Fibromyalgia: Causes & Protocols: Part I

References

According to the American College of Rheumatology, fibromyalgia is a common condition that originates in muscles and soft tissues and is associated with widespread aching, stiffness and fatigue. People with fibromyalgia are found to have multiple tender points in specific muscle areas. Most individuals complain of aching and stiffness in areas around the neck, shoulders, upper back, lower back and hip areas. Many patients have no underlying disorders, while others who develop fibromyalgia may have conditions such as rheumatoid arthritis, spinal arthritis or Lyme disease. Some people have symptoms of irritable bowel syndrome, tension headaches and numbness or tingling of the extremities. Depression is also not unusual in fibromyalgia patients.

Researchers believe there isn’t a single cause of fibromyalgia. Rather, a number of factors may contribute. Some people with fibromyalgia appear to have alterations in the regulation of certain neurotransmitters, particularly serotonin, which is linked to depression, migraines and gastrointestinal distress; and substance P, a brain chemical associated with pain, stress and anxiety, as well as depression.

Disturbed sleep patterns may also be a cause, rather than just a symptom, of fibromyalgia. Some researchers believe a viral or bacterial infection may trigger fibromyalgia; although no single viral or bacterial agent has been implicated, it may be that a number of such agents are capable of triggering fibromyalgia. Abnormalities of the autonomic (sympathetic) nervous system may play a role, while other possible causes include changes in muscle metabolism, such as deconditioning and decreased blood flow, psychological stress, hormonal changes, and injury or trauma, particularly in the upper spinal region. Since any combination of the aforementioned factors may play a role in the etiology of fibromyalgia, a multifaceted treatment approach may be necessary.

Despite the prevalence of fibromyalgia, no drugs have been developed or approved specifically for its treatment. Therefore, doctors presently prescribe a wide variety of medications to treat specific symptoms of fibromyalgia. For example, because sleep disturbance is common in fibromyalgia, some of the most effective remedies are those that promote restful sleep. But traditional sleep aids aren’t necessarily the answer. Many doctors and patients find that some antidepressants, including tricyclic antidepressants, as well as benzodiazepines can promote deep, restorative sleep when taken at bedtime. Also, selective serotonin reuptake inhibitors (SSRIs) may be taken along with tricyclics to increase energy. Muscle relaxants and other medications may be used to decrease muscle pain and spasms experienced by many people with the condition, and a seizure medication called gabapentin (Neurontin) may ease the leg pain, numbness and tingling sensations that come with the condition.

One of the major categories of complementary or alternative treatments for fibromyalgia is the natural serotonin modulators, including L-tryptophan, 5-HTP, and Hypericum perforatum (St. John’s wort). Evidence from multiple sources supports the concept of decreased flux through the serotonin pathway in fibromyalgia patients. The use of serotonin substrates plays a correcting role in aforementioned chemical changes in the brain relating to serotonin. In addition, the improvement in quality sleep that is likely to occur from supplementation may also help correct the abnormally low levels of somatomedin C. Serotonin substrate supplementation, via L-tryptophan (1,500 mg daily) or 5-hydroxytryptophan (5-HTP, 100 mg three times daily), has been shown to improve symptoms of depression, anxiety, insomnia and somatic pains in a variety of patient cohorts. Identification of low serum tryptophan and serotonin levels may be a simple way to identify persons who will respond well to this approach.^1,2,3,4

The clinical evidence is overwhelming in favor of St. John’s wort (300 mg, three times daily) as a relatively risk-free antidepressant suited for the treatment of mild to moderate depression. This alone may be beneficial for fibroymaliga patients with this type of depression. Of particular interest is one of hypericum’s mechanisms of action. Namely, a primary mechanism of action seems to be that it increases serotonin levels, much by the same mechanism of action that Prozac® exerts.⁵ Such an increase may be beneficial for fibromyalgia patients in any case. In addition, Hypericum has demonstrable antiviral properties,⁶ another potential benefit for fibromyalgia patients.

Fibromyalgia patients also appear to have low levels of vitamin B12; studies report women with fibromyalgia and CFS have increased homocysteine levels and increased fatiguability.⁷ Others have been observed to have high hair calcium and magnesium levels, indicative of low corresponding tissue levels; supplementation with the minerals may be indicated to help with tender points.⁸ Other research has revealed individuals with fibromyalgia had a lower average bone mineral density than matched controls; and a higher incidence of osteoporosis in subjects 51-60 years of age.⁹ The authors of the study concluded “early detection and implementation of appropriate nutritional supplementation (calcium/vitamin D), resistive and weight bearing exercise, and specific bone mineral enhancing pharmacological therapy may be indicated in pre, peri, and postmenopausal subjects.”

In recent years, evidence has accumulated to suggest fibromyalgia may be, at least in part, the result of local hypoxia (oxygen deficiency) in the muscles. It has been hypothesized that in hypoxic muscle tissues part of energy metabolism is inhibited, reducing ATP synthesis. This stimulates a process which results in the breakdown of muscle proteins to amino acids that can be utilized to make ATP. This muscle tissue breakdown, which has been observed in muscle biopsies taken from fibromyalgia patients, is hypothesized to result in the muscle pain characteristic of fibromyalgia.^10,11

Malic acid (magnesium malate) is a natural substance both derived from food sources and synthesized in the body though the citric acid cycle. Since it plays a central role in energy production, especially during hypoxic conditions, malic acid supplements have been examined for their effects on fibromyalgia.

Subjective improvement in pain was observed within 48 hours of supplementation with 300 to 600 mg magnesium and 1,200 to 2,400 milligrams of malic acid; this improvement was lost following the discontinuation of malic acid for 48 hours.¹² While this study also used magnesium supplements, due to the fact that magnesium is often low in fibromyalgia patients, the rapid improvement following malic acid, as well as the rapid deterioration after discontinuation, suggests that malic acid is the most important component. A double blind trial by the same research group using 300 mg magnesium and 1,200 mg malic acid per day found no reduction in symptoms, suggesting the higher dosages may be necessary.¹³

S-adenosyl-L-methionine (SAMe) is a natural molecule synthesized from the amino acid methionine in the presence of magnesium and adenosine triphosphate (ATP). A study of 17 fibromyalgia patients revealed a significant improvement in both pain at trigger points and depression following SAMe treatment.¹⁴ In another study, 34 fibromyalgia patients receiving SAMe experienced improvement in pain and overall well being, although these improvements were not considered “statistically significant.”¹⁵ It is interesting to note that several of the symptoms that SAMe is know for treating—such as inflammation, moodiness, pain and migraine headaches— are also present in fibromyalgia.

Many practitioners have recognized that true progress will not be made in the treatment of fibromyalgia until correction of the sleep disturbances first takes place. Hence it is not surprising that researchers have tested melatonin supplementation on fibromyalgia patients in a preliminary trial.¹⁶ When 3 mg of melatonin was given at bedtime, there was a reduction in tender points, and an improvement in sleep and other measures of disease severity (though pain and fatigue improved only slightly).

It is hypothesized that the relative deficiency in the branched chain amino acids (BCAAs) may play a role in the pathophysiology of fibromyalgia, since the BCAAs supply energy to the muscle and regulate protein synthesis in the muscles. In one study, patients with fibromyalgia had significantly lower plasma concentrations of the three BCAAs (valine, leucine and isoleucine) and phenylalanine than did normal controls.¹⁷ The authors of the study stated, “A supplemental trial with BCAAs in fibromyalgia appears to be justified.”

References

"Fibromyalgia: Causes & Protocols: Part I" References

1. Juhl JH. "Fibromyalgia and the serotonin pathway." Alt Med Rev. 3, 5:367-75, 1989.

2. Puttini PS, Caruso I. "Primary fibromyalgia syndrome and 5-hydroxy-L-tryptophan: a 90-day open study." J Int Med Res. 20, 2:182-9, 1992.

3. Byerley WF et al. "5-Hydroxytryptophan: a review of its antidepressant efficacy and adverse effects." J Clin Psychopharmacol. 7, 3:127-37, 1987.

4. Caruso I et al. "Double-blind study of 5-hydroxytryptophan versus placebo in the treatment of primary fibromyalgia syndrome." J Int Med Res. 18, 3:201-9, 1990.

5. Müller W, Rossol R. "Effects of Hypericum extract on the expression of serotonin receptors." J Geriatr Psychiat Neurol. 7, Suppl 1:S63-4, 1994.

6. Mills S, Bone K. Principles and Practice of Phytotherapy. Churchill Livingstone, Edinburgh, Scotland, 2000.

7. Regland B et al. "Increased concentrations of homocysteine in the cerebrospinal fluid in patients with fibromyalgia and chronic fatigue syndrome." Scand J Rheumatol. 26, 4:301-7, 1997.

8. Ng SY. "Hair calcium and magnesium levels in patients with fibromyalgia: a case center study." J Manipulative Physiological Ther. 22, 9:586-93, 1999.

9. Swezey RL, Adams J. "Fibromyalgia: a risk factor for osteoporosis." J Rheumatol. 26, 12:2642-4, 1999.

10. Eisinger J, Plantamura A, Ayavou T. "Glycolysis abnormalities in fibromyalgia." J Am Coll Nutr. 13, 2:144-8, 1994.

11. [No author listed]. "Is fibromyalgia caused by glycosis impairment?" Nutr Rev. 52, 7:248-50, 1994.

12. Abraham G, Flechas J. "Management of fibromyalgia: Rationale for the use of magnesium and malic acid." J Nutr Med. 3:49-59, 1992.

13. Russell J et al. "Treatment of fibromyalgia syndrome with SuperMalic: A randomized, double-blind, placebo-controlled, crossover pilot study." J Rheumatol. 22, 5:953-7, 1995.

14. Tavoni A et al. "Evaluation of S-adenosylmethionine in primary fibromyalgia. A double-blind crossover study." Am J Med. 83, 5A:107-10, 1987.

15. Volkmann H et al. "Double-blind, placebo-controlled crossover study of intravenous S-adenosyl-L-methionine in patients with fibromyalgia." Scand J Rheum. 26, 3:206-11, 1997.

16. Citera G et al. "The effect of melatonin in patients with fibromyalgia: a pilot study." Clin Rheumatol. 19: 9-13, 2000.

17. Maes M et al. "Branched-chain-amino acids in fibromyalgia." Psychiatry Res. 97, 1:11-20, 2000.

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