Hey Dr JMW - what are your thoughts on the below info?
(reposted from Trevdog at AF)
Maybe we shouldn't run T3 with GH
Thoughts on this?
Here is one of Nandi12's posts on the subject.
"There is another study I like a lot; it took me a minute to dig the xerox copy out of my files. They looked at combinations of T3, T3 plus GH, and T3 plus anavar on weight loss and nitrogen retention in several subjects. As an illustrative example, in their patient #4, for 12 days with a washout period between treatments, they gave either T3 (150 mcg/day); T3 plus GH (5 mg/day = 15 IU/day) or T3 plus anavar (10 mg/day)
The weight loss in gm/day was as follows:
T3: 513 gm/day; T3+GH: 107gm/day; T3+anavar: 100gm/day
The nitrogen excretion in gm/3days was:
T3: 37; T3+GH: 32; T3+anavar: 26; placebo: 32
So just like in the other study on combining T3 and GH, you can see that here the nitrogen excretion of the T3+GH was exactly the same as placebo. In other words, the T3 cancelled all anabolic benefit of the GH. Giving T3 and anavar @ 10mg/day gives almost the same weight loss as GH+T3, but preserves much more lean body mass.
It makes no sense to combime GH and T3. Combining T3 with a low dose of AAS is a much wiser strategy for losing weight and preserving muscle
J Clin Endocrinol Metab 1971 Aug;33(2):293-300
Effects of triiodothyronine, growth hormone and anabolic steroids on nitrogen excretion and oxygen consumption of obese patients.
Bray GA, Raben MS, Londono J, Gallagher TF Jr."
Here is another one of his posts from the same thread, at
http://www.cuttingedgemuscle.com/Fo...ighlight=growth
There are a couple of things about the second study I find interesting. One is how much weight these obese patients were losing on the T3: over a pound a day.
The other thing is how the GH interfered with the weight loss. That is a feature of a number of other studies where large doses of GH were used; in this one 15 IU/day. Insulin resistance becomes an important factor hindering weight loss at those large GH doses. Normally the insulin like effect of IGF-1 helps by lowering the endogenous output of insulin to some degree. IGF-1 as the name implies has an insulin like effect on glucose metabolism, but without interfereing with lipolysis like insulin. So in the presence of elevated IGF-1, the body secretes less insulin, improving fat loss. The problem here I suspect is that by impairing bioavailability of IGF-1, as T3 has been shown to do, the T3 negated the fat burning effect of GH.
Water retention caused by GH is a big factor as well. This is an old study (1970) so when measuring weight loss during GH administration, they did not have access to the sophisticated equipment available today to accurately measure changes in muscle and fat mass. They probably just weighed the subjects and because of the GH induced water retention it looks like they were not losing as much fat as they possibly were.
Here is another one of Nandi12's posts on the subject.
T3 and GH use are incompatible. T3 elevates levels of IGF binding protein to the point that they render IGF-1 unbioavailable.
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.
Department of Medicine M (Endocrinology and Diabetes), Aarhus University Hospital, Denmark.
BACKGROUND/AIMS: A decline in urea excretion is seen following long-term growth hormone administration, reflecting overall protein anabolism. Conversely, hyperthyroidism is characterized by increased urea synthesis and negative nitrogen metabolism. These seemingly opposite effects are presumed to reflect different actions on peripheral protein metabolism. The extent to which these hormonal systems have different direct effects on hepatic urea genesis has not been fully characterized. METHODS: We measured urea nitrogen synthesis rates and blood alanine levels concomitantly before, during, and after a 4-h constant intravenous infusion of alanine (2 mmol.kg bw-1.h-1). Urea nitrogen synthesis rate was estimated hourly as urinary excretion corrected for gut hydrolysis and accumulation in body water. The slope of the linear relationship between urea nitrogen synthesis rate and alanine concentration represents the liver function as to conversion of amino-N, and is denoted the functional hepatic nitrogen clearance. Eight normal male subjects (age 21-27 years; body mass index 22.4-27.0 kg/m2) were randomly studied four times: 1) after 10 days of subcutaneous saline injections, 2) after 10 days of subcutaneous growth hormone injections (0.1 IU/kg per day), 3) after 10 days of triiodothyronine administration (40 micrograms on even dates, 20 micrograms on uneven dates) and 4) after 10 days given 2)+3). All injections were given at 20 00 h. 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.
T3 blocks IGF-1 in the liver.
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Thanks for the input.
...bd
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