Guaifenesin protocol

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Guaifenesin protocol is an unapproved treatment for fibromyalgia suggested in the 1990s by R. Paul St. Amand. The protocol involves three parts: titrating the guaifenesin dosage, avoiding salicylates, and following a low-carbohydrate diet if the patient is hypoglycemic. Guaifenesin has not been approved by the FDA for the treatment of fibromyalgia, and the protocol has not been shown to be effective in clinical trials. Despite the demonstrated lack of clinical efficacy, the protocol has been adopted by many due to anecdotal evidence of success.[1][2][3]

Treatment details[edit]

Avoiding salicylates[edit]

Salicylates in even tiny amounts block guaifenesin from being absorbed by the kidneys, especially when absorbed through the skin or mucous membranes. One must be cautious of personal care products such as flavouring in dental products and gum, body lotions, cosmetics, hair care products, hand sanitizers, and anything that can be absorbed through the skin. Normal food amounts of salicylate will not obstruct the process of excretion with Guaifenesin. The exception to this rule is mint. Even a small dose of any member of the mint family will block guaifenesin absorption in the kidneys. Ingesting concentrated amounts of salicylate such as tea or herbal concentrations can be too much for the liver to process and salicylate can thus pass the liver and then block the receptor site for Guaifenesin in the kidneys' renal tubules. Salicylates can also be found in drugs such as aspirin, Salsalate, Disalcid, Anacin, and Excedrin. Plants produce salicylic acid, so herbal medications must be avoided as well as plant oils, gels and extracts in cosmetics and any product that touches the skin. These ingredients include but are not limited to aloe, castor oil, camphor, and pycnogenol, mint. Any plants can be eaten, however, because the small amount of salicylic acid present in food is broken down in the digestive system and tagged with glycine by the liver before reaching the kidneys. Juicing of vegetables, however, can be too concentrated of an amount of salicylate for the liver to handle, so the receptor site for Guaifenesin in the kidneys may become occupied by salicylate and block Guaifenesin.


This hypothesis involves phosphate accumulation in cells that eventually reach a level to impede the ATP process, possibly caused by a kidney dysfunction or missing enzyme that prevents the removal of excess phosphates from the blood stream. This theory posits that fibromyalgia is an inherited disorder, and that phosphate build up in cells is gradual (but can be accelerated by trauma or illness). Calcium is required to buffer the excess phosphate when it enters the cells. The additional phosphate slows down the ATP process; however the excess calcium prods the cell to action. The causative mechanism in the kidneys is unknown.

The phosphate build-up hypothesis is said to explain the myriad symptoms present in fibromyalgia and provides an underlying cause, but remains theoretical; there is no clinical evidence that the phosphate build-up theory is correct, or that Guaifenesin protocol is effective.


Results of the only reported randomized clinical trial in 1996 found that guaifenesin had no significant effects on pain, other symptoms, or laboratory measures (serum and urinary levels of uric acid and phosphate) over 12 months in a sample of people diagnosed with fibromyalgia syndrome,[2] The lead author of the study has suggested a number of reasons why some patients may have previously reported benefits on this protocol, concluding "St. Amand has unknowingly used guaifenesin as a powerful focus in a program of cognitive behavioral therapy, in which his empathy, enthusiasm and charisma were the real instruments in effecting a beneficial change."[4] St. Amand, who participated as a "Study Advisor" to this clinical trial, has stated that the study did not control for salicylate use, and therefore did not study the protocol as a whole. He has recommended a follow-up study be conducted which controls for all elements of the protocol.[5][6] The lead author of the study counters that none of the subjects exhibited any signs of salicylate use.[2]


This hypothesis arose when St. Amand noticed that patients with fibromyalgia symptoms had an increase of tartar on the teeth in the form of calcium phosphate. Crystals are also often found on urinalysis, which further points to calcium phosphate, and muscle biopsies show an steady state of phosphate in the cytosol as well as a dearth of ATP and phosphocreatine. The implication is that insufficient energy formation is the basis for the generalized cellular fatigue expressed in many tissues of fibromyalgia. Lesions of muscles, tendons, and ligaments can be felt by simple palpation. St. Amand calls this 'mapping' and uses it to confirm the diagnosis and in followup reversal of fibromyalgia. He feels that a genetically induced retention of phosphate also draws excess quantities of calcium into cells and exhorts them into overdrive. Contracted musculoskeletal tissues are the result and they produce the palpable lesions.

The treatment was discovered serendipitously when the physician found that uricosuric drugs for treating gout also coincided with relief of fibromyalgia symptoms. Guaifenesin is mildly uricosuric but, unlike standard uricosuric drugs, has almost no side-effects. St. Amand therefore began to study whether guaifenesin might relieve the symptoms of fibromyalgia while causing fewer side-effects than the earlier medications.


  1. ^ Bennett, R.; deGarmo, P.; Clark, S. (1996), Arthritis and Rheumatism (Conference presentation), American College College of Rheumatology 60th National Scientific Meeting; Association of Rheumatology Health Professionals 31st Scientific Meeting (Orlando, FL) 39 (Suppl. S9): S212, doi:10.1002/art.1780391402.  Missing or empty |title= (help); |chapter= ignored (help)
  2. ^ a b c Bennett, R.M.; Clark, S.R; De Garmo, P. "Report on a randomized, prospective, 12 month study to compare the efficacy of guaifesin versus placebo in the management of fibromyalgia". Fibromyalgia Information Foundation. 
  3. ^ "Is one placebo better than another? -- The guaifenesin story". Consumer Alerts. Coping Resources. Fibromyalgia Network. 
  4. ^ Bennett, R. "Speculation as to the mechanism whereby some of Dr. St. Amand's fibromyalgia patients experienced improvement while taking guaifenesin". Fibromyalgia Information Foundation. Retrieved 2008-01-06. 
  5. ^ St. Amand, R.P. "A Response To The Oregon Study's Implication". Fibromyalgia Treatment Center. 
  6. ^ St. Amand, R.P.; Potter, C. (1997). "The use of uricosuric agents in fibromyalgia: Theory, practice, and a rebuttal to the Oregon study of guaifenesin treatment". Clinical Bulletin of Myofascial Therapy 2 (4): 5–17. doi:10.1300/J425v02n04_02.