As
@Worldsfastestfatty mentioned, I put together a post about T4 & its combination with rhGH in
The Definitive Thyroid Hormone Thread (T3, T4, some implications for rhGH).
A member of ours, M@NU (who is impossible to tag - possibly by design - because of the @ in his username) has suffered overt thyrotoxycosis, which is a theoretical risk with rhGH + T4 - but I am unsure whether it was due to rhGH & T4 in combination.
Aside from this risk however, the combined use of T4 & rhGH is just not well supported. Its popularity seems to originate from an Anthony Roberts article, from 2006 (when Roberts may have held a financial interest in supplying T4; but this is unconfirmed). With respect to that article, the crux of Roberts' argument was:
Now, as we’ve seen, GH is HIGHLY synergistic with T3 in the body, and as a mater of fact, if you’ve been paying any attention up until this point, you’ll note that the limiting factor on GH’s ability to exert many of it’s effects, is mediated by the amount of T3 in the body.
As noted before, T3 enhances many effects of GH by several mechanisms, including (but not limited to): increasing IGF-1 levels, IGF-1 mRNA levels, and finally by actually mediating the control of the growth hormone gene transcription process as seen below:
Comparison of the kinetics of L-T3-receptor binding abundance to changes in the rate of transcription of the GH gene.(3)
As you can see, T3 levels are directly correlative to GH gene transcription. The scientists who conducted the study which provided the graph above concluded that the amount of T3 present is a regulatory factor on how much GH gene transcription actually occurs. And gene transcription is what actually gives us the effects from GH. This last fact really seems to shed some light on why we need T3 levels to be supraphysiological if we’re going to be using supraphysiological levels of GH, right?
There's rodent data that intramuscular IGF-I is related to replacement doses of rat GH+T3 (rat GH is an entirely different molecule than human GH) 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 Roberts was thinking. But combined rhGH & T4 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 & T4. 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 (i.e., in skeletal muscle) 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 (only in part). 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, and comes with the risk of inducing overt thyrotoxycosis. If you do see a decrement to sub-normal T4 levels on blood-work, then that indicates
preexisting central hypothyroidism (rather than rhGH as a cause), and you can more wisely decide to use exogenous T4.