The Role of Guaifenesin in Fibromyalgia

The Truths and Myths of the use of Guaifenesin for Fibromyalgia or Guaifenesin:  One Medicine, Several Effects | by Mark London

This article by Mark London, Systems Programmer/Analyst for the Plasma Science and Fusion Center at MIT, gives a full analysis of what effects guaifenesin might have on the body and mind.  His 20,000 words contain 150 links to other articles, most from PubMed, supporting his points (and explaining more than I can understand).

Below I’ve annotated the two most pertinent sections explaining how guaifenesin affects various body systems and how these effects may alleviate fibromyalgia pain:

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 known, is because guaifenesin 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 with similar properties, were found to be more effective.

Researchers continued to study these drugs to find a longer lasting form.  In the 1950s, such a form was created, known as a carbamate.

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

Patients on guaifenesin for fibromyalgia take anywhere from 600 to 3600mg per day

Additionally, in the previously mentioned study that compared Robaxin and guaifenesin, it was found that the two drugs had comparable muscle relaxant effects at similar dose levels.

Since the maintenance dose for Robaxin is 1500mg, we can infer that the same level dose of guaifenesin would also have significant relaxant effects.  And in fact, many people with who take guaifenesin, take a dose that is close to that amount.

Guaifenesin was being used as an expectorant, well before propanediols were discovered, as it can be derived from the bark of the guaiac tree.

It is worth noting that guaifenesin’s relaxant effect on the nervous system might be the reason for its expectorant property

Guaifenesin’s Analgesic Effect

But guaifenesin’s effect on the nervous system is not simply limited to acting as a muscle relaxant

guaifenesin, may indeed have the ability to lower fibromyalgia pain levels.

The related drug carisoprodol (soma) also appears to have an analgesic effect which is separate from its muscle relaxant effect

However, even at low doses, at which guaifenesin doesn’t exhibit any of its own analgesic or muscle relaxing effect, it still may have neurological properties that could be useful for fibromyalgia.

As an aside, neurontin at low doses is able to potentiate the anaglesic property of opioids such as morphine.  This potentiating property is likely due to an antagonistic effect on excitatory amino acids.  Increased levels of EAAs are known to cause tolerance and the loss of antinociceptive response to morphine, and neurontin has been shown to reduce morphine tolerance.

Given the possibly unique mode of action of guaifenesin, i.e. an anti-excitatory amino acid effect, it might explain why some people with fibromyalgia have noticed an effect from it, while others have not.  Many drugs used for fibromyalgia have varying success between patients.

Many people who take guaifenesin, often do so because they either haven’t found any meds that have worked for them, or they can’t tolerate the side effects from such medicines.  In other words, the guaifenesin study might have not accurately reflected the population who have found the most benefit from taking guaifenesin.

Unfortunately, propanediol drugs often have hemolytic side effects, which is why they are not being used to treat pain.  For example, the propanediol drug felbamate, was definitely was definitely found to be able to reduce neuropathic pain.   But research on it was discontinued, when significant hemolytic side effects were discovered

Additionally, the rate of metabolism of guaifenesin appears to have a wide range of variance between 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 have a slower metabolic rate, and that this could account for why some people with fibromyalgia find it useful, while others do not, and why the effective dose varies widely between people.

extracts of the guaiac tree, have a long history of being used for rheumatism

The fact that guaifenesin has a history of treating various ailments, supports the theory that it has a more general analgesic effect, rather than a specific effect that only treats fibromyalgia.

Guaifenesin’s Anticoagulant Effect

Guaifenesin has another effect that might be useful for some people with fibromyalgia.  It has a known anticoagulant effect,

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:

Hypoglycemia is one of the more interesting conditions related to serotonin, as it is especially common in fibromyalgia.

However, hypoglycemia can be influenced by a serotonin release


Guaifenesin is not a simple drug, and fibromyalgia is not a simple disease.  Because of this, it’s possible that there are a number of reasons why guaifenesin might help someone with fibromyalgia.  I’ve presented several alternative reasons, that are based on what is known about fibromyalgia and guaifenesin from the medical literature.

On the other hand, the medical literature contains little support for the phosphate theory.  In order for the phosphate theory to be valid, not only would it contradict what is known about fibromyalgia and guaifenesin, but it would also contradict what is known about phosphate metabolism, kidney functioning, and the effects of uricosuric drugs, not to mention the dubious claims regarding salicylates.

Fibromyalgia is a syndrome of symptoms.  It often is triggered by a wide range of other health problems, i.e. a sleep disorder, hypothyroidism, lyme disease, chronic myofascial pain, to name just a few.  In many cases, fibromyalgia is secondary to these other problems, and treating these primary problems can often significantly relieve the fibromyalgia

Hypothyroidism is another condition which can be a primary reason for fibromyalgia

Other hormonal imbalances, such as a deficiency of either progesterone or testosterone, can play a major role in fibromyalgia symptoms.  Progesterone not only has hormonal effects, but also has many neurological ones.

Low levels of testosterone, both in men and women, can also play a role in chronic pain.

What these examples show is that there are many conditions that can be the primary cause of fibromyalgia symptoms.  However, even when fibromyalgia is the primary problem, other conditions may still be present as secondary problems, affecting the severity of the fibromyalgia symptoms..  And fibromyalgia by itself can cause other problems which take a life on their own, such as chronic myofascial pain.

Fibromyalgia (FM) pain is frequent in the general population but its pathogenesis is only poorly understood. Many recent studies have emphasized the role of central nervous system pain processing abnormalities in FM, including central sensitization and inadequate pain inhibition.

However, increasing evidence points towards peripheral tissues as relevant contributors of painful impulse input that might either initiate or maintain central sensitization, or both. It is well known that persistent or intense nociception can lead to neuroplastic changes in the spinal cord and brain, resulting in central sensitization and pain. This mechanism represents a hallmark of FM and many other chronic pain syndromes,

This theory of fibromyalgia explains why so many widely different treatments are claimed to help fibromyalgia.  Treating any source of pain will reduce fibromyalgia symptoms

A treatment that directly affects muscle pain, would likely have the most success.  Muscle pain has been found to be particularly efficient at stimulating centralized pain, so that muscle pain may especially cause fibromyalgia to persist.  One possible reason for muscle pain in fibromyalgia, is the reduction of microcirculation blood flow in muscles, which has been seen in some studies.  Some researchers theorize that this is the most common reason for fibromyalgia.

For a description of this theory, see the 2005 article written by Professor Charles J. Vierck, former head of the Department of Neuroscience at the University of Florida College of Medicine, who has published a number of studies on fibromyalgia.

In that article, he concludes:

“Evidence presented here supports the view that the majority of FM cases develop as a consequence of a peripheral insult and associated nociceptive input [pain resulting from injury] that is long-lasting because of inadequate healing.

Tissue injury and nociceptive input generate central nociceptive sensitization, involving inflammatory influences and synaptic processes of spatial radiation and temporal summation.

Centrally enhanced nociceptive input produces sympathetic activation.

Also, chronic, persistent pain from any source, local or generalized, is as effective a stressor as can be imagined.

Nociceptive input to the cerebral cortex and limbic system elicits stress reactions involving the HPA and sympathetic nervous system. Abnormally high sympathetic activation produces peripheral vasoconstriction, and this leads over time to a spatially distributed peripheral ischemia of deep tissues.

Muscle nociceptors are highly sensitive to ischemia, and this accounts for referral of clinical FM pain to deep tissues.

Therefore, focal pain of peripheral origin can produce widespread peripheral effects with chronicity and with magnification by central nociceptive processing. An increased spatial distribution of nociceptive input from sensitized deep nociceptors in ischemic tissue enhances the sympathetic activation responsible for peripheral ischemia.

Input from muscle nociceptors sensitizes central cells that receive convergent projections from the skin, accounting for the generalized allodynia and hyperalgesia which is observed for FM subjects. Also, central convergence of somatic and visceral afferents appears to create a predisposition toward development of IBS and interstitial cystitis by FM patients.”

In any event, if it is true that reduced blood flow in muscles is capable of causing the persistence of fibromyalgia, then the beneficial effects from muscle relaxants may be due to an improvement of blood flow.

The paper includes several other chapters and you can read it in full at:

Here’s a personal account from someone who has tried it as recently as 2012: My Fibromyalgia and the Guaifenesin Protocol Story

5 thoughts on “The Role of Guaifenesin in Fibromyalgia

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