GODT240 super promo--Pharma grade HGH 240iu only 264$

Your T4 is low!
At 4 IU daily you see that you can use T4 to upper your level...
It's good to see that, bc is like if you use max 4 IU per day you DON'T have to need to supplement T4.
But you can see the result is low and also T3 is not really high.
I think T4 will be enough to raise both up.
...

Thanks a lot for your results posted
The last lab was from a few months ago. It's closest I have to a baseline. I have ordered some t4 to run with it though. I'm a little nervous about it though as last time I tried to run t3 it started giving me bad anxiety. If 411 on my igf1 decent for 4iu? From what I understand it process of converting t4 to t3 that makes it work synergistically with gh. Is that correct? Can you she'd any other light on the benifits of it or point me towards some studies/articles. First run with gh.
 
The last lab was from a few months ago. It's closest I have to a baseline. I have ordered some t4 to run with it though. I'm a little nervous about it though as last time I tried to run t3 it started giving me bad anxiety. If 411 on my igf1 decent for 4iu? From what I understand it process of converting t4 to t3 that makes it work synergistically with gh. Is that correct? Can you she'd any other light on the benifits of it or point me towards some studies/articles. First run with gh.
Using T4 is better than T3 on HGH for the reason you stated: synergy. But after a few weeks (6-8) on HGH your T3 levels should rebound. Suppression is temporary.
 
Sorry guys this is the best you get. I'm driving (currently my wife is actually) across state lines and won't be home until Monday. This is at 4iu for 4 weeks. Bloods was in afternoon around 3-4 with last injection being 8-9pm the night before. Technically don't have a baseline but I tested a few months back on semorelin ghrp6/2 and my score was 260 something. Was on the semorelin 6-8 weeks when tested. If it's in the same files I'll post it up after this.View attachment 50518


4iu for 4 weeks, IGF1 from 235 to 411. its good number. 4iu is not high dose. only 4 weeks. if u run 2 weeks more, it might touch 500s.


IGF1 reference range : 88--246. i see most of baseline of IGF1 between 90 and 130 (without running any gh ). u run ghrp6/2, your IGF1 got 235 a few months ago, but once u stop it for a few months, your IGF1 level should go back to normal level. then u use gh for 4 weeks, u got 411. so your baseline should be less than 235. its just my thought.
 
another IGF1 test posted couple days ago, quite similar as yours

week 1 , 2iu
week 2, 3iu
week 3, 4iu
week 4, 4iu
baseline 170, 4 weeks later: IGF1 537

blood test: Pictures - IGF bloods GODT240
Hold off on self promoting OP. Meso will soon have the legitimate evidence to how good your stuff is. You're either gonna be very very busy soon so be prepared or this thread is gonna die instantly lol GL OP I'm actually rooting for you believe it or not ;)
 
trial kit 188$ ,one kit limited. paypal guaranteed. after assay, the price will go back to 300$ per kit.
 
Using T4 is better than T3 on HGH for the reason you stated: synergy. But after a few weeks (6-8) on HGH your T3 levels should rebound. Suppression is temporary.
Send to



Clin Endocrinol (Oxf). 2000 Aug;53(2):183-9.
Changes in serum thyroid hormones levels and their mechanisms during long-term growth hormone (GH) replacement therapy in GH deficient children.
Portes ES1, Oliveira JH, MacCagnan P, Abucham J.
Author information

Abstract
OBJECTIVE:
The effects of GH therapy on thyroid function among previous reports have shown remarkable discrepancies, probably due to differences in hormone assay methods, degree of purification of former pituitary-derived GH preparations, dosage schedules, diagnostic criteria, patient selection, duration of treatment and study design. These considerations motivated us to investigate whether and how GH replacement therapy changes serum thyroid hormone levels, including the much less studied rT3 levels, in a group of unequivocally GH-deficient children receiving long-term recombinant human GH therapy.

PATIENTS AND DESIGN:
Twenty clinically and biochemically euthyroid children were studied in two therapeutic conditions: on GH replacement therapy for at least 6 months and without GH replacement, either before GH was started or after GH was withdrawn for 30-60 days. Eight patients were on thyroxine replacement treatment and thyroxine doses were kept constant during the study. Blood was collected before and after 15, 20 and 60 minutes of TRH administration in both therapeutic conditions (with GH and without GH).

MEASUREMENTS:
Concentrations of thyroid hormone levels were determined only in sera obtained before TRH administration. FT4, T3 and TSH were measured by immunoflourimetric assays and rT2 was measured by immunoradioassay.

RESULTS:
Patients were classified into two groups, according to basal TSH levels: group I (TSH > 0.4 mU/l, n = 12) and group II (on thyroxine and TSH < 0.05 mU/l, n = 8). In both groups, serum FT4 levels decreased (17. 0 +/- 1.1 vs. 14.3 +/- 0.9 mU/l, P < 0.001, and 18.0 +/- 1.7 vs. 14. 2 +/- 1.7 mU/l, P < 0.01, respectively), serum T3 levels increased (1.8 +/- 0.1 vs. 2.4 +/- 0.2 nmol/l, P < 0.001, and 1.9 +/- 0.3 vs. 2.4 +/- 0.2 nmol/l, P < 0.05, respectively), and serum rT3 levels decreased (0.35 +/- 0.03 vs. 0.25 +/- 0.03 nmol/l, P < 0.01, and 0. 48 +/- 0.06 vs. 0.34 +/- 0.06 nmol/l, P < 0.01, respectively). Basal (3.2 +/- 0.50 vs. 2.6 +/- 0.72 mU/l, P = 0.28, paired t-test), TRH-stimulated peak TSH levels (13.9 +/- 5.3 vs. 15.9 +/- 8.0 mU/l, P = 0.35, paired t-test) and TRH-stimulated TSH secretion, expressed as area under the curve (609 +/- 97 vs. 499 +/- 53 mU/l.minutes-1, P = 0.15, paired t-test), remained unchanged during GH replacement in group I patients. Low serum FT4 and high serum T3 levels were observed in only one patient each, but low serum rT3 levels were found in six patients (four in group I and two in group II) during GH replacement.

CONCLUSIONS:
These results show that long-term GH replacement therapy in children with unequivocal GHD significantly decreases serum FT4 and rT3 levels and increases serum T3 levels; that these changes are independent of TSH and result from increased peripheral conversion of T4 to T3 and that GH replacement therapy in GH deficient children does not induce hypothyroidism, but simply reveals previously unrecognized cases whose serum FT4 values fall in the low range during GH replacement.

PMID:

There is not really a synergy persay going on here and I believe you should of stated t4 instead of t3.

By no means do I think you shouldn't use t4 with gh use. We just need to understand why it helps.

Here is another study. That you might find interesting.

Send to



Int J Clin Pharmacol Ther. 2004 Jan;42(1):30-4.
Effects of recombinant growth hormone therapy on thyroid hormone concentrations.
Kalina-Faska B1, Kalina M, Koehler B.
Author information

Abstract
BACKGROUND AND OBJECTIVE:
There are numerous, often contradictory reports on the effects of growth hormone (GH) therapy on thyroid function. The aim of this study was to assess the effect of such therapy on serum concentrations of thyroid hormones in GH-deficient children euthyroid prior to the treatment, and to determine the necessity of thyroid hormone administration in these patients.

MATERIAL AND METHODS:
The study included 32 GH-deficient patients in the first stage of sexual development, in whom disorders of thyroid function could be excluded. The inclusion criteria were based on clinical examination and levels of thyroxine (T4), triiodothyronine (T3), free thyroxine (fT4), free triiodothyronine (fT3), reverse triiodothyronine (rT3), thyrotropin (TSH) before and after stimulation with thyrotropin-releasing hormone (TRH). Recombinant growth hormone (rGH) (Genotropin 16U, Pharmacia) was administered at a dose of 0.7 U/kg/week. Fasting blood samples were drawn before treatment and after 3, 6, 9 and 12 months of therapy. Thyroid hormones were measured using RIA and IRMA methods.

RESULTS:
There were no physical signs of hypothyroidism in the patients examined during 12 months of rGH administration, and the satisfactory growth rate was achieved. T4 levels decreased in the first 3 months but remained within the normal range, and then returned to the values prior to the treatment. A similar trend was observed for fF4, with 28.5% of patients exhibiting fF4 levels below the normal in the 3rd month. An increase during the first 3 months of therapy was observed in the cases of T3 (statistically non-significant) and fT3, and these values then fell to levels within the normal range of patients' age. During treatment, TSH levels decreased but remained within the normal range.

CONCLUSIONS:
A transient decrease in T4 concentrations in the 3rd month with unchanged T3 and an increase in fT3 concentrations probably result from the effect of rGH on the peripheral metabolism of thyroid hormones. The results obtained do not support the use of thyroid hormone therapy with levothyroxine during the first year of rGH therapy in patients who are initially euthyroid.

PMID:

14756384
[PubMed - indexed for MEDLINE]

mands
 
Last edited:
Send to



Clin Endocrinol (Oxf). 2000 Aug;53(2):183-9.
Changes in serum thyroid hormones levels and their mechanisms during long-term growth hormone (GH) replacement therapy in GH deficient children.
Portes ES1, Oliveira JH, MacCagnan P, Abucham J.
Author information

Abstract
OBJECTIVE:
The effects of GH therapy on thyroid function among previous reports have shown remarkable discrepancies, probably due to differences in hormone assay methods, degree of purification of former pituitary-derived GH preparations, dosage schedules, diagnostic criteria, patient selection, duration of treatment and study design. These considerations motivated us to investigate whether and how GH replacement therapy changes serum thyroid hormone levels, including the much less studied rT3 levels, in a group of unequivocally GH-deficient children receiving long-term recombinant human GH therapy.

PATIENTS AND DESIGN:
Twenty clinically and biochemically euthyroid children were studied in two therapeutic conditions: on GH replacement therapy for at least 6 months and without GH replacement, either before GH was started or after GH was withdrawn for 30-60 days. Eight patients were on thyroxine replacement treatment and thyroxine doses were kept constant during the study. Blood was collected before and after 15, 20 and 60 minutes of TRH administration in both therapeutic conditions (with GH and without GH).

MEASUREMENTS:
Concentrations of thyroid hormone levels were determined only in sera obtained before TRH administration. FT4, T3 and TSH were measured by immunoflourimetric assays and rT2 was measured by immunoradioassay.

RESULTS:
Patients were classified into two groups, according to basal TSH levels: group I (TSH > 0.4 mU/l, n = 12) and group II (on thyroxine and TSH < 0.05 mU/l, n = 8). In both groups, serum FT4 levels decreased (17. 0 +/- 1.1 vs. 14.3 +/- 0.9 mU/l, P < 0.001, and 18.0 +/- 1.7 vs. 14. 2 +/- 1.7 mU/l, P < 0.01, respectively), serum T3 levels increased (1.8 +/- 0.1 vs. 2.4 +/- 0.2 nmol/l, P < 0.001, and 1.9 +/- 0.3 vs. 2.4 +/- 0.2 nmol/l, P < 0.05, respectively), and serum rT3 levels decreased (0.35 +/- 0.03 vs. 0.25 +/- 0.03 nmol/l, P < 0.01, and 0. 48 +/- 0.06 vs. 0.34 +/- 0.06 nmol/l, P < 0.01, respectively). Basal (3.2 +/- 0.50 vs. 2.6 +/- 0.72 mU/l, P = 0.28, paired t-test), TRH-stimulated peak TSH levels (13.9 +/- 5.3 vs. 15.9 +/- 8.0 mU/l, P = 0.35, paired t-test) and TRH-stimulated TSH secretion, expressed as area under the curve (609 +/- 97 vs. 499 +/- 53 mU/l.minutes-1, P = 0.15, paired t-test), remained unchanged during GH replacement in group I patients. Low serum FT4 and high serum T3 levels were observed in only one patient each, but low serum rT3 levels were found in six patients (four in group I and two in group II) during GH replacement.

CONCLUSIONS:
These results show that long-term GH replacement therapy in children with unequivocal GHD significantly decreases serum FT4 and rT3 levels and increases serum T3 levels; that these changes are independent of TSH and result from increased peripheral conversion of T4 to T3 and that GH replacement therapy in GH deficient children does not induce hypothyroidism, but simply reveals previously unrecognized cases whose serum FT4 values fall in the low range during GH replacement.

PMID:

There is not really a synergy persay going on here and I believe you should of stated t4 instead of t3.

By no means do I think you shouldn't use t4 with gh use. We just need to understand why it helps.

Here is another study. That you might find interesting.

Send to



Int J Clin Pharmacol Ther. 2004 Jan;42(1):30-4.
Effects of recombinant growth hormone therapy on thyroid hormone concentrations.
Kalina-Faska B1, Kalina M, Koehler B.
Author information

Abstract
BACKGROUND AND OBJECTIVE:
There are numerous, often contradictory reports on the effects of growth hormone (GH) therapy on thyroid function. The aim of this study was to assess the effect of such therapy on serum concentrations of thyroid hormones in GH-deficient children euthyroid prior to the treatment, and to determine the necessity of thyroid hormone administration in these patients.

MATERIAL AND METHODS:
The study included 32 GH-deficient patients in the first stage of sexual development, in whom disorders of thyroid function could be excluded. The inclusion criteria were based on clinical examination and levels of thyroxine (T4), triiodothyronine (T3), free thyroxine (fT4), free triiodothyronine (fT3), reverse triiodothyronine (rT3), thyrotropin (TSH) before and after stimulation with thyrotropin-releasing hormone (TRH). Recombinant growth hormone (rGH) (Genotropin 16U, Pharmacia) was administered at a dose of 0.7 U/kg/week. Fasting blood samples were drawn before treatment and after 3, 6, 9 and 12 months of therapy. Thyroid hormones were measured using RIA and IRMA methods.

RESULTS:
There were no physical signs of hypothyroidism in the patients examined during 12 months of rGH administration, and the satisfactory growth rate was achieved. T4 levels decreased in the first 3 months but remained within the normal range, and then returned to the values prior to the treatment. A similar trend was observed for fF4, with 28.5% of patients exhibiting fF4 levels below the normal in the 3rd month. An increase during the first 3 months of therapy was observed in the cases of T3 (statistically non-significant) and fT3, and these values then fell to levels within the normal range of patients' age. During treatment, TSH levels decreased but remained within the normal range.

CONCLUSIONS:
A transient decrease in T4 concentrations in the 3rd month with unchanged T3 and an increase in fT3 concentrations probably result from the effect of rGH on the peripheral metabolism of thyroid hormones. The results obtained do not support the use of thyroid hormone therapy with levothyroxine during the first year of rGH therapy in patients who are initially euthyroid.

PMID:

14756384
[PubMed - indexed for MEDLINE]

mands
Right, my mistake on the typo. Obviously meant T4 would rebound.
 
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