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LETTER TO THE EDITOR

The Effect of Coenzyme Q10 on Symptoms of Mother and Son with Fibromyalgia Syndrome

, , , , , & show all
Pages 118-119 | Published online: 23 Mar 2011

To the Editor

Coenzyme Q10 [CoQ10] plays a crucial role in cellular metabolism, acting as the electron carrier between complexes I and II and complex III of the mitochondrial respiratory chain, and regulates uncoupling proteins, the transition pore, β-oxidation of fatty acids, and nucleotide pathway. Additionally, it has antioxidant and membrane-stabilizing properties (Citation1). CoQ10 is often reduced in patients with myopathy, either as a primary or a secondary event (Citation2), and patients with all forms of CoQ10 deficiency [primary and secondary] have shown clinical improvements after initiating oral CoQ10 supplementation (Citation3), and have been observed to experience a decrease in muscle pain associated with statin treatment by CoQ10 supplementation (Citation4).

Fibromyalgia syndrome [FMS] is a common chronic pain syndrome accompanied by other symptoms such as fatigue, headache, sleep disturbances, and depression. It is diagnosed according to the classification criteria established by the American College of Rheumatology (Citation5). Pathophysiological mechanisms of FMS are difficult to identify, and current drug therapies demonstrate limited effectiveness, so drugs used to treat FMS have been focused to the management of single symptoms. Recently, we have observed CoQ10 deficiency in blood mononuclear cells [BMCs] in FMS patients (Citation6). Oral CoQ10 supplementation in FMS seemed to provide beneficial effects in FMS patients in a previous pilot study, although this could be also due to the presence of Ginkgo biloba (7).

We now describe the results of oral CoQ10 supplementation in mother and son patients with FMS and CoQ10 deficiency. Four years ago, a mother, a 42-year-old woman, and son, a 16-year-old boy, were diagnosed with FMS by exclusion of other diseases and syndromes and in accordance with the American College of Rheumatology. The mother had daily episodes of intense musculoskeletal pain, stiffness, anxiety, migraine, and sleep disturbance. The son had daily episodes of intense musculoskeletal pain and sleep disturbance. Routine laboratory test yielded normal results. For treatment, they only used paracetamol on demand. Their visual analog scale scores were 7 and 6, respectively. The Fibromyalgia Impact Questionnaire scores were 60 and 51, respectively, and tender points were 17 and 11, respectively []. Both mother and son participated in a study on mitochondrial dysfunction in BMCs showing higher levels of mitochondrial reactive oxygen species production and lipid peroxidation, reduced mitochondrial membrane potential and mitochondrial mass, low levels of CoQ10, and higher levels of mitochondrial degradation [mitophagy] (Citation6). Oxidative stress and mitochondrial degradation were reduced by CoQ10 supplementation in BMCs (Citation6).

Table 1 Charasteristic Findings of the Patients Pre- and Post-treatment with CoQ10

After informed consents were obtained, both mother and son were treated with 300 mg CoQ10 divided in three doses. They experienced no adverse effects, and after three months, both mother and son reported a decrease in their symptoms. Specifically, they noted an improvement in sleep, mental alertness, a marked decrease in joint pain, and decrease of episodes and intensity of headache. After six months of treatment, the patients were evaluated and we observed an important decrement in visual analog scale, Fibromyalgia Impact Questionnaire, and tender point scores, given in . Lipid peroxidation in BMCs was significantly reduced by 56 percent in the mother and by 42 percent in the son, and CoQ10 levels were increased in BMCs by 71 percent in the mother and by 79 percent in the son.

At the time of this writing, the patients were continuing to take CoQ10 and were satisfied that the symptoms had abated. According to our results, we think that CoQ10 might be a promising therapeutic agent in the treatment of symptoms in patients with FMS and CoQ10 deficiency.

Mario D. Cordero

Centro Andaluz de Biología del Desarrollo

Universidad Pablo de Olavide-CSIC

Carretera de Utrera Km 1, Sevilla 41013, Spain

Email: [email protected]

REFERENCES

  • Turunen M, Olsson J, Dallner G: Metabolism and function of coenzyme Q. Biochim Biophys Acta 1660:171–199, 2004.
  • Littarru GP, Tiano L: Clinical aspects of coenzyme Q10: an update. Nutrition 26: 3:250–254, 2010.
  • Haas RH: The evidence basis for coenzyme Q therapy in oxidative phosphorylation disease. Mitochondrion 7 Suppl:S136–S145, 2007.
  • Caso G, Kelly P, McNurlan MA, Lawson WE: Effect of coenzyme q10 on myopathic symptoms in patients treated with statins. Am J Cardiol 99: 10:1409–1412, 2007.
  • Wolfe F, Smythe HA, Yunus MB, Bennett RM, Bombardier C, Goldenberg DL, Tugwell P, Campbell SM, Abeles M, Clark P, Fam AG, Farber SJ, Fiechtner JJ, Franklin CM, Gatter RA, Hamaty D, Lessard J, Lichtbroun AS, Masi AT, McCain GA, Reynolds WJ, Romano TJ, Russell IJ, Sheon RP: The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Arthritis Rheum 33:160–172, 1990.
  • Cordero MD, De Miguel M, Moreno-Fernández AM, Carmona-López IM, Garrido-Maraver J, Cotán D, Gómez Izquierdo L, Bonal P, Campa F, Bullon P, Navas P, Sánchez-Alcázar JA: Mitochondrial dysfunction and mitophagy activation in blood mononuclear cells of fibromyalgia patients: implication in the pathogenesis of the disease. Arthritis Res Ther 12: 1:R17, 2010.
  • Lister RE: An open, pilot study to evaluate the potential benefits of coenzyme Q10 combined with Ginkgo biloba extract in fibromyalgia syndrome. J Int Med Res 30: 2:195–199, 2002.

Fibromyalgia Syndrome and Coenzyme Q10: Out of the Labyrinth?

Fibromyalgia syndrome [FMS] is a multifactorial condition, often associated with perpetuating factors such as peripheral stimuli [myofascial trigger points] or chronic illness [hypothyroidism and resistance to insulin (Citation1)]. Several biological abnormalities have been reported in FMS with respect to neurotransmitters [substance P (Citation2)], free radical production [malondialdehyde (Citation3)], or cellular signaling disorders (Citation4).

On the other hand, therapeutics based on antioxidant agents, such as magnesium, selenium, taurine, and vitamin A or E, are without effect in our experience, whereas adenosylmethionine and superoxide dismutase are poorly efficient in FMS. A recent trial on coenzyme Q10 [CoQ10] demonstrates that this treatment is efficient in a FMS patient family group associated with blood CoQ10 changes (Citation5).

The number of potential variables linked to FMS metabolic disorders is considerable, and their management is complex. However, even if CoQ10 effects on Parkinson's disease or chronic fatigue syndrome are controversial, new therapeutic approaches are promising and need further investigations.

J Eisinger, D Starlanyl and T Ayavou

Hôpital G. Clemenceau BP1412

83056 Toulon, France

REFERENCES

  • Starlanyl DJ, Copeland ME: Fibromyalgia and Chronic Myofascial Pain: A Survival Manual. New Harbinger, Oakland, 2001.
  • Russell IJ: Neurochemical pathogenesis of fibromyalgia syndrome. J Musculoskelet Pain 4: 1/2:61–92, 1996.
  • Eisinger J, Gandolfo C, Zakarian H, Ayavou T: Reactive oxygen species, antioxidant status and fibromyalgia. J Musculoskelet Pain 5:5–11, 1997.
  • Eisinger J. Fibromyalgia: Terra incognita. J Musculoskelet Pain 14: 4: 2006.
  • Cordero MD, Alcocer-Gómez E, Cano-García FJ, de Miguel M, Campa F, Bonal P, Moreno Fernández AM: The effect of coenzyme Q10 on symptoms of mother and son with fibromyalgia syndrome. J Musculoskelet Pain, 19:2-118–119.
  • Lister RE: An open, pilot study to evaluate the potential benefits of coenzyme Q10 combined with Ginkgo biloba extract in fibromyalgia syndrome. J Int Med Res 30: 2:195–199, 2002.

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