Detecting when you might need t3 when on hgh?

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    Detecting when you might need t3 when on hgh?


    Hello im on a cycle of hgh along with an aas stack. Really love it so far. What signs should i be looking for if im in need of t3. Im also taking clen and albuterol. I am eating along during the day to maintain sugar levels.

    Regards

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    i dont know but im interestead. My friend just got some somatropin and he mentioned using T3 i said i never heard of using it while on GH....

    ear on door....
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    Most sites and sources tend to say that for gh to really work well you need a synergistic stack of insulin, t3 along with gh. Well both insulin and t3 can be really dangerous. So far my experience with gh has been great at 4 iu a day. Along with A stack of equi, masteron, and clen, albuterol. I think the its important to eat a lot of meals during the day to keep insulin levels up.
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    You will need both T3/T4, like armor thryroid.
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    Post How do you know you need T3 when on hGH?


    ...well, you know you need T3 if you wake up tomorrow morning, and its really 2 weeks later

    Seriously, when on cycle along with hGH or even just stand alone, it is very difficult to use "lethargy" as a gauge to justify you need T3 and how much...
    Best to get full thyroid blood workup: TSH, Free T4, Free T3, possibly even Reverse T3.

    The general study info points to hGH affecting thyroid function via changes in specific types of deiodinaise enzymes (increase Type I or "D1") responsible for an increased conversion of T4 to T3 (in peripheral tissue) . However, some newer research points to a decrease in D3 (Type III) being the reason, which would normally breakdown T3 and T4 into inactive forms. Either way the end result is eventual increases in T3 levels.
    It is speculated that the increase in T3 eventually leads to the negative feedback response, thus appropriately decreasing TSH and thus thyroid hormone levels.
    Increases in Somatostatin (GH/IGF-1 mediated) have also been proposed to influence Thyroid, as SS is also a contributing factor in thyroid function.

    Here is some info regarding this:

    At least two mechanisms have been suggested to underlie the recorded changes. The first points to an increase in peripheral conversion of T4 to T3 along with a decreased conversion of T4 to rT3, selectively mediated by GH (Sato et al., 1977; Grunfeld et al., 1988; Jørgensen et al., 1989; Salomon et al., 1989; Burman et al., 1996; Portes et al., 2000). The second suggests an inhibition of TSH release (Cobb et al., 1981; Grunfeld et al., 1988) via either an increased somatostatinergic tone or a T3-negative feedback mechanism within the pituitary, due to increased T3 production from T4 deiodination (Oliner & Ballantine, 1968; Porter et al., 1973; Sato et al., 1977; Rezvani et al., 1981; Cabello & Wrutniak, 1989; Salomon et al., 1989; Jørgensen et al., 1994).
    Specific type I and type III deiodinase tests (5'D-I and 5D-III), however, show that GH has no effect at all on the amount of hepatic type I enzyme (catalyzing T4 deiodination to T3) but acutely decreases the amount of type III enzyme (catalyzing T3 deiodination). This suggests that the GH-induced increase in plasma T3 is not due to an increased T3 production, but is the result of a decreased T3 breakdown.
    Take Care.
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    you need t4, t3 and gh fight for the same receptors. t4 converts into t3, supplementing t3 will greatly diminish the gh's effectiveness. SO I HAVE BEEN TOLD.
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    Quote Originally Posted by king1033 View Post
    you need t4
    In fact, exogenous T4 or T3 is fine. Some claim that exogenous T4 will be less suppressive on the thyroid. Truth is I see no evidence, but do see the facts that both T4 and T3 individually impart a negative feedback resoponse on the Hypothalmus-Pituitary-Thyroid Axis, decreasing TRH and TSH...
    With T4 you are just letting your body determine how much additional T3 it can convert the surplus of T4 into...

    t3 and gh fight for the same receptors.
    Ahhh, the mysterious G3 receptor? j/k

    Not true my friend. Although hormones do agonize a variety "non native" receptors (ex. hGH -->GHR & PRLR),
    there is no "fight" between GH and T3.
    T3's effects are mediated by TR (thyroid receptor)alpha and beta. GH's effects are mediated by the GHR as well as the GH mediated IGF-1 that agonizes IGF-1 receptors
    T3 upregulates both GHR and IGF-1R mRNA which obviously makes GH more efficient at carring out its task.
    GH on the otherhand is responsible for eventually lowering T3 levels (see my previous post). You can see how the relationship is structured. There is MUCH more to the Thyroid-GH/IGF-1 relationship than just this....

    t4 converts into t3
    True. Iodothyronine Deiodinase Type 1 and 2 are responsible for the conversion of Thyroxine (T4) to Tri-iodothironine (T3).
    Deiodinase Type 3 is responsible for conversion of T4 and T3 into inactive forms.

    supplementing t3 will greatly diminish the gh's effectiveness. SO I HAVE BEEN TOLD.
    Sorry, I do not agree with this.

    The actual issue (in the BB arena) started with an article by Anthony Roberts. Although many of his facts in the article were properly cited, his own conclusions were flawed in my opinion (and many others who understand the specifics).

    http://mesomorphosis.com/articles/an...th-hormone.htm

    In summary, he concluded that increasing T3 (exogenously) in the presence of decreased T4, which occurs via the increased (GH mediated) peripheral T4 to T3 conversion, would lead to upregulated deiodinase Type 3 (D3) and downregulated D1 and D2. This was his basis for supporting that T3 would be ineffective comapared to T4. High D3 would "negate" T3's intended effects (as it would convert T3 to inactive metabolites). Actually, his way of stating his reasoning is much more bizaar as he states that it is the T4 to T3 conversion process that is responsible for the effects of T3 and NOT T3 in itself. This is the most bizaar statement in the whole article and defies the whole concept and target of Thyroid Hormone function.
    In reality this is all much more complex than any of this and there are missing pieces in the conclusions above.
    The fact is that the up and downregulation of deiodinases is only one piece and what is not taken into account is that both T4 AND T3 are targets (of "inactivation") of D3, NOT just T3 as Anthony proposes. This greatly changes things.
    Even in spite of this proposed possibility, exogenous doses are "exogenous" and adjustible and ultimately not necessarily limited by any of the bodies endogenous adjustments...

    The only thing I see in all this is that there really is not much difference in the end, between T4 or T3 supplementation. neither in protocol efficiency, nor in the suppression of the H-P-Thyroid Axis.
    Nothing, at least, that I have seen concrete evidence of.

    If anyone has any info that could enlighten me as to anything talked about here please feel free to chime in...

    Take care.
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    good info bobaslaw, im part of a couple good BB forums and have read many things this is what i stumbled across as well up until this point is where im stuck at but through much debate and reading i am more comfortable with supplementing with t4 until this issue can be straightend out. other than that perhaps the t3/t4 mixture pills might be good to give a go? also what do you guys feel would be symtoms that your thyroid is being interfered with. in other words symptoms that gh is starting to lower your thyroid.

    Quote Originally Posted by Bobaslaw View Post
    In fact, exogenous T4 or T3 is fine. Some claim that exogenous T4 will be less suppressive on the thyroid. Truth is I see no evidence, but do see the facts that both T4 and T3 individually impart a negative feedback resoponse on the Hypothalmus-Pituitary-Thyroid Axis, decreasing TRH and TSH...
    With T4 you are just letting your body determine how much additional T3 it can convert the surplus of T4 into...



    Ahhh, the mysterious G3 receptor? j/k

    Not true my friend. Although hormones do agonize a variety "non native" receptors (ex. hGH -->GHR & PRLR),
    there is no "fight" between GH and T3.
    T3's effects are mediated by TR (thyroid receptor)alpha and beta. GH's effects are mediated by the GHR as well as the GH mediated IGF-1 that agonizes IGF-1 receptors
    T3 upregulates both GHR and IGF-1R mRNA which obviously makes GH more efficient at carring out its task.
    GH on the otherhand is responsible for eventually lowering T3 levels (see my previous post). You can see how the relationship is structured. There is MUCH more to the Thyroid-GH/IGF-1 relationship than just this....



    True. Iodothyronine Deiodinase Type 1 and 2 are responsible for the conversion of Thyroxine (T4) to Tri-iodothironine (T3).
    Deiodinase Type 3 is responsible for conversion of T4 and T3 into inactive forms.



    Sorry, I do not agree with this.

    The actual issue (in the BB arena) started with an article by Anthony Roberts. Although many of his facts in the article were properly cited, his own conclusions were flawed in my opinion (and many others who understand the specifics).

    Thyroid Hormone + Growth Hormone by Anthony Roberts with James Daemon, Ph.D.

    In summary, he concluded that increasing T3 (exogenously) in the presence of decreased T4, which occurs via the increased (GH mediated) peripheral T4 to T3 conversion, would lead to upregulated deiodinase Type 3 (D3) and downregulated D1 and D2. This was his basis for supporting that T3 would be ineffective comapared to T4. High D3 would "negate" T3's intended effects (as it would convert T3 to inactive metabolites). Actually, his way of stating his reasoning is much more bizaar as he states that it is the T4 to T3 conversion process that is responsible for the effects of T3 and NOT T3 in itself. This is the most bizaar statement in the whole article and defies the whole concept and target of Thyroid Hormone function.
    In reality this is all much more complex than any of this and there are missing pieces in the conclusions above.
    The fact is that the up and downregulation of deiodinases is only one piece and what is not taken into account is that both T4 AND T3 are targets (of "inactivation") of D3, NOT just T3 as Anthony proposes. This greatly changes things.
    Even in spite of this proposed possibility, exogenous doses are "exogenous" and adjustible and ultimately not necessarily limited by any of the bodies endogenous adjustments...

    The only thing I see in all this is that there really is not much difference in the end, between T4 or T3 supplementation. neither in protocol efficiency, nor in the suppression of the H-P-Thyroid Axis.
    Nothing, at least, that I have seen concrete evidence of.

    If anyone has any info that could enlighten me as to anything talked about here please feel free to chime in...

    Take care.
  

  
 

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