To clarify things and address your original question. No hgh does cause hypothyroidism. there will be a supression in tsh and t4,
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Thyroid. 2008 Dec;18(12):1249-54.
Long-term effects of growth hormone replacement therapy on thyroid function in adults with growth hormone deficiency.
Losa M, Scavini M, Gatti E, Rossini A, Madaschi S, Formenti I, Caumo A, Stidley CA, Lanzi R.
Source
Department of Neurosurgery, Istituto Scientifico San Raffaele, Università Vita-Salute, Milan, Italy.
Abstract
BACKGROUND:
Clinical studies on the effect of growth hormone (GH) on thyroid function in patients with GH deficiency are contradictory. Further, the majority of published observations are limited to the first 6-12 months of GH replacement therapy. The aim of our study was to estimate the incidence of clinically relevant hypothyroidism in a cohort of patients with adult GH deficiency (AGHD) during long-term therapy with recombinant human GH (rhGH).
METHODS:
The study was designed as a retrospective collection of data on thyroid function in 49 AGHD patients of whom 44 (90%) had multiple hormone deficiency. Thirty-seven patients (76%) were on stable levothyroxine (LT4) replacement therapy (HYPO), and 12 (24%) were euthyroid (EUT). Therapy with rhGH was started at a dose of 3.5 microg/kg body weight and adjusted according to insulin-like growth factor-I (IGF-I) levels. At baseline, 6 months, 12 months, and yearly thereafter we measured free triiodothyronine (fT3), free thyroxine (fT4), thyroid-stimulating hormone, and IGF-I. Study outcome was fT4 level below the normal range (9 pmol/L), irrespectively of fT3 or thyroid-stimulating hormone levels.
RESULTS:
During a follow-up of 115 patient-years,
mean fT4 level decreased significantly, although remaining within the normal range (p = 0.0242; month 48 vs. baseline). The largest decrease was between baseline and month 6, when fT4 decreased of 1.43 pmol/L (95% confidence interval, 0.33-2.53) per 1 unit (microg/kg body weight) increase in rhGH dose. The incidence of hypothyroidism was 1.2 (HYPO group) and 6.7 (EUT group) events per 100 patient-years.
CONCLUSION:
We confirm that in patients with AGHD, rhGH therapy is associated with a small, although significant, decrement of fT4 in the first 6 months of replacement therapy. However, the incidence of hypothyroidism is low. Monitoring of thyroid function during rhGH therapy is advisable, particularly in the first year of therapy when the largest decrease in fT4 occurs.
But it increase the conversion of t4 into t3 and decreases the likely hood of t4 converting into reverse t3.-
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Pediatr Res. 1981 Jan;15(1):6-9.
Action of human growth hormone (hGH) on extrathyroidal conversion of thyroxine (T4) to triiodothyronine (T3) in children with hypopituitarism.
Rezvani I, DiGeorge AM, Dowshen SA, Bourdony CJ.
Abstract
To study the action of human growth hormone (hGH) on peripheral metabolism of serum thyroxine (T4), an oral loading dose of levothyroxine (1.2 mg/m2) was administered to seven children with hypopituitarism before initiation of hGH therapy. Serum concentrations of triiodothyronine (T3), T4, reverse triiodothyronine (rT3), and thyroxine-binding globulin (TBG) capacity were measured sequentially for 6 days. The study was repeated after 4 wk of treatment with hGH. Serum concentrations of T4 were not affected by hGH therapy. In contrast, mean basal serum concentration of T3 increased significantly after treatment with hGH. Also, changes in serum concentrations of T3 and in the ratio of T3/T4 after an oral dose of levothyroxine were significantly augmented during hGH therapy. Serum concentrations of rT3 changed in the opposite direction of T3 during therapy. After treatment with hGH, the mean basal level of serum rT3 decreased, and increases in serum concentrations of rT3 after oral levothyroxine were significantly attenuated. No changes in mean serum concentrations of thyroid stimulating hormone (TSH) and TBG capacity were observed. These data suggest that
administration of hGH to children with hypopituitarism enhances the extrathyroidal conversion of T4 to T3 and concomitantly decreases the serum concentration of rT3.
), but I'm going to ask this anyway: GH is said to sometimes shut down thyroid activity. To counter this, it is suggested that cycles of T3 be run. T3 mimics the effects of Thyroid activity so all sides from lack of thyroid activity are now covered. But by doing this, won't T3 use also shut down the thyroid, so when the T3 is stopped, one will be worse off than before? What, exactly, does T3 do for one when on a GH run?
). And I'm still going to get checked by a cardiologist even though my ECG was pretty good. All I want to know on this forum is whether Human Growth Hormone could be contributing to this condition (since it had started long before I began my current AAS cycle). Otherwise, I'm just tired or dizzy all the time, yet still trucking on, so I'm in the hands of the medical community (to whom, at this point, I have not revealed my steroid or hGH use).
