T4+HGH off test cycle, advisable?

A more appropriate term rather than "caused" would be resulted in.

However routine supplementation of thyroxine is NOT recommended since, as this study revealed, the resultant rise in TSH from GH use will normalize thyroxine levels in due course.

Consequently thyroxine supplementation in this instance only negates those physiologic processes designed to remedy it.

Can I read this as "use GH, but don't add T3 or T4?"?
 
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.

Just another study to add that goes along with an earlier posted study in this thread.

mands
 
Just another study to add that goes along with an earlier posted study in this thread.

mands

Nice cut and paste but it doesn't support your claim that T4 "enhances the effects of the GH."

Okay here it is.. when you are running Gh and then add t4 you actually increase the conversion of t4 to t3 . This will give you a greater effect. So, basically adding t4 to a Gh cycle you are making the GH more effective.

I posted why I use it. It enhances the effects of the GH.

What evidence do you have to support these statements? So far you've posted none.

GH leading to transient decreases in T4 and increased T4 to T3 diiodination is well established in the literature, but that doesn't support the idea that supplemental T4 somehow makes GH work better in euthyroid users. It's bro lore.


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.

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.

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.
 
Nice cut and paste but it doesn't support your claim that T4 "enhances the effects of the GH."





What evidence do you have to support these statements? So far you've posted none.

GH leading to transient decreases in T4 and increased T4 to T3 diiodination is well established in the literature, but that doesn't support the idea that supplemental T4 somehow makes GH work better in euthyroid users. It's bro lore.


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.

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.

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.
I was looking into and found some others I thought were interesting. I didn't post it for you CBS. You can keep coming after me for calling you out I don't really mind. I've made my feelings known and that's all I needed to do.

It will be hard to find a study on what you are actually asking me to do but I have been looking. Not to prove you wrong but to show there is a significance difference for me personally and others when combining the two. Synergy is very common in PED's as you know. As for the actual action that takes place as you can see in my earlier posts and yours that there is something going on when they are introduced.

You could always help me search CBS. You are better than myself at fining scientific evidence and studies. :)

Hey I did say I would post pics of my 3-4 weeks when I added t4 to my gh.

mands
 
It will be hard to find a study on what you are actually asking me to do but I have been looking. Not to prove you wrong but to show there is a significance difference for me personally and others when combining the two. Synergy is very common in PED's as you know. As for the actual action that takes place as you can see in my earlier posts and yours that there is something going on when they are introduced.


Synergy is common with PEDs but thyroid hormone isn't a PED. When GH enhances the diiodination of T4 to T3, the body compensates by making less T4 and TSH. If it didn't, your T3 levels would go supraphysiological.

So when you add even more T4, what do you think is going to happen? You get more T3.

If you're noticing anything going on, it's hyperthyroidism. A stimulant effect. It's no surprise that a stimulant can eliminate the drowsiness and fatigue that everyone complains about when they're on GH.

You see the same phenomenon on thyroid forums, adrenal forms, chronic fatigue forums, etc. You have a bunch of tired people with normal labs that still believe they have hypothyroidism. When their fatigue goes away after starting thyroid hormone, they think that proves they were right. All it proves is too much thyroid hormone acts like a stimulant.
 
If you're noticing anything going on, it's hyperthyroidism. A stimulant effect. It's no surprise that a stimulant can eliminate the drowsiness and fatigue that everyone complains about when they're on GH.

You see the same phenomenon on thyroid forums, adrenal forms, chronic fatigue forums, etc. You have a bunch of tired people with normal labs that still believe they have hypothyroidism. When their fatigue goes away after starting thyroid hormone, they think that proves they were right. All it proves is too much thyroid hormone acts like a stimulant.

I certainly enjoy this effect rather than feeling like a zombie on GH alone..

Let me ask you this, do you think there is any real downside to supplementing T4 with GH?
 
I certainly enjoy this effect rather than feeling like a zombie on GH alone..

Let me ask you this, do you think there is any real downside to supplementing T4 with GH?

Yes, I posted about it earlier. Obviously, the degree of risk associated with hyperthyroidism will depend on severity and duration, but unlike with AAS, there is lots of evidence showing the adverse effect it has on the heart.

Hyperthyroidism for only a few weeks is usually pretty safe, but most are using it for months and months at a time. If you're going to use it, get bloods and keep the dose as low as possible. Don't let your TSH or T4 go out of range. And watch your BP and HR. If it's high - or especially if you're getting those big palpitations that feel like they're going 'boom' when you're lying in bed at night, lower the dose.

It's worth pointing out that thyroid use is not without risk, particularly cardiovascular. Inducing subclinical, and in many cases, overt hyperthyroidism is usually harmless enough in the short term but atrial fibrillation, increased left ventricular mass and septal wall thickening, etc., have all been associated with subclinical hyperthyroidism. Obviously the risks increase the longer you remain in that state and there is lots of evidence demonstrating the risk is real. And keep in mind, cardiomegaly (although a debatable AAS side effect) is already a concern with AAS use. Adding thyroid hormone increases the risk even further.
 
Yes, I posted about it earlier. Obviously, the degree of risk associated with hyperthyroidism will depend on severity and duration, but unlike with AAS, there is lots of evidence showing the adverse effect it has on the heart.

Hyperthyroidism for only a few weeks is usually pretty safe, but most are using it for months and months at a time. If you're going to use it, get bloods and keep the dose as low as possible. Don't let your TSH or T4 go out of range. And watch your BP and HR. If it's high - or especially if you're getting those big palpitations that feel like they're going 'boom' when you're lying in bed at night, lower the dose.

Well duh!! But will it have a negative effect on those GH "gainz"?! haha

Thanks for the info..
 
For what it's worth I was taking t4 for a couple months with my seros. 6iu ed avg (sometimes 9, down to 4 when I can't feel my hands) with 200mcg t4. I had heart palpitations anything over 200 and sometimes at 200. I stopped taking it a month ago and I was tired for a week. Now I'm fine with no other noticeable differences. I'm all for taking the least amount of shit I can- so fuck a t4. Totally anecdotal, but whateva.
 
For what it's worth I was taking t4 for a couple months with my seros. 6iu ed avg (sometimes 9, down to 4 when I can't feel my hands) with 200mcg t4. I had heart palpitations anything over 200 and sometimes at 200. I stopped taking it a month ago and I was tired for a week. Now I'm fine with no other noticeable differences. I'm all for taking the least amount of shit I can- so fuck a t4. Totally anecdotal, but whateva.

That makes sense. Full replacement for most adults is 100 - 125 mcg/day. Since you're quite a bit bigger than most people, a full replacement dose for you is probably a bit higher but it seems 200 was too much and made you hyperthyroid.
 
For what it's worth I was taking t4 for a couple months with my seros. 6iu ed avg (sometimes 9, down to 4 when I can't feel my hands) with 200mcg t4. I had heart palpitations anything over 200 and sometimes at 200. I stopped taking it a month ago and I was tired for a week. Now I'm fine with no other noticeable differences. I'm all for taking the least amount of shit I can- so fuck a t4. Totally anecdotal, but whateva.
That sucks man. I'm good at 200mcg buy I haven't take more than that and I started at 75mcg to 150mcg to 200mcg. I feel great and not tired and have had no heart issues thus far.

@CensoredBoardsSuck hasn't already been discussed and studies that the thyroid levels are decreased in the first weeks or longer during the start of gh use? Then normalizes later during use?

I agree that you should use any drug under close scrutiny and monitor at all times.

mands
 
Synergy is common with PEDs but thyroid hormone isn't a PED. When GH enhances the diiodination of T4 to T3, the body compensates by making less T4 and TSH. If it didn't, your T3 levels would go supraphysiological.

So when you add even more T4, what do you think is going to happen? You get more T3.

If you're noticing anything going on, it's hyperthyroidism. A stimulant effect. It's no surprise that a stimulant can eliminate the drowsiness and fatigue that everyone complains about when they're on GH.

You see the same phenomenon on thyroid forums, adrenal forms, chronic fatigue forums, etc. You have a bunch of tired people with normal labs that still believe they have hypothyroidism. When their fatigue goes away after starting thyroid hormone, they think that proves they were right. All it proves is too much thyroid hormone acts like a stimulant.
I have never had the stimulant effect from t4! Hell I can't even take a preworkout. So I guess my levels don't go super-physiological when supplementing t4 with my gh.

mands
 
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