Taking T3 alongside HGH.....DRjmw/Einstein??!?!?!!

[Whacked]

I read somewhere that T3 or THBG/TBG somehow interferes with the absorption of somatotropin and/or somatomedin (IGF-1) if taken simultaneously or within a similar time frame (HGH has a short half life). I would HATE to waste money on HGH if T3 would simply BIND IT/render it ineffective.

Thoughts........

And while ON this subject......what about the timing of simple carbohydrates alongside HGH injects. Couldn't carbohydrates ALSO interefere with somatotropin's effectiveness!?!?!!?

 

[Whacked]

From JohhnyB: "T3 produces IGF-1 binding proteins which negates the IGF-1 that would come from using HGH".


From Nandi: "Countering T3 induced muscle loss with AAS or prohormones makes sense from a physiological viewpoint as well. Thyroid hormone muscle protein breakdown is mainly mediated via the so-called ubiquitin-proteasome pathway. (12). (There are several independent metabolic pathways of protein breakdown in the body. For instance, another pathway, the lysosomal pathway, is responsible for the accelerated rate of muscle protein breakdown during and after exercise.) Testosterone administration has been shown to decrease ubiquitin-proteasome activity. (13) So AAS specifically target the muscle protein breakdown process stimulated by T3.

What may not be an effective strategy to maintain muscle mass during a T3 cycle is the use of exogenous growth hormone (GH). Studies have shown that when GH and T3 are administered concurrently, the increased nitrogen retention normally associated with GH use is abolished. This has been attributed to the observation that T3 increases levels of insulin like growth factor binding protein, reducing the bioavailability of igf-1 (14). "

"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. "

"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. "

Can anyone put everything here into perspectoive and give us any PROOF one way or the other?

DOES THBG render HGH (IGF-1) useless if taken together?

 

[JP@Ironology]

Bump.

 

[DrJMW]

For fat loss, this is not a problem. In any case, I have not seen this phenomenon in any of my client's blood testing. IGF-1 blood tests as well as IGFBP-3 levels are normal even with the subject taking t3 with HGH. I think the key is using dosing of cytomel below therapeutic levels--which is what I recommend. Theory and "studies" are one thing--actual results with athletes is another. Sometimes we have to go contrary. It is up to the individual to decide.

 

[Whacked]

Thanks......"low dose" being less than ?? (~25 mcg's)??

 

[DrJMW]

I start the men out at 50mcg daily before breakfast. If they feel uncomfortable, I drop them to 25mcg. I would say that 99% of the male clients using HGH/cytomel stay at 50mcg.

 

[Thom]

I guess you are checking theire bodyfat percentage along with weight... do they experience much muscleloss (from T3 being catabolic)? I know this also depends on diet though...

And, just for curiousity, what doses of hgh does your male clients use?

 

[Whacked]

I start the men out at 50mcg daily before breakfast. If they feel uncomfortable, I drop them to 25mcg. I would say that 99% of the male clients using HGH/cytomel stay at 50mcg.

thanks DOC

 

[einstein1905]

I really only see it beneficial to add T3 to the mix if fatloss is your primary goal. T3 does raise IGFBPs, but that of course is dose-dependent, as is everything. Many hear that GH suppresses endogenous T3 levels, which is true, but again, to what extent? Not very significant IMO. GH is regulated by the balance of somatostatin and GHRH. Somatostatin also has suppressive effects on thyroid hormones. Typical daily production of T3 is roughly 25mcg, and I'd bet money that GH suppression of endo T3 wouldn't be more than 10% or so, which makes supplementing with exo T3 somewhat unimportant to compensate for this minor loss, if significant at all (keep in mind it's dose-dependent).

 

[Whacked]

I really only see it beneficial to add T3 to the mix if fatloss is your primary goal. T3 does raise IGFBPs, but that of course is dose-dependent, as is everything. Many hear that GH suppresses endogenous T3 levels, which is true, but again, to what extent? Not very significant IMO. GH is regulated by the balance of somatostatin and GHRH. Somatostatin also has suppressive effects on thyroid hormones. Typical daily production of T3 is roughly 25mcg, and I'd bet money that GH suppression of endo T3 wouldn't be more than 10% or so, which makes supplementing with exo T3 somewhat unimportant to compensate for this minor loss, if significant at all (keep in mind it's dose-dependent).

Thanks Brain-child

Could you give us your spin on my 1st post? The binding of HGH (Igf-1) from exo-T-3 use. If fat loss is the primary goal, then MOST would suggest a T3/HGH combo. But it almost seems like Nandi feels that T3 use will render exo-HGH "ineffective".......so essentially you're JUST getting the adipolytic activity of T3 (and little if any from HGH)

Thank you for your time.

 

[einstein1905]

Thanks Brain-child

Could you give us your spin on my 1st post? The binding of HGH (Igf-1) from exo-T-3 use. If fat loss is the primary goal, then MOST would suggest a T3/HGH combo. But it almost seems like Nandi feels that T3 use will render exo-HGH "ineffective".......so essentially you're JUST getting the adipolytic activity of T3 (and little if any from HGH)

Thank you for your time.

T3 doesn't affect the actions of GH but rather the actions of IGF-1 (which is increased in response to GH). T3 increases IGFBPs, which will bind IGF-1 and render it unable to mediate its effects. The % increase in IGFBPs due to T3 isn't clear though......you need to quantify these things......we hear terms like "hinders" and inhibits", but we need to consider that they are dose-dependent effects and also that they may not be significant levels of "hindrance" in the first place. The doc mentioned above that he hadn't seen any significant increases in IGFBPs due to exo T3 doses, so it appears not to be a significant factor in the real world.

 

[Whacked]

Nice .....thanks Einstein (........AND DrJMW)

 

[DrJMW]

I start the men out with 4IU, sc, six days on and one day off. The women use half the amount, but the same frequency. The athletes and I keep an eye on symptoms at this level (joint pain, unusual swelling mostly). If symptoms do develop, I have the athlete reduce the dosing by 1IU until symptoms subside.

When I have athletes using HGH with AAS for size/strength purposes, I do not have them use any cytomel. So, it seems we are all in agreement for the most part. Again, HGH with low-dose cytomel for fat loss only. The athletes do not experience any muscle loss, for their diet (high protein, low carb, moderate fat) and training prevent this. I have not seen any LBM loss as a result of this fat loss stack. The reason I do not have the athlete using low-dose AAS is because of the HPTA suppression caused by it. With fat loss cycles lasting anywhere from three to six months or more, I do not want the HPTA suppressed for that long. Obviously, with those people whose natural testos is low to begin with, they should be using low-dose AAS anyway.

If I would to introduce a "cure" for obesity, I would simply put the overweight and obese on HGH/low-dose Cytomel; high protein, low carb diet, and proper training. I would introduce low-dose AAS and adjust dosing of HGH and cytomel based on the blood tests I recommend. Interestingly, most overweight and obese individuals are deficient (or low-normal) in GH, Testos, and T3. The benefits are safe, rapid results. Maintenance is easy: continuing low-dose AAS, cyclical ketogenic dieting, training. Many of these folks may not need but occasional HGH cycles. Some of these folks, once their BF% are dropped to normal levels, regain youthful levels of GH on their own. Again, blood testing can verify this.

 

[thx9000]

Interestingly, most overweight and obese individuals are deficient (or low-normal) in GH, Testos, and T3.

These conditions also seem to come along with another problem that accompanies high BF...insulin resistance or type II diabetes. High circulating insulin levels doesn't seem to lead to good things at all.

 

[DrJMW]

Low carb diets were specifically invented for the insulin resistent and type II diabetics. High Insulin levels come down within days of carb cutting. As you know, HGH basically converts the body into a fat burning machine. As the BF% corrects, many of the symptoms of obesity correct.

Now, the aging problem. It is a fact that insulin resistence expresses itself as certain people age (typically the endomorphs--people battling their weight problems their whole lives). Once the fat is lost, then these folks can be evaluated to see if they still suffer significant insulin resistance and/or hyperinsulinemia. Continued diet modification and/or medications like metformin can help these folks even after the HGH/cytomel fat loss cycle--part of their maintenance. the process is complex, but it is well-thought-out.