T4 with HGH - Why?
Posted: Wed Apr 08, 2020 2:16 am
T4 with HGH - Why?
Let's talk about the very significant of using T4 Human growth hormone? Is it necessary?
Only bloods will tell..
Listen - Upon taking GH and increasing levels due to a exogenous source it will increase the fat burning properties via vast mechanisms...However, this effect is amplified by the activity through the T3 hormone...This effect is rather unique, in the fashion by the enzyme 5'(prime) Deiodinase is significantly/drastically enhanced.. The process now amplifies the conversion ratio within stored T4 into active T3, thus more bio-active T3 in circulation, inducing a fold in the fat burning rate.. Unfortunately, the endocrine has a limited amount or T4, in storage and total.. It's gone before you know it!
What's exactly does this all translate into? If the ratio is being used faster then production, due to the increased conversion/activity, there is now a deficiency.. Supply and demand!
This is were the suggestion concerning the protocol of adding T4 through an exogenous channel is recommended.. Now at some point the level of T4 will go extremely low effecting conversion, thus interfering with the fat burning process by slowing down, decreasing.. Now I'm not stating that GH will no long possess fat burning properties but like anything else, the effects will begin to halt..
The hack to this situation to continue and restore the feeding process with GH boosting fat burning by implementing the addition is T4, at a low to moderate dose (you don't need much)..
There is a drastic shift in T4/T3 levels during GH usage, get bloods as often as one can during treatment, this will indicate exactly where you are..
Always provide every compound, agent, pep/GH or AAS with what they need to be a fully function mechanism (this includes food)..GH cost enough as it is, get the most out of it, and supply GH with what it needs to assist and achieve your desired goal...Now with the addition of T4, GH has more to work with "again".. sustain it, and it will convert and pump out t3 (it will take what it needs)..This is a hack in terms to optimizing the effects of GH for your advantage!
Thyroid function during growth hormone therapy.
Jørgensen JO1, Møller J, Skakkebaek NE, Weeke J, Christiansen JS.
Abstract
Administration of growth hormone (GH) in GH-deficient patients has been reported to cause a variety of perturbations in thyroid function. Reports range from decreased sensitivity of thyrotropin (TSH) to thyrotropin-releasing hormone (TRH) stimulation and induction of hypothyroidism to increased energy expenditure and enhanced peripheral thyroxine (T4) to triiodothyronine (T3) conversion. Some of the diversities may relate to the fact that earlier studies were uncontrolled case reports, which furthermore employed pituitary GH preparations, which may have been contaminated with TSH. A confounding variable in terms of incipient TSH insufficiency in some patients may also have been present. Data from a placebo-controlled crossover study of 4-months GH therapy in GH-deficient adults, some of whom were on ongoing T4 substitution, revealed that the most prominent effect on thyroid function was increased peripheral T4 to T3 conversion without significantly affecting TSH levels or secretion from the thyroid gland. It was furthermore observed that T3 levels during placebo were significantly decreased compared to an untreated healthy control group. Comparable findings have been made in a controlled study of 6-months GH therapy in adult-onset GH-deficient patients. More recent data suggest that these effects prevail after long-term (16 months) therapy. Similar findings have also been reported in healthy subjects receiving pharmacological GH doses. It is likely that this effect is not caused by GH per se inasmuch as reduced T4 to T3 conversion is a common observation in catabolic states with concomitant GH hypersecretion. It remains to be shown whether insulin-like growth factor I (IGF-I) stimulates peripheral deiodination.
Effects of growth hormone therapy on thyroid function of growth hormone-deficient adults with and without concomitant thyroxine-substituted central hypothyroidism.
Administration of human GH to GH-deficient patients has yielded conflicting results concerning its impact on thyroid function, ranging from increased resting metabolic rate to induction of hypothyroidism. However, most studies have been casuistic or uncontrolled and have used pituitary-derived GH of varying purity, often contaminated with TSH. Therefore, we conducted a double blind, placebo-controlled cross-over study of the effect of 4 months of biosynthetic human GH therapy (Norditropin; 2 IU/m2.day) on thyroid function in GH-deficient adults (8 females and 14 males; mean +/- SE age, 23.8 +/- 1.2 yr). One group (I) was euthyroid without T4 substitution (n = 13), whereas the other (group II) received T4 (n = 9). Serum T4 (nanomoles per L) decreased in both groups after GH treatment [group I, 100 +/- 8 (mean +/- SE) vs. 89 +/- 8 (P less than 0.01); group II, 145 +/- 18 vs. 115 +/- 10 (P less than 0.05)]. Conversely, GH treatment caused an increase in serum T3 (nanomoles per L) in both groups [group I, 1.9 +/- 0.1 vs. 2.0 +/- 0.1 (P less than 0.1); group II, 1.7 +/- 0.1 vs. 1.9 +/- 0.1 (P less than 0.05)]. Similar changes were seen in serum free T4 and T3. The serum T3 level during the placebo period of group I was significantly lower than that in an age-matched reference group (P less than 0.02). Serum rT3 (nanomoles per L) was low in group I and decreased significantly, as in group II, after GH treatment [group I, 0.26 +/- 0.02 (placebo) vs. 0.20 +/- 0.02 (GH; P less than 0.01); group II, 0.38 +/- 0.05 (placebo) vs. 0.29 +/- 0.02 (GH; P less than 0.01)]. Serum TSH decreased in both groups during GH therapy, though not significantly. Serum thyroglobulin was unaltered and did not differ from that in the reference group. In conclusion, our data are consistent with a GH-induced enhancement of peripheral deiodination of T4 to T3. GH thus seems to play an important role, either directly or indirectly, in the regulation of peripheral T4 metabolism.
PMID: 2685007 [PubMed - indexed for MEDLINE]
Let's talk about the very significant of using T4 Human growth hormone? Is it necessary?
Only bloods will tell..
Listen - Upon taking GH and increasing levels due to a exogenous source it will increase the fat burning properties via vast mechanisms...However, this effect is amplified by the activity through the T3 hormone...This effect is rather unique, in the fashion by the enzyme 5'(prime) Deiodinase is significantly/drastically enhanced.. The process now amplifies the conversion ratio within stored T4 into active T3, thus more bio-active T3 in circulation, inducing a fold in the fat burning rate.. Unfortunately, the endocrine has a limited amount or T4, in storage and total.. It's gone before you know it!
What's exactly does this all translate into? If the ratio is being used faster then production, due to the increased conversion/activity, there is now a deficiency.. Supply and demand!
This is were the suggestion concerning the protocol of adding T4 through an exogenous channel is recommended.. Now at some point the level of T4 will go extremely low effecting conversion, thus interfering with the fat burning process by slowing down, decreasing.. Now I'm not stating that GH will no long possess fat burning properties but like anything else, the effects will begin to halt..
The hack to this situation to continue and restore the feeding process with GH boosting fat burning by implementing the addition is T4, at a low to moderate dose (you don't need much)..
There is a drastic shift in T4/T3 levels during GH usage, get bloods as often as one can during treatment, this will indicate exactly where you are..
Always provide every compound, agent, pep/GH or AAS with what they need to be a fully function mechanism (this includes food)..GH cost enough as it is, get the most out of it, and supply GH with what it needs to assist and achieve your desired goal...Now with the addition of T4, GH has more to work with "again".. sustain it, and it will convert and pump out t3 (it will take what it needs)..This is a hack in terms to optimizing the effects of GH for your advantage!
Thyroid function during growth hormone therapy.
Jørgensen JO1, Møller J, Skakkebaek NE, Weeke J, Christiansen JS.
Abstract
Administration of growth hormone (GH) in GH-deficient patients has been reported to cause a variety of perturbations in thyroid function. Reports range from decreased sensitivity of thyrotropin (TSH) to thyrotropin-releasing hormone (TRH) stimulation and induction of hypothyroidism to increased energy expenditure and enhanced peripheral thyroxine (T4) to triiodothyronine (T3) conversion. Some of the diversities may relate to the fact that earlier studies were uncontrolled case reports, which furthermore employed pituitary GH preparations, which may have been contaminated with TSH. A confounding variable in terms of incipient TSH insufficiency in some patients may also have been present. Data from a placebo-controlled crossover study of 4-months GH therapy in GH-deficient adults, some of whom were on ongoing T4 substitution, revealed that the most prominent effect on thyroid function was increased peripheral T4 to T3 conversion without significantly affecting TSH levels or secretion from the thyroid gland. It was furthermore observed that T3 levels during placebo were significantly decreased compared to an untreated healthy control group. Comparable findings have been made in a controlled study of 6-months GH therapy in adult-onset GH-deficient patients. More recent data suggest that these effects prevail after long-term (16 months) therapy. Similar findings have also been reported in healthy subjects receiving pharmacological GH doses. It is likely that this effect is not caused by GH per se inasmuch as reduced T4 to T3 conversion is a common observation in catabolic states with concomitant GH hypersecretion. It remains to be shown whether insulin-like growth factor I (IGF-I) stimulates peripheral deiodination.
Effects of growth hormone therapy on thyroid function of growth hormone-deficient adults with and without concomitant thyroxine-substituted central hypothyroidism.
Administration of human GH to GH-deficient patients has yielded conflicting results concerning its impact on thyroid function, ranging from increased resting metabolic rate to induction of hypothyroidism. However, most studies have been casuistic or uncontrolled and have used pituitary-derived GH of varying purity, often contaminated with TSH. Therefore, we conducted a double blind, placebo-controlled cross-over study of the effect of 4 months of biosynthetic human GH therapy (Norditropin; 2 IU/m2.day) on thyroid function in GH-deficient adults (8 females and 14 males; mean +/- SE age, 23.8 +/- 1.2 yr). One group (I) was euthyroid without T4 substitution (n = 13), whereas the other (group II) received T4 (n = 9). Serum T4 (nanomoles per L) decreased in both groups after GH treatment [group I, 100 +/- 8 (mean +/- SE) vs. 89 +/- 8 (P less than 0.01); group II, 145 +/- 18 vs. 115 +/- 10 (P less than 0.05)]. Conversely, GH treatment caused an increase in serum T3 (nanomoles per L) in both groups [group I, 1.9 +/- 0.1 vs. 2.0 +/- 0.1 (P less than 0.1); group II, 1.7 +/- 0.1 vs. 1.9 +/- 0.1 (P less than 0.05)]. Similar changes were seen in serum free T4 and T3. The serum T3 level during the placebo period of group I was significantly lower than that in an age-matched reference group (P less than 0.02). Serum rT3 (nanomoles per L) was low in group I and decreased significantly, as in group II, after GH treatment [group I, 0.26 +/- 0.02 (placebo) vs. 0.20 +/- 0.02 (GH; P less than 0.01); group II, 0.38 +/- 0.05 (placebo) vs. 0.29 +/- 0.02 (GH; P less than 0.01)]. Serum TSH decreased in both groups during GH therapy, though not significantly. Serum thyroglobulin was unaltered and did not differ from that in the reference group. In conclusion, our data are consistent with a GH-induced enhancement of peripheral deiodination of T4 to T3. GH thus seems to play an important role, either directly or indirectly, in the regulation of peripheral T4 metabolism.
PMID: 2685007 [PubMed - indexed for MEDLINE]