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The Growth Hormone FAQ

poantrex said:
The FAQ above mentions that thyroid replacement should be used during GH? That is absolutely not true - GH *signifigantly* RAISES Free T3 levels. I've seen 3 studies that have indicated this, i'll find them later.

i would like to see that, since most of the time i see recommendations on t3 supplementation due to gh causing you to feel lethargic
 
Great read even if its old. What about some users experience and how your body composition changed ?
 
Well, the theory is based on the fact that exo-HGH will reduce free T4 levels, and when this was noted by some scientists they speculated that thyroid supplementation (with t4 obviously) was needed. But the latest studies show a deactivation of deiodinase, which increases levels of free T3 hormone very signifigantly- So apparently exo-HGH increases T4-T3 conversion which is why T4 levels are reduced.
T4 is unimportant in this case because T3 is the metabolically active thyroid hormone.

Hold on a sec, i'll dig the studies up right now
 
I better get K for this :(



Anyway here are the studies

Effects of recombinant growth hormone therapy on thyroid hormone concentrations.

Kalina-Faska B, Kalina M, Koehler B.

Department of Pediatric Endocrinology and Diabetes, Medical University of Silesia, Katowice, Poland. [email protected]

BACKGROUND AND OBJECTIVE: There are numerous, often contradictory reports on the effects of growth hormone (GH) therapy on thyroid function. The aim of this study was to assess the effect of such therapy on serum concentrations of thyroid hormones in GH-deficient children euthyroid prior to the treatment, and to determine the necessity of thyroid hormone administration in these patients. MATERIAL AND METHODS: The study included 32 GH-deficient patients in the first stage of sexual development, in whom disorders of thyroid function could be excluded. The inclusion criteria were based on clinical examination and levels of thyroxine (T4), triiodothyronine (T3), free thyroxine (fT4), free triiodothyronine (fT3), reverse triiodothyronine (rT3), thyrotropin (TSH) before and after stimulation with thyrotropin-releasing hormone (TRH). Recombinant growth hormone (rGH) (Genotropin 16U, Pharmacia) was administered at a dose of 0.7 U/kg/week. Fasting blood samples were drawn before treatment and after 3, 6, 9 and 12 months of therapy. Thyroid hormones were measured using RIA and IRMA methods. RESULTS: There were no physical signs of hypothyroidism in the patients examined during 12 months of rGH administration, and the satisfactory growth rate was achieved. T4 levels decreased in the first 3 months but remained within the normal range, and then returned to the values prior to the treatment. A similar trend was observed for fF4, with 28.5% of patients exhibiting fF4 levels below the normal in the 3rd month. An increase during the first 3 months of therapy was observed in the cases of T3 (statistically non-significant) and fT3, and these values then fell to levels within the normal range of patients' age. During treatment, TSH levels decreased but remained within the normal range. CONCLUSIONS: A transient decrease in T4 concentrations in the 3rd month with unchanged T3 and an increase in fT3 concentrations probably result from the effect of rGH on the peripheral metabolism of thyroid hormones. The results obtained do not support the use of thyroid hormone therapy with levothyroxine during the first year of rGH therapy in patients who are initially euthyroid.

PMID: 14756384 [PubMed - indexed for MEDLINE]

Effects of short-term growth hormone treatment on PTH, calcitriol, thyroid hormones, insulin and glucagon.

Brixen K, Nielsen HK, Bouillon R, Flyvbjerg A, Mosekilde L.

University Department of Endocrinology and Metabolism, Aarhus County Hospital, Denmark.

We measured changes in serum insulin-like growth factor-1 (IGF-1), calcitriol, parathyroid hormone (PTH), thyroid hormones, insulin, and plasma glucagon in response to seven days of treatment with a pharmacological dosage of recombinant human growth hormone (r-hGH) (0.1 IU/kg sc twice daily) or placebo in 20 normal male volunteers to evaluate whether the effect of r-hGH on biochemical bone markers could be attributed to changes in these hormones. Serum IGF-1 (p < 0.001) and vitamin D-binding protein (p < 0.001) increased steadily during treatment returning to baseline at day 14. Total calcitriol (p < 0.01) and free calcitriol index (p < 0.001) increased transiently at day 4. Furthermore, serum insulin (p < 0.001) and both total (p < 0.001) and free triiodothyronine (p < 0.02) increased during treatment, while serum PTH and plasma glucagon remained unchanged. In conclusion, pharmacological doses of r-hGH increased not only IGF-1 but also free-calcitriol index, insulin, and free T3. The increase in these hormones may be co-responsible for some of the observed effects of r-hGH on bone turnover and calcium homeostasis.

Publication Types:

* Clinical Trial
* Controlled Clinical Trial


PMID: 1449044 [PubMed - indexed for MEDLINE]
 
poantrex said:
But the latest studies show a deactivation of deiodinase, which increases levels of free T3 hormone very signifigantly- So apparently exo-HGH increases T4-T3 conversion which is why T4 levels are reduced.

This doesn't make sense since deiodinase enzyme is the one that induces the T4>T3 conversion in liver/kidneys.
I agree on the point of T4 as being impertinent as the measure of thyroid function: all that matters is the free plasma T3 levels unbound by the TBH.

Recombinant hGH replacement therapy and the hypothalamus-pituitary-thyroid axis in children with GH deficiency: when should we be concerned about the occurrence of central hypothyroidism?

RESULTS: Serum IGF-I levels normalized in all patients. In both groups, a significant reduction in FT4 levels (P < 0.01) occurred during rhGH therapy. No patient in group A had FT4 values into the hypothyroid range, while in four of six patients in group B, fell FT4 levels into the hypothyroid range during rhGH. In particular, the two euthyroid children developed central hypothyroidism during rhGH treatment, and their height velocities did not normalize until the achievement of euthyroidism through appropriate LT4 substitution. No variation in serum FT3 and TSH levels was recorded in either groups. CONCLUSION: Contrary to that observed in patients with MPHD, rhGH replacement therapy does not induce central hypothyroidism

The influence of growth hormone and thyroxine on iodothyronine deiodinase activity in the liver, kidney and brown adipose tissue in hypophysectomized rats.

In conclusion, GH stimulates iodothyronine deiodinase activity of the liver and kidney in hypophysectomized rats. Moreover, when GH is administered together with T4, the T4-stimulated enzyme activity in the liver and kidney is downregulated, suggesting that GH attenuates (or modulates) the T4 effect on this specific enzyme activity.
 
Yeah, I got that part backwards....but the point stands that newer studies done on humans are showing an increase in FT3 during exo-HGH therapy.
 
In all honesty, I am not even quite sure as to why or where the myth of mandatory T3 adjunct therapy with r-hGH regimen originated. But somehow everyone is led to believe that r-hGH co-administration will precipitate impaired thyroid function :o
 
very interesting indeed, as i always read that t3 was a must with gh. but im still confused. so does this mean that would t4 maybe be a better choice than t3 in conjunction with gh, or to use neither?
 
genarr3 said:
Originally posted by The Man Child on www.EliteFitness.com
Also - information taken from ironmaster posts


True Story on Growth Hormone by Death On The Field
Growth Hormone

Rating: (1 being the lowest, 5 being the highest)
Strength-4
Weight Gain-4
Fat Loss-4
Side Effects-2
Keep Gains--4

_______________________________________________
this is far from true. from my experience, as well as others i train with, GH alone is a rating of 0 for strength, weight gain. maybe a 1 for fat loss. ive ran it for about 8 months. i did notice a huge magnifying effect when combined with 17AA as well as test. the GH seemed to magniify the effects.
 
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