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C F S
- Information International Growth Hormone and CFS/
FM
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Growth Hormone - the axis
The Growth Hormone (GH)-IGF-1
homeostasis is the 'bottom' step of a 3-level axis which regulates GH
secretion and homeostasis
by numerous interactions and counteractions. GH is produced and
secreted by the pituitary on top of which the hypothalamus is situated, not
just physically, but also in terms of secretory control. The hypothalamus
secretes Growth Hormone Releasing Hormone (GHRH), which causes the pituitary
to release GH. There is a negative feed-back build in the system.
Pituitary surgery may result in GH deficiency, and a small 2001-study found
FM symptoms in 4 of 10 operated patients, Hallegua et al., 2001. Growth Hormone secretagogues
Some well-known simple peptides
has been shown to cause release of GH, and these
peptides were thus named secretagogues. The Belgian CFS-research team
tested one secretagogue (acclydine) on CFS patients and found it to improve
GH secretion,
De Becker et al., 2001. Growth Hormone in FM/ CFS
Researchers have focused on GH
deficiency in FM for some years,
Bennett, 1998, Bagge et al., 1998, and others have focused
on similar findings in CFS,
Berwaerts et al., 1998. A 1999-study found low spontaneous GH
secretion in FM,
Leal-Cerro et al., 1999. These findings have resulted in attempts to
treat the respective conditions,
Bennett et al., 1998,
Moorkens et al., 1998. In a 2000-study, GH homeostasis was found
somewhat disturbed in FM but not as in significant GH deficiency, Dinser et al., 2000. Although only
30% of adult FM patients show GH deficiency, which is a potentially treatable
condition, Bennett, 2002. One study
found no deficits in the GH-IGF-1 axis in FM women compared to
controls, McCall et al., 2003. One study found no defects in the GH-IGF-1 system, Cleare et al., 2000, others found
significant impairment of GH response during insulin-induced hypoglycemia and
a low nocturnal GH secretion in CFS patients, Moorkens et al., 2000. Low
GH-secretion in CFS may be the cause - or the effect - of the disease, Berwaets et al., 1998. A
2001-study of GH and prolactin demonstrated decreased nocturnal hormone
values in FM,
Landis et al., 2001. Following exercise GH secretion in FM differs
from normal,
Gursel et al., 2001. A 2002-study addressed the reduced GH
secretion after exercise to increased somatostatin, Paiva et al., 2002, news, Paiva et al., 2002. Low levels of the IGF-1 cytokine may predispose CFS
patients to bone mineral resorption and osteopenia, Nijs et al., 2003. A review: Suboptimal growth hormone secretion is
important in rheumatic diseases, bennett04.txt. Six months of treatment
with pyridostigmine and tri-weekly exercise fails to improve Insulin-Like
Growth Factor-I levels in FM, jones.etal07.txt. A subpopulation of FM patients with low
serum IGF-I levels will fail the GHRH-arginine test, yuen.etal07.txt. Growth Hormone and HPA axis
Somatostatin has significant
effect on the "parallel" hypothalamus/pituitary/adrenal axis, the
corticosteroid regulatory hormones. In FM patients normal exercise
regulated GHR responses are inhibited by somatostatin, Riedel et al., 2002. The HPG - axis
The HPG [hypothalamus -
pituitary - gonadal, or lactotropic] axis has been
studied in CFS and FM also. One study did not find disturbances, Korszun et al., 2000. A case study found FM to have been caused by
administration of Gt-RH analogue, Toussirot & Wendling, 2001, and according
to this press news, oxytocin has been linked to FM, press, oxytocin, 2001. CFS and Leptin
Low dose hydrocortisone therapy
caused increases in plasma leptin levels, cleare.etal01.txt. |
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