ketsugo
MuscleHead
- Sep 10, 2011
- 2,652
- 486
I keep a folder on the PC with all my all time informative and favorite articles, after browsing and brushing up , this one is from 2002 and still one of the best I ever seen with tons of intersting points
Most people who are taking the plunge into Human Growth Hormone use have reached a dead end with their use of anabolics, and need to push through that wall. Im sure youve heard about the synergistic combination of using Human Growth Hormone along with Anabolic Steroids, IGF, insulin and T3 (* usually synthroid, a thyroid medication). The reason is that when these hormones are used correctly together, theyll produce a large amount of synergy, the insulin is able to shuttle nutrients into your muscle, the thyroid hormone increases your fat-burning capability, the IGF will cause muscle growth as well as helping to grow new cartilage (thus preventing injury), and the anabolic steroids like testosterone, specifically (in addition to being anabolic) can increase IGF-1, in muscle tissue(11), and maybe even increase your bodys ability to use it. Also, usually, an increased amount of IGF usually tells your body to stop producing Human Growth Hormone, but testosterone actually blunts this part of the Negative FeedBack Loop (12)! And the addition of an Aromatase Inhibitor will also stop conversion of testosterone into estrogen; estrogen reduces IGF levels.(13)(14) Finally, the Human Growth Hormone does, well everything I just spent the last few pages telling you about!
Thus, IGF, Testosterone (and of course other steroids), Insulin, thyroid meds, and Human Growth Hormone will all combine to produce a pretty damned effective fat-burning and muscle building cycle! You know what else? Human Growth Hormone is virtually undetectable on any sort of currently used drug-screening tests. Human Growth Hormone, Insulin, Thyroid meds, and IGF may also be used pretty safely by those who may be subject to drug screening tests, or as a non-HPTA suppressive "bridge" between cyclesPeople on thyroid medications may benefit significantly from hgh use. HGH has the effect of increasing the effectiveness of nearly every gland and organ in the body and the thyroid is no exception. The thyroid gland and hormone regulate and maintains the metabolism of every human.The condition that benefits most from hgh supplementation related to the thyroid is Hyperthyroidism. This is caused my a malfunctioning thyroid gland which is overworking itself. There are a vast number of symptoms of this disease and it is hard to tell if one actually has it without tests.The thyroid is often improved slowly but surely after beginning to supplement with HGH. However, any person with hyperthyroidism should not take any HGH product unless it is prescribed to them by their personal physician.Growth Hormone and T4: Anabolic Synergy By Mark Stent (B.Sc, Dipl Dat, SPN, and Muscle Growth hormone and thyroid hormones have been standard drugs in the arsenals of bodybuilders for years. Growth hormone has been used for its anabolic, muscle cell increasing, fat loss and anti aging properties. Thyroid hormones have been used for the fat loss, stimulatory and (to a lesser extent) anabolic effects. In this article I will look at the synergies between the two different types of thyroid hormone (T4 and T3) and Growth hormone (GH) and their applications in bodybuilding.Before we get into the juicy stuff, we need to start with a little ‘geek-talk’ and some physiology.The body produces two thyroid hormones, the first is thyroxine (T4) and the second is triiodothyronine (T3), which is the most widely used thyroid hormone in the world of muscle building. T4 is the inactive thyroid hormone and needs to be converted to T3 to exert thyroid-specific effects. This is done by the enzymes in the deiodinase group, of which there are 3 types – D1 and D2, which involved in the initiation of the process of conversion of T4 to T3 and D3, which is involved in the deactivation process.The secretion of T4 is created in the thyroid gland and is stimulated by Thyroid stimulating hormone (TSH), which in turn is stimulated by Thryrotropin Releasing hormone (TRH). So, when T3 levels rise, the body says, ‘hey, I have enough T3 floating around, so I need to cut back’, which it does by suppressing TSH (this is known as a ‘negative feedback loop’). Incidentally, thyroid hormones require insulin or IGF-1 to trigger their effects.Growth hormone (GH) is produced in the pituitary gland and is regulated by factors such as hormones and enzymes. It is regulated by two hormones Somatostatin (SS) and Growth hormone releasing hormone (GHRH). When there is too much GH circulating the body another negative feedback loop tells it to produce SS to decrease GH levels. When the body has too little GH, GHRH is produced. GH has the ability to stimulate the conversion of T4 to T3, making thyroid hormones partially dependent on GH. Somatostatin (which is secreted when GH levels are too high) can also inhibit TSH secretion or reduce TRH secretion, which means it can limit the amount of T4 produced by the body. This means that although GH increases the conversion of T4 to T3, which means more T3, it may actually mean lower than normal T4 levels.GH gene transcription is what gives GH its wonderful effects (such as muscle growth, fat loss etc) and T3 enhances these effects, making GH and T3 extremely synergistic, in fact, T3 is the limiting factor in exogenous GH usage. Here we now have a contradiction: T3 and GH are synergistic, but too much T3 decreases the anabolic effects of GH.This is where Anthony Roberts (a self professed steroid and performance enhancing drugs expert) hypothesised that it is the conversion process of T4 to T3 that is important. Let me explain. When there is too much T3 in the body and normal levels of T4, the thyroid sends a signal to produce less D1 and D2 (the activators) and more of D3 (the in-activator) and thus inhibits many of the synergistic effects of T3. When D3 levels are high, growth factors such as IGF-1 are stimulated, which means D3 is an important part of the equation with regards to the anabolic effects of GH.Now for the part you have all been waiting for, the summary and conclusion…When growth hormone is taken, along with T3, the GH will stop converting T4 to T3 after a certain point, which means it will shut of the good, anabolic effects of GH by killing the pathway that creates them! This, to me, seems like a bad thing! Now if we add T4 into a GH cycle, we would enhance this pathway, giving the GH more anabolic effects!Remember that T4 alone is pretty ineffective for our purposes and requires something like GH to be made effective.I have actually seen how effective using T4 in conjunction with GH is, first hand. An athlete I was working with was dieting for a show using GH and T3 (along with many other anabolic compounds), but was seeing no change in his fat to muscle ratio. Even with changes in his diet, such as lowering carbs, increasing cardio and even lowering calories, there were minimal changes, at best. T4 was introduced and within 1 week a change of 2.5% body fat and an increase of 1kg of muscle was measured! This is a pretty drastic change in any book.The way I see it, growth hormone costs a lot, and, if it were me, I would want to maximise it as much as possible to get a better ‘bang for my buck’, T4 seems to be the catalyst here and without it, GH is a waste of moneySo we want elevated T3 levels when we take GH, or we won’t be getting ANYWHERE NEAR the full anabolic effect of our injectable GH
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."
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.
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..
AAS lower T3 levels(Specially Fina) thats how the exert most of their anti-catabolic effects.
Adding T3 at a low dosage will simply bring your T3 levels back up to normal. Nothing more.
We are not talking about supra-physiological dosing, just optimization.
Adding a low dosage of T3 while on AAS+GH is a good idea. Now, if its only GH+T3, thats a different story. I would not run T3 while only on GH. I would run 7-Keto DHEA instead of the T3. Maybe even an ECA stack to increase peripheral T4-T3 conversion.
GH also gives you a mild case of insulin resistance(As do some AAS), therefore adding R-ALA is definately a good idea as well.
"Great minds talk about ideas, average minds talk about facts, and weak minds talk about people"
AAS LOWERS T-3 MYTH OR FACT?
This is essentially another bodybuilding myth. Please ask the person who made the statement about tren lowering BIOAVAILABLE T3 to produce the research. I have read the studies, of which there are a grand total of two on tren in animals, and only total T4 was examined. This is not the same as free T4. Anabolic steroids lower thyroid binding globulin, which lowers total thyroid hormone levels. However, the body compensates by increasing thyroid hormone production, keeping free T3/T4, ie the bioavailable fraction, normal.
I have done a meta-analysis of all published studies on the effects of androgens/AAS on thyroid function. It will be out not this month in Mind & Muscle but in the subsequent issue. Here is a passage from the study:
"Can we make any sense out of the seeming hodgepodge of conflicting data? The only parameters that are consistent from study to study, where they were measured, are depressed total T3 and T4, and TBG. As we have discussed, androgens typically lower TBG, along with total T4 and T3 since the latter are a function of TBG levels...In conclusion then AAS seem to have little if any effect on thyroid function per se.
"The reports by Deyssig & Weissel, and Daly et al suggest the possibility of a direct action of AAS on the thyroid or pituitary, but their results are inconsistent: The former researchers detected elevated stimulated TSH while the latter saw an increase in basal TSH. Free T4 was unchanged in former group, while it was elevated in the latter. The only consistently reported effect is a depression in total T4, total T3 and TBG. If there is a direct effect of AAS on the thyroid, pituitary, or hypothalamus the studies conducted so far shed little light on the mechanism due to their inconsistent results. And as stressed by Deyssig & Weissel any direct effect of anabolic steroids on the thyroid would likely be of no clinical significance due to its small magnitude."
In the total medline database there are eight studies where the effects of androgens/AAS on free thyroid levels were examined. Only one of those studies showed a small clinically insignificant drop in free thyroid hormones. Two actually showed an increase in free thyroid hormones, again clinically insignificant. The remainder showed no effect.
I think adding T3 to a steroid cutting cycle is an excellent idea. I have stressed that point many times, and I always do it. What I think is a bad idea, unless all one is concerned about is weight loss and not preservation of lean body mass is to combine T3 with GH.
Anonymous poster
"Great minds talk about ideas, average minds talk about facts, and weak minds talk about people"
Most people who are taking the plunge into Human Growth Hormone use have reached a dead end with their use of anabolics, and need to push through that wall. Im sure youve heard about the synergistic combination of using Human Growth Hormone along with Anabolic Steroids, IGF, insulin and T3 (* usually synthroid, a thyroid medication). The reason is that when these hormones are used correctly together, theyll produce a large amount of synergy, the insulin is able to shuttle nutrients into your muscle, the thyroid hormone increases your fat-burning capability, the IGF will cause muscle growth as well as helping to grow new cartilage (thus preventing injury), and the anabolic steroids like testosterone, specifically (in addition to being anabolic) can increase IGF-1, in muscle tissue(11), and maybe even increase your bodys ability to use it. Also, usually, an increased amount of IGF usually tells your body to stop producing Human Growth Hormone, but testosterone actually blunts this part of the Negative FeedBack Loop (12)! And the addition of an Aromatase Inhibitor will also stop conversion of testosterone into estrogen; estrogen reduces IGF levels.(13)(14) Finally, the Human Growth Hormone does, well everything I just spent the last few pages telling you about!
Thus, IGF, Testosterone (and of course other steroids), Insulin, thyroid meds, and Human Growth Hormone will all combine to produce a pretty damned effective fat-burning and muscle building cycle! You know what else? Human Growth Hormone is virtually undetectable on any sort of currently used drug-screening tests. Human Growth Hormone, Insulin, Thyroid meds, and IGF may also be used pretty safely by those who may be subject to drug screening tests, or as a non-HPTA suppressive "bridge" between cyclesPeople on thyroid medications may benefit significantly from hgh use. HGH has the effect of increasing the effectiveness of nearly every gland and organ in the body and the thyroid is no exception. The thyroid gland and hormone regulate and maintains the metabolism of every human.The condition that benefits most from hgh supplementation related to the thyroid is Hyperthyroidism. This is caused my a malfunctioning thyroid gland which is overworking itself. There are a vast number of symptoms of this disease and it is hard to tell if one actually has it without tests.The thyroid is often improved slowly but surely after beginning to supplement with HGH. However, any person with hyperthyroidism should not take any HGH product unless it is prescribed to them by their personal physician.Growth Hormone and T4: Anabolic Synergy By Mark Stent (B.Sc, Dipl Dat, SPN, and Muscle Growth hormone and thyroid hormones have been standard drugs in the arsenals of bodybuilders for years. Growth hormone has been used for its anabolic, muscle cell increasing, fat loss and anti aging properties. Thyroid hormones have been used for the fat loss, stimulatory and (to a lesser extent) anabolic effects. In this article I will look at the synergies between the two different types of thyroid hormone (T4 and T3) and Growth hormone (GH) and their applications in bodybuilding.Before we get into the juicy stuff, we need to start with a little ‘geek-talk’ and some physiology.The body produces two thyroid hormones, the first is thyroxine (T4) and the second is triiodothyronine (T3), which is the most widely used thyroid hormone in the world of muscle building. T4 is the inactive thyroid hormone and needs to be converted to T3 to exert thyroid-specific effects. This is done by the enzymes in the deiodinase group, of which there are 3 types – D1 and D2, which involved in the initiation of the process of conversion of T4 to T3 and D3, which is involved in the deactivation process.The secretion of T4 is created in the thyroid gland and is stimulated by Thyroid stimulating hormone (TSH), which in turn is stimulated by Thryrotropin Releasing hormone (TRH). So, when T3 levels rise, the body says, ‘hey, I have enough T3 floating around, so I need to cut back’, which it does by suppressing TSH (this is known as a ‘negative feedback loop’). Incidentally, thyroid hormones require insulin or IGF-1 to trigger their effects.Growth hormone (GH) is produced in the pituitary gland and is regulated by factors such as hormones and enzymes. It is regulated by two hormones Somatostatin (SS) and Growth hormone releasing hormone (GHRH). When there is too much GH circulating the body another negative feedback loop tells it to produce SS to decrease GH levels. When the body has too little GH, GHRH is produced. GH has the ability to stimulate the conversion of T4 to T3, making thyroid hormones partially dependent on GH. Somatostatin (which is secreted when GH levels are too high) can also inhibit TSH secretion or reduce TRH secretion, which means it can limit the amount of T4 produced by the body. This means that although GH increases the conversion of T4 to T3, which means more T3, it may actually mean lower than normal T4 levels.GH gene transcription is what gives GH its wonderful effects (such as muscle growth, fat loss etc) and T3 enhances these effects, making GH and T3 extremely synergistic, in fact, T3 is the limiting factor in exogenous GH usage. Here we now have a contradiction: T3 and GH are synergistic, but too much T3 decreases the anabolic effects of GH.This is where Anthony Roberts (a self professed steroid and performance enhancing drugs expert) hypothesised that it is the conversion process of T4 to T3 that is important. Let me explain. When there is too much T3 in the body and normal levels of T4, the thyroid sends a signal to produce less D1 and D2 (the activators) and more of D3 (the in-activator) and thus inhibits many of the synergistic effects of T3. When D3 levels are high, growth factors such as IGF-1 are stimulated, which means D3 is an important part of the equation with regards to the anabolic effects of GH.Now for the part you have all been waiting for, the summary and conclusion…When growth hormone is taken, along with T3, the GH will stop converting T4 to T3 after a certain point, which means it will shut of the good, anabolic effects of GH by killing the pathway that creates them! This, to me, seems like a bad thing! Now if we add T4 into a GH cycle, we would enhance this pathway, giving the GH more anabolic effects!Remember that T4 alone is pretty ineffective for our purposes and requires something like GH to be made effective.I have actually seen how effective using T4 in conjunction with GH is, first hand. An athlete I was working with was dieting for a show using GH and T3 (along with many other anabolic compounds), but was seeing no change in his fat to muscle ratio. Even with changes in his diet, such as lowering carbs, increasing cardio and even lowering calories, there were minimal changes, at best. T4 was introduced and within 1 week a change of 2.5% body fat and an increase of 1kg of muscle was measured! This is a pretty drastic change in any book.The way I see it, growth hormone costs a lot, and, if it were me, I would want to maximise it as much as possible to get a better ‘bang for my buck’, T4 seems to be the catalyst here and without it, GH is a waste of moneySo we want elevated T3 levels when we take GH, or we won’t be getting ANYWHERE NEAR the full anabolic effect of our injectable GH
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."
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.
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..
AAS lower T3 levels(Specially Fina) thats how the exert most of their anti-catabolic effects.
Adding T3 at a low dosage will simply bring your T3 levels back up to normal. Nothing more.
We are not talking about supra-physiological dosing, just optimization.
Adding a low dosage of T3 while on AAS+GH is a good idea. Now, if its only GH+T3, thats a different story. I would not run T3 while only on GH. I would run 7-Keto DHEA instead of the T3. Maybe even an ECA stack to increase peripheral T4-T3 conversion.
GH also gives you a mild case of insulin resistance(As do some AAS), therefore adding R-ALA is definately a good idea as well.
"Great minds talk about ideas, average minds talk about facts, and weak minds talk about people"
AAS LOWERS T-3 MYTH OR FACT?
This is essentially another bodybuilding myth. Please ask the person who made the statement about tren lowering BIOAVAILABLE T3 to produce the research. I have read the studies, of which there are a grand total of two on tren in animals, and only total T4 was examined. This is not the same as free T4. Anabolic steroids lower thyroid binding globulin, which lowers total thyroid hormone levels. However, the body compensates by increasing thyroid hormone production, keeping free T3/T4, ie the bioavailable fraction, normal.
I have done a meta-analysis of all published studies on the effects of androgens/AAS on thyroid function. It will be out not this month in Mind & Muscle but in the subsequent issue. Here is a passage from the study:
"Can we make any sense out of the seeming hodgepodge of conflicting data? The only parameters that are consistent from study to study, where they were measured, are depressed total T3 and T4, and TBG. As we have discussed, androgens typically lower TBG, along with total T4 and T3 since the latter are a function of TBG levels...In conclusion then AAS seem to have little if any effect on thyroid function per se.
"The reports by Deyssig & Weissel, and Daly et al suggest the possibility of a direct action of AAS on the thyroid or pituitary, but their results are inconsistent: The former researchers detected elevated stimulated TSH while the latter saw an increase in basal TSH. Free T4 was unchanged in former group, while it was elevated in the latter. The only consistently reported effect is a depression in total T4, total T3 and TBG. If there is a direct effect of AAS on the thyroid, pituitary, or hypothalamus the studies conducted so far shed little light on the mechanism due to their inconsistent results. And as stressed by Deyssig & Weissel any direct effect of anabolic steroids on the thyroid would likely be of no clinical significance due to its small magnitude."
In the total medline database there are eight studies where the effects of androgens/AAS on free thyroid levels were examined. Only one of those studies showed a small clinically insignificant drop in free thyroid hormones. Two actually showed an increase in free thyroid hormones, again clinically insignificant. The remainder showed no effect.
I think adding T3 to a steroid cutting cycle is an excellent idea. I have stressed that point many times, and I always do it. What I think is a bad idea, unless all one is concerned about is weight loss and not preservation of lean body mass is to combine T3 with GH.
Anonymous poster
"Great minds talk about ideas, average minds talk about facts, and weak minds talk about people"
