enzyme for the metabolism of guaifenesin is O-Demethylase. However, the activity of this enzyme is greatly dependent on ATP, and it is well known that some people with fibromyalgia have low levels of ATP. Thus, people with fibromyalgia might metabolize guaifenesin at a slower rate. Any future studies on guaifenesin might want to test the metabolic rate, as this might explain why it works better in some people.

    What About Salicylates?
    Dr. St. Amand and many patients on guaifenesin, believe that salicylates block guaifenesin's effects. The theory behind this is that uricosuric drugs compete with each other for transport into the kidneys. Thus, if you take enough salicylates, you can block guaifenesin from entering part of the kidneys, and therefore in theory block any of guaifenesin's effects on the urine. Dr. St. Amand and some of his patients claim that obstaining from salicylates have helped them feel guaifenesin's effects. Assuming this is true, then this appears to indicate that all of guaifenesin's effects are due to it's urinary effects. However, it been noticed that some patients are very sensitive to any products containing even very small amounts of salicylates, while others do not find this at all. Additionally, some people have stated that they noticed a difference in their fibromyalgia symptoms as soon as they stopped salicylates. Thus, some have questioned whether salicylates themselves has a direct effect on fibromyalgia.
    The claim that very small amounts of salicylates can block guaifenesin's effects, is itself a claim that lacks medical proof. For example, Dr. St. Amand believes that sunscreen lotions can be a significant source of salicylates, yet a lab test has shown that less than 1% of the salicylates over a 48 hour period are absorbed from the lotions. But even if such lotions were the source of a significant amount of low levels of salicylates, there is no process in the kidneys that would allow a small amount of salicylates to block a very large amount of guaifenesin. Salicylates, guaifenesin, uric acid, and other similar acidic substances, compete via a process known as active transport. It's mainly a competitive process for binding sites, meaning that dose amounts play a large role in determining which substance is transportted.. It wouldn't explain how small amounts of salicylates can supposedly block much larger doses of guaifenesin, often larger by many magnitudes. In fact, people with gout, who take uricosuric medications such as probenecid, who are also warned to avoid salicylates, are not told to worry about such small amounts of salicylates. And even if a small amount of one substance could block large amounts of another substance, since guaifenesin is known to have a stronger uricosuric effect than salicylates, that is, it can block more uric acid at the same dose, one could then infer that guaifenesin might be more likely to block salicylates, than the other way around.

    However, whatever the truth is regarding the blocking effect of salicylates on guaifenesin in the kidneys, it is also well known in the medical literature that some people are adversely affected by salicylates. Sensitivity and side effects from salicylates has long been claimed by many people to be able to affect many different health problems. While many of these claims lack proper studies, a well documented sensitivity is known to exist in people with asthma and chronic sinusitis. Aspirin sensitive asthma is not only a reality, but it affects a very significant amount of people with asthma, especially those who also have allergies. This is significant, since many people with fibromyalgia also have asthma, sinus problems, and allergies. And this effect may be related to aspirin's effect on platelets. Aspirin is usually known to reduce platelet activity. However, when aspirin is introduced to platelets from aspirin sensitive asthmatics, the platelets become more activated.. This appears to be due to aspirin's ability to inhibit cyclooxygenase. In these people, salicylate sensivity could therefore be adversely affecting people with fibromyalgia, and blocking the anticoagulant effect of guaifenesin, which will be discussed later.

    Salicylate sensitivity has also been associated with low levels of glutathione-peroxidase activity. This may be significant, as some people believe that chronic fatigue syndrome is partially due to low levels of glutathione, and many people with fibromyalgia also have CFS. Some people with CFS have found that taking whey supplements help them, and whey contains amino acids that increase glutathione production. And, in fact, some people taking guaifenesin are also taking whey, as there is an internet discussion group devoted to people taking both supplements. Therefore, perhaps low glutathione levels might make some people with fibromyalgia likely to be sensitive to salicylates, and avoiding them would help to alleviate fibromyalgia symptoms.

    And salicylate sensitivity is not just restricted to asthma For example, salicylates appear to aggravate symptoms of people with celiac disease, i.e. gluten intolerance, and anecdotally it appears that this disease is quite common in people with fibromyalgia. Salicylates also compete with other substances to binding to serum albumin. This includes T4 thyroid hormone. If you have low serum albumin, it's possible that salicylates can lower the level of thyroid hormones by lowering the amount that can bind to albumin.

    By the way, even if people with asthma and sinus problems aren't aspirin sensitive, they might be helped on the guaifenesin protocol from the well known expectorant effect of guaifenesin. Relieving congestion would not only improve sleep, but would also help to avoid infections, both effects which could help to relieve fibromyalgia symptoms.

    Salicylates can also block Vitamin K. This may be important for some people with fibromyalgia, as easy bruising is a common symptom in some people with fibromyalgia, and a vitamin K deficiency could cause this. However, Vitamin K does much more than this. It is also a significant antioxidant, controls insulin release, and is important in protecting osteoporosis. Additionally, vitamin K reduces IL-6, an inflammatory cytokine, which some people theorize places a role in creating fibromyalgia pain. Vitamin K deficiencies have also been linked to mitral valve prolapse and hypermobility, both conditions which also commonly overlap in some people with fibromyalgia. Therefore, reducing salicylates may be helping some people with fibromyalgia by increasing levels of vitamin K

    In any event, salicylates can have a wide range of effects on the body, and therefore it's impossible to tell what is the result of avoiding salicylates, without proper lab tests or studies.

    Guaifenesin's Anticoagulant Effect
    Possibly a very important effect for fibromyalgia is guaifenesin's known anticoagulant effect, an effect which Dr. St. Amand notes in his book. However, both of the previous uricosuric drugs that Dr. St. Amand used for fibromyalgia, i.e. anturane and probenecid, also have an anticoagulant effect. This effect is relevant, because it has been found that some people with CFS/FMS have hypercoagulant activity, and initial studies have shown some success with using heparin and other anticoagulant drugs. The anticoagulant effect was first noticed in 1994 by a Dr. John Couvaras, an infertility doctor, who began using heparin for fertility problems, and discovered that it helped many symptoms of his patients who also had CFS and fibromyalgia. Perhaps not so coincidentally, guaifenesin is also known to have the ability to increase fertility (originally it was thought that this effect from guaifenesin was due to thinning of cervical mucus. But guaifenesin has not been found to have a direct effect on thinning mucus, but instead simply stimulates mucus glands to allow more mucus to flow, possibly by irritating gastric linings. This effect is not likely to occur in the cervix, because little if any guaifenesin could appear there. Plus, it's the thinning of the mucus which is important, not increased mucus flow. Thinning mucus occurs due to a raise in estrogen levels, and coincidentally estrogen inhibits platetlet aggregation.)
    There are several reasons given as to possibly why anticoagulants have helped some people. But there is one specific effect that might be very relevant for fibromyalgia. In a recent study on fibromyalgia, it's been found that some fibromyalgia symptoms coorelate with lower levels of serum serotonin and higher levels of plasma serotonin. See:


    But platelet activation, which causes platelet aggregation, also causes the release of serotonin, resulting in high plasma serotonin In addition, only in the last few years has it been recognized that serotonin influences many other problems, such as migraines, hypoglycemia, asthma, Raynaud's, and IBS, all conditions which are associated with fibromyalgia. Some of these conditions are exacerbated due to serotonin's ability to cause constriction. However, Dr. Couvaras has said that migraines, irritable bowel syndrome, and pelvic pain, all went away when he put his patients on heparin. Interestingly, Dr. St. Amand has also claimed that guaifenesin is able to treat many different conditions. An imbalance of serotonin in the blood could be the link that connects all these conditions.

    Hypoglycemia is one of the more interesting conditions related to serotonin, as it is especially common in fibromyalgia. It is so common, that Dr. St. Amand himself regularly prescribes a diet for hypoglycemia to many of his patients, and it is often an integral part of his treatment in combination with guaifenesin. However, hypoglycemia can be influenced by a serotonin release, as serotonin has been shown to increase insulin levels. Not only that, but platelet aggregation sensitivity is increased due to hypoglycemia. Thus, this is one possible explanation of why hypoglycemia is so common. (As an aside, low carbohydrate diets, such as diets for hypoglycemia, have been found to help many people with fibromyalgia, even those not taking guaifenesin. So much so, that anyone considering going on the guaifenesin protocol and the diet, might want to first try the diet alone, in order to be able to tell which effects are occurring from diet, and effects are from the guaifenesin.)

    Other commonly seen conditions also have a serotonin link. For example, plasma serotinin in celiac patients has been found to be elevated. Problems associated with blood pressure, such as Neurally Mediated Hypotension, are also influenced by serotonin.

    In addition, platelet activity causes a release of other substances that might be affecting fibromyalgia. For example, ATP is also released, and this might be the cause of reduced levels of ATP found in red blood cells of people with fibromyalgia.

    Both of the previous uricosuric drugs used by Dr. St. Amand, anturane and probenecid, also affect platelet activity. Anturane (sulphinpyrazone) is well known for having antiplatelet activity. Probenecid's effect is a bit different. It's able to block a number of different aggregating agents. And it's main effect may be due to it's ability to inactivate thrombin, which is the cause of platelet activation which leads to the secretion of serotonin from the serum to the plasma. See the following studies:



    But what's more is that an anticoagulant effect might be the reason for the increased phosphate excretion. The clue to this possibility is a recent report of a patient being treated with probenecid for calcinosis:



    According to most studies, probenecid does not cause phosphate excretion in either non-gout or gout patients. However, there are several reports in the medical literature of it occurring. But they are so rare, that whenever a case occurs, it's reported in a medical journal. In the above report, the patient had Juvenile Dermatomyositis which led to calcinosis, a condition where calcium is abnormally deposited around bones, causing severely limited mobility. The patient also had hyperphosphatemia, and probenecid was able to reverse this condition by increasing phosphate excretion, and this led to reversing the calcinosis.

    However, it's possible that the hyperphosphatemia seen in this patient was due to a drug that she was taking, which was Cyclosporin A. This drug is known to cause platelet aggregation and high plasma serotonin levels:



    This paper mentions that impaired renal functioning and reduced renal plasma flow also occur with this drug. The impaired renal functioning could lead to phosphate retention. If an anticoagulant could improve renal flow, then theoretically this could cause increased phosphate excretion.

    And there is possible proof that the phosphate excretion from probenecid is due to an effect other than the uricosuric effect. Here is a study of an earlier case of probenecid being successfully used for calcinosis:


    In that case, phoshate excretion occurred even without a significant increase in uric acid excretion. In other words, the two effects might be unrelated.

    This would also explain the puzzle of why uricosuric drugs produce increased uric acid excretion in normal people, yet phosphate excretion does not occur. They are two separate effects, and the phosphate excretion would only occur in people who had impaired platelet functioning.

    But it should be pointed out that not all anticoagulants affect the impaired renal functioning which is caused by platelet aggregation. This is not surprising, as there are several different pathways involved in platelet aggregation Thus, different drugs inhibit aggregation in different ways.. In the following study, renal impairment was induced by endotoxin, a platelet growth factor which causes aggregation. In high enough doses, endotoxin is able to cause reduced phosphate excretion. Heparin had no effect on the renal impairment, while aspirin was able to restore proper renal functioning:



    Heparin is strictly an anticoagulant, while aspirin is an antiplatelet drug. This study theorized that only antiplatelet drugs could reverse the renal impairment caused by platelet aggregation, but perhaps the real reason is how the kidneys handle the drugs. Drugs such as uricosuric drugs and salicylates are actively secreted into the kidneys. Thus, uricosuric drugs might be the only anticoagulant drugs that are able to reverse all the affects of platelet aggregation.

    What is causing the platelet aggregation? There are many possible reasons. A magnesium deficiency can be the cause. Another interesting possibility is that low levels of certain antioxidants factors, glutathione and thiols, can also be the cause. This is interesting because some people with fibromyalgia and CFS appear to have this condition, and people have found benefit from taking supplements that increase glutathione, such as special forms of whey. Elevated blood homocysteine levels is also a possible cause. This can be due to a B12 deficiency, and many people with CFS and fibromyalgia find benefit from taking B12 shots. Homocysteine levels are also increased in hypothyroidism , and hypothyroidism is commonly found in fibromyalgia patients. Estrogen may be a factor in women, since it's known to inhibit platelet aggregation. Fibromyalgia is more likely to occur in older women, when estrogen levels are decreasing. One study showed lowered basal levels of estrogen in women with fibromyalgia. Another study showed that fibromyalgia symptoms were worse during part of the cycle with the lowest level of estrogen. Certain infections, such as candida, can increase platelet activity, as platetets secrete toxins against infections. Lyme disease might also increase platelet aggregation.

    It's quite possible that a number of factors can be increasing platelet aggregation. This is true in other conditions, such as diabetes, where where platelet aggregation exists, and different treatments have been found to be useful, One treatment of specific interest is the use of amino acids which have been found to be low in diabetes. Taurine and arginine have been successfully used to reduce platelet aggregation. Since amino acid levels have been found to abnormal in both fibromyalgia and CFS, this is another possible factor.

    If platelet activity is a factor in fibromyalgia, then how is it that other drugs and supplements for fibromyalgia are also effective, yet they don't have any effect on platelet activity? The answer is that coincidentally (or perhaps not), most other drugs and supplements for fibromyalgia do inhibit platelet aggregation. All of the following have some affect on platelet activity: Some antidepressants, especially tricyclics, benzodiazepines such as xanax and valium, antihistamines such as benadryl, anesthetics such as procaine, supplements such as MSM, ginko, pycnogenol, quercetin, and bromelain, magnesium, B12 (homocysteine increases platelet aggregation), whey (treats glutathione deficiency, which causes platelet aggregation), some amino acids such as taurine and arginine, and relaxin (presently experimentally used for fibromyalgia). Thus, like guaifenesin, all of these substances are recommended for use for fibromyalgia, but they also have some ability to inhibit platelet aggregation

    In fact, one could hypothesize that some of the people in the guaifenesin study, who did not see any benefit from guaifenesin, might have already been taking a supplement or medicine that inhibitted platelet activation, and thus were not affected by the addition of guaifenesin. This hypothesis gains further strength from the fact that Dr. St. Amand recommends to people to avoid most supplements, because he feels they are not necessary, so that his own patients would be less likely to be exposed to such remedies. Additionally, many of the supplements that inhibit platelet activation, may contain traces of salicylates, so they are avoided by people taking guaifenesin. The fact that both guaifenesin and many salicylate containing supplements are able to inhibit platelet aggregation is not simply a coincidence. Both guaifenesin and many of these supplements are derived from the skins and barks of plants, so they are likely to have similar effects. However, guaifenesin is now artifically produced, rather than being naturally derived, so it doesn't have the traces of salicylates that the other supplements might have.

    This anticoagulant effect could have other consequences, in conjunction with other aspects of guaifenesin. For example, the flow of the lymphatic system can be improved by increased blow flow. But lymph flow is also improved by increased physical and muscle activity, which could occur from using a muscle relaxant. Could Dr. St. Amand's lumps be also related to the lymphatic system, perhaps a very mild form of lymphedema? Perhaps, something to look into.

    Regardless of whether the anticoagulant theory is correct, people should be aware of this effect from guaifenesin, as many other drugs and supplements also have anticoagulant effects. The combination of several such drugs could causes side effects. Too much of an anti-platelet effect can destroy platelets, resulting in a much larger release of serotonin and histamine. Also, if guaifenesin doesn't help your platelet aggregation problem, it could be that you need a different type of anticoagulant, as platelet activation is caused by several different effects. Additionally, guaifenesin's effect is dependent on how long it stays in the blood stream. However, guaifenesin is rapidly metabolized and removed from the blood, so that it doesn't necessarily make for the best anticoagulant drug. And it also has other effects which are not found in other anticoagulants.

    So what are the lumps that Dr. St. Amand claims to find in his patients?
    One of the main diagnostic tools which Dr. St. Amand uses to determine if a patient is correctly responding to guaifenesin, is by examining lumps which he detects on a patient. He maps the body for such lumps. While the definition of fibromyalgia includes the presence of tender points in the body, these points are not necessarily lumpy. Plus, Dr. St. Amand finds many more lumps than the number of known tender points. Such lumps are not described by any other fibromyalgia researcher, and are not a part of the description of fibromyalgia. Some fibromyalgia researchers used to wonder if perhaps there were major abnormalities in the muscles that could be the reason for the pain. However, no major differences could be found that would be responsible for the pain. Therefore, they no longer believe that the primary cause of fibromyalgia originates from the muscles themselves, but in the neurological and immune system. Any abnormalities found in muscles and tissues surrounding them are believed to be secondary effects. Thus, any changes in the muscles due not necessarily reflect whether the primary cause of fibromyalgia is being treated. And anecdotally, I've spoken with people who have taken guaifenesin for over a year, and had all their lumps reduced, creating a clear map, yet their level of fibromyalgia pain was still quite high.
    At first, Dr. St. Amand believed that these lumps contained phosphate deposits. However, biopsies on fibromyalgia tissues have found no such abnormalities. He then changed his theory to believe that the phosphates were being stored in the cells themselves. Therefore, even according to his own phosphate theory, these lumps do not necessarily reflect a direct reflection of the cause of fibromyalgia.

    So what exactly are these lumps? Could they be myofascial trigger points or knots in the muscles? Possibly. However, Dr. St. Amand has stated he does not feel for areas which are painful or tender, but which are swollen to the touch. Thus, if they are swollen, another possible explaination is that they are related to edema, or water retention. Edema can be caused by an excess of anything that causes vasodilation, which then leads to capillary permeability. Abnormally high levels of cortisol are known to cause this, and studies have shown higher that levels are increased in some people with fibromyalgia. Other substances such as serotonin and histamine can also cause vasodilation. These substances are released when blood platelets are activated. Thus, the antiplatelet effect of guaifenesin might be responsible for reducing such lumps. And it's interesting to note that the study that looked at guaifenesin's analgesic properties, also looked looked at possible anti-inflammatory effects. In comparison with aspirin, guaifenesin was found to affect certain inflammation effects, but not all of them. One of those effects happened to be a reduction in edema lesions. The fact that guaifenesin didn't act as a full anti-inflammatory, could lead one to speculate that the effect was not a true anti-inflammatory one, but that it was a different effect that was at work, such as the antiplatelet effect.

    Uricosuric Drugs and Phosphate Excretion

    Dr. St. Amand believes that the increased phosphate excretion is the reason for guaifenesin's benefit, and that by reducing excess phosphate in the body onecan totally reverse fibromyalgia. While I believe guaifenesin to have some benefit, there is no evidence that it can reverse fibromyalgia, nor is there any evidence that phosphate is the cause of fibromyalgia.

    Before Dr. St. Amand used guaifenesin for treating fibromyalgia, he used anturane and probenecid. Both are used for gout, due to their ability to increase urinary uric acid. However, neither is known for be able to enhance phosphate excretion. The medical literature appears to have no references to any studies which tests anturane for this ability. However, there are several studies which have tested for this effect in probenecid.

    Probenecid is believed to increase urinary uric acid by reducing the amount that is reabsorbed via the kidneys back into the serum. The section of the kidneys where this occurs is known as the proximal tubule. Probenecid is secreted into the proximal tubule via a process known as renal tubular secretion, which only occurs for certain weak acids. One of those acids includes salicylates. Since this process has a limited capacity, acids compete with each other for secretion. If salicylate levels are too high, they block probenecid from being secreted.

    Once in the proximal tubule fluid, probenecid is believed to act as an anion transport inhibitor, which is to say it prevents the kidneys from reabsorbing negatively charged substances, including such acids as uric acid. The following study that looked extensively at the effects of probenecid on urinary electrolytes, and did not find any increase in urinary phosphate.

    Can Med Assoc J. 1970 Sep 12;103(5):473-83 AUTHORS: Garcia DA, Yendt ER (No abstract available in MEDLINE)

    Additionally, other studies have confirmed that probenecid does not increase urinary phosphate excretion, such as the following:



    In that study, the action of probenecid was monitored in connection with Didronel, a drug used for osteoporosis. Didronel has a known side effect of increasing serum phosphate levels, an effect which lasts from 2-4 weeks after discontinuing the drug. Probenecid was tested to see if it would cause any increase in phosphate excretion, which it did not. Interestingly, Dr. St. Amand actually recommends Didronel for osteoporosis for his patients, and it does not appear to cause any worsening of fibromyalgia symptoms, even in people who exhibit a rise in phosphate levels. This casts doubt on the phosphate theory, since a rise in serum phosphate levels should offset the effect of guaifenesin, but it does not.

    With regard to guaifenesin, unfortunately there have been very few published studies on it's urinary effects. There is only one published study that studied its effect on urinary uric acid.



    It showed a definite, although weak, uricosuric effect (using 1800mg in a 6 hour period). And since it's been reported that guaifenesin's action is blocked by salicylates, it probably is secreted into the kidneys via the same path that probenecid uses. However, guaifenesin is rapidly metabolized, and its metabolites have been found in urine. And its major metabolite has been found in kidney stones that occurred in individuals who took high doses of guaifenesin:



    Thus, guaifenesin can form an insoluble salt with calcium. And it's interesting to note that in Bennett's study of guaifenesin on fibromyalgia, while he did not find any increase in either urinary uric acid or phosphate, the study did show a significant increase in urinary calcium in the guaifenesin group: So while I've previously noted that probenecid has caused phosphate excretion in rare cases, and that this might be linked to an anticoagulant effect, there is not a lot of evidence to show that this actually is occurring in people with fibromyalgia, nor is there evidence to show that excess phosphate could be the cause of fibromyalgia symptoms. Even if coagulation problems do exist in people with fibromyalgia, this would not necessarily mean that the problem is worse enough to impair renal functioning. If that was the case, then decreased phosphate excretion would be noted in patients with fibromyalgia. Not only is this not true, but people with fibromyalgia have found benefit from guaifenesin without observing any increased phosphate excretion. As for the urine tests which Dr. St. Amand has said he has done with some patients, it should be noted that many drugs initially cause side effects that gradually disappear. This is especially true of phosphate excretion which is very much dependent on hormonal levels. If a drug initially disrupted hormone levels, it could take many weeks before hormone levels restabilized. For example, prednisone initially causes increased phosphate excretion, but this effect disappears after long term term. Thus, long term testing would be needed in order to determine if a change in phosphate excretion was a permanent effect.

    No Medical Evidence that Excess Phosphate Can Cause Fibromyalgia Symptoms

    Dr. St. Amand conducted a few urinary tests on some of his patients, and found that both urinary calcium and phosphate levels were raised. Since phosphate levels were raised the most, Dr. St. Amand believes it is this effect that helps to treat fibromyalgia. The following quote is taken from his web page: "My theory, simplistically stated, is that minimal phosphate retention year after year is leading to gradual excesses. An elevated phosphate in the blood is not tolerated since it would depress calcium levels. The parathyroid glands will not allow this and phosphate must be spread evenly not only in body fluids but also within cells."

    Phosphorus, commonly referred to as phosphate, is one of the most common and most necessary minerals in the body. Phosphate is used everywhere, from the building of bones, to balancing the body's PH, and most important, for providing energy to run the body, via the formation of ATP. However, since it is so common in the foods we eat, both phosphate deficiency and phosphate excess are rare. The kidneys are known to be able to keep phosphate serum levels well regulated, which is critical, since the body obtains it's phosphate from the serum. The kidneys can keep phosphate serum steady even when phosphate intake is several times larger than normal. Thus, the kidneys are crucial to proper phosphate metabolism. Additionally, the parathyroid glands influences kidney phosphate excretion rates via production of PTH. Thus, phosphate problems mainly occur in cases of kidney or parathyroid problems.

    If phosphate excretion is too low, phosphate serum levels rise, resulting in the condition known as hyperphosphatemia This is normally due to either kidney failure, parathyroid deficiency (hypoparathyroidism), or due to the body not reacting properly to parathyroid hormone. The Merck Manual pages that relate to this condition are found here:

    Such a condition is easily detected via a blood test. Initially, this condition is symptomless. The main symptoms occur due to the excess phosphate combining with calcium. This causes a calcium deficiency, which is the main source of symptoms in hyperphosphatemia. However, if phosphate levels are high enough, eventually metastatic calcification occurs, in which deposits of calcium phosphate accumulate in soft tissues, including the heart, lungs, blood vessels, kidneys, brain, eyes, peri-articular tissues, and skin. However, no such condition has been found in fibromyalgia, so there is no direct proof that excess phosphate is present and is creating any problem.

    Dr. St. Amand used to believe that phosphate deposits existed in the knots and lumps which he observed in the muscle of his patients. However, studies have found no such deposits in the muscles of people with fibromyalgia. He has since changed his theory, and now believes that excess phosphate is being stored in cells, causing the lower levels of ATP which is found in fibromyalgia. However, studies have shown no relationship to the level of ATP and actual fibromyalgia symptoms. And there have been no published studies which have found that excess phosphate is associated with ATP depletion, or for that matter, any fibromyalgia symptoms. But there are studies which show that ATP deficiencies are found in people with phosphate deficiencies, not surprising, since ATP requires phosphate. In fact, one study has found that some people with chronic fatigue syndrome have phosphate diabetes, a condition caused by kidneys excreting too much phosphate.

    Not only that, but studies show that muscle cells appear to be somewhat protected from serum phosphate levels changes. This might be why calcification from hyperphosphatemia initially occurs in soft tissues, and not in muscles. Furthermore, phosphate uptake in muscle cells is increased by a compound known as IGF-1, the insulin-like growth factor 1. IGF-1 also causes kidneys to reabsorb more phosphate, and thus excrete less. IGF-1 is produced from growth hormone. However, levels of both compounds have often been found to be low in fibromyalgia, possibly due to a deficiency of stage 4 sleep, which stimulates growth hormone secretion. Thus, fibromyalgia people are low in a factor which increases phosphate uptake into muscle cells, making it even less likely that phosphate excess is occurring in muscles.

    Some people have pointed to studies which show that fibromyalgic muscles contain low levels of ATP and high levels of inorganic phosphate as being proof of the phosphate theory. However, these same abnormalities have been known for a while, and are quite common in other conditions. For example, studies have shown that similar muscle conditions occur due to hormonal disorders, such as a hypothyroidism. In fact, it occurs in normal people, after exercise that causes muscle fatigue. But studies on exercise show that these phosphate abnormalities are reduced if muscles are properly trained beforehand. Thus, this condition can occur if muscles are unconditioned, which is often the case for people with fibromyalgia. Many people have thus come to the conclusion that fibromyalgia studies on muscles do not show any conditions which are the primary cause of fibromyalgia, and that fibromyalgia is not related to any muscle disorder.

    So there presently is no proof to support the phosphate theory, nor is there any proof that ATP depletion could cause all the immune, hormonal, and brain disfunctions which have been found in fibromyalgia, or for that matter chronic fatigue syndrome, which Dr. St. Amand believes is the same disease as fibromyalgia. This is the reason why, that although ATP levels were found to be abnormal as far back as the early 1990s, present day research is not focused on that as being the primary cause of fibromyalgia or chronic fatigue syndrome symptoms.

    But even if we accept this theory, we must also believe that guaifenesin can lower the serum phosphate level to the point where it would cause phosphate to be released by the cells into the serum and be excreted. Such an effect would have to be quite significant, in order to create a large enough gradient between the blood and the cells to make the phosphate want to move into the blood. And it has to be large enough to allow the released phosphate to be excreted, rather than simply being reabsorbed by other cells. Such a significant effect would be easily noticed in lab tests. And in fact, such a test should probably be used as a parameter for how much guaifenesin is needed, in order to make sure that phosphate isn't being lowered too much. Phosphate blood and urine levels are usually extremely constant, and assuming one is taking a timed release version of guaifenesin to achieve a steady decrease of phosphate, a blood test should be quite reliable. However, such tests have not been published, nor are they being used for verifying the dose of the drug. Increasing excretion of minerals can theoretically lead to many health problems. Yet, Dr. St. Amand only uses symptoms as his guide for doses. In fact, his treatment protocol expects that you will initially feel worse when taking guaifenesin, which makes one wonder how one is supposed to know if one is feeling bad or good effects, without a proper lab test.

    Dr. St. Amand himself has said his theory is purely theoretical, and that perhaps guaifenesin is changing the excretion level of some other anion. His main reason for originally believing in the phosphate theory was due to what he had observed in his patients, such things as weaknesses in teeth and nails, which he believed was due to calcium deposits resulting from the high level of phosphate. However, weak and abnormal bone formations can be due to a phosphate diabetes, which we have previously described. And it can also be due to a much more common problem, which is a magnesium deficiency. Bones are not only formed from calcium and phosphate, but also from magnesium. Without magnesium, the resulting formations will be soft. Teeth will have soft enamel, nails will be brittle, symptoms which match Dr. St. Amand's observations.

    Magnesium is extremely necessary for proper ATP synthesis, because ATP is stored in the body as a combination of magnesium and ATP, which is known as MgATP. ATP requires magnesium in order to be stable. Without magnesium, ATP would easily break down into other components, ADP and inorganic phosphate.

    Magnesium deficiency is very common in the general US population. Not only is our daily intake low, but we eat a diet which increases the demand for magnesium. And unfortunately, urinary magnesium loss can be increased by many factors, both physical and emotional. Magnesium loss increases in the presence of certain hormones. Stress can greatly increase magnesium loss. Even loud noises can extra magnesium loss. One article on the web goes so far as to say that that almost everyone is the United States is at least marginally deficient in magnesium. So there is an excellent chance that a person with fibromyalgia has a magnesium deficiency. But since people with fibromyalgia often have high levels of stress, and a disrupted hormonal system, they are more likely to be candidates for magnesium deficiency. Plus, sleep deprivation has been shown to cause lower magnesium levels:



    Magnesium is known to regulate or inhibit many nerve receptors, such as NMDA or 5-HT3, which have been considered as sources of certain types of fibromyalgia pain. Neurontin, for example, is used because of it's ability to regulate NMDA. Since magnesium also blocks NMDA receptors, studies have used intravenous magnesium therapy to try and treat similar types of neuropathic pain:



    And it's because of magnesium's ability to regulate nerve functions that other fibromyalgia symptoms occur. Migraine headaches, mitral valve prolapse, and Raynaud's phenomenon, all problems commonly found in people with fibromyalgia, are also problems that have been associated with a magnesium deficiency. Without enough magnesium, nerves fire too easily from even minor stimuli. Noises will sound excessively loud, lights will seem too bright, emotional reactions will be exaggerated, and the brain will be too stimulated to sleep, all symptoms commonly found in fibromyalgia. And if the oversensitivity to light and noise reminds you of someone suffering from a hangover, they are one and the same problem, as alcohol is known for decreasing magnesium levels, and magnesium supplementation has been found to relieve hangover symptoms.

    Another commonly found condition in fibromyalgia which has nervous related symptoms is reactive hypoglycemia. Anxiety related symptoms occur after carbohydrate intake, and this is believed to be due to either an excess release of adrenaline, or a higher sensitivity to adrenaline. In either case, a deficiency of magnesium could be a factor, as "magnesium has been found to slow the release of both adrenaline and noradrenaline, and to partially block adrenergic receptors."

    A magnesium deficiency also increases levels of substance P, a chemical which has been implicated as being responsible for increased pain levels in FMS. Several studies, such as the following, show this:

    And also of interest is that a magnesium deficiency can cause platelet aggregation;



    Unfortunately, magnesium deficiency is not easily detected, as serum levels do not reflect the levels of magnesium in tissues. This is the reason why it is so overlooked and ignored, both by doctors and by studies. And unfortunately, oral magnesium supplementation can be difficult because of absorption problems. Digestion and diet play a key role in absorption. People with fibromyalgia often have conditions like Irritable Bowel System, gluten intolerance, or other problems that might limit absorption. Phosphate can bind to magnesium in the gut, creating magnesium phosphate, an insoluble salt that can't be utilized. Many forms of oral magnesium supplements are hard to assimilate. The most common, magnesium oxide and citrate, happen to be the worst to assimilate, which is why both have a strong laxative effect. If you suffer from that effect when you take magnesium, it is often not because you are taking too much, but because you are not assimilating it well. And it may take long term use of supplements before magnesium levels are raised in all the tissues, and for damaged cell functions to be restored.

    Therefore, the symptoms which Dr. St. Amand has attributed to an excess of phosphate, would more likely be due to a magnesium deficiency.

    Did the Oregon study prove anything?

    The Oregon study was designed assuming that the effects of guaifenesin were due to urinary ones, so that lab tests mainly studied urinary functioning. It only excluded people and medicine that would not conflict with this ability. Thus, it was not well designed for looking at other guaifenesin effects.

    Did it prove or dispove anything about guaifenesin's urinary effects? Dr. Bennett believes it did, because he states that if low levels of salicylates were blocking guaifenesin, then the salicylates would have reduced urinary uric acid. However, while I've not seen a proper rebuttal to that point in print on the web, it should be mentioned that the study wasn't designed to test for this possibility. Salicylates, and other uricosuric agents, at very low doses, do reduce urinary uric acid. As the dose increases, urinary uric acid increases, first becoming normal, and then at higher doses it causes urinary uric aicd to increase to above normal. In theory, there could have been enough salicylates to block guaifenesin, while not being enough to decrease urinary uric acid. The presence of guaifenesin, also a uricosuric agent, also must be considered.. There are a number of possible conditions which could have existed that would have allowed uric acid to be normal, but for a significant amount of guaifenesin to be blocked.

    On the other hand, one could also create situations where guaifenesin was not blocked, and that urinary uric acid would still be normal. Dr. St. Amand points to the fact that uric acid was normal as proof that the guaifenesin was blocked. However, while guaifensin is known to be a uricosuric agent, the only study on this behavior used non-timed released guaifenesin, given in 600mg doses every 2 hours for 6 hours. In other words, we don't know what the effects are of timed released guaifenesin, which was used in the Bennett study. Any uricosuric agent at low doses decreases urinary uric acid, and it most reach a high enough dose before it causes an increase in urinary uric acid. It could be that the dose used in the study was simply not high enough for a significant change in uric acid.

    Dr. St. Amand also believes the study was flawed because it did not exclude people with hypoglycemia. However, other studies on treatments for fibromyalgia don't makes this exclusion, yet are still able to show benefits from treatments. Additionally, Dr. St. Amand says himself that "Failure to comply with these [hypoglycemic] dietary recommendations would not delay the reversal of fibromyalgia."

    On the other hand, it is curious to note that urinary calcium excretion was increased. I've not seen that point mentioned by anyone, but to me that means that possibly guaifenesin wasn't blocked, and that it doesn't increase phosphate excretion, but that it does increase phosphate excretion.


    Is Guaifenesin causing the excretion of any
  2. klutzo

    klutzo New Member

    It was VERY interesting though. I am scientifically trying to control my experiments with Guai and give it a fighting chance. I will report when done. I don't trust any speculation until I test it myself.
    I would just like to note that the last sentence of this piece before it cut off contained contradictory statements.
    I'd also like to note that Mg Citrate does not have the laxative effect of Mg Oxide as he says it does.
    Klutzo
  3. Mikie

    Mikie Moderator

    This is VERY interesting information even if it is a lot to try to digest. I guess the info in a nutshell is that the Guai may be beneficial in the treatment of FMS but not necessarily for the reasons espoused by Dr. St. Amand.

    I put absolutely no creedence in the Oregon study as it was so flawed as to be unuseable. Dr. St. A knows that too little was known at the time about the Guai and the sals for the study to be significant; however, as the author points out, the study may have been flawed for reasons other than what Dr. St. A. believes.

    It does appear that there are benefits to be had from the Guai treatment though. There have been a lot of people, including me, who have been helped by the Guai. I used to have the tender bumps which would make me cry from even a slight touch. These are mostly gone and the few which are left are much less tender. Any massage therapist will tell you that toxins produced by stress can build up in the soft tissue and become very tender.

    I can see what I used to believe is phosphate debris in my urine. After reading this, I'm not sure if it is phosphate debris, but it is something like powder or crystals.

    Since being on the Guai, I no longer use pain meds, so regardless of how it is working its magic, the improtant thing to me is that it is working. When I took a magnesium supplement which turned out to be veggie based, it blocked the Guai's benefits after a time, and my pain and tender spots returned. As soon as I stopped taking the supplement, the Guai benefits returned.

    So, in a nutshell, for me, the Guai is working. It may not be for the reasons I previously thought, but it is working. Bottom line, that is what counts.

    There will probably never be another Guai study because there is nothing financial to be gained by doing one. There will most likely just be an ongoing duel of theories like this comprehensive article. All info is valuable to us in trying to figure out what helps and why. I thank you for providing this for us. I would ask, however, that you please go through and remove URL's from the article. I have edited it and hope I got them all.

    Love, Mikie
  4. Dayle

    Dayle New Member

    but for what ever reason the guiafenesin is working for me. I however could not believe that I was hypoglycemic & did not stop eating carbs until after taking the guia, I discovered that I felt terribly ill whenever I ate carbs. This protocol is not for everyone it can be difficult & if as Mark London claims he & others took it in the 90s before all info was in; I salute them & encourage them to try 1 more time. But follow the complete protocol; it has helped me. After only 2 months I have had 2 weeks of happiness & excitement & 80% relief from fibro. symptoms. Lucky for me I found a Doc. near by who is helping me. I also have Dr. St.Amands book which is a must. Good luck to all who are willing to give it a try. Regards,D.
    [This Message was Edited on 02/26/2003]