Type-IIx
Well-known Member
The problem with taking exogenous T3 and rhGH is at least additive protein breakdown and dysregulation of the HPT axis (hypothalamo-thyro). If talking exogenous T4+T3, then you're increasing the risk for overt thyrotoxicosis.Last quote from:
Fat Loss via other mechinisms
What compounds promote fat loss by other mechanisms besides appetite suppression? Which allow for a caloric deficit. So if you eat at maintenance yet use these various compounds you will still lose body fat, due to other mechanisms at play. I know some increase temperature, so thermogenic. I...thinksteroids.com
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?
T3 causes net protein breakdown (yes it increases protein turnover, resulting in more protein loss). Further, it preferentially catabolizes hypertrophied muscle (reflected by reduction to type IIA fiber cross-sectional area).
Did you ever read the thyroid hormone effects on protein turnover (Peter Bond Article)?. Most noteworthy, 75 µg of exogenous T3 increases RMR by 15% and 100 µg exogenous T3 for 2 weeks reduced type IIA fiber CSA (this reflects hypertrophied muscle) in line with this increased RMR (though there may be some compensatory mechanism that antagonizes the protein catabolic effects over longer periods, staving off further muscle loss).