T3 - Growth Hormone - HOW???

[proud13]

I have spoken to a friend who is getting out of profesional bodybuilding and I asked him about T3 and slin with my current growth cycle. He told me to use slin 15 minutes before the end of my wkouts and only on the days I workout. T3 go up to 50 mcg a day broken up 3x (am, noonish, afternoon). He said I could stay on for 8 wks but not to go too high and when coming down do so slowly and gradually ending with 12.5 mcg.

I'm currently using the slin and growth but still waiting on the T3.

 

[nandi12]

Is t-3 even THAT important to do whil on growth if your not using INSULIN?

There are some conflicting studies, but generally research shows that GH itself increases T3 levels by increasing the conversion of T4 to T3 (1). This is thought to account in part for GH's fat burning effects. So you may not need T3 supplementation.

There is also some disturbing research showing that taking relatively low doses of T3 (40mcg/day) along with GH completely eliminates the ability of GH to increase nitrogen retention (2). The "long term" in the title of the paper refers to 10 days of treatment!

Here is the gist of the study:

RESULTS: Growth hormone decreased functional hepatic nitrogen clearance (l/h) by 30% (from 33.8 +/- 3.2 l/h (control) to 23.8 +/- 1.5 l/h (10 days growth hormone) (mean +/- SE) (ANOVA; p < 0.01)). Triiodothyronine did not change functional hepatic nitrogen clearance (36.7 +/- 3.2 l/h), but triiodothyronine given together with growth hormone abolished the effect of growth hormone functional hepatic nitrogen clearance (38.8 +/- 4.8 l/h). CONCLUSIONS: The results show that long-term growth hormone administration acts on liver by decreasing functional hepatic nitrogen clearance, thereby retaining amino-N in the body. Triiodothyronine has no effect on functional hepatic nitrogen clearance, but given together with growth hormone, it abolishes the effect of growth hormone on functional hepatic nitrogen clearance.A possible mechanism is the known effect of thyroid hormones in reducing the bioavailability of insulin-like growth factor-I. Thus, the effects of growth hormone and triiodothyronine on amino-N homeostasis are interdependent and to some extent exerted via interplay in their regulation of liver function as to amino-N conversion.

As far as staying on T3 for extended preiods damaging your thyroid, this is a myth.

There have been studies of people who were misdiagnosed as being hypothyroid and put on thyroid hormone replacement for as long as 30 years. When the medication was withdrawn, their thyroids returned to normal. (Greer,M. N Engl J Med 244:385, 1951)

Here is a remark about Greer's classic paper from a later author:

"In 1951, Greer reported the pattern of recovery of thyroid function after stopping suppressive treatment with thyroid hormone in euthyroid [normal] subjects based on sequential measurements of their thyroidal uptake of radioiodine. He observed that after withdrawal of exogenous thyroid therapy, thyroid function, in terms of radioiodine uptake, returned to normal in most subjects within two weeks. He further observed that thyroid function returned as rapidly in those subjects whose glands had been depressed by several years of thyroid medication as it did in those whose gland had been depressed for only a few days" (3)

These results have been subsequently verified in several studies. Basically you could stay on T3 indefinitely.


(1) Eur J Endocrinol 1996 May;134(5):563-
Insulin-like growth factor I alters peripheral thyroid hormone metabolism in humans: comparison with growth hormone.
Hussain MA, Schmitz O, Jorgensen JO, Christiansen JS, Weeke J, Schmid C, Froesch ER.

(2) : J Hepatol 1996 Mar;24(3):313-9
Effects of long-term growth hormone (GH) and triiodothyronine (T3) administration on functional hepatic nitrogen clearance in normal man.
Wolthers T, Grofte T, Moller N, Vilstrup H, Jorgensen JO.

(3) N Engl J Med 1975 Oct 2;293(14):681-4
Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy.
Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH

 

[Elapid]

I think Nandhi's right. I've done two t-3 cycles, one for the "safe" 6 weeks never going over 100mcg. The second one I got bold, bolstered by reading a similar study as this and by the fact that I've never heard of anyone fucking their thyroid up forever by using t-3, it was 10 weeks.

After my 10 wk cycle my thyroid bounced back to normal even with a minimal taper.

I don't understand why so many people are afraid to use t-3 but theres constant posts of people using ecstacy and other hard drugs that we know can fuck up us up permantly and sometimes fatally.


















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[SUST-MAN]

Thanks guys...

You were very helpful

 

[nandi12]

I wanted to add this abstract last night but it was on my computer at work, so it had to wait. Anyway, the mechanism by which thyroid hormones decrease the bioavailability of IGF-1 is by elevating levels of IGF-1 binding protein. This lowers the amount of free IGF-1 in circulation.

Clin Endocrinol (Oxf) 1993 May;38(5):547-51

Thyroxine treatment increases circulating levels of insulin-like growth factor binding protein-1: a placebo-controlled study.

Angervo M, Tiihonen M, Leinonen P, Valimaki M, Seppala M.

First Department of Obstetrics and Gynaecology, Helsinki University Central Hospital, Finland.

OBJECTIVE: Thyroid hormones affect carbohydrate metabolism in the liver, and hepatic insulin-like growth factor binding protein-1 (IGFBP-1) participates in glucose counter-regulation, so we studied the effects of oral thyroxine on serum IGFBP-1. DESIGN: The study was performed on a placebo-controlled cross-over basis covering 3 months' thyroxine and 3 months' placebo administration. PATIENTS: Eight patients taking anticonvulsant medication and four patients with hypothalamic hypothyroidism were given thyroxine, 150-200 micrograms daily for 3 months, or placebo. MEASUREMENTS: Serum IGFBP-1, sex hormone binding globulin, free T3 and free T4, TSH and IGF-I levels were measured after an overnight fast before treatment, and at the end of each 3-month period. RESULTS: Anticonvulsant medication had no significant effect on serum IGFBP-1. After 3 months' thyroxine treatment the serum IGFBP-1 levels (69; 58-167 micrograms/l; median and interquartile range, respectively) were significantly higher than those after placebo treatment (44; 23-58 micrograms/l; P = 0.002), or the pretreatment levels (54; 19-81 micrograms/l, P = 0.005). The IGFBP-1 levels rose in all 12 patients after thyroxine treatment, the median rise being 2.1-fold compared to placebo levels. No change was found in serum IGF-I concentrations. CONCLUSIONS: Oral thyroxine produces a rise in serum IGFBP-1 levels without a change in serum IGF-I concentration.

 

[SUST-MAN]

And this is bad....right?

 

[nandi12]

Yeah. Total IGF = Free IGF + Bound IGF. Increasing the binding protein levels increases the bound fraction of the IGF. If total IGF is unchanged, then the free portion goes down. That is bad.

 

[SUST-MAN]

OK....i wont use T-3 while on growth...

But why does anyone use it?

I am not the first person that wants to use it...

I hear all the time that T-3 & slin must be used...

 

[nandi12]

As far as using T3 and GH, most people probably do it assuming that if both increase lipolysis, then the combination would be doubly better. Some may do this out of simple lack of knowledge of the way the two interact. Others may know that T3 blocks the ability of IGF-1 to enhance nitrogen retention, but think that the lipolytic effects of GH are independent of IGF-1 action, and that IGF-1 actually promotes lipogenesis. This latter notion is the classic picture of GH action: GH itself promotes fat burning, and IGF-1 is responsible for muscle growth, and because of its insulin like action, fat deposition.

It's more complicated than this though. A lot of experiments have looked at the lipolytic effects of IGF-1 administration. When you inject IGF, it reduces GH production. Nevertheless, lipolysis is stimulated. When you examine the studies, IGF-1 administration either causes no net fat change, or a decrease. The lipolytic effects of IGF-1 seem to be greater than its insulin like effect.

Additionally, GH administration causes insulin resistance, while IGF-1 administration along with GH reverses that resistance (1) (2). It makes sense that by lowering free IGF-1 levels with T3 you exacerbate the GH induced insulin resistance. If you are using slin along with the GH, the T3 will just make the insulin less effective.

It just doesn't make sense to spend a fortune on GH and block a significant portion of its effects with a dirt cheap drug like T3.


(1) J Clin Invest 1993 Nov;92(5):2249-56
Insulin-like growth factor I stimulates lipid oxidation, reduces protein oxidation, and enhances insulin sensitivity in humans.
Hussain MA, Schmitz O, Mengel A, Keller A, Christiansen JS, Zapf J, Froesch ER.

(2) J Clin Invest 1994 Sep;94(3):1126-33
Comparison of the effects of growth hormone and insulin-like growth factor I on substrate oxidation and on insulin sensitivity in growth hormone-deficient humans.
Hussain MA, Schmitz O, Mengel A, Glatz Y, Christiansen JS, Zapf J, Froesch ER.

 

[SUST-MAN]

Its people like you who really keep us on this board. Thanks for everything!