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HGH does shutdown T3
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Because of the extra free T3 caused by the hGH, your TSH levels go down, which means when the H is stopped your T3 levels will drop, too. That's why longterm H users take T3 and nothing more!
Growth hormone administration stimulates energy expenditure and extrathyroidal conversion of thyroxine to triiodothyronine in a dose dependent manner and suppresses circadian thyrotrophin levels: studies in GH deficient adults.
Author
Jørgensen JO; Møller J; Laursen T; Orskov H; Christiansen JS; Weeke J
Address
Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, Denmark.
Source
Clin Endocrinol (Oxf), 41(5):609 14 1994 Nov
Abstract
OBJECTIVE: The impact of exogenous GH on thyroid function remains controversial although most data add support to a stimulation of peripheral T4 to T3 conversion. For further elucidation we evaluated iodothyronine and circadian TSH levels in GH deficient patients as part of a GH dose response study. PATIENTS: Eight GH deficient adults, who received stable T4 substitution due to central hypothyroidism; two patients, who were euthyroid without T4 supplementation were studied separately. DESIGN: All patients were initially studied after at least 4 weeks without GH followed by 3 consecutive 4 week periods in fixed order during which they received daily doses of 1, 2 and 4 IU of GH/m2 body surface area. The patients were hospitalized for 24 hours at the end of each period. MEASUREMENTS: Circulating total and free concentrations of T4 and T3, total rT3 and TSH were measured once at the end of each study period. Circadian TSH levels were recorded during the period without GH and during GH treatment with 2 IU GH. RESULTS: Highly significant GH dose dependent increases in total and free T3 and a reduction in rT3 were observed. The T3/T4 ratio also increased with increasing GH dosages (P < 0.001). In seven patients subnormal T3 levels were recorded in the period off GH, despite T4 levels well within the normal range. Resting energy expenditure also increased and correlated with free T3 levels (r = 0.47, P < 0.05). The circadian TSH levels exhibited a significant nocturnal increase during the period without GH, whereas GH therapy significantly suppressed the TSH levels and blunted the circadian rhythm (mean TSH levels (mU/l) 0.546 +/ 0.246 (no GH) vs 0.066 +/ 0.031 (2 IU GH) (P < 0.05)). The two euthyroid non T4 substituted patients exhibited qualitatively similar changes in all parameters. CONCLUSIONS: GH administration stimulated peripheral T4 to T3 conversion in a dose dependent manner. Serum T3 levels were subnormal despite T4 substitution when the patients were off GH but normalized with GH therapy. Energy expenditure increased with GH and correlated with free T3 levels. GH caused a significant blunting of serum TSH. These findings suggest that GH plays a distinct role in the physiological regulation of thyroid function in general, and of peripheral T4
Question?
Does IGF produce the same effect on thyroid function as GH does? I guess it depends on if the effects from GH is before its conversion to IGF in the liver or a byproduct of it not directly linked to IGF; or it is the IGF causing it. I'd be very interested, if any knows which ones is the case and why?
Answer:
I have not found, nor have I seen any evidence that I affects T3. IN fact, in head to head studies done with I+T3 against hGH alone, the I+T3 was beaten by the H and they couldn't/can't figure out what caused it.
Now yes, that T rise from the H could be the prime reason for fat loss, but the I created by the H or I alone if using it, cause a DIRECT change in the FAT CELLS which keeps them from adding any more calories and more likely to be in lipolysis.
It could be that mechanism which is affected after 1 month of I and then you have to add in H if you want gains to continue, HOWEVER, it could just be the T3 which may enable the gains to continue as that is the biggest contributor of H!
HGH does shutdown T3
--------------------------------------------------------------------------------
Because of the extra free T3 caused by the hGH, your TSH levels go down, which means when the H is stopped your T3 levels will drop, too. That's why longterm H users take T3 and nothing more!
Growth hormone administration stimulates energy expenditure and extrathyroidal conversion of thyroxine to triiodothyronine in a dose dependent manner and suppresses circadian thyrotrophin levels: studies in GH deficient adults.
Author
Jørgensen JO; Møller J; Laursen T; Orskov H; Christiansen JS; Weeke J
Address
Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, Denmark.
Source
Clin Endocrinol (Oxf), 41(5):609 14 1994 Nov
Abstract
OBJECTIVE: The impact of exogenous GH on thyroid function remains controversial although most data add support to a stimulation of peripheral T4 to T3 conversion. For further elucidation we evaluated iodothyronine and circadian TSH levels in GH deficient patients as part of a GH dose response study. PATIENTS: Eight GH deficient adults, who received stable T4 substitution due to central hypothyroidism; two patients, who were euthyroid without T4 supplementation were studied separately. DESIGN: All patients were initially studied after at least 4 weeks without GH followed by 3 consecutive 4 week periods in fixed order during which they received daily doses of 1, 2 and 4 IU of GH/m2 body surface area. The patients were hospitalized for 24 hours at the end of each period. MEASUREMENTS: Circulating total and free concentrations of T4 and T3, total rT3 and TSH were measured once at the end of each study period. Circadian TSH levels were recorded during the period without GH and during GH treatment with 2 IU GH. RESULTS: Highly significant GH dose dependent increases in total and free T3 and a reduction in rT3 were observed. The T3/T4 ratio also increased with increasing GH dosages (P < 0.001). In seven patients subnormal T3 levels were recorded in the period off GH, despite T4 levels well within the normal range. Resting energy expenditure also increased and correlated with free T3 levels (r = 0.47, P < 0.05). The circadian TSH levels exhibited a significant nocturnal increase during the period without GH, whereas GH therapy significantly suppressed the TSH levels and blunted the circadian rhythm (mean TSH levels (mU/l) 0.546 +/ 0.246 (no GH) vs 0.066 +/ 0.031 (2 IU GH) (P < 0.05)). The two euthyroid non T4 substituted patients exhibited qualitatively similar changes in all parameters. CONCLUSIONS: GH administration stimulated peripheral T4 to T3 conversion in a dose dependent manner. Serum T3 levels were subnormal despite T4 substitution when the patients were off GH but normalized with GH therapy. Energy expenditure increased with GH and correlated with free T3 levels. GH caused a significant blunting of serum TSH. These findings suggest that GH plays a distinct role in the physiological regulation of thyroid function in general, and of peripheral T4
Question?
Does IGF produce the same effect on thyroid function as GH does? I guess it depends on if the effects from GH is before its conversion to IGF in the liver or a byproduct of it not directly linked to IGF; or it is the IGF causing it. I'd be very interested, if any knows which ones is the case and why?
Answer:
I have not found, nor have I seen any evidence that I affects T3. IN fact, in head to head studies done with I+T3 against hGH alone, the I+T3 was beaten by the H and they couldn't/can't figure out what caused it.
Now yes, that T rise from the H could be the prime reason for fat loss, but the I created by the H or I alone if using it, cause a DIRECT change in the FAT CELLS which keeps them from adding any more calories and more likely to be in lipolysis.
It could be that mechanism which is affected after 1 month of I and then you have to add in H if you want gains to continue, HOWEVER, it could just be the T3 which may enable the gains to continue as that is the biggest contributor of H!
