rHGH in abstaining AAS users

Not a good idea to have the sodium, TSH and T4 changed huh?

well the increase in sodium accounts for any bloating experienced but is only temporary. Likewise the tsh and t4. I take a little armour to offset that.

jb

Posted by: jboldman

well the increase in sodium accounts for any bloating experienced but is only temporary. Likewise the tsh and t4. I take a little armour to offset that.

jb

The problem with the sodium is the increase of blood pressure to unhealthy levels.

t3 helps with both.

Posted by: Seabiscuit Hogg

T3 helps with both.

Please, elaborate.

yes, how does the T3 help with sodium levels?

jb

It doesn't help with sodium but it does help prevent water retention. Don't ask for studies this is just my personal experience.

i take a little hctz for that!

jb

Posted by: guijr

The problem with the sodium is the increase of blood pressure to unhealthy levels.

Posted by: Seabiscuit Hogg

It doesn't help with sodium but it does help prevent water retention. Don't ask for studies this is just my personal experience.

Thanks.

Posted by: guijr

The problem with the sodium is the increase of blood pressure to unhealthy levels.

Posted by: jboldman

I wish the abstract indicated the dose, this is very interesting particularly for those who want to bridge.

jb

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Curr Neurovasc Res. 2007 Feb;4(1):9-18.
Recombinant human growth hormone in abstinent androgenic-anabolic steroid use: psychological, endocrine and trophic factor effects.Graham MR, Davies B, Kicman A, Cowan D, Hullin D, Baker JS.
Department of Exercise and Health Science, School of Applied Science, University of Glamorgan, Pontypridd, Wales, United Kingdom.

This study examined whether six days recombinant human growth hormone (rhGH) affected psychological profile in an abstinent androgenic-anabolic steroid (AAS) abusing group, compared with an abstinent AAS control group. Male subjects (n = 48) were assigned in a random fashion into one of two groups: (1): (n=24) control group (C); (2): (n=24) rhGH group (GH). A hospital anxiety scale (HADS) questionnaire was completed by all subjects. Physiological responses investigated included anthropometry. Biochemical markers examined included; serum glucose, sodium, urea, lipid profile, high sensitivity C-reactive protein (hsCRP), homocysteine (HCY), tetra-iodothyronine (T4), thyroid stimulating (TSH), luteinising (LH) and follicle stimulating (FSH) hormones, testosterone (T), prolactin (PRL), cortisol and insulin like growth factor-1 (IGF-I). HADS questionnaire significantly decreased in both anxiety (A) and depression (D) symptoms within GH (P<0.017) and compared with C (P<0.05). Body mass index (BMI) and fat-free mass index (FFMI) significantly increased (both P<0.017) while body fat significantly decreased within GH (P<0.017)[/b]. IGF-I significantly increased within GH (P<0.017) and significantly increased compared with C (P<0.05). Serum sodium significantly increased (P<0.017) and serum HCY, hsCRP, TSH and T4, significantly decreased within GH (all P<0.017).PRL significantly increased and T4 significantly decreased compared with C (both P<0.05). The findings of this study suggest that short term use of rhGH has beneficial effects on mental state in individuals who were previous abusers of AAS and appeared to have a beneficial effect on cardiovascular risk markers associated with adverse mental health.

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water retention come from prolactin or prl like.

Growth Horm IGF Res. 2000 Aug;10(4):187-92.

Differences in the effects of 20 K- and 22 K-hGH on water retention in rats.

Satozawa N, Takezawa K, Miwa T, Takahashi S, Hayakawa M, Ooka H.

Medicinal Research Department, Institute of Biological Science, Mitsui Pharmaceuticals Inc., Chiba, Japan.

Antidiuretic actions induced by two growth hormone (GH) isoforms (20 K- and 22 K-hGH; 0.2 and 2.0 mg/kg) were evaluated in rats, as fluid retention may cause oedema, one of the adverse effects of GH. Both GH isoforms (2.0 mg/kg) suppressed urine excretion in hypophysectomized rats (P< 0.01), but only the 22 K-hGH isoform (2.0 mg/kg) suppressed urine excretion in intact rats (P< 0.01). In addition, prolactin (PRL) suppressed urine excretion in intact rats (P< 0.05). In conclusion, 20 K-hGH has less potency in causing urine retention than 22 K-hGH and since 20 K-hGH is missing 15 amino acids found in 22 K-hGH, these amino acids may be important for the antidiuretic action of GH. Since prolactin suppressed urine excretion, a part of the antidiuretic action of GH may be related to PRL-R activation

Mol Endocrinol. 2006 Mar;20(3):661-74.

Two wrongs can make a right: dimers of prolactin and growth hormone receptor antagonists behave as agonists.

Langenheim JF, Tan D, Walker AM, Chen WY.

Department of Biological Sciences, Clemson University, Clemson, SC 29634-0326, USA.

Prolactin (PRL) and GH have two distinct binding sites (site 1 with high affinity; site 2 with low affinity) that each interact with a PRL receptor (PRLR) to form a functional receptor dimer that activates signal transduction. The G129R mutation in PRL and the G120R mutation in GH disrupt the structural integrity of site 2 such that the ligands retain the ability to bind to the first receptor with high affinity, but act as receptor antagonists. In this study, we examined the ability of monomeric and dimeric forms of these ligands, human (h) PRL and hGH, and their antagonists (hPRL-G129R and hGH-G120R) to 1) bind to PRLRs; 2) induce conformational changes in PRLRs; 3) activate signaling pathways associated with the PRLR; and 4) mediate cell proliferation in vitro. In contrast to monomeric hPRL-G129R, homodimeric hPRL-G129R induced PRLR dimerization; activated Janus family of tyrosine kinases 2/signal transducer and activator of transcription 5, Ras/Raf/MAPK kinase/Erk, and phosphatidylinositol 3-kinase/Akt signaling; and stimulated Nb2 cell proliferation. Similarly, homodimeric hGH-G120R was able to mediate signaling via the PRLR and to stimulate Nb2 cell proliferation. These experiments demonstrate that a ligand must have two functional binding sites, but that these may be site 1 plus site 2 or two site 1's, to elicit receptor-mediated signal transduction. The size of the ligand plays less of a role in receptor activation, suggesting that the extracellular portion of the PRLR (and possibly the GH receptor) is rather flexible and can accommodate larger ligands. These findings may have implications for designing multifunctional therapeutics that target this class of cytokine receptors.

Last edited by oswaldosalcedo on 04-24-2007 at 07:42 PM

I knew someone would notice that. we need solutions here. perhaps it is time to dust off a prl antagonist.

jb

Naltrexone. (owned)

because bromo and caber are very nasty.

amen to the bromo being nasty! naltrexone, hmm most likely LDN?

jb

=========

Possible dopaminergic system involvement in LH and PRL responses to naltrexone treatment.Yogev L, Gottreich A, Homonnai ZT, Paz GF.
Institute for the Study of Fertility, Serlin Maternity Hospital, Tel-Aviv Medical Center, Israel.

Naltrexone (Nalt) causes a rapid increase in luteinizing hormone (LH) level. This short term increase of LH concentration declines to baseline levels in less than 1 hour. Addition of pimozide (0.1 mg) caused a blunted response to Nalt challenge, with significantly reduced LH peak values compared with Nalt treatment alone. Pimozide alone caused a delayed decrease compared with baseline LH values. By following plasma prolactin (PRL) levels it was shown that pimozide administration increased PRL levels rapidly for more than 2 hours. Addition of Nalt to pimozide-treated rats significantly decreased plasma PRL values compared with pimozide alone. Nalt injected by itself attenuated PRL baseline levels. Thus, the mechanism by which pimozide caused PRL elevated level is via the dopaminergic as well as the opioid system. It is suggested that the opioid system controls plasma PRL and LH levels through other hypothalamic neurotransmitters in addition to dopamine.

Nandro can share with HGH the same mechanism in water retention,
prolactin secretion:

J Pharmacol Exp Ther. 1999 Jan;288(1):260-9
Dynorphin A1-13 causes elevation of serum levels of prolactin through an opioid receptor mechanism in humans

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Peptides. 2007 Apr;28(4):851-8.

Enzymatic conversion of dynorphin A in the rat brain is affected by administration of nandrolone decanoate.

Magnusson K, Hallberg M, Bergquist J, Nyberg F.

Department of Pharmaceutical Biosciences, Division of Biological Research on Drug Dependence, Uppsala University, Biomedical Center, Box 591, 751 24 Uppsala, Sweden.