How much T4 do you take? Is the effect really that noticeable vs running only HgH?
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T4+HGH off test cycle, advisable?
- Thread starter NeoNepomuk
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How much T4 do you take? Is the effect really that noticeable vs running only HgH?
I haven't posted any studies in this thread. You, on the other hand, did. And I didn't need a study to prove your article was BS.
The enzyme utilized from the t4 to t3 process makes gh more effective
Do you taper or just start/stop?
I've always tapered and advised others too a well. Basically it comes down to finding what dose works for you.
On these forums the majority can go by standards others may not. Bloods are important. What might be okay for me might not be for another.
mands
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I don't know what dosage Mands uses but 99% of those who are using T4 with their GH are using subphysiological doses, and that is about as effective as using subphysiological doses of testosterone.
It's worth pointing out that thyroid use is not without risk, particularly cardiovascular. Inducing subclinical, and in many cases, overt hyperthyroidism is usually harmless enough in the short term but atrial fibrillation, increased left ventricular mass and septal wall thickening, etc., have all been associated with subclinical hyperthyroidism. Obviously the risks increase the longer you remain in that state and there is lots of evidence demonstrating the risk is real. And keep in mind, cardiomegaly (although a debatable AAS side effect) is already a concern with AAS use. Adding thyroid hormone increases the risk even further.
A beneficial effect for supplemental thyroid hormone in euthyroid GH users is noticeable only in the bro lore. Monitor your thyroid indices. If your T4 decreases or TSH increases, replace with enough levothyroxine to bring your TSH and T4 back into range. Ideally, you'll do this under your physician's supervision.
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Cite your evidence.
Here is a study for the OP that's interesting.
The Acute Effects of Human Growth Hormone Administration on Thyroid Function in Normal Men
http://press.endocrine.org/action/doSearch?text1=GRUNFELD%2C+C&field1=Contribhttp://press.endocrine.org/doi/abs/10.1210/jcem-67-5-1111#fn2, http://press.endocrine.org/action/doSearch?text1=SHERMAN%2C+B+M&field1=Contrib, andhttp://press.endocrine.org/action/doSearch?text1=CAVALIERI%2C+R+R&field1=Contrib
Address requests for reprints to: Barry Sherman, M.D., Genentech, Inc., 460 Point San Bruno Boulevard, South San Francisco, California 94080.
*This work was supported in part by grants from the V.A. Research Service, the NIH (DK-37102), and Genentech, Inc.
†Clinical Investigator with the V.A.
DOI: http://dx.doi.org/10.1210/jcem-67-5-1111
Received: March 15, 1991
First Published Online: July 01, 2013
GH replacement therapy may lead to alterations in serum TSH and/or thyroid hormone values in GH-deficient patients, but there is no consensus on the explanation for these changes. We examined the effect of GH administration (0.125 mg, sc, daily for 4 days) on thyroid function in 20 normal men. Serum T4 levels decreased by 8%, and serum free T4 index values decreased by 5%. In contrast, serum T3 levels increased by 21%; serum rT3 did not change. These changes were accompanied by a 54% decrease in the mean serum TSH level. While it is not possible to draw conclusions about hormone production and disposal rates from changes in serum levels, these data are most consistent with enhanced extrathyroidal (including intrapituitary) conversion of T4 to T3 and a compensatory decrease in TSH secretion.
Affiliations
http://press.endocrine.org/action/doSearch?text1=J%C3%B8RGENSEN%2C+J+O+L&field1=Contrib, http://press.endocrine.org/action/doSearch?text1=PEDERSEN%2C+S+A&field1=Contrib, http://press.endocrine.org/action/doSearch?text1=LAURBERG%2C+P&field1=Contrib, http://press.endocrine.org/action/doSearch?text1=WEEKE%2C+J&field1=Contrib, http://press.endocrine.org/action/doSearch?text1=SKAKKEB%C3%86K%2C+N+E&field1=Contrib, andhttp://press.endocrine.org/action/doSearch?text1=CHRISTIANSEN%2C+J+S&field1=Contrib
Address requests for reprints to J. O. L. Jørgensen, Second University Clinic of Internal Medicine, Aarhus kommunehospital, DK-8000 C, Denmark.
*This work was supported in part by Aarhus University Research Foundation, the National Danish Health Foundation (H 11/84-87 and H 11/26-88), and the Danish Medical Research Council (12-7452).
DOI: http://dx.doi.org/10.1210/jcem-69-6-1127
Received: April 03, 1989
First Published Online: July 01, 2013
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 < 0.01); group II, 145 + 18 vs. 115 + 10 (P < 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< 0.1); group II, 1.7 + 0.1 vs. 1.9 + 0.1 (P < 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 < 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 < 0.01); group II, 0.38 + 0.05 (placebo) vs. 0.29 + 0.02 (GH; P < 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 T4to T3. GH thus seems to play an important role, either directly or indirectly, in the regulation of peripheral T4metabolism. (J Clin Endocrinol Metab 69: 1127, 1989)
Affiliations
The Acute Effects of Human Growth Hormone Administration on Thyroid Function in Normal Men
http://press.endocrine.org/action/doSearch?text1=GRUNFELD%2C+C&field1=Contribhttp://press.endocrine.org/doi/abs/10.1210/jcem-67-5-1111#fn2, http://press.endocrine.org/action/doSearch?text1=SHERMAN%2C+B+M&field1=Contrib, andhttp://press.endocrine.org/action/doSearch?text1=CAVALIERI%2C+R+R&field1=Contrib
Address requests for reprints to: Barry Sherman, M.D., Genentech, Inc., 460 Point San Bruno Boulevard, South San Francisco, California 94080.
*This work was supported in part by grants from the V.A. Research Service, the NIH (DK-37102), and Genentech, Inc.
†Clinical Investigator with the V.A.
DOI: http://dx.doi.org/10.1210/jcem-67-5-1111
Received: March 15, 1991
First Published Online: July 01, 2013
- http://press.endocrine.org/doi/abs/10.1210/jcem-67-5-1111
- http://press.endocrine.org/doi/pdf/10.1210/jcem-67-5-1111
- http://press.endocrine.org/doi/citedby/10.1210/jcem-67-5-1111
GH replacement therapy may lead to alterations in serum TSH and/or thyroid hormone values in GH-deficient patients, but there is no consensus on the explanation for these changes. We examined the effect of GH administration (0.125 mg, sc, daily for 4 days) on thyroid function in 20 normal men. Serum T4 levels decreased by 8%, and serum free T4 index values decreased by 5%. In contrast, serum T3 levels increased by 21%; serum rT3 did not change. These changes were accompanied by a 54% decrease in the mean serum TSH level. While it is not possible to draw conclusions about hormone production and disposal rates from changes in serum levels, these data are most consistent with enhanced extrathyroidal (including intrapituitary) conversion of T4 to T3 and a compensatory decrease in TSH secretion.
Affiliations
- Department of Medicine, University of California-San Francisco
San Francisco, California 94121 - The Metabolism Section, Medical Service and Nuclear Medicine Service, Veterans Administration Medical Center
San Francisco, California 94121 - The Department of Clinical Research, Genentech, Inc.
http://press.endocrine.org/action/doSearch?text1=J%C3%B8RGENSEN%2C+J+O+L&field1=Contrib, http://press.endocrine.org/action/doSearch?text1=PEDERSEN%2C+S+A&field1=Contrib, http://press.endocrine.org/action/doSearch?text1=LAURBERG%2C+P&field1=Contrib, http://press.endocrine.org/action/doSearch?text1=WEEKE%2C+J&field1=Contrib, http://press.endocrine.org/action/doSearch?text1=SKAKKEB%C3%86K%2C+N+E&field1=Contrib, andhttp://press.endocrine.org/action/doSearch?text1=CHRISTIANSEN%2C+J+S&field1=Contrib
Address requests for reprints to J. O. L. Jørgensen, Second University Clinic of Internal Medicine, Aarhus kommunehospital, DK-8000 C, Denmark.
*This work was supported in part by Aarhus University Research Foundation, the National Danish Health Foundation (H 11/84-87 and H 11/26-88), and the Danish Medical Research Council (12-7452).
DOI: http://dx.doi.org/10.1210/jcem-69-6-1127
Received: April 03, 1989
First Published Online: July 01, 2013
- http://press.endocrine.org/doi/abs/10.1210/jcem-69-6-1127
- http://press.endocrine.org/doi/pdf/10.1210/jcem-69-6-1127
- http://press.endocrine.org/doi/citedby/10.1210/jcem-69-6-1127
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 < 0.01); group II, 145 + 18 vs. 115 + 10 (P < 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< 0.1); group II, 1.7 + 0.1 vs. 1.9 + 0.1 (P < 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 < 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 < 0.01); group II, 0.38 + 0.05 (placebo) vs. 0.29 + 0.02 (GH; P < 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 T4to T3. GH thus seems to play an important role, either directly or indirectly, in the regulation of peripheral T4metabolism. (J Clin Endocrinol Metab 69: 1127, 1989)
Affiliations
- Second University Clinic of Internal Medicine and Institute of Experimental Clinical Research, Aarhus Kommunehospital, and University of Aarhus
Aarhus - University Department of Pediatrics, Hvidovre Hospital
Copenhagen, Denmark
CBS its there on the web ill let u do ur thing
No sir! You made the claim, the onus is on you to prove it.
It looks like you are in range on all three and your FSH looks good to me. .5 or under would be considered hypo and over 5.0 most would consider hyper.
mands
I think you reversed that... Over 5 is hypo. I had a doctor tell me the new number they're using on tsh is 3.5 so he's really close to that number. Most people say tsh isn't enough to make a diagnosis on its own though... Further tasting is required.
I believe you are right, Over 5 is hypo because when tsh is high, it means the body is trying to produce more t4-t3 but if t3-t4 are low it means the pituary is not working well.
I'm not sure this is the way it works but it's more or less like lh and fsh.
if they are sky high and your TT is low, well there is a problem huston
Correct, there was a push to change the upper reference range from ~5 to 3.5 for the TSH panel. I don't know that it ever passed but many specialists do use the 3.5 value as the limit. Also TSH alone isn't enough to make a full diagnosis of what's wrong if anything. Further testing of things like FT3 and 4 would be suggested.
Yes you are correct!!!
HIGHER TSH = UNDERACTIVE THYROID / HYPOTHYROIDISM.
Sorry about that. I knew what I meant but posted the wrong info.
mands
[QUOTE="
Taking more than 50/75mcg of T3 starts to eat into my muscles when off cycle.[/QUOTE]
There is no reason to use Thyroxine when taking Tren, but it seems you know that and are using it for "cutting".
Regarding to your question. It really should not matter whether your using an AAS or not, "high" levels of thyroxine result in a catabolic state.
I suspect the reason your noticing a catabolic state while cycling is the AAS your using are offsetting the difference.
So because T3-T4 enhances lipolysis and facilitates muscle wasting it's use should be restricted to VERY SHORT several week intervals as in pre-contest preparation.
What's even more important, bc hyperthyroidism is CLEARLY associated with untoward cardiovascular effects, the practice of routinely supplementing Thyroxine to induce a
hypermetabolic state MUST BE STRONGLY DISCOURAGED!
Finally although there are some folk who don't convert T-4 to T-3 as readily as others, whether this makes a difference from a clinical perspective is UNLIKELY, IMO.
Taking more than 50/75mcg of T3 starts to eat into my muscles when off cycle.[/QUOTE]
There is no reason to use Thyroxine when taking Tren, but it seems you know that and are using it for "cutting".
Regarding to your question. It really should not matter whether your using an AAS or not, "high" levels of thyroxine result in a catabolic state.
I suspect the reason your noticing a catabolic state while cycling is the AAS your using are offsetting the difference.
So because T3-T4 enhances lipolysis and facilitates muscle wasting it's use should be restricted to VERY SHORT several week intervals as in pre-contest preparation.
What's even more important, bc hyperthyroidism is CLEARLY associated with untoward cardiovascular effects, the practice of routinely supplementing Thyroxine to induce a
hypermetabolic state MUST BE STRONGLY DISCOURAGED!
Finally although there are some folk who don't convert T-4 to T-3 as readily as others, whether this makes a difference from a clinical perspective is UNLIKELY, IMO.
Here is a study for the OP that's interesting.
The Acute Effects of Human Growth Hormone Administration on Thyroid Function in Normal Men
http://press.endocrine.org/action/doSearch?text1=GRUNFELD%2C+C&field1=Contribhttp://press.endocrine.org/doi/abs/10.1210/jcem-67-5-1111#fn2, http://press.endocrine.org/action/doSearch?text1=SHERMAN%2C+B+M&field1=Contrib, andhttp://press.endocrine.org/action/doSearch?text1=CAVALIERI%2C+R+R&field1=Contrib
Address requests for reprints to: Barry Sherman, M.D., Genentech, Inc., 460 Point San Bruno Boulevard, South San Francisco, California 94080.
*This work was supported in part by grants from the V.A. Research Service, the NIH (DK-37102), and Genentech, Inc.
†Clinical Investigator with the V.A.
DOI: http://dx.doi.org/10.1210/jcem-67-5-1111
Received: March 15, 1991
First Published Online: July 01, 2013
Abstract
- http://press.endocrine.org/doi/abs/10.1210/jcem-67-5-1111
- http://press.endocrine.org/doi/pdf/10.1210/jcem-67-5-1111
- http://press.endocrine.org/doi/citedby/10.1210/jcem-67-5-1111
GH replacement therapy may lead to alterations in serum TSH and/or thyroid hormone values in GH-deficient patients, but there is no consensus on the explanation for these changes. We examined the effect of GH administration (0.125 mg, sc, daily for 4 days) on thyroid function in 20 normal men. Serum T4 levels decreased by 8%, and serum free T4 index values decreased by 5%. In contrast, serum T3 levels increased by 21%; serum rT3 did not change. These changes were accompanied by a 54% decrease in the mean serum TSH level. While it is not possible to draw conclusions about hormone production and disposal rates from changes in serum levels, these data are most consistent with enhanced extrathyroidal (including intrapituitary) conversion of T4 to T3 and a compensatory decrease in TSH secretion.
Affiliations
Effects of Growth Hormone Therapy on Thyroid Function of Growth Hormone-Deficient Adults with and without Concomitant Thyroxine-Substituted Central Hypothyroidism
- Department of Medicine, University of California-San Francisco
San Francisco, California 94121- The Metabolism Section, Medical Service and Nuclear Medicine Service, Veterans Administration Medical Center
San Francisco, California 94121- The Department of Clinical Research, Genentech, Inc.
http://press.endocrine.org/action/doSearch?text1=J%C3%B8RGENSEN%2C+J+O+L&field1=Contrib, http://press.endocrine.org/action/doSearch?text1=PEDERSEN%2C+S+A&field1=Contrib, http://press.endocrine.org/action/doSearch?text1=LAURBERG%2C+P&field1=Contrib, http://press.endocrine.org/action/doSearch?text1=WEEKE%2C+J&field1=Contrib, http://press.endocrine.org/action/doSearch?text1=SKAKKEB%C3%86K%2C+N+E&field1=Contrib, andhttp://press.endocrine.org/action/doSearch?text1=CHRISTIANSEN%2C+J+S&field1=Contrib
Address requests for reprints to J. O. L. Jørgensen, Second University Clinic of Internal Medicine, Aarhus kommunehospital, DK-8000 C, Denmark.
*This work was supported in part by Aarhus University Research Foundation, the National Danish Health Foundation (H 11/84-87 and H 11/26-88), and the Danish Medical Research Council (12-7452).
DOI: http://dx.doi.org/10.1210/jcem-69-6-1127
Received: April 03, 1989
First Published Online: July 01, 2013
Abstract
- http://press.endocrine.org/doi/abs/10.1210/jcem-69-6-1127
- http://press.endocrine.org/doi/pdf/10.1210/jcem-69-6-1127
- http://press.endocrine.org/doi/citedby/10.1210/jcem-69-6-1127
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 < 0.01); group II, 145 + 18 vs. 115 + 10 (P < 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< 0.1); group II, 1.7 + 0.1 vs. 1.9 + 0.1 (P < 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 < 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 < 0.01); group II, 0.38 + 0.05 (placebo) vs. 0.29 + 0.02 (GH; P < 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 T4to T3. GH thus seems to play an important role, either directly or indirectly, in the regulation of peripheral T4metabolism. (J Clin Endocrinol Metab 69: 1127, 1989)
Affiliations
mands
- Second University Clinic of Internal Medicine and Institute of Experimental Clinical Research, Aarhus Kommunehospital, and University of Aarhus
Aarhus- University Department of Pediatrics, Hvidovre Hospital
Copenhagen, Denmark
A more appropriate term rather than "caused" would be resulted in.
That's bc it's been reasonably well established GH supplementation results In an enhanced utilization of thyroxine with the net effect being increased conversion of T-4 into T-3 out of necessity.
However routine supplementation of thyroxine is NOT recommended since, as this study revealed, the resultant rise in TSH from GH use will normalize thyroxine levels in due course.
Consequently thyroxine supplementation in this instance only negates those physiologic processes designed to remedy it.
The only exception being those patients with "borderline" hypothyroidism (based on Thyroid indices) since they may develop overt hypothyroidism with GH supplementation.
