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Dr. Paul St. Amand believes fibromyalgia (FM) is likely an inherited disorder. In his patient examinations he often finds a family history of FM symptoms or of osteoarthritis that also "maps" with the same muscular, tendon and ligament lesions as in fibromyalgia. The age spread at FM onset suggests multiple genes are involved in its development, and a 4:1 ratio of affected women to men indicates that at least one of these should lie on the X chromosome. Symptoms are even noticeable in adolescence or earlier if both parents are afflicted, with the child commonly showing a history of "growing pains."
Dr. St. Amand feels that fibromyalgia is a retention disease, similar to most cases of gout, but with more varied tissue dispersion. Though patients respond to uricosuric agents, urates are not involved in FM. The widespread symptoms and number of affected organs point to a metabolic disruption caused by the build up of an anion different from urates. This ion wreaks havoc throughout many body systems but does not cause an inflammatory response.
The Role of Phosphate
Through extensive clinical observations, Dr. St. Amand suspects a partial role for inorganic phosphate (Pi) in FM. Patients often note cyclic chipping or peeling of their fingernails (calcium phosphate) while dental calculus (calcium phosphate) often breaks off, and sometimes no longer forms during guaifenesin treatment. Calcium added to meals allows lower dosages of medication, since calcium binds to phosphate and increases fecal elimination. Dr. St. Amand’s examination of 24-hour urine samples of patients who had begun guaifenesin treatment show large increases in the excretion of phosphate and, in lesser amounts, calcium and oxalate. Though other anions might be involved, his observations suggest a primary defect in phosphate (and possibly pyrophosphate) metabolism.
Research on biopsied fibromyalgic lesions reported roughly a 20-percent decrease in ATP levels2 and noted a similar decrease in phosphocreatine, the high energy reservoir used by cells. No such changes were present in unaffected muscle and a decrease in red blood cell ATP was also documented. Dr. St. Amand believes an energy deficit in affected cells would explain the entire fibromyalgia syndrome, including all symptoms and the multiple chemical abnormalities.
Buildup and Blockage
Dr. St. Amand’s theory as to the cause of fibromyalgia is ATP generation from a fully operational citric acid (Krebs') cycle becomes defective, and produces heat instead of energy. According to St. Amand, 80 to 90 percent of ingested phosphate is absorbed into the body, which depends on proximal renal tubular function for coordinating the retention or excretion of phosphate according to need. He believes an enzyme, receptor or pump defect leads to systemic buildup of phosphate. Phosphates readily enter cells and maintain balance with phosphates already in the outer mitochondrial chamber. Excess H+ (phosphoric acid in equilibrium with phosphate) in this system would seriously block the movement of H+ from the matrix to the outer chamber. Electron generation and transport for ATP formation depend on reversal of H+ direction back to the matrix. Even a minor inborn error anywhere in the sequence including ATP synthesis would increase susceptibility to phosphate blockages.
A person with cycling fibromyalgia meets full energy demands, on occasion, barely, or not at all. Moments of adequate energy availability permit some bursts of effort, but expenditures from activating any system readily deplete the marginal energy bank. Thus, an accident, emotional stress, infection, or surgery may initiate the first attack of fibromyalgia. In muscle, whatever anion is involved it must be cleared from the cell to allow cessation of activities peculiar to the cell. Failure to remove it forces an attempt by the cell to continue reactions that lead to eventual cellular "fatigue" and malfunction. Muscular contractions of rigor mortis are an extreme example of this process as ATP formation ceases and calcium accumulates freely in the dying structure.
Fibromyalgia and Hypoglycemia
Many people with fibromyalgia gain considerable weight. Arguably, this is due to diminished activity imposed by the disease. However, the multiple, over stimulated areas of fibromyalgia tend to burn fuel steadily. This results in sugar-cravings as a futile attempt to create energy. Increasing carbohydrate intake yields little, due to the impediment to ATP formation. Sugars and starches induce repetitive insulin surges that, in susceptible individuals, initiate a "hypoglycemia" syndrome. Some 40 percent of fibromyalgic females and 20 percent of males suffer from this as manifested by frontal headaches, tremulousness, sweats, heart palpitations or pounding, often with tachycardia and the sudden feeling of anxiety. Symptoms occur a few hours after eating and often at night. Episodes last approximately 20 to 30 minutes.
Studies have reported the release of counter-regulatory hormones during glucose tolerance tests on normal individuals3. Blood samples taken every few minutes showed an epinephrine rise fully 10 minutes before the sample reached its lowest blood sugar level. One-half of these young, healthy subjects became maximally symptomatic as epinephrine neared its peak, some at perfectly normal glucose levels. Every individual has a set point for glucose tolerance. Below this threshold, well-defined, corrective measures are induced by the body. Epinephrine is the trigger for the preceding symptoms, which when most intense, are labeled as "panic attacks.”
Dr. St. Amand notes that the central nervous system becomes accustomed to repetitive hypoglycemic attacks, and as a result, mounts no neurohormonal, counter-regulatory response. Epinephrine symptoms cease, "panic attacks" end, but cognitive disorders continue.4 This situation can only be surmised by the past history. Within two weeks of proper carbohydrate restriction, epinephrine signaling of dietary indiscretion is restored.
According to Dr. St. Amand, this syndrome overlaps strikingly with fibromyalgia but is distinguishable mainly by the epinephrine symptoms. Patients with the dual afflictions do not feel better without dietary control, although examination reveals the anticipated, cyclic resolution of guaifenesin-treated fibromyalgia. Therefore, despite improved physical findings documented on mapping, there would be no change in the standard, patient wellness questionnaire.
Those with carbohydrate cravings, whether or not fully intolerant, suggest an added factor. Insulin causes increased reabsorption of phosphates and sodium in the proximal renal tubules -- a known effect of that hormone. Insulin also drives tryptophan into cells, as it does other amino acids, where they are metabolized. The lowered serum levels of L-tryptophan diminishes availability for brain uptake and formation of serotonin. These higher insulin surges probably account for lowered serum levels of several amino acids as well as serotonin. Thus, the more patients yield to sugar-craving, the more confusing and intense is the interplay of hypoglycemia and fibromyalgia.
Conclusion
According to Dr. St. Amand, Guaifenesin has proven the most effective medication to date for FM. Any source of salicylate will block guaifenesin's benefit at a renal, tubular level as it does in gout. All plants make varying amounts of salicylates, and are readily absorbed through skin.7,8,9,10 Even small amounts in cosmetics and other topicals will negate or slow the effects of guaifenesin. Dr. St. Amand has made many maps during treatment that illustrate lesions becoming static or worsening in previously improving patients who, unwittingly, began using such preparations. Once warned, some patients find that over one-half of their usual skin preparations could have contained salicylates. Susceptibility to phosphate blockade seems genetically determined and highly variable. Some patients are blocked by tiny amounts of offending agents, yet others improve despite moderate usage. Many patients are carbohydrate intolerant and must also be treated with diet.
References
- Physicians' Desk Reference, Medical Economics Co., Inc., Montvale, NJ, 1996.
- Bengtsson, A. and Henriksson, K. G.: The Muscle in Fibromyalgia: A Review of Swedish Studies. J. Rheumatol., 16(Suppl. 19): 144-149, 1989.
- Genter, P. and Ipp, E.: Plasma Glucose Thresholds for Counter regulation After an Oral Glucose Load. Metabolism, 43(1): 98-103, 1994.
- Hvidberg, A., Fanelli, C.G., Hershey, T., et al.: Impact of recent antecedent hypoglycemia on hypoglycemic cognitive dysfunction in nondiabetic humans. 45(1):1030-1036, 1996.
- Eisinger, J.; Plantamura, A.; and Ayavou, T.: Glycolysis abnormalities in fibromyalgia. J.Am. Coll. of Nutri., 13(2)144-148,1994.
- Delaney, T.P. Uknes, S., Vernooij, B., et al.: A central role of salicylic acid in plant disease resistance. Science, 266: 1247-1249, 1994.
- Winter, R.: A Consumer's Dictionary of Cosmetic Ingredients. New York, Crown Trade Paperbacks, 1994
- Taylor J.R., Halprin K.M.: Percutaneous absorption of salicylic acid. Arch. Dermatol. 111(6):740-743, 1975.
- Brubacher J.R., Hoffman R.S.: Salicylism from topical salicylates: review of the literature. J.Toxicol. 34 (4) : 431-436, 1996.
- Yip A.S., Chow W.H., Tai Y.T., Cheung K.L.: Adverse effect of topical methylsalicylate ointment on warfarin anticoagulation: an unrecognized potential hazard. Postgrad Med J. 66 (775): 367-369, 1990.
- Bennett, R.: Poster presentation of the Oregon guaifenesin study, Academy of Rheumatology meeting, Orlando, FL, 1996.
(Source: www.guaidoc.com)
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