MESO-Rx
Anabolic Steroids
Let's grow October 24th - January 30th
- Thread starter Wunderpus
- Start date
" It was furthermore observed that T3 levels during placebo were significantly decreased compared to an untreated healthy control group. "
I believe you are having great experience with those three no doubt.
GH doesn't suppress T3 levels. It will actually increase them. I think L. Rea is incorrect here. RIP.
mands
Any resources on that? I've never heard this... Even Dr Jim has commented on it in the past however, it typically does not need to be supplemented because normal t3 levels will return in time.
I've also always read that T4 is virtually useless because the body will not convert any more T4 to T3 even if there is an abundance of T4 in the body. hGH is supposed to suppress the conversion.
Send to
Int J Clin Pharmacol Ther. 2004 Jan;42(1):30-4.
Effects of recombinant growth hormone therapy on thyroid hormone concentrations.
Kalina-Faska B1, Kalina M, Koehler B.
Author information
Abstract
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.
mands
Int J Clin Pharmacol Ther. 2004 Jan;42(1):30-4.
Effects of recombinant growth hormone therapy on thyroid hormone concentrations.
Kalina-Faska B1, Kalina M, Koehler B.
Author information
Abstract
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.
mands
I know, that's what I found interesting, too. I wasn't using that to back up my claim, I found it to be interesting and contradictory to my claim...
Clin Endocrinol (Oxf). 1994 Nov;41(5):609-14.
Growth hormone administration stimulates energy expenditure and extrathyroidal conversion of thyroxine to triiodothyronine in a dose-dependent manner and suppresses circadian thyrotrophin levels: studies in GH-deficient adults.
Jørgensen JO1, Møller J, Laursen T, Orskov H, Christiansen JS, Weeke J.
Author information
Abstract
OBJECTIVE:
The impact of exogenous GH on thyroid function remains controversial although most data add support to a stimulation of peripheral T4 to T3 conversion. For further elucidation we evaluated iodothyronine and circadian TSH levels in GH-deficient patients as part of a GH dose-response study.
PATIENTS:
Eight GH-deficient adults, who received stable T4 substitution due to central hypothyroidism; two patients, who were euthyroid without T4 supplementation were studied separately.
DESIGN:
All patients were initially studied after at least 4 weeks without GH followed by 3 consecutive 4-week periods in fixed order during which they received daily doses of 1, 2 and 4 IU of GH/m2 body surface area. The patients were hospitalized for 24 hours at the end of each period.
MEASUREMENTS:
Circulating total and free concentrations of T4 and T3, total rT3 and TSH were measured once at the end of each study period. Circadian TSH levels were recorded during the period without GH and during GH treatment with 2 IU GH.
RESULTS:
Highly significant GH dose-dependent increases in total and free T3 and a reduction in rT3 were observed. The T3/T4 ratio also increased with increasing GH dosages (P < 0.001). In seven patients subnormal T3 levels were recorded in the period off GH, despite T4 levels well within the normal range. Resting energy expenditure also increased and correlated with free T3 levels (r = 0.47, P < 0.05). The circadian TSH levels exhibited a significant nocturnal increase during the period without GH, whereas GH therapy significantly suppressed the TSH levels and blunted the circadian rhythm (mean TSH levels (mU/l) 0.546 +/- 0.246 (no GH) vs 0.066 +/- 0.031 (2 IU GH) (P < 0.05)). The two euthyroid non-T4 substituted patients exhibited qualitatively similar changes in all parameters.
CONCLUSIONS:
GH administration stimulated peripheral T4 to T3 conversion in a dose-dependent manner. Serum T3 levels were subnormal despite T4 substitution when the patients were off GH but normalized with GH therapy. Energy expenditure increased with GH and correlated with free T3 levels. GH caused a significant blunting of serum TSH. These findings suggest that GH plays a distinct role in the physiological regulation of thyroid function in general, and of peripheral T4 metabolism in particular.
mands
Growth hormone administration stimulates energy expenditure and extrathyroidal conversion of thyroxine to triiodothyronine in a dose-dependent manner and suppresses circadian thyrotrophin levels: studies in GH-deficient adults.
Jørgensen JO1, Møller J, Laursen T, Orskov H, Christiansen JS, Weeke J.
Author information
Abstract
OBJECTIVE:
The impact of exogenous GH on thyroid function remains controversial although most data add support to a stimulation of peripheral T4 to T3 conversion. For further elucidation we evaluated iodothyronine and circadian TSH levels in GH-deficient patients as part of a GH dose-response study.
PATIENTS:
Eight GH-deficient adults, who received stable T4 substitution due to central hypothyroidism; two patients, who were euthyroid without T4 supplementation were studied separately.
DESIGN:
All patients were initially studied after at least 4 weeks without GH followed by 3 consecutive 4-week periods in fixed order during which they received daily doses of 1, 2 and 4 IU of GH/m2 body surface area. The patients were hospitalized for 24 hours at the end of each period.
MEASUREMENTS:
Circulating total and free concentrations of T4 and T3, total rT3 and TSH were measured once at the end of each study period. Circadian TSH levels were recorded during the period without GH and during GH treatment with 2 IU GH.
RESULTS:
Highly significant GH dose-dependent increases in total and free T3 and a reduction in rT3 were observed. The T3/T4 ratio also increased with increasing GH dosages (P < 0.001). In seven patients subnormal T3 levels were recorded in the period off GH, despite T4 levels well within the normal range. Resting energy expenditure also increased and correlated with free T3 levels (r = 0.47, P < 0.05). The circadian TSH levels exhibited a significant nocturnal increase during the period without GH, whereas GH therapy significantly suppressed the TSH levels and blunted the circadian rhythm (mean TSH levels (mU/l) 0.546 +/- 0.246 (no GH) vs 0.066 +/- 0.031 (2 IU GH) (P < 0.05)). The two euthyroid non-T4 substituted patients exhibited qualitatively similar changes in all parameters.
CONCLUSIONS:
GH administration stimulated peripheral T4 to T3 conversion in a dose-dependent manner. Serum T3 levels were subnormal despite T4 substitution when the patients were off GH but normalized with GH therapy. Energy expenditure increased with GH and correlated with free T3 levels. GH caused a significant blunting of serum TSH. These findings suggest that GH plays a distinct role in the physiological regulation of thyroid function in general, and of peripheral T4 metabolism in particular.
mands
These were hGH deficient kids as well, I'm wondering what part that might play....
I was stating for anyone else that was reading big guy. I knew why you posted it.
mands
Looks like they are doing .7 units per kg of body weight, per week? So, for me that would be 102 x .7 = 71.4, so roughly 10iu/day?
Morning boys and girls. Quick update, I ordered some IGF-1 LR3 from Maxim Peptides earlier this week, and gave a shot of 50mcg's ~40 minutes pre workout a try yesterday. This is EXACTLY what I would've expected from IGF-1... Transformix made me feel this way too... Kind of hypo, but full and SUPER pumped and hard. I wanted to not take any orals or a pre workout to make sure it was the IGF-1... Seems to be pretty solid. Now, is this a perfect way to test/review this product? No.... But, it certainly did SOMETHING! I was VERY full hours after my workout, as well... Just my quick review of that product.
Oh, and I will have 2 kits on the way of IGF-1 LR3 from Karl shortly.... Standby for reviews on those as well.
Oh, and I will have 2 kits on the way of IGF-1 LR3 from Karl shortly.... Standby for reviews on those as well.
2Dumb2Plumb
Banned
I'm expecting some IFBB level mass from this log... by the way isn't igf suppose to be taken after a workout?
Yes, and no. It really depends, but the general consensus is yes. HOWEVER, I wanted to test it out, and I know what it feels like pre workout, if you know what I mean? I won't use it pre workout for my protocol, but I knew that was a good way to see it's effects.
@Wunderpus, have you ever used injectable superdrol? I got some as an extra a few months back and I'm thinking I'm going to run it the last few weeks leading into my next meet in the summer. If you have what are your thoughts on it? I can't find much in the way of first hand experience and I think I remember you mentioning it at some point.
2Dumb2Plumb
Banned
There's no merit in this. But do you follow YouTube peeps like Rich Piana? He had a video up that skewered Boston Loyds claims that peptide companies can make pure igf1 lr3. The claim he makes that there is only two licensed companies that are FDA approved to make igf and he goes on to claim that what peptide companies are selling is garbage.
He also has said he doesn't use synthol/PMMA/Collagen and that it's impossible to brew gear at or above 300mgs/ml... Soooooo
Also, as a follow-up to this... I have spoken many times with Bostin now. We've chatted about just about anything and everything, I've used his peptides back in the day as well as his synthol. He's MUCH more intelligent and knowledgeable than he comes off in his videos... He kind of has a curse of the "bro" way of speaking, and also is about as horrible of a typer as a human can be.... BUT, he does know WAYYYY more than you'd ever guess about just about every aspect of bodybuilding... Rich on the other hand, i've never had any first hand experience with. I can tell by the way he talks about shit, and by looking at him, he's a lying sack of shit.
ronin17
New Member
Yeah, piana is a perfect example of someone who has lost thier fucking mind on these drugs. He regularly spouts his opinion as fact.
Ever noticed how jaundiced looking he is? I wouldnt take anything that guy says as fact.
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