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Serious what happens when i dont use Thyroid Support (T4) when taking HGH? (1 Viewer)

Serious what happens when i dont use Thyroid Support (T4) when taking HGH?
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i really want to know what happens if i dont take Thyroid Support (T4) while using HGH, what really change?
 

Dexter

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GH and TSH are both reciprocally inhibited by somatostatin (SST). when you administer exogenous rhGH you create supraphysiological levels of GH. this triggers a negative feedback loop that increases somatostatin tone

elevated somatostatin directly inhibits thyrotropin releasing hormone from the hypothalamus and TSH from the pituitary. so exogenous HGH suppresses TSH secretion
for a thyroid gland to produce thyroxine and triiodothyronine it requires TSH stimulation. if TSH is suppressed by HGH the thyroid gland downregulates its synthetic output

wo thyroid support, this will happen
1) latent central hypothyroidism: peripheral conversion of T4 to T3 (via deiodinase type 2, D2) usually maintains intracellular T3 in the brain and pituitary but HGH alters deiodinase activity and iirc often accelerating T4 catabolism while simultaneously reducing T4 production. you enter a state of euthyroid sick syndrome induced by the HGH itself
2) IGF1 attenuation: the efficacy of the HGH gets fucked. youre injecting HGH but your hepatic cells cant translate that signal into IGF1 production. the anabolic and metablic effects are fucked then
and,

HGH is lipolytic and thyroid hormone is calorigenic. without T4 the synergistic effect is gone
lipid metabolism: T3 upregulates beta adrenergic receptors on adipocytes. without T4/T3 the lipolytic effect of HGH is shit which causes paradoxical lipid accumulation despite high GH levels
protein synthesis: in a hypothyroid state protein synthesis stops. yeah HGH pushes for nitrogen retention but the absence of T3 results in a catabolic state in lean tissue. the net effect shifts from anabolism to fatigue and sarcopenia over time
 

NotGrayCellBTWtheway

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GH and TSH are both reciprocally inhibited by somatostatin (SST). when you administer exogenous rhGH you create supraphysiological levels of GH. this triggers a negative feedback loop that increases somatostatin tone

elevated somatostatin directly inhibits thyrotropin releasing hormone from the hypothalamus and TSH from the pituitary. so exogenous HGH suppresses TSH secretion
for a thyroid gland to produce thyroxine and triiodothyronine it requires TSH stimulation. if TSH is suppressed by HGH the thyroid gland downregulates its synthetic output

wo thyroid support, this will happen
1) latent central hypothyroidism: peripheral conversion of T4 to T3 (via deiodinase type 2, D2) usually maintains intracellular T3 in the brain and pituitary but HGH alters deiodinase activity and iirc often accelerating T4 catabolism while simultaneously reducing T4 production. you enter a state of euthyroid sick syndrome induced by the HGH itself
2) IGF1 attenuation: the efficacy of the HGH gets fucked. youre injecting HGH but your hepatic cells cant translate that signal into IGF1 production. the anabolic and metablic effects are fucked then
and,

HGH is lipolytic and thyroid hormone is calorigenic. without T4 the synergistic effect is gone
lipid metabolism: T3 upregulates beta adrenergic receptors on adipocytes. without T4/T3 the lipolytic effect of HGH is shit which causes paradoxical lipid accumulation despite high GH levels
protein synthesis: in a hypothyroid state protein synthesis stops. yeah HGH pushes for nitrogen retention but the absence of T3 results in a catabolic state in lean tissue. the net effect shifts from anabolism to fatigue and sarcopenia over time
Mirin iq😍
 

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