Fibromyalgia is caused by a mycoplasmal infection in the neuroendocrine system.
Justification:
The advances in research on Fibromyalgia Syndrome (FMS) over the last 5 years has targeted specific links and correlations which might indicate a dysregulation or imbalance of the neuroendocrine system, especially the HPA axis, which may well explain many of the seemingly unrelated symptoms presented by FMS patients. Research supports that various components of the central nervous system appear to be involved, including the hypothalamic pituitary axes, pain-processing pathways, and autonomic nervous system.
The advances in gene research during this same time peroid has provided new evidence in the identification and pathogenesis of specific species of mycoplasmas which might have the ability to cause a dysregulation of the neuroendocrine system. To learn more about mycoplasmas, how they deregulate cellular functions and cause a wide range of diseases and syndromes in the body. In this section we are going to try to answer:-
What is a Mycoplasma?
What diseases can they cause?
Treatment Options
Nutritional Protocols
Laboratory Testing for Mycoplasmas
Medical Research and Studies on Mycoplasmas
(There are more in-depth links on Mycoplasmas at the end of this page)
Fibromyalgia is an extremely common chronic condition that can be challenging to manage. Although the etiology remains unclear, characteristic alterations in the pattern of sleep and changes in neuroendocrine transmitters such as serotonin, substance P, growth hormone, thyroid hormones, estrogen and cortisol suggest that dysregulation of the autonomic and neuroendocrine system now appears to be the basis of the syndrome.
Evidence of neuroendocrine system dysfunction in Fibromyalgia:
Thyroid
Virtually every feature of fibromyalgia corresponds to signs or symptoms associated with failed transcription regulation by thyroid hormone.(See Table) In the late 1980’s to early 1990’s some diagnoses of fibromyalgia and rheumatic diseases were subsequently changed to a hypothyroidism diagnosis after thyroid testing was performed.(4, 6, 7) In a 1992 german study thyroid function was tested in 13 female patients with primary fibromyalgia syndrome (FMS) 10 healthy age matched controls by intravenous injection of 400 micrograms thyrotropin-releasing hormone (TRH). Basal thyroid hormone levels of both groups were in the normal range. However, patients with primary FMS responded with a significantly lower secretion of thyrotropin and thyroid hormones to TRH, within an observation period of 2 h, and reacted with a significantly higher increase of prolactin. Total and free serum calcium and calcitonin levels were significantly lower in patients with primary FMS, while both groups exhibited parathyroid hormone levels in the normal range. This phenomenon would not be discovered in a doctor’s routine thyroid tests of measuring T3, T4, and TSH since it is indicative of secondary hypothyroidism (Euthyroid) rather than primary hypothyroidism. Recent research suggests the cause of this phenomenon to be a newly discovered gene mutation reporting: “in hypothyroid fibromyalgia, failed transcription regulation would result from thyroid-hormone deficiency. In euthyroid fibromyalgia, failed transcription regulation may result from low-affinity thyroid hormone receptors coded by a mutated c-erbA beta 1 gene, yielding partial peripheral resistance to thyroid hormone. The result would be tissue-specific hypothyroid-like symptoms despite normal circulating thyroid-hormone levels.”(1)
In clinical practice is has been demonstrated that a significant percentage of FMS patients are tested with secondary hypothyroidism (euthyroid). This is missed by many health practitioners who routinely test thyroid function by measuring common thyroid hormones T3, T4, and TSH (Thyroid stimulating hormone). The majority of FMS patients will test in normal ranges. However, thyroid dysfunction is often revealed in FMS patients when a TRH stimulus test (Thyrotropin-releasing hormone) is administered. Medical practitioners have been able to manage symptoms of FMS patients with some degree of success by administering thryoid homone replacement therapy for several years now.(2) Other researchers suggest that FMS patients may have a form of thryoid autoimmunity, reporting the prevalence of thyroid microsomal antibodies were significantly higher in persons with than without chronic widespread musculoskeletal complaints. (3)
The thyroid produces hormones that increase oxygen use in cells and stimulate vital processes in every part of the body. These thyroid hormones have a major impact on growth, use of energy, heat production, and infertility. They affect the use of vitamins, proteins, carbohydrates, fats, electrolytes, and water, and regulate the immune response in the intestine. They can also alter the actions of other hormones and drugs. The two key thyroid hormones are thyroxine (T4) and L-triiodothyronine (T3). Iodine is the raw material used in the manufacture of these hormones; it is extracted from the blood and trapped by the thyroid gland where 80% of the body’s iodine is stored. The thyroid mostly produces thyroxine, which in turn, is converted into T3, the more biologically active thyroid hormone. Only about 20% of T3 is actually formed in the thyroid gland, however; the rest is manufactured from circulating thyroxine in tissues outside the thyroid. The whole process of iodine trapping and thyroid hormone production is directly influenced by another important hormone, thyroid-stimulating hormone (TSH or thyrotropin). This hormone is secreted by the pituitary gland and monitored by thyrotropin-releasing hormone (TRH), which is produced in the hypothalamus gland. Both glands are located in the brain. Any abnormality in this intricate system of glands and hormone synthesis and production can have far-reaching consequences.
In autoimmune diseases, the body’s immune system attacks its own cells; in the case of autoimmune thyroiditis, the cells under attack are in the thyroid gland. Experts do not know why the immune system starts to injure the thyroid. One theory is that a virus or bacteria with a protein resembling a thyroid protein might trigger the response. This theory is backed up to some extent by the presence of recent infections in people with autoimmune disease.
Footnotes:
(1) Lowe JC, Mutations in the c-erbA beta 1 gene: do they underlie euthyroid fibromyalgia? Med Hypotheses. 1997 Feb;48(2):125-35. [MEDLINE]
(2) Dr. John C. Lowe, The Metabolic Treatment of Fibromyalgia.
(3) Aarflot T, et.al., Association between chronic widespread musculoskeletal complaints and thyroid autoimmunity. Results from a community survey. Scand J Prim Health Care. 1996 Jun;14(2):111-5. [MEDLINE]
(4) Keenan GF, et.al., Rheumatic symptoms associated with hypothyroidism in children. J Pediatr. 1993 Oct;123(4):586-8.[MEDLINE]
(5) Neeck G, Thyroid function in patients with fibromyalgia syndrome. J Rheumatol. 1992 Jul;19(7):1120-2.
(6) Carette S,et.al., Fibrositis and primary hypothyroidism. J Rheumatol. 1988 Sep;15(9):1418-21. MEDLINE
(7) Wilke WS, et.al., Hypothyroidism with presenting symptoms of fibrositis. J Rheumatol. 1981 Jul-Aug;8(4):626-31. [MEDLINE]
TABLE 1
Symptoms of Hypothyroidism Symptoms of Fibromyalgia
Chronic fatigue Chronic fatigue
Muscle and joint aches Muscle and joint aches
Muscle cramps Muscle cramps
Muscle weakness Muscle weakness
Concentration and memory problems Concentration and memory problems
Depression and mood swings Depression and mood swings
Weight gain Weight gain
Constipation Irritable bowel including constipation
Obstructive sleep apnea Sleep disorders and insomnia
Heavy menstruation
Dry skin
Dry coarse hair
Flaky or split fingernails
Hair loss
Myxedema (round puffy face, swelling in hands and feet )
Husky voice
Numbness of arms and legs
Sensitivity to cold
Impaired sex drive
Infertility
Low blood pressure
Headaches
Visual disturbance
High cholesterol
The hypothalamic pituitary adrenal axis
The brain and the immune system are the two major adaptive systems of the body. During an immune response the brain and the immune system “talk to each other” and this process is essential for maintaining homeostasis. Two major pathway systems are involved in this cross-talk: the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS).(6) Living organisms survive by maintaining an immensely complex dynamic equilibrium of the internal milieu or homeostasis. The systemic sympathetic and adrenomedullary (sympathetic) system (SNS) and the HPA axis are the peripheral limbs of the stress system, whose main function is to maintain both basal and stress-related homeostasis. At rest catecholamines (CA) maintain homeostasis as major regulators of fuel metabolism, heart rate, blood vessel tone, and thermogenesis. When homeostasis is disturbed or threatened by internal or external challenges, both the SNS and HPA axis become activated, resulting in increased peripheral levels of CAs and glucocorticoids that act in concert to keep the steady state of the internal milieu.
Researchers around the world have published articles and research which indicate “defects in the hypothalamus-pituitary-adrenal axis have been observed in autoimmune and rheumatic diseases, chronic inflammatory disease, chronic fatigue syndrome and fibromyalgia.”(3) Research as early as 1989 indicated data suggesting alteration in the pituitary hypothalamic axis with respect to cortisol secretion in fibromyalgia syndrome.(4) A1998 German study discovered: “We found in FMS patients elevated basal values of ACTH and cortisol, lowered basal values of insulin-like growth factor I (IGF-I) and of triiodothyronine (T3), elevated basal values of follicle-stimulating hormone (FSH) and lowered basal values of estrogen. Following injection of the four releasing-hormones, we found in FMS patients an augmented response of ACTH, a blunted response of TSH, while the prolactin response was exaggerated. The effects of LHRH stimulation were investigated in six FMS patients and six controls and disclosed a significantly blunted response of LH in FMS. We explain the deviations of hormonal secretion in FMS patients as being caused by chronic stress, which, after being perceived and processed by the central nervous system (CNS), activates hypothalamic CRH neurons. CRH, on the one hand, activates the pituitary-adrenal axis, but also stimulates at the hypothalamic level somatostatin secretion which, in turn, causes inhibition of GH and TSH at the pituitary level.”(1) In several studies, histologic muscle abnormalities of membranes, mitochondria, and fiber type have been well described at both the light microscopic and ultrastructural levels. These abnormalties found in muscle tissues of FM patients have been reported to be “consistent with neurologic findings and disturbances in the hypothalamic-pituitary-adrenal axis” and suggests, “muscle abnormalities may be elicited by intrinsic changes within the muscle tissue itself and/or extrinsic neurologic and endocrine factors.(5) Another research group found “The influence of maximum exercise has been studied in 10 patients with primary fibromyalgia syndrome (PFS) and 10 healthy sedentary control persons. The exercise consisted of a bicycle ergometertest and a steptest, both till exhaustion. In both tests, the mean maximum workload of the PFS patients was lower than that of the controls. Significantly lower values of serum creatinekinase, myoglobin, cortisol, epinephrine and norepinephrine were found in PFS patients. A striking finding was a lower heart rate in PFS patients compared to the controls under the same workload. The lower (nor)epinephrine concentration together with the lower heart rate suggests a disturbance of the sympathetic activity in PFS patients. The preliminary conclusion is that there is a disturbed reactivity of the sympathetic system as well as of the HPA axis in PFS.”(7)
(1) Riedel W, et.al., Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones. Z Rheumatol. 1998;57 Suppl 2:81-7. [MEDLINE]
(2) Clauw DJ, et.al., Chronic pain and fatigue syndromes: overlapping clinical and neuroendocrine features and potential pathogenic mechanisms.euroimmunomodulation. 1997 May-Jun;4(3):134-53. [MEDLINE]
(3) Anisman H, et.al., Neuroimmune mechanisms in health and disease: 2. Disease. CMAJ. 1996 Oct 15;155(8):1075-82. [MEDLINE]
(4) McCain GA, Diurnal hormone variation in fibromyalgia syndrome: a comparison with rheumatoid arthritis. J Rheumatol Suppl. 1989 Nov;19:154-7. [MEDLINE]
(5) Park JH, et.al., Evidence for Metabolic Abnormalities in the Muscles of Patients with Fibromyalgia. Curr Rheumatol Rep. 2000 Apr;2(2):131-140. [MEDLINE]
(6) Elenkov IJ, et al., The sympathetic nerve-An integrative interface between two supersystems:
the brain and the immune system. Pharmacol Rev 2000 Dec;52(4):595-638 [MEDLINE]
(7) van Denderen JC, et al., Physiological effects of exhaustive physical exercise in primary fibromyalgia syndrome (PFS): is PFS a disorder of neuroendocrine reactivity? Scand J Rheumatol 1992;21(1):35-7
Elenkov IJ, et al., The sympathetic nerve-An integrative interface between two supersystems: the brain and the immune system. Pharmacol Rev 2000 Dec;52(4):595-638
Elam M, Johansson G and Wallin BG (1992) Do patients with primary fibromyalgia have an altered muscle sympathetic nerve activity? Pain 48: 371-375 [Medline].
Qiao ZG, Vaeroy H and Morkrid L (1991) Electrodermal and microcirculatory activity in patients with fibromyalgia during baseline, acoustic stimulation and cold pressor tests. J Rheumatol 18: 1383-1389 [Medline].
Clauw DJ and Chrousos GP (1997) Chronic pain and fatigue syndromes: Overlapping clinical and neuroendocrine features and potential pathogenic mechanisms. Neuroimmunomodulation 4: 134-153 [Medline].
Clauw DJ, Radulovic D, Antonetti D, Bagati R, Baraniuk J and Barbey JT (1996a) Tilt table tasting in fibromyalgia. Arthritis Rheum 39 (9S): S276.
Clauw DJ, Radulovic D, Heshmat Y and Barbey JT (1996b) Heart rate variability as a measure of autonomic dysfunction in patients with fibromyalgia. Arthritis Rheum 39 (9S): S276.
van Denderen JC, Boersma JW, Zeinstra P, Hollander P and van Neerbos BR (1992) Physiologic effects of exhaustive physical exercise in primary fibromyalgia syndrome (PFS): Is PFS a disorder of neuroendocrine reactivity? Scand J Rheumatol 21: 35-37 Medline.
Rowe PC, Bou-Holaigah I, Kan JS and Calkins H (1995) Is neurally mediated hypotension an unrecognized cause of chronic fatigue? Lancet 345: 623-624 Medline.
Hasko G, Elenkov IJ, Kvetan V and Vizi ES (1995a) Differential effect of selective block of alpha 2-adrenoreceptors on plasma levels of tumour necrosis factor-alpha, interleukin-6 and corticosterone induced by bacterial lipopolysaccharide in mice. J Endocrinol 144: 457-462 [Medline].
Elenkov IJ, Papanicolaou DA, Wilder RL and Chrousos GP (1996) Modulatory effects of glucocorticoids and catecholamines on human interleukin-12 and interleukin-10 production: Clinical implications. Proc Assoc Am Physicians108: 374-381 [Medline].
Hypothalmus
Recent research this year has demonstrated FMS patients have a decrease in GH (growth hormone) over healthy subjects suggesting “Severe GH deficiency is not a significant pathogenic factor in most patients with FMS. We observed an impaired reactivity of the somatotropic axis in one-third of patients with FM, in keeping with a functional alteration of the hypothalamus.”(1) “Patients with fibromyalgia were found to have an impaired ability to activate the hypothalamic pituitary portion of the hypothalamic pituitary adrenal axis as well as the sympathoadrenal system, leading to reduced corticotropin and epinephrine response to hypoglycemia.” (2) In fact, FMS patients complaining of “fibro-fog” have later been diagnosed with intermitent hypoglycemia which is causing sort term memory loss, periods of confusion or “fog” and even stupor-like states as blood sugar levels drop unexpectedly. This intermittent hypoglycemia may result from this impaired hypothalamic pituitary function.
(1) Dinser R, et.al., Stringent endocrinological testing reveals subnormal growth hormone secretion in some patients with fibromyalgia syndrome but rarely severe growth hormone deficiency. J Rheumatol. 2000 Oct;27(10):2482-8. [Medline]
(2) Buskila D. Fibromyalgia, chronic fatigue syndrome, and myofascial pain syndrome. Curr Opin Rheumatol. 2000 Mar;12(2):113-23. Review. [Medline]
Clinical Research supporting Neuroendocrine factors in Fibromyalgia
Dysregulation and/or significant abnormalties of the neuroendocrine system
Millea PJ, et.al., Treating fibromyalgia. Am Fam Physician. 2000 Oct 1;62(7):1575-82, 1587.
Bradley LA, et.al., Pain Complaints in Patients with Fibromyalgia Versus Chronic Fatigue Syndrome. Curr Rev Pain. 2000;4(2):148-157.
Klimas N. Pathogenesis of chronic fatigue syndrome and fibromyalgia. Growth Horm IGF Res. 1998 Apr;8 Suppl B:123-6.
Korszun A, et.al., Follicular phase hypothalamic-pituitary-gonadal axis function in women with fibromyalgia and chronic fatigue syndrome. J Rheumatol. 2000 Jun;27(6):1526-30.
Dessein PH, et.al., Neuroendocrine deficiency-mediated development and persistence of pain in fibromyalgia: a promising paradigm? Pain. 2000 Jun;86(3):213-5.
Crofford LJ. Neuroendocrine abnormalities in fibromyalgia and related disorders. Am J Med Sci. 1998 Jun;315(6):359-66.
Morand EF, et.al., Advances in the understanding of neuroendocrine function in rheumatic disease. Aust N Z J Med. 1996 Aug;26(4):543-51.
Moldofsky H. Sleep, neuroimmune and neuroendocrine functions in fibromyalgia and chronic fatigue syndrome. Adv Neuroimmunol. 1995;5(1):39-56. Review.
van Denderen JC, et.al., Physiological effects of exhaustive physical exercise in primary fibromyalgia syndrome (PFS): is PFS a disorder of neuroendocrine reactivity? Scand J Rheumatol. 1992;21(1):35-7.
Torpy DJ, et.al., The three-way interactions between the hypothalamic-pituitary-adrenal and
gonadal axes and the immune system Baillieres Clin Rheumatol 1996 May;10(2):181-98
HPA axis dysfunction/dysregulation
Neeck G, et.al., Neuroendocrine perturbations in fibromyalgia and chronic fatigue syndrome. Rheum Dis Clin North Am. 2000 Nov;26(4):989-1002.
Crofford LJ. The hypothalamic-pituitary-adrenal stress axis in fibromyalgia and chronic fatigue syndrome. Z Rheumatol. 1998;57 Suppl 2:67-71.
Crofford LJ, et.al., Neurohormonal perturbations in fibromyalgia. Baillieres Clin Rheumatol 1996 May;10(2):365-78
Clauw DJ, et.al., Chronic pain and fatigue syndromes: overlapping clinical and neuroendocrine
features and potential pathogenic mechanisms. Neuroimmunomodulation 1997 May-Jun;4(3):134-53
Griep EN, et.al., Function of the hypothalamic-pituitary-adrenal axis in patients with fibromyalgia and low back pain. J Rheumatol. 1998 Jul;25(7):1374-81.
McCain GA, et.al., Diurnal hormone variation in fibromyalgia syndrome: a comparison with rheumatoid arthritis. J Rheumatol Suppl 1989 Nov;19:154-7
Demitrack MA, Evidence for and pathophysiologic implications of hypothalamic-pituitary- adrenal axis dysregulation in fibromyalgia and chronic fatigue syndrome. Ann N Y Acad Sci. 1998 May 1;840:684-97.
Bellometti S, et.al., Function of the hypothalamic adrenal axis in patients with fibromyalgia syndrome undergoing mud-pack treatment. Int J Clin Pharmacol Res. 1999;19(1):27-33.
Scott LV, et.al., The neuroendocrinology of chronic fatigue syndrome: focus on the hypothalamic-pituitary-adrenal axis. Funct Neurol. 1999 Jan-Mar;14(1):3-11.
Adler GK, et.al., Reduced hypothalamic-pituitary and sympathoadrenal responses to hypoglycemia in women with fibromyalgia syndrome. Am J Med. 1999 May;106(5):534-43.
Torpy DJ, et.al., The three-way interactions between the hypothalamic-pituitary-adrenal and gonadal axes and the immune system. Baillieres Clin Rheumatol. 1996 May;10(2):181-98.
Schneider MJ. Et.al., Tender points/fibromyalgia vs. trigger points/myofascial pain syndrome: a need for clarity in terminology and differential diagnosis. J Manipulative Physiol Ther. 1995 Jul-Aug;18(6):398-406. Review.
Griep EN, Altered reactivity of the hypothalamic-pituitary-adrenal axis in the primary fibromyalgia syndrome. J Rheumatol. 1993 Mar;20(3):469-74.
van Denderen JC, et.al., Physiological effects of exhaustive physical exercise in primary fibromyalgia syndrome (PFS): is PFS a disorder of neuroendocrine reactivity? Scand J Rheumatol. 1992;21(1):35-7.
Hypothalamus dysregulation
Riedel W, Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in
patients with fibromyalgia syndrome following systemic injection of the relevant
hypothalamic-releasing hormones. Z Rheumatol 1998;57 Suppl 2:81-7
Neeck G. et.al., Neuroendocrine and hormonal perturbations and relations to the serotonergic system in fibromyalgia patients. Scand J Rheumatol Suppl. 2000;113:8-12.
Neeck G, et.al., Hormonal pertubations in fibromyalgia syndrome. Ann N Y Acad Sci. 1999 Jun 22;876:325-38;
Adrenal insufficiency
Griep EN, Altered reactivity of the hypothalamic-pituitary-adrenal axis in the primary fibromyalgia syndrome. J Rheumatol. 1993 Mar;20(3):469-74.
Growth Hormone secretion deficiency:
Bennett RM, A randomized, double-blind, placebo-controlled study of growth hormone in the treatment of fibromyalgia. Am J Med 1998 Mar;104(3):227-31
Bennett RM, Disordered growth hormone secretion in fibromyalgia: a review of recent findings and a hypothesized etiology. Z Rheumatol 1998;57 Suppl 2:72-6
Schlienger JL, [Growth hormone: a magical potion]? Rev Med Interne 1998 Apr;19(4):279-85
Bennett R, Fibromyalgia, chronic fatigue syndrome, and myofascial pain. Curr Opin Rheumatol 1998 Mar;10(2):95-103
Bennett RM, Hypothalamic-pituitary-insulin-like growth factor-I axis dysfunction in patients with fibromyalgia. J Rheumatol 1997 Jul;24(7):1384-9
Dinser R, et.al., Stringent endocrinological testing reveals subnormal growth hormone secretion in some patients with fibromyalgia syndrome but rarely severe growth hormone deficiency. J Rheumatol. 2000 Oct;27(10):2482-8.
Riedel W, Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones. Z Rheumatol 1998;57 Suppl 2:81-7
Bagge E, et.al., Low growth hormone secretion in patients with fibromyalgia–a preliminary report on 10 patients and 10 controls. J Rheumatol 1998 Jan;25(1):145-8
Crofford LJ, et.al., Neurohormonal perturbations in fibromyalgia. Baillieres Clin Rheumatol 1996 May;10(2):365-78
Griep EN, et.al., Pituitary release of growth hormone and prolactin in the primary fibromyalgia syndrome. J Rheumatol. 1994 Nov;21(11):2125-30.
Lowered basal values of insulin-like growth factor 1 (IGF-1)
Neeck G, Neuroendocrine and hormonal perturbations and relations to the serotonergic system in fibromyalgia patients. Scand J Rheumatol Suppl 2000;113:8-12
Berwaerts J, et.al., Secretion of growth hormone in patients with chronic fatigue syndrome. Growth Horm IGF Res 1998 Apr;8 Suppl B:127-9
Leal-Cerro A, et.al, The growth hormone (GH)-releasing hormone-GH-insulin-like growth factor-1 axis in patients with fibromyalgia syndrome. J Clin Endocrinol Metab 1999 Sep;84(9):3378-81
Riedel W, Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones. Z Rheumatol 1998;57 Suppl 2:81-7
Bennett RM, A randomized, double-blind, placebo-controlled study of growth hormone in the treatment of fibromyalgia. Am J Med 1998 Mar;104(3):227-31
Bagge E, et.al., Low growth hormone secretion in patients with fibromyalgia–a preliminary report on 10 patients and 10 controls. J Rheumatol 1998 Jan;25(1):145-8
Bennett RM, Hypothalamic-pituitary-insulin-like growth factor-I axis dysfunction in patients with fibromyalgia. J Rheumatol 1997 Jul;24(7):1384-9
Griep EN, et.al., Pituitary release of growth hormone and prolactin in the primary fibromyalgia syndrome. J Rheumatol. 1994 Nov;21(11):2125-30.
Inverse correlation between low density lipoprotein levels and maximal GH concentration
Dinser R, et.al., Stringent endocrinological testing reveals subnormal growth hormone secretion in some patients with fibromyalgia syndrome but rarely severe growth hormone deficiency. J Rheumatol. 2000 Oct;27(10):2482-8.
Alteration at the hypothalamic level in the neuroendocrine control and release of GH
Leal-Cerro A, et.al, The growth hormone (GH)-releasing hormone-GH-insulin-like growth factor-1 axis in patients with fibromyalgia syndrome. J Clin Endocrinol Metab 1999 Sep;84(9):3378-81
Lowered basal values and/or secretion of Somatomedin C
Neeck G, Neuroendocrine and hormonal perturbations and relations to the serotonergic system in fibromyalgia patients. Scand J Rheumatol Suppl 2000;113:8-12
Bennett AL, et.al., Somatomedin C (insulin-like growth factor I) levels in patients with chronic fatigue syndrome. J Psychiatr Res. 1997 Jan-Feb;31(1):91-6.
Griep EN, et.al., Pituitary release of growth hormone and prolactin in the primary fibromyalgia syndrome. J Rheumatol. 1994 Nov;21(11):2125-30.
Bennett RM, Low levels of somatomedin C in patients with the fibromyalgia syndrome. A possible link between sleep and muscle pain. Arthritis Rheum. 1992 Oct;35(10):1113-6.
Elevated basal values and/or activation of ACTH
Neeck G, Neuroendocrine and hormonal perturbations and relations to the serotonergic system in fibromyalgia patients. Scand J Rheumatol Suppl 2000;113:8-12
Riedel W, Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones. Z Rheumatol 1998;57 Suppl 2:81-7
Griep EN, et.al., Pituitary release of growth hormone and prolactin in the primary fibromyalgia syndrome. J Rheumatol. 1994 Nov;21(11):2125-30.
Griep EN, Altered reactivity of the hypothalamic-pituitary-adrenal axis in the primary fibromyalgia syndrome. J Rheumatol. 1993 Mar;20(3):469-74.
Griep EN, et.al., Function of the hypothalamic-pituitary-adrenal axis in patients with fibromyalgia and low back pain. J Rheumatol. 1998 Jul;25(7):1374-81.
Lentjes EG, et.al., Glucocorticoid receptors, fibromyalgia and low back pain. Psychoneuroendocrinology. 1997 Nov;22(8):603-14.
Elevated basal values of follicle-stimulating hormone (FSH),
Neeck G, Neuroendocrine and hormonal perturbations and relations to the serotonergic system in fibromyalgia patients. Scand J Rheumatol Suppl 2000;113:8-12
Riedel W, Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones. Z Rheumatol 1998;57 Suppl 2:81-7
Lowered basal values of cortisol
Crofford LJ, et.al., Neurohormonal perturbations in fibromyalgia. Baillieres Clin Rheumatol 1996 May;10(2):365-78
McCain GA, et.al., Diurnal hormone variation in fibromyalgia syndrome: a comparison with rheumatoid arthritis. J Rheumatol Suppl 1989 Nov;19:154-7
Riedel W, Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones. Z Rheumatol 1998;57 Suppl 2:81-7
Neeck G, Neuroendocrine and hormonal perturbations and relations to the serotonergic system in fibromyalgia patients. Scand J Rheumatol Suppl 2000;113:8-12
Heim C, et.al., The potential role of hypocortisolism in the pathophysiology of stress-related bodily disorders. Psychoneuroendocrinology. 2000 Jan;25(1):1-35.
van Denderen JC, et.al., Physiological effects of exhaustive physical exercise in primary fibromyalgia syndrome (PFS): is PFS a disorder of neuroendocrine reactivity? Scand J Rheumatol. 1992;21(1):35-7.
Hyposecretion of adrenal androgens (DHEAS and Testosterone)
Dessein PH, et.al., Hyposecretion of adrenal androgens and the relation of serum adrenal steroids, serotonin andinsulin-like growth factor-1 to clinical features in women with fibromyalgia. Pain. 1999 Nov;83(2):313-9.
Abnormal dexamethasone suppression
McCain GA, et.al., Diurnal hormone variation in fibromyalgia syndrome: a comparison with rheumatoid arthritis. J Rheumatol Suppl 1989 Nov;19:154-7
Lowered basal values of norepinephrine
Crofford LJ, et.al., Neurohormonal perturbations in fibromyalgia. Baillieres Clin Rheumatol 1996 May;10(2):365-78
van Denderen JC, et.al., Physiological effects of exhaustive physical exercise in primary fibromyalgia syndrome (PFS): is PFS a disorder of neuroendocrine reactivity? Scand J Rheumatol. 1992;21(1):35-7.
Decreased serotonergic activity
Crofford LJ, et.al., Neurohormonal perturbations in fibromyalgia. Baillieres Clin Rheumatol 1996 May;10(2):365-78
Decreased thyroid homone production in reponse to thyrotropin-releasing hormone (TRH)
Neeck G, Thyroid function in patients with fibromyalgia syndrome. J Rheumatol 1992 Jul;19(7):1120-2
Lowered basal values of seratonin
Lowe JC, et.al., Mutations in the c-erbA beta 1 gene: do they underlie euthyroid fibromyalgia? Med Hypotheses 1997 Feb;48(2):125-35
Thyroid autoimmunity relating to dysregulation of thyrotropin releasing hormone.(TRH)
Aarflot T, Association between chronic widespread musculoskeletal complaints and thyroid autoimmunity. Results from a community survey. Scand J Prim Health Care 1996 Jun;14(2):111-5
Lowered basal values of seratonin
Lowe JC, et.al., Mutations in the c-erbA beta 1 gene: do they underlie euthyroid fibromyalgia? Med Hypotheses 1997 Feb;48(2):125-35
Lowered basal values of free triiodothyronine (FT3)
Neeck G, Neuroendocrine and hormonal perturbations and relations to the serotonergic system in fibromyalgia patients. Scand J Rheumatol Suppl 2000;113:8-12
Riedel W, Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones. Z Rheumatol 1998;57 Suppl 2:81-7
Lowered basal values of oestrogen.
Neeck G, Neuroendocrine and hormonal perturbations and relations to the serotonergic system in fibromyalgia patients. Scand J Rheumatol Suppl 2000;113:8-12
Riedel W, Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones. Z Rheumatol 1998;57 Suppl 2:81-7
Increased secretion of ACTH and prolactin
Neeck G, Neuroendocrine and hormonal perturbations and relations to the serotonergic system in fibromyalgia patients. Scand J Rheumatol Suppl 2000;113:8-12
Riedel W, Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones. Z Rheumatol 1998;57 Suppl 2:81-7
Neeck G, Thyroid function in patients with fibromyalgia syndrome. J Rheumatol 1992 Jul;19(7):1120-2
Griep EN, et.al., Pituitary release of growth hormone and prolactin in the primary fibromyalgia syndrome. J Rheumatol. 1994 Nov;21(11):2125-30.
Blunted response of TSH
Riedel W, Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones. Z Rheumatol 1998;57 Suppl 2:81-7
Lowered hypothalmic function
Neeck G, Neuroendocrine and hormonal perturbations and relations to the serotonergic system in fibromyalgia patients. Scand J Rheumatol Suppl 2000;113:8-12
Elevated activity of Hypothalamic CRH neurons (corticotropin-releasing hormone)
Neeck G, Hormonal pertubations in fibromyalgia syndrome. Ann N Y Acad Sci 1999 Jun 22;876:325-38;
The Correlation between Fibromyalgia and Mycoplasmas
Mycoplasmas require a large amount of cholesterol and other sterols for growth and reproduction. If mycoplasmas are present and are competing for these sterols intracellularly, less is available to the body and especially the neuroendocrine system for the sythesis and manufacture of steroids like estrogens, growth hormones and cortisols which many FMS patients have been found to be deficent in.
Mycoplasmas also need and utilize proteins derived from amino acids. Amino acids are the core building blocks in the neuroendocrine system for the synthesis of most chemicals produced and used in the complex intricate pathways of the neuroendocrine system including thyroid hormone production and other chemicals taken up and used in the HPA. This may cause the deregulation of the neuroendocrine system thru the loss of vital nutrients required to maintain regulation.
Mycoplasma maintains a defense mechanism which encodes tryptophan to hide from normal immune responses. If enough tryptophan was utilized from host cells in the neuroendocrine system for this purpose, less would be available to the body for the normal synthesis of tryptophan to seratonin, thus possibly deregulating or lowering seratonin levels and causing depression and sleep disorders most FMS patients present.
Mycoplasmas have the ability to attached to any cell in the body and cause that cell to malfunction, acting differently, thereby causing different interactions with other cells. If mycoplasmas invaded and attached to various cells in endocrine organs, it could cause the widespread deregulation of the entire endocrine system described in the previous research shown above, because of the complex interactions between these organs and the chemicals they produce and utilize.
For more information on how mycoplasmas cause disease and deregulation of systems, organs and cells, see the Simple File on Mycoplasmas which also includes treatment protocols or the more Technical file on Mycoplasmas which provides more links to clinical research published about their actions and pathogenisis.
