Fibromyalgia: Nutritional Support

Fibromyalgia syndrome (FMS) is a rheumatic syndrome that is characterized by generalized musculoskeletal pain and stiffness, chronic aching, fatigue and multiple areas of local tenderness called "tender points" that are easily identified during physical examination. These tender points have become the primary diagnostic factor for FMS. Research studies suggest that FMS may be the result of any condition that could lead to constant muscle hypoxia and it has been postulated that FMS patients may be deficient in certain compounds required for the synthesis of adenosine triphosphate (ATP). Various conventional treatment modalities have been tested in FMS patients, all with poor results. Evidence suggests that FMS patients may be deficient in certain nutrients required for ATP synthesis and the respiratory chain, such as magnesium, malic acid, manganese and thiamin. Nutritional approaches to the treatment of FMS include supplementation with these nutrients to optimize the nutritional status of the patient.

Who's affected by fibromyalgia?

Fibromyalgia syndrome (FMS), a mysteriously debilitating rheumatic syndrome, is taking an increasing toll on our population. The condition, which bears a striking resemblance to chronic fatigue syndrome (CFS), mainly affects women aged 25 to 50 years (female to male ratio is at least 5:1).(1,2) Both syndromes are characterized by a broad spectrum of physical and emotional symptoms, and both are receiving increasing attention from the medical community.(3)

FMS, which is generally classified as a soft tissue musculoskeletal condition,(4) resembles CFS in several ways.(5) Both syndromes plague patients with symptoms of chronic musculoskeletal pain, aching, stiffness, disturbed sleep, depression and fatigue (Table 1).(2,3,5-7) While not all patients experience all symptoms, those with FMS have a peculiar sensation of tenderness in specific areas of their body.(1,2,6-8)

The tender point examination (i.e., tenderness in at least 11 of 18 defined points) has become the primary diagnostic factor for FMS and helps doctors to differentiate the syndrome from CFS.(8) Tender points are localized areas where slight to moderate pressure elicits a sensation of pain. They are located over muscles and tendon insertions, and can range from mildly irritating to completely debilitating (Figure 1).(7,8) Pain in FMS patients has been attributed in part to an unusually high degree of gluconeogenesis. This increased level of muscle tissue breakdown has been hypothesized as one of the main reasons for pain, aching and fatigue.(9)

In order to better understand the origin of the disease, scientists in Sweden have conducted several studies on patients with FMS. Muscle morphology, chemistry, and physiology were carefully examined, as were the most prominent symptoms, including muscle pain, muscle fatigue and muscle stiffness. The authors of a comprehensive review of these studies found that victims of the syndrome appear to have microcirculation disturbances, along with mitochondrial damage and abnormally low phosphate counts -- strongly suggesting an energy deficient state in the muscle tissues.(10) These scientists hypothesized that FMS might be the result of any condition that could lead to constant muscle hypoxia, specifically through the establishment of abnormal motor patterns.

Conventional treatments fall short

Despite long years of research and study, the treatment and management of FMS is still not satisfactory. A tricyclic agent known as amitriptyline has been shown to provide some short-term relief; however, the drug is also known to have adverse side effects, including myocardial infarction, stroke, arrhythmia, coma, seizure and alopecia. Long-term effects of the drug are still not known. One study found ibuprofen to be no more beneficial than a placebo.11 Of the variety of conventional treatment modalities that have been tested on FMS patients, all have yielded unsatisfactory results.

Adenosine triphosphate (ADP) synthesis and the critical role of magnesium

Some research suggests that FMS patients may be deficient in certain compounds required for the synthesis of adenosine triphosphate (ATP).(12) ATP synthesis requires the presence of oxygen, magnesium, substrate, adenosine diphosphate (ADP) and phosphate. Optimal concentrations of each of these allow healthy mitochondrial respiration and the concomitant production of biological energy. Deficiencies, on the other hand, may slow the Krebs cycle, increase anaerobic glycolysis, increase lactic acid formation and cause a reduction of maximum lung capacity. This combination of factors may lead to the symptoms of fatigue, depression and muscle pain.

Some evidence suggests that magnesium, one of the most crucial elements for ATP synthesis, may be below normal ranges in FMS patients.(12,13) Magnesium is a critical nutrient for the production of ATP. Mitochondrial uptake and accumulation of magnesium are directly related to the uptake of phosphate required for ADP phosphorylation. Thus, the entire Krebs cycle is a magnesium-dependent mechanism and even a slight deficiency may potentially impair its optimal function. Related problems caused by magnesium deficiency include mitochondrial swelling, increased membrane permeability, decreased selectivity of mitochondrial innermembrane, uncoupling of oxidative phosphorylation and possibly aluminum toxicity.

Aluminum toxicity

Aluminum toxicity may play a role in symptoms experienced by magnesium-deficient FMS patients since magnesium is needed to help the body block the toxic effects of aluminum. This needs to be acknowledged and addressed, since aluminum inhibits glycolysis and oxidative phosphorylation resulting in decreased intramitochondrial ATP production.(12) Additionally, due to its high affinity for phosphate groups, aluminum blocks the absorption and utilization of phosphates vital to the synthesis of ATP. This may further contribute to the problem of intramitochondrial phosphate deficiency.

Since it has become widely recognized that aluminum overload can lead to major metabolic disturbances, some researchers have carefully studied means of eliminating the toxic metal, especially from the body's vital organs.(14) They found that, in addition to adequate amounts of magnesium (which helps prevent the toxic effects of aluminum), supplemental malic acid may support aluminum detoxification. Malic acid is a known chelator of aluminum.(12)

Magnesium, malic acid and fibromyalgia

The Journal of Nutritional Medicine published a study on the combined effects of magnesium and malic acid on FMS patients.(12) The researchers used oral magnesium and malic acid preparations in an open clinical setting. Fifteen patients (ages 32 to 60) ingested 1,200 to 2,400 milligrams of malic acid with 300 to 600 milligrams of magnesium for a testing period of four to eight weeks. The results of the study were encouraging: all patients reported significant relief of pain within 48 hours of treatment and, within four to eight weeks, all patients had a significant and measurable decrease in the Tender Point Index (TPI). TPI scores were about 20 prior to treatment and between about eight and seven after treatment. Following the eight-week study period, six patients were switched to placebo tablets for an additional two weeks. The TPI values increased from about six to about 21. These results indicate the possibility of a very promising nutritional approach for FMS.

Manganese and thiamin

Fatigue is one of the most prominent features of FMS syndrome, and both CFS and FMS may have a common link in manganese-dependent neuroendocrine changes, especially along the hypothalamic-pituitary thyroid axis.15 The cycle begins with hypothalamic production of thyrotrophin-releasing hormone (TRH). TRH stimulates the pituitary gland to produce thyroid stimulating hormone (TSH), which in turn stimulates thyroid production of thyroxin. This is important, since thyroxin regulates the metabolic rate. And with fatigue as one of the major complaints among both FMS and CFS patients, hypometabolism due to secondary hypothyroidism fits very nicely into this hypothesis. Manganese, which directly influences the metabolic rate through its involvement in this hypothalamic-pituitary-thyroid axis, may therefore be an important trace mineral for CFS and FMS patients.

Thiamin also plays a role in the respiratory chain. In addition, thiamin deficiency symptoms are strikingly similar to many of the symptoms experienced by FMS patients. These include apathy, confusion, fatigue, insomnia, depression, paresthesia (numbness or burning in the hands and feet), low blood pressure, low metabolism and shortness of breath.

Considering the lack of medical treatments and evidence of nutritional factors, it makes sense to implement the use of dietary supplements to optimize the nutritional status of people with FMS. To summarize the first part of our discussion, the nutrients to consider here are:

• Magnesium and malic acid to support ATP synthesis and aluminum detoxification (the addition of vitamin B6 can support this process)
• Manganese to support neuroendocrine changes
• Thiamin to support the respiratory chain

The disease-toxicity connection

As with all degenerative conditions, it is highly beneficial to carefully investigate the relationship between toxicity and the presenting condition. This involves a close look at the role of the GI tract, liver function, lymph and cardiovascular function, nervous system balance (sympathetic/parasympathetic) and immune regulation.

With a functional understanding of the important role each of these systems play in both the onset and effective management of FMS, and indeed most degenerative illnesses, it becomes clear that a comprehensive clinical approach is required. Such an approach focuses on the following characteristics:

• Mental/emotional states and effective stress management skills
• Dietary patterns, i.e., diet (with careful attention to both macro- and micronutrient balance) and dietary habits (with attention to habits that facilitate or inhibit proper digestion)
• Postural and exercise habits and biomechanics

The clinical thrust is to restore key organ system function, and in the case of FMS, special attention should be given to resuscitating mitochondrial function. In addition, some evidence suggests that cardiovascular fitness training can help alleviate some of the symptoms of FMS as well. According to a study published in the American Journal of Medicine, "It is concluded that cardiovascular fitness training is feasible in patients with fibrositis/fibromyalgia and that such training improves subjective measurements of pain-reporting behavior."(16) In addition to nutritional support and mild exercise, massage, heat treatments and rest may also help. Improvements resulting from these treatment modalities can be measured by decreased sensitivity at the tender points and improved stamina, energy and mobility.

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References

1. Smythe HA. Nonarticular Rheumatism and Psychogenic Musculo- skeletal Syndromes. In: McCarty DJ, ed. Arthritis and Allied Conditions. 9th ed. Philadelphia: Lea & Febiger, 1989:1241-54.

2. Wolfe F. The clinical syndrome of fibrositis. Am J Med 1986;81:7-13.

3. Masi AT, Yunus MB. Concepts of illness in populations as applied to fibromyalgia syndromes. Am J Med 1986;81:19-25.

4. Campbell SM, et al. Clinical characteristics of fibrositis. A blinded controlled study of symptoms and tender points. Arthritis Rheum 1983;26:817-24.

5. Goldenberg DL, et al. High frequency of fibromyalgia in patients with chronic fatigue seen in a primary care practice. Arthritis Rheum 1990;33:381-87.

6. Henrikson KG, Bengtson A. Fibromyalgia - a clinical entity? Can J Physiol Pharmacol 1991;69:672-77.

7. Smythe HA. "Fibrositis" and Other Diffuse Musculoskeletal Syndromes. In: Kelley WN, et al., eds. Textbook of Rheumatology. 1st ed. Philadelphia: WB Saunders, 1985:481-89.

8. Wolfe F, et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum 1990;33:160-72.

9. Lund N, et al. Muscle tissue oxygen pressure in primary fibromyalgia. Scand J Rheumatol 1986;15:165-73.

10. Bengtson A, Henrikson KG. The muscle in fibromyalgia-A review of Swedish studies. J Rheumatol 1989;16 (suppl 19):144-49.

11. Yunus MB, et al. Short term effects of ibuprofen in primary fibromyalgia syndrome. J Rheumatol 1989;16:527-32.

12. Abraham GE, Flechas JD. Management of fibromyalgia: rationale for the use of magnesium and malic acid. J Nutr Med 1992;3:49-59.

13. Romano TJ, et al. Magnesium deficiency in fibromyalgia syndrome. J Nutr Med 1994;4:165-67.

14. Domingo JL, et al. Citric, malic and succinic acids as possible alternatives to deferoxamine in aluminum toxicity. Clin Tox 1988;26:67-79.

15. Ferraccioli G, et al. Neuroendocrinologic findings in primary fibromyalgia (soft tissue chronic pain syndrome) and in other chronic rheumatic conditions (rheumatoid arthritis, low back pain). J Rheumatol 1990;17:869-73

16. McCain GA. Role of physical fitness training in the fibrosis/ fybromyalgia syndrome. Am J Med 1986;81:73-77.

 

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