Hgh length?

I've commented on the 2006 Anthony Roberts article before making these claims based on rodent data (note that rat GH is a different compound altogether from 22-K hGH).

The crux of that article is that:

There's rodent data that intramuscular IGF-I is related to replacement doses of rat GH+T3 (remember different GH molecule) in rats whose thyroid was removed. There's some statistical evidence suggesting similarilities in gene transcription between rat GH & T3 binding... This is such tangential, unrelated minutae to supraphysiological rhGH use that it's baffling. I have not seen evidence of tethering between thyroid function & growth hormone function in human genomic work.

Frankly, I don't really know what AR was thinking. But this was never supported in human data & is a wild outlier (it's bro science with a very convoluted pseudoscientific spin). This article is the only source that has ever existed that makes these claims regarding hGH. They have not withstood the test of time well (except being raised as support for the notion that T4+rhGH is a good idea on bodybuilding forums).

T3 increases with exogenous rhGH administration due to peripheral conversion of T4 to T3. Great. The increase in T3 contributes about 50% to GH's increase in REE. GH's primary lipolytic mechanisms have nothing to do with REE nor thyroid. That alone should tell you the unbelievable irrelevance of this 2006 article today.

If you want to keep taking T4 with your rhGH, by all means! It's just unnecessary.

Exactly !!!
Broscience:rolleyes:
T4 is not essential with GH.
 
I've commented on the 2006 Anthony Roberts article before making these claims based on rodent data (note that rat GH is a different compound altogether from 22-K hGH).

The crux of that article is that:

There's rodent data that intramuscular IGF-I is related to replacement doses of rat GH+T3 (remember different GH molecule) in rats whose thyroid was removed. There's some statistical evidence suggesting similarilities in gene transcription between rat GH & T3 binding... This is such tangential, unrelated minutae to supraphysiological rhGH use that it's baffling. I have not seen evidence of tethering between thyroid function & growth hormone function in human genomic work.

Frankly, I don't really know what AR was thinking. But this was never supported in human data & is a wild outlier (it's bro science with a very convoluted pseudoscientific spin). This article is the only source that has ever existed that makes these claims regarding hGH. They have not withstood the test of time well (except being raised as support for the notion that T4+rhGH is a good idea on bodybuilding forums).

T3 increases with exogenous rhGH administration due to peripheral conversion of T4 to T3. Great. The increase in T3 contributes about 50% to GH's increase in REE. GH's primary lipolytic mechanisms have nothing to do with REE nor thyroid. That alone should tell you the unbelievable irrelevance of this 2006 article today.

If you want to keep taking T4 with your rhGH, by all means! It's just unnecessary.
Excellent post! I'm so glad I started this discussion. I'll keep taking it just because there's no harm, but I understand it isn't nessesary. You should make a post on HGH and Insulins synergy and possible dosage guidelines!
 
I wanted to run HGH for 9-10 months but some people in other threads say 6 and a month break. Is there any reason I can't? Any harm? Looking at 5iu everyday
check out your IGF-1 before. If you'll get more than 200 you don't need HGH
 
The main possible reason is an increase in the number of antibodies to growth hormone in your body. Recombinant growth hormone is a foreign molecule that, in any case, will cause the body's immune response to administration. After their number is too high, the growth hormone will simply stop working. In order for the antibodies to decrease, it is necessary to take a break between your HGH courses.
 
The main possible reason is an increase in the number of antibodies to growth hormone in your body. Recombinant growth hormone is a foreign molecule that, in any case, will cause the body's immune response to administration. After their number is too high, the growth hormone will simply stop working. In order for the antibodies to decrease, it is necessary to take a break between your HGH courses.
Nonsense. The antigenicity arising due to rhGH, which is very rare (1.4 - 2.8%), with long-term use has no clinical relevance (no effect on GH response). Rather, the decrement in serum IGF-I that occurs is likely due to receptor or signaling desensitization or possibly binding protein dynamics.

Anyhow it does happen. Practical protocols for rhGH should be cyclical in design.
 
Nonsense. The antigenicity arising due to rhGH, which is very rare (1.4 - 2.8%), with long-term use has no clinical relevance (no effect on GH response). Rather, the decrement in serum IGF-I that occurs is likely due to receptor or signaling desensitization or possibly binding protein dynamics.

Anyhow it does happen. Practical protocols for rhGH should be cyclical in design.
Is exogenous gh stronger then endogenous. 2 iu genotropin vs 2 iu your body
 
I've commented on the 2006 Anthony Roberts article before making these claims based on rodent data (note that rat GH is a different compound altogether from 22-K hGH).

The crux of that article is that:

There's rodent data that intramuscular IGF-I is related to replacement doses of rat GH+T3 (remember different GH molecule) in rats whose thyroid was removed. There's some statistical evidence suggesting similarilities in gene transcription between rat GH & T3 binding... This is such tangential, unrelated minutae to supraphysiological rhGH use that it's baffling. I have not seen evidence of tethering between thyroid function & growth hormone function in human genomic work.

Frankly, I don't really know what AR was thinking. But this was never supported in human data & is a wild outlier (it's bro science with a very convoluted pseudoscientific spin). This article is the only source that has ever existed that makes these claims regarding hGH. They have not withstood the test of time well (except being raised as support for the notion that T4+rhGH is a good idea on bodybuilding forums).

T3 increases with exogenous rhGH administration due to peripheral conversion of T4 to T3. Great. The increase in T3 contributes about 50% to GH's increase in REE. GH's primary lipolytic mechanisms have nothing to do with REE nor thyroid. That alone should tell you the unbelievable irrelevance of this 2006 article today.

If you want to keep taking T4 with your rhGH, by all means! It's just unnecessary.


Interesting. I could have sworn I saw blood tests posted here and other forums with T4 dropping and T3 increasing upon administration of hgh - and guys taking 75-100 of T4 to offset this. Of course I can't find an example now . . .
 
Is exogenous gh stronger then endogenous. 2 iu genotropin vs 2 iu your body
No. I won't confuse you getting into the ~6% 20 kDa GH we have in circulation, since it's not clinically nor practically relevant. For all intents & purposes, rhGH is equipotent to endogenous GH.
Interesting. I could have sworn I saw blood tests posted here and other forums with T4 dropping and T3 increasing upon administration of hgh - and guys taking 75-100 of T4 to offset this. Of course I can't find an example now . . .
Yes, there is a decrement in serum T4. This happens for everyone due to increased peripheral conversion to T3. It does not follow that you have to supplement it. If someone's T4 falls out of range (low) after rhGH, then it indicates they had pre-existing central hypothyroidism that was as yet undetected.
 
Yes, there is a decrement in serum T4. This happens for everyone due to increased peripheral conversion to T3.
ome of them you absolutely should not use in synergy, e.g. yohimbine and clen, or clen and the ECA stack, or yohimbine and the ECA stack, for example. T3 and rhGH also. T4 and rhGH watch for potential thyrotoxicosis.
Last quote from:

What is the reason behind NOT using rHGH and T3 ( for those who are hypothyroidal, e.g. 100/25 T4/T3) that you stated?
I guess not to shutdown your thyroid and fuck T4 production, but for those of us who already take T4 and T3 is there any problem regarding rHGH not doing its job properly or not letting it pheripherically convert T4 to T3 due to the supplementation of T3?
Or was more like what you said about the T4 supplementation and higher converstion to T3 ending in thyrotoxicosis?
 
Yes, there is a decrement in serum T4. This happens for everyone due to increased peripheral conversion to T3. It does not follow that you have to supplement it. If someone's T4 falls out of range (low) after rhGH, then it indicates they had pre-existing central hypothyroidism that was as yet undetected.
My t4 went to 4.9 and then 4.4 on hgh.
 
Anyone got and tested gold tops in the meantime?

Nonsense. The antigenicity arising due to rhGH, which is very rare (1.4 - 2.8%), with long-term use has no clinical relevance (no effect on GH response). Rather, the decrement in serum IGF-I that occurs is likely due to receptor or signaling desensitization or possibly binding protein dynamics.

Anyhow it does happen. Practical protocols for rhGH should be cyclical in design.

Do you see a problem with being on 3-4 iu long term without breaks? For angi aging
 
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