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Journal of the American College of Nutrition, Vol. 17, No. 3, 300-303 (1998)
Published by the American College of Nutrition

Letter

Fibromyalgia—A Hidden Link?

Barbara A. Monroe, MS, RD, CNSD

Nutrition Department
Spaulding Rehabilitation Hospital
Boston, MA

A number of similarities exist between Fibromyalgia (FM) and thiamin deficiency. They include irritability, frequent headaches, unusual fatigue, muscle tenderness upon pressure palpitation, muscular weakness, irritable bowel syndrome, and sleep disturbances [1–3]. Studies published in JACN have demonstrated abnormalities of thiamin metabolism in FM [4,5]. Thiamin deficiency, in developed society, stems mostly from excessive alcohol intake. It is suggested that studies be done to look at both alcohol consumption and thiamin status in patients diagnosed with FM. The literature currently lacks this type of investigation in FM.

REFERENCES

  1. Tanphaichitr V: Thiamin. In Shils EM, Olson JA, Shike M (eds): "Modern Nutrition in Health and Disease," 8th ed. Philadelphia: Lea & Febiger, pp 359–365, 1994.
  2. Anderson CE: Vitamins. In Schneider HA, Anderson CE, Coursin DB (eds): "Nutritional Support of Medical Practice." New York: Harper & Row, pp 24–56, 1977.
  3. Wolfe F, Ross K, Anderson J, Russell IJ: Aspects of fibromyalgia in the general population: sex, pain threshold, and fibromyalgia symptoms. J Rheum 22: 151–156, 1995.[Medline]
  4. Eisinger J, Plantamura A, Ayavou T: Glycolysis abnormalities in fibromyalgia. J Am Coll Nutr 24(2): 144–148, 1994.
  5. Eisinger J, Ayavou T: Transkctolase stimulation in Fibromyalgia. J Am Coll Nutr 9(1): 56–57, 1990.[Medline]
 

Response

Jean Eisinger, MD, FACN

Service de Rhumatologie,
Centre Hospitalier de Toulon-La Seyne,
BP 1412-F 83056 Toulon FRANCE

Author’s Reply

Alcohol, Thiamin and Fibromyalgia

Fibromyalgia (FM) symptoms such as widespread muscular pain and fatigue or sleep disorders have been explained, in part, by neurotransmitters and muscle metabolism abnormalities.

A "hidden link" between FM and excessive alcohol intake has been hypothesized by Monroe [1] that could be in line with several findings: 1) eating disorders and, to a lesser extent, alcohol abuse have been demonstrated in FM, correlated with increased prevalence of previous physical or sexual abuse, in a comparative study vs. other rheumatic diseases [2]. It is noteworthy that FM clinical improvement has been reported by some patients with low doses of aperitif or wine [3]; 2) excessive alcohol intake induces energy metabolism, antioxidant defenses and vitamin B1 abnormalities [4] similar to these observed in FM [5–11].

However, alcohol usually aggravates FM [3] and FM patients are probably not heavy drinkers since blood transaminases or erythrocyte volume are unchanged and gamma glutamyl transferases are markedly increased in less than 8% of our patients (Mechtouf K, in press). Similarly, lipid peroxidations as well as magnesium (Mg) or vitamin deficiency associated with chronic alcoholism are not observed in FM: leucocyte Mg, vitamin A or E values are increased, erythrocyte Mg or vitamin B2 status are only slightly impaired [5,6] and malondialdehyde or vitamin B6 status [6,7], 25 hydroxyvitamin D, cobalamin or folates [12] are normal. Moreover, we have demonstrated [7–10] several significant differences between FM patients and biological findings in alcoholics (Table 1) [5,6].


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  		Table 1. Energy Metabolism and B Vitamin (Whole Blood, Plasma or Erythrocytes*) Investigations in Fibromyalgia (FM) and Chronic Alcoholics

 
Therefore the vitamin B1 abnormalities demonstrated in FM [7,10] are not induced by nutritional deficiency (low dosages of thiamin, per os or IM, are poorly [11] efficient) and are probably related to a reduced activation of thiamin into thiamin pyrophosphate (cocarboxylase), linked to high energy phosphates deficit [5,13] (Fig. 1). On the other hand, the significant decrease of thiamin-dependent enzymes affinity for cocarboxylase reported in FM [10,14] similar to that observed in Wernicke-Korsakoff or senile dementia [10,15], is related to structural enzymatic abnormalities.



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  		Fig. 1. Nutritional factors impairing B1 metabolism include mainly alcohol or excessive intake of carbohydrates. Transketolase (B1 dependent) abnormalities induce pentose pathway impairment and nicotinamide adenosine dinucleotide phosphate reduced (NADPH) deficit. NADPH is involved in reduced glutathione (GSH) and nitric oxid (NO) synthesis and therefore in muscle microcirculation and antioxidant defenses. Pyruvate dehydrogenase (B1 dependent) abnormalities induce adenosine triphosphate (ATP) deficit. ATP is involved in phosphorylations (peculiarly B1 activation) and performances. Thiamin deficiency is associated with brain serotonin depletion. Serotonin is involved in pain perception, mood and nutritional habits. It is noteworthy that pain and fatigue induce detraining that aggravates these metabolic abnormalities.

Details in reference 6 and 10.

 
These complex thiamin abnormalities might explain reduced nitric oxid (and impaired muscle relaxation and microcirculation) or glutathione (and muscle soreness) [6], impaired glycolysis (and muscle fatigue) [5] or even serotonin depletion (and decreased pain threshold) [10] observed in FM.

Whatsoever, even if excessive alcohol intake is not a FM risk factor, conversely to hypothyroidism or detraining, appropriate metabolic treatment is needed, particularly when blood pyruvate is elevated [5]. Cocarboxylase (IM or sublingual) is markedly more efficient than thiamin alone [11] or magnesium [16] and further studies on other B vitamins (pyridoxal phosphate, riboflavine, folates, thioctic acid), minerals (Mg, manganese, selenium), amino acids (arginine, S-adenosyl methionine, cysteine) or drugs stimulating pyruvate dehydrogenase activity (trimetazidine, carnitine) and phosphorylations (phosphocreatinine, piracetam) are needed [6,10,15].

Thiamin and its derivatives have been prescribed for years in order to treat neurotransmitter dysfunction and chronic pain [15,17–19] or to improve glycolysis abnormalities and athletic performances [5,20], with significant results and few adverse effects. Even, if cocarboxylase is not easily available, there is no reason to deprive FM patients of a treatment more appreciated [16] than antidepressants.

REFERENCES

  1. Monroe BA: Fibromyalgia—A Hidden Link? J Am Coll Nutr 17: 300, 1998.[Free Full Text]
  2. Boisset-Pioro MH, Esdaile JM, Fitz-Charles MA: Sexual and physical abuse in women with fibromyalgia syndrome. Arthritis Rheum 38: 235–241, 1995.[Medline]
  3. Mechtouf K, Collard O, Eisinger J: Depression and pain evolution in Fibromyalgia. Z Rheumatol, 56: 378, 1997.
  4. Lieber CS: Alcohol, liver and nutrition. J Am Coll Nutr 10: 602–632, 1991.[Abstract]
  5. Eisinger J, Plantamura A, Ayavou T: Glycolysis abnormalities in fibromyalgia. J Am Coll Nutr 13: 144–148, 1994.[Abstract]
  6. Eisinger J, Gandolfo C, Zakarian H, Ayavou T: Reactive oxygenspecies, antioxidant status and fibromyalgia. J Musculoske Pain 5(4): 5–15, 1997.[Medline]
  7. Eisinger J, Zakarian H, Mathieu F, Ayavou T: Statut vitaminique B1 B6 et pathologie fonctionnelle. Lyon Med Med 25: 12365–12369, 1989.
  8. Eisinger J, Clairet D, Zakarian H, Ayavou T: ATP érythrocytaire et appareil locomoteur: action de la calcitonine. Lyon Med Med 26: 326–328, 1990.
  9. Eisinger J, Plantamura A, Arroyo PH, Arroyo H, Ayavou T: Thiamine pyrophosphate (TPP), enzymes TPP-dependants et pathologie neuromusculaire. Lyon Med Med 29: 1319–1321, 1993.
  10. Eisinger J, Zakarian H, Plantamura A, Clairet D, Ayavou T: Studies of transketolase in chronic pain. J Adv Med 5: 105–114, 1992.
  11. Eisinger J, Ayavou T: Transketolase stimulation in fibromyalgia. J Am Coll Nutr 9: 56–57, 1990.[Medline]
  12. Bengtsson A, Henriksson CG, Jorfeldt L, Kagedal B, Lennmarken C, Lindstrom F: Primary fibromyalgia. A clinical and laboratory study of 55 patients. Scand J Rheumatol 15: 340–347, 1986.[Medline]
  13. Russell IJ, Vipraio GA, Abraham GE: Red cell nucleotide (RCN) abnormalities in fibromyalgia syndrome (FS). Arthritis Rheum 36: S223, 1993.
  14. Eisinger J, Ayavou T, Zakarian H, Plantamura A: Thiamin-dépendent enzymes abnormalities in fibromyalgia. J Musculoske Pain 3(S1): 112, 1995.
  15. Eisinger J: Thiamin and cognitive impairment. J Am Coll Nutr 16: 96–98, 1997.[Medline]
  16. Mechtouf K, Collard O, Eisinger J: Pain treatment in Fibromyalgia. Z Rheumatol 56: 377, 1997.
  17. Quirin H: Pain and vitamin B1 therapy. Biblthca Nutr Dieta 387: 110–111, 1986.
  18. Sbinden G: Therapeutic use of vitamin B1 in diseases other than beriberi. Ann NY Acad Sci 98: 551–561, 1962.
  19. Lonsdale D: Allithiamin and its synthetic derivatives. J Nutr Med 2: 305–311, 1991.
  20. Howald H: Moyens d’influences médicales pharmacologiques de la performance dans le sport d’élite. Med et Hyg 37: 3274–3279, 1979.



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Fibromyalgia--A Hidden Link?
J. Am. Coll. Nutr., June 1, 1998; 17(3): 300 - 303.
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