To T-3 or not to T-3 with HGH?
- Thread starter maxmurph
- Start date
Drveejay11
I am banned!
I vote NOT. AS have the ability to negate any catabolic effects Thyroxine may induce; typical HGH doese would not (near as effectively).
T3 increases SHBG as well.
T3 increases SHBG as well.
Drveejay11
I am banned!
maxmurph said:
If you decide to opt FOR; just keep doses low (20-25 mcg's); you should be fine. My comments (above) were based solely on a "typical" run of T3 and NOT based on a mere 'supplemental' protocol of <25 mcg's.
Last edited:
From the PDR, this is from Serono:
Because human growth hormone may induce a state of insulin resistance, patients should be observed for evidence of glucose intolerance. Human growth hormone should be used with caution in patients with diabetes mellitus or a family history of diabetes mellitus.
Hypothyroidism may develop during Saizen® therapy. Untreated hypothyroidism will jeopardize the response to growth hormone. Therefore, thyroid hormone determinations should be performed periodically during Saizen® administration and thyroid hormone replacement should be initiated when indicated.
Just talk to those stacking T3 or Armour with HGH. I have never received any negative feedback from T3 orArmour/HGH users. The key is to keep the T3 dose steady at 25-50mcg daily in the AM or 60mg Armour in the AM. Just enough to normalize thyroid output.
Because human growth hormone may induce a state of insulin resistance, patients should be observed for evidence of glucose intolerance. Human growth hormone should be used with caution in patients with diabetes mellitus or a family history of diabetes mellitus.
Hypothyroidism may develop during Saizen® therapy. Untreated hypothyroidism will jeopardize the response to growth hormone. Therefore, thyroid hormone determinations should be performed periodically during Saizen® administration and thyroid hormone replacement should be initiated when indicated.
Just talk to those stacking T3 or Armour with HGH. I have never received any negative feedback from T3 orArmour/HGH users. The key is to keep the T3 dose steady at 25-50mcg daily in the AM or 60mg Armour in the AM. Just enough to normalize thyroid output.
ironmaster
Community Veteran, HGH Guru
And what about this, Dr J ?
Recombinant hGH replacement therapy and the hypothalamus-pituitary-thyroid axis in children with GH deficiency: when should we be concerned about the occurrence of central hypothyroidism?
Giavoli C, Porretti S, Ferrante E, Cappiello V, Ronchi CL, Travaglini P, Epaminonda P, Arosio M, Beck-Peccoz P.
Institute of Endocrine Sciences, University of Milan, Ospedale Maggiore IRCCS, Milan, Italy.
OBJECTIVE: Recombinant hGH treatment may alter thyroid hormone metabolism and we have recently reported that 50% of patients with GH deficiency (GHD) due to organic lesions, previously not treated with thyroxine, developed hypothyroidism during treatment with recombinant human GH (rhGH). These results prompted us to evaluate the impact of rhGH treatment on thyroid function in children with GHD. DESIGN: Open study of GH treatment up to 12 months. Investigations were performed at baseline, and after 6 and 12 months of GH therapy. MEASUREMENT AND STUDY SUBJECTS: Serum TSH, FT4, FT3, AbTg and AbTPO, IGF-I, height and weight, were evaluated in 20 euthyroid children (group A) with idiopathic isolated GHD and in six children (group B) with multiple pituitary hormone deficiencies (MPHD) due to organic lesions. Among the latter, four already had central hypothyroidism and were on adequate LT4 replacement therapy, while two were euthyroid at the beginning of the study. RESULTS: Serum IGF-I levels normalized in all patients. In both groups, a significant reduction in FT4 levels (P < 0.01) occurred during rhGH therapy. No patient in group A had FT4 values into the hypothyroid range, while in four of six patients in group B, fell FT4 levels into the hypothyroid range during rhGH. In particular, the two euthyroid children developed central hypothyroidism during rhGH treatment, and their height velocities did not normalize until the achievement of euthyroidism through appropriate LT4 substitution. No variation in serum FT3 and TSH levels was recorded in either groups. CONCLUSION: Contrary to that observed in patients with MPHD, rhGH replacement therapy does not induce central hypothyroidism in children with idiopathic isolated GHD, further supporting the view that in children with MPHD, as in adults, GHD masks the presence of central hypothyroidism. Slow growth (in spite of adequate rhGH substitution and normal IGF-I levels) is an important clinical marker of central hypothyroidism, therefore a strict monitoring of thyroid function is mandatory in treated children with MPHD.
PMID: 14974926 [PubMed - in process]
Recombinant hGH replacement therapy and the hypothalamus-pituitary-thyroid axis in children with GH deficiency: when should we be concerned about the occurrence of central hypothyroidism?
Giavoli C, Porretti S, Ferrante E, Cappiello V, Ronchi CL, Travaglini P, Epaminonda P, Arosio M, Beck-Peccoz P.
Institute of Endocrine Sciences, University of Milan, Ospedale Maggiore IRCCS, Milan, Italy.
OBJECTIVE: Recombinant hGH treatment may alter thyroid hormone metabolism and we have recently reported that 50% of patients with GH deficiency (GHD) due to organic lesions, previously not treated with thyroxine, developed hypothyroidism during treatment with recombinant human GH (rhGH). These results prompted us to evaluate the impact of rhGH treatment on thyroid function in children with GHD. DESIGN: Open study of GH treatment up to 12 months. Investigations were performed at baseline, and after 6 and 12 months of GH therapy. MEASUREMENT AND STUDY SUBJECTS: Serum TSH, FT4, FT3, AbTg and AbTPO, IGF-I, height and weight, were evaluated in 20 euthyroid children (group A) with idiopathic isolated GHD and in six children (group B) with multiple pituitary hormone deficiencies (MPHD) due to organic lesions. Among the latter, four already had central hypothyroidism and were on adequate LT4 replacement therapy, while two were euthyroid at the beginning of the study. RESULTS: Serum IGF-I levels normalized in all patients. In both groups, a significant reduction in FT4 levels (P < 0.01) occurred during rhGH therapy. No patient in group A had FT4 values into the hypothyroid range, while in four of six patients in group B, fell FT4 levels into the hypothyroid range during rhGH. In particular, the two euthyroid children developed central hypothyroidism during rhGH treatment, and their height velocities did not normalize until the achievement of euthyroidism through appropriate LT4 substitution. No variation in serum FT3 and TSH levels was recorded in either groups. CONCLUSION: Contrary to that observed in patients with MPHD, rhGH replacement therapy does not induce central hypothyroidism in children with idiopathic isolated GHD, further supporting the view that in children with MPHD, as in adults, GHD masks the presence of central hypothyroidism. Slow growth (in spite of adequate rhGH substitution and normal IGF-I levels) is an important clinical marker of central hypothyroidism, therefore a strict monitoring of thyroid function is mandatory in treated children with MPHD.
PMID: 14974926 [PubMed - in process]
roccodart440
New member
I've heard to run T-4 with HGH not T3
Similar threads
