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PLEASE CLICK ON THE FIBROMYALGIA SECTION FOR MORE INFORMATION It has been shown that chronic fatigue syndrome and fibromyalgia patients have abnormal sleep patterns with a deficiency in stage 4 sleep (1). Stage 4 sleep is closely related to the pulsatile secretion of growth hormone and 80% of the total daily secretion of growth hormone is during this stage. It has also been shown that chronic fatigue syndrome/fibromyalgia patients are unable to mount a normal growth hormone response to exercise as compared to healthy individuals (2). Thus, it is not a surprise that growth hormone secretion is shown to be deficient in chronic fatigue syndrome/fibromyalgia patients (2-5), with lower than average IGF-1 levels (a marker for growth hormone secretion) (4,6,7). Supplementation of this deficiency with growth hormone is shown to result in significant symptomatic improvement in these conditions (6). As is the case with thyroid and cortisol production in these patients, where there are significant deficiencies in these hormones despite seemingly normal standard testing (8,9), it has also been shown that these patients have a relative growth hormone deficiency despite typically “normal” or low-normal serum markers of IGF-1 (2-4,7). Bennett et al found that 92% of patients with fibromyalgia have pituitary dysfunction that results in low growth hormone secretion and that fibromyalgia patients have significantly lower IGF-1 levels that averaged 138 +/- 56 versus 215 +/- 86 (p = 0.00000000001) in non-fibromyalgia patients, demonstrating significant growth hormone deficiency despite IGF-1 levels in the “normal” range (4). This is consistent with another study that also found that fibromyalgia patients had deficient growth hormone as demonstrated by IGF-1 levels that averaged 124 +/- 47 ng/ml versus 175 +/- 60 ng/ml (p = 0.000001) in normal healthy individuals. The authors conclude, “These findings indicate that there is a distinctive disruption of the growth hormone-somatomedin C (IGF-1) neuroendocrine axis in a majority of fibromyalgia patients (7).”
In a subsequent double-blind, placebo-controlled study, the effectiveness of growth hormone supplementation in fifty women with fibromyalgia and low normal IGF-1 levels (< 160 ng/ml) was studied. Patients were treated with growth hormone to maintain an IGF-1 of 250 ng/ml for 9 months. It was found that fibromyalgia patients treated with growth hormone had significant improvement in symptoms as measured by the Fibromyalgia Impact Questionnaire and a significant reduction in muscle pain as measured by the tender point score compared to placebo. The treatment group also noted an increased sense of well-being and an increased ability to sustain increased levels of activity without the usual increase in muscle pain. The authors conclude, “Women with fibromyalgia and low IGF-1 levels experienced an improvement in their overall symptomatology and number of tender points after 9 months of daily growth hormone therapy. This suggests that a secondary growth hormone deficiency may be responsible for some of the symptoms of fibromyalgia (6).” There was a lag of about 6 months before patients noted improvements, but other studies, as well as our own experience, demonstrate that beneficial effects typically occur approximately 2-3 months after starting replacement.
Conclusion: Chronic fatigue syndrome and fibromyalgia patients are shown to have a relative deficiency of growth hormone and supplementation with growth hormone can be of significant benefit. A clinical diagnosis of growth hormone deficiency, often with support of low or low-normal IGF-1 levels, are the most appropriate means of making the diagnosis of relative growth hormone deficiency. Growth hormone stimulation tests are shown to be inaccurate, unreliable, highly variable, risky, non-physiologic and lack adequate sensitivity to detect relative growth hormone deficiencies. Thus, the growth hormone stimulation tests generally do not add significant useful information in the clinical management of these patients and are not recommended in this patient population.
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