Metabolic Basis for Fibromyalgia
Thyroid hormones and skeletal muscle-new insights and potential implications.    2014 Apr;10(4):206-14. doi: 10.1038/nrendo.2013.238. Epub 2013 Dec 10.

In The Thyroid Solution by Ridha Arem, M. D he states, “Thyroid hormone imbalance affects the functioning of most bodily organs How severely it affects organs, however, differs from one person to the next Imagine two people having the same level of hypothyroidism They may have some symptoms in common, such as dry skin, constipation , and weight gain One of them, however, may have severe headaches, which then become the main concern for both the patient and the physician Joint and muscle pain is another symptom that often triggers unnecessary testing and leads to the wrong diagnosis Doctors frequently consider neurological or rheumatologica conditions in such patient rather than a thyroid condition. Because many of the emotional and physical symptoms are also symptoms of fibromyalgia and chronic fatigue syndrome (conditions that typically cause severe fatigue), hypothyroid patients may also end up misdiagnosed with one of these two conditions.”

Chronic Fatigue Syndrome, Fibromyalgia, and Autoimmune Thyroid Disease

Mary Shomon's Practitioner Perspectives Series Fibromyalgia Aches and Pains as a "Symptom" of Hypothyroidism:

The Journal of Family Practice Letters

Further studies on the treatment of fibromyalgia

To the editor:
I wish to comment upon the POEM “Useful treatments for fibromyalgia syndrome” (J Fam Pract 2005; 54:105, citing JAMA 2004; 292:2388–2395).1 Drs Goldenberg, Burckhardt, and Crofford did only a partial job of covering the readily accessible literature. Unfortunately, a useful set of randomized controlled trials2-4 escaped their search strategy. Furthermore, there is a major error in their conclusions that is inconsistent with the body of the discussion.

In 1997 the cause of the symptoms of fibromyalgia was strongly linked to partial peripheral resistance to thyroid hormone in 3 studies published in an off-Medline journal, the Clinical Bulletin of Myofascial Therapy. This choice of journals, a regrettable decision, consigned the studies to obscurity.

Barnes5 first suggested, because of observed high rates of hypometabolism, that resistance to thyroid hormone must be fairly common. That same year, the famous Albright6 guessed the same thing for the same reason given by Barnes. In 1981 Kaplan7 finally reported the biological parameters of a prototypical case. Since then, textbooks in endocrinology and thyroid disease in particular8 make routine reference to thyroid hormone resistance. While the emphasis in these texts is upon genetic lesions, acquired lesions are also suggested.

Our research group9 has given doses far in excess of those given to the Kaplan patient, ranging up to 1350 μg of liothyronine (T3) (T4 equivalence 5400 μg) on multiple occasions without thyrotoxic effects. This is prima facie evidence that we have learned to accurately recognize partial peripheral resistance to thyroid hormone, for the consequences of this dosing would otherwise be catastrophic. The 3 studies cited above2-4 exhaustively document our initial experience with subjects in doses up to 150 μg of liothyronine (T3) (T4 equivalence 600 μg). Symptomatic responses of these patients were dramatically clinically significant as well as statistically significant to tiny values of P.

This establishes thyroid hormone resistance as the most evidence-based proposed cause of fibromyalgia. I know of no evidence refuting this. Also, this information is available from Cochrane, so the authors’ search strategy failed. Lastly, our group has had personal communication with the authors, and still they do not acknowledge it.

Thyroid hormone resistance is the most evidence-based proposed cause

Since 1997 our group has concentrated upon refinement of the use of supraphysiological doses of thyroid hormone for the ablation of fibromyalgia symptoms. We have also worked out much of the biological bases of the acquired causes of thyroid resistance. This latter work10 is summarized in a recent review. Thus the state of the art has moved beyond establishing the etiology of fibromyalgia as T3 resistance, to the causes and successful treatments of that resistance.

As for the error in the conclusions of this review, the paper states that there is strong evidence for efficacy of tricyclic antidepressants (TCAs). In the discussion, however, it is correctly noted that there is no evidence for such efficacy except in the first 12 weeks of treatment; even then only a tiny percentage respond. After that, there is no difference between TCA and placebo. I wish the myth of TCA effectiveness would go away, but this paper perpetuates it.

Richard L. Garrison, MD
San Jacinto Methodist Hospital, Family Practice
Residency Training Program; Baylor College of
Medicine, Department of Family and Community
Medicine, Baytown, Texas


  • Goldenberg DL, Burchhardt C, Crofford L. Management of fibromyalgia syndrome. JAMA 2004;292:2388–2395.
  • Lowe JC, Garrison RL, Reichman AJ, Yellin J, Thompson M, Kaufman D. Effectiveness and safety of T3 (triiodothyronine) therapy for euthyroid fibromyalgia: a double-blind placebo-controlled response-driven crossover study. Clin Bull Myofascial Ther 1997;2:31–58.
  • Lowe JC, Reichman AJ, Yellin J. The process of change during T3 treatment for euthyroid fibromyalgia: a double-blind placebo-controlled crossover study. Clin Bull Myofascial Ther 1997;2:91–124.
  • Lowe JC, Garrison RL, Reichman AJ, Yellin J. Triiodothyronine (T3) treatment of euthyroid fibromyalgia: a small-n replication of a double-blind placebo-controlled crossover study. Clin Bull Myofascial Ther 1997;2:71–88.
  • Barnes BO. Basal temperature versus basal metabolism. JAMA 1942;119:1072–1074.
  • Albright F, Burnett CH, Smith PH, Parson W. Pseudohypoparathyroidism: an example of “Seabright-Bantam syndrome.” Endocrinology 1942;30:922–932.
  • Kaplan MM, Swartz SL, Larsen PR. Partial peripheral resistance to thyroid hormone. Am J Med 1981;70:1115–1121.
  • Usala SJ. Thyroid hormone resistance syndromes. In: SA Falk (ed). Thyroid Disease: Endocrinology, Surgery, Nuclear Medicine, and Radiotherapy. 2nd ed. Philadelphia, Pa: Lippincott-Raven; 1997:223-230.
  • The Fibromyalgia Research Foundation website. Boulder, Colo.
  • Garrison RL, Breeding PC. A metabolic basis for fibromyalgia and its related disorders: the possible role of resistance to thyroid hormone. Med Hypotheses 2003;61:182–189.The Journal of Family Practice ©2005 Dowden Health Media

    Curr Rheumatol Rep 2000 Apr;2(2):131-40
    Evidence for metabolic abnormalities in the muscles of patients with fibromyalgia.

    Park JH, Niermann KJ, Olsen N.

    Vanderbilt University School of Medicine, Department of Radiology, Division of Rheumatology and Immunology, Department of Medicine, 3219 Medical Center North, Vanderbilt University, Nashville, TN 37232-2681, USA.

    Widespread muscle pain, fatigue, and weakness are defining characteristics of patients with fibromyalgia (FM). The aim of this review is to summarize recent investigations of muscle abnormalities in FM, which can be classified as structural, metabolic, or functional in nature. Histologic muscle abnormalities of membranes, mitochondria, and fiber type have been well described at both the light microscopic and ultrastructural levels. These structural abnormalities often correlate with biochemical abnormalities, defective energy production, and the resultant dysfunction of FM muscles. The observed abnormalities in FM muscles are consistent with neurologic findings and disturbances in the hypothalamic-pituitary-adrenal axis. Functional changes in FM muscles are assessed most directly by strength and endurance measurements, but pain and psychologic factors may interfere with accurate assessments. To compensate for diminished effort, the decreased efficiency of the work performance by patients with FM can be verified from P-31 magnetic resonance spectroscopy (MRS) data by calculation of the work/energy-cost ratio for various tasks. In the disease course, muscle abnormalities may be elicited by intrinsic changes within the muscle tissue itself and/or extrinsic neurologic and endocrine factors. The accurate assignment of intrinsic or extrinsic factors has been substantially clarified by a recent surge of experimental findings. Irrespective of the multifaceted causes of muscle dysfunction and pain, an in-depth understanding of the muscle defects may provide ideas for characterization of the underlying pathogenesis and development of new therapeutic approaches for fibromyalgia syndrome.

    Publication Types:
    PMID: 11123050 [PubMed - indexed for MEDLINE]