# Thyroid Hormone + Growth Hormone with James Daemon, Ph.D. (Must Read)



## Supra (Sep 20, 2012)

Thyroid Hormone + Growth Hormone 
(If You Aren’t Using T4 with Your GH, You’re Not Doing It Right)

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with James Daemon, Ph.D.

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Posted July 23, 2006. 

Discussion of pharmaceutical agents below is presented for information only. Nothing here is meant to take the place of advice from a licensed health care practitioner. Consult a physician before taking any medication.

Quite some time ago, I wrote a book on Anabolics, and since then, I’ve received quite a bit of feedback on it. Some of the information contained in the book is based on the 50-60 profiles I completed for Steroid.com’s main page. As a result, I get feedback on certain portions of the book from people who have read them online. 

When someone takes the time to send an e-mail to Steroid.com or AnabolicBooks LLC, they’re screened, and eventually some of them make their way to my e-mail account. AnabolicBooks LLC is publisher- a little known fact is that my book is actually wasn’t edited by me, nor do I own the rights to any of it. When they forward an e-mail to me, I typically consider it very carefully, and reply to the original sender. If amendments or additions are useful for anything I’ve previously written (readers frequently send me recently published studies), I typically reply and thank the person for their help. 

This time, something odd happened. I was forwarded an e-mail from AnabolicBooks, and the reader seemed to know what he was talking about, but (I thought) mistaken about interactions between Growth Hormone and Thyroid medication. I took a look at the e-mail, and knew that I could quickly find a study that I had saved previously, to send to the reader, to verify that the claims in my work on GH were sound. 

In this particular case- James Daemon, PhD- was the reader, and was correct in his assessment of the interaction between thyroid hormone and Growth Hormone. And, in direct contradiction, so was I. Thyroid medication decreases the anabolic effect of Growth Hormone. And it increases it. 

Huh? 

There’re some leaps here, because research in some of the necessary areas is sketchy (or not done yet), but if you read the entirety of this article, you’ll learn how to get a significantly more gains from Growth Hormone, for pennies a day, by the addition of a readily available (and cheap) addition to it. And yeah, it’s a drug you can get anywhere on the ‘net, very easily. And no, it’s not a steroid.

In fact, I’ll go so far as to say you’re throwing away a substantial portion of your gains from growth hormone if you are not using this drug with it.

Ok…I’ll explain things a bit further. First, a brief explanation of Thyroid Hormone as well as Growth Hormone may be necessary. 

Your thyroid gland secretes two hormones that are going to be of primary importance in understanding Thyroid/GH interaction. The first is thyroxine (T4) and the second is triiodothyronine (T3). T3 is frequently considered the physiologically active hormone, and consequently the one on which most athletes and bodybuilders focus their energies on. T4, on the other hand, is converted in peripheral tissue into T3 by the enzymes in the deiodinase group, of which there are three types- the three iodothyronine deiodinase either catalyze the initiation (D1, D2) or termination (D3) of thyroid hormone effects. The majority of the body's T3 (about 80%) comes from this conversion via the first two types of deiodinase, while conversion to an inactive state is accomplished by the third type. 

It’s important to note that not all of the body’s T4 is converted to T3, however- some remains unconverted. The secretion of T4 is under the control of Thyroid Stimulating Hormone (TSH) which is produced by the pituitary gland. TSH secretion is in turn controlled through release of Thyrotropin Releasing Hormone which is produced in your hypothalamus. So, when T3 levels go up, TSH secretion is suppressed, due to the body’s self regulatory system known as the "negative feedback loop" . This is also the mechanism whereby exogenous thyroid hormone suppresses natural thyroid hormone production. However, it should be noted that thyroid stimulating hormone (like all other hormones) can not work in a vacuum. TSH also requires the presence of Insulin or Insulin-like Growth Factor to stimulate thyroid function (1) When thyroid hormone is present without either insulin or IGF -1, it has no physiological effect (ibid).

Most people think that T3 is just a physiologically active hormone that regulates bodyfat setpoint and has some minor anabolic effects, but in actuality, in some cases of delayed growth in children, T3 is actually too low, while GH levels are normal, and this has a growth limiting effect on several tissues (2) This could be due to T3’s ability to stimulate the proliferation of IGF-1 mRNA in many tissues (which would, of course, be anabolic), or it could be due to the synergistic effect T3 has on GH, specifically on regulation of the growth hormone gene. Although it is largely overlooked in the world of performance enhan***ent, regulation of the growth hormone response is predominantly determined by positive control of growth hormone gene transcription which is proportional to the concentration of thyroid hormone-receptor complexes, which are influenced by T3 levels. (3)

At this point, just to give you a better understanding of what’s going on, I think it’s prudent to also give a brief explanation of Growth Hormone (GH) as well. 

Your body’s GH is regulated by many internal factors, such as hormones and enzymes. hormones. A change in the level of your body’s GH output begins in the hypothalamus with somatostatin (SS) and growth hormone-releasing hormone (GHRH). Somatostatin exerts its effect at the pituitary to decrease GH output, while GHRH acts at the pituitary to increase GH output. Together these hormones regulate the level of GH you have in your body. In many cases, GH deficiency presents with a low level of T3, and normal T4(4). This is of course because conversion of T4-T3 is partially dependant on GH (and to some degree GH stimulated IGF-1), and it’s ability to stimulate that conversion process of T4 into T3.

Interestingly, the hypothalamus isn’t the only place where SS is contained; the thyroid gland also contains Somatostatin-producing cells. This is of interest to us, because in the case of the thyroid, it’s been noted that certain hormones which were previously thought only to govern GH secretion can also influence thyroid hormone output as well. SS can directly act to inhibit TSH secretion or it may act on the hypothalamus to inhibit TRH secretion. So when you add GH into your body from an outside source, you are triggering the body into releasing SS, because your body no longer needs to produce its own supply of GH…and unfortunately, the release of SS can also inhibit TSH, and therefore limit the amount of T4 your body produces. 

But that’s not the only interaction we see between the thyroid and Growth Hormone. 

As we learned in high-school Biology class, the body likes to maintain homeostasis, or "normal" operating conditions. This is the body’s version of the status quo, and it fights like hell to maintain the comfort of the status quo (much like moderators on most steroid discussion boards). What we see with thyroid/GH interplay is that physiological levels of circulating thyroid hormones are necessary to maintain normal pituitary GH secretion, due to their directly stimulatory actions. However, when serum concentrations of thyroid hormone increase above the normal range we see an increase in hypothalamic somatostatin action, which suppresses pituitary GH secretion and overrides any stimulatory effects that the thyroid hormone may have had on GH. The suppression of GH secretion by thyroid hormones is probably mediated at the hypothalamic level by a decrease in GHRH release(5). 

In addition, as IGF-I production is increased in the hypothalamus after T3 administration and T3 may participate in IGF-1 mediated negative feedback of GH by triggering either increased somatostatin tone and/or decreased GHRH production (6). IGF, interestingly, has the ability to mediate some of T3’s effects independent of GH, but not to the same degree GH can (7.) In fact, IGF-I production is increased in the hypothalamus after T3, administration it may plausibly participate in negative feedback by triggering either increased somatostatin tone and/or decreased GHRH production. So we know that GH lowers T4 (more about this in a sec), but an increase in T3 upregulates GH receptors (8) as well as IGF-1 receptors (9,10).

As can be previously stated, and due to the ability of GH to convert inactive T4 into active T3, GH administration in healthy athletes shows us an entirely predicatble increase in mean free T3 (fT3), and a decrease in mean free T4 (fT4) levels.(11) 




Interaction between GH, IGF-I, T3, and GC. GH stimulates hepatic IGF-I secretion and local production of growth plate IGF-I, and exerts direct actions in the growth plate. Circulating T3 is derived from the thyroid gland and by enzymatic deiodination of T4 in liver and kidne.. The regulatory 5'-DI and 11ßHSD type 2 enzymes may also be expressed in chondrocytes to control local supplies of intracellular T3 and GC. Receptors for each hormone (GHR, IGF-IR, TR, GR) are expressed in growth plate chondrocytes.

So, with the use of GH, what we see is an increased conversion of T4-T3, and possible inhibition of Thyroid Releasing Hormone by Somatostatin, and therefore even though T3 levels may rise, there is no increase in T4 (logically, we see a decrease). Now, as we’ve seen, GH is HIGHLY synergistic with T3 in the body, and as a mater of fact, if you’ve been paying any attention up until this point, you’ll note that the limiting factor on GH’s ability to exert many of it’s effects, is mediated by the amount of T3 in the body. 

As noted before, T3 enhances many effects of GH by several mechanisms, including (but not limited to): increasing IGF-1 levels, IGF-1 mRNA levels, and finally by actually mediating the control of the growth hormone gene transcription process as seen below:


Comparison of the kinetics of L-T3-receptor binding abundance to changes in the rate of transcription of the GH gene.(3)

As you can see, T3 levels are directly correlative to GH gene transcription. The scientists who conducted the study which provided the graph above concluded that the amount of T3 present is a regulatory factor on how much GH gene transcription actually occurs. And gene transcription is what actually gives us the effects from GH. This last fact really seems to shed some light on why we need T3 levels to be supraphysiological if we’re going to be using supraphysiological levels of GH, right? Otherwise, the GH we’re using is going to be limited by the amount of T3 our body produces. However, since we’re taking GH, and it is converting more T4 into T3, T4 levels are lowered substantially, and this is the problem with GH. and may actually be THE limiting factor on GH…if we assume that at least some of GH’s effects are enhanced by thyroid hormone, and specifically T3, then what we are looking at is the GH that has been injected is being limited by a lack of T3. But that doesn’t make sense, because if we use T3 + GH, we get a decrease in the anabolic effect of GH. 

This is where Mr. Daemon, who had contacted me via an e-mail to my publisher, about Thyroid + GH interaction, was able to shed some light on things. You see, I knew that it couldn’t just be the actual presence of enough T3 along with the GH that was limiting GH’s anabolic effect, because, simply adding T3 to a GH cycle will reduce the anabolic effect of the GH (12.). 

Originally, he had said to me that T3 was synergistic with GH, wheras I said that T3 actually reduced the anabolic effects of GH- now I realize we were both correct. Logically this presents a bit of a problem, which I believe can be solved. This came from reading several studies provided to me by Dr.Daemon. the trend I was seeing was that even when Growth Hormone therapy was used, T3 levels needed to be elevated in order to treat several conditions caused by a lack of natural growth hormone. And even if the patient was on GH, T3 levels still needed to be elevated. And what I noticed was that those levels were elevated successfully by using supplemental T4 but not T3. 

Here’s why I think this is:

Additional T3 is not all that’s needed here. What’s needed is the actual conversion process of T4-T3, and the deiodinase presence and activity that it involves. This is because Local 5'-deiodination of l-thyroxine (T4) to active the thyroid hormone 3,3',5-tri-iodothyronine (T3) is catalyzed by the two 5'-deiodinase enzymes (D1 and D2). These enzymes not only "create" T3 out of T4, but actually regulates various T(3)-dependent functions in many tissues including the anterior pituitary and liver. So when there is an excess of T3 in the body, but normal levels of T4, the body’s thyroid axis sends a negative feedback signal., and produces less (D1 and D2) deiodinase, but more of the D3 type, which signals the cessation of the T4-T3 conversion process, and is inhibitory of many of the synergistic effects that T3 has! Remember, Type 3 iodothyronine deiodinase (D3) is the physiologic INACTIVATOR of thyroid hormones and their effects (13) and is well known to have independent interaction with growth factors (which is what GH and IGF-1 are).(14) This is because with adequate T4 and excess T3, (D1 and D2) deiodinase is no longer needed for conversion of T4 into T3, but levels of D3 deiodinase will be elevated. When there is less of the first two types of deidinase, it would seem that the T3 which has been converted to T4 can not exert it’s protein sparing (anabolic effects), as those first two types are responsible for mediation of many of the effects T3 has on the body. This seems to be one of the ways deiodinase contributes to anabolism in the presence of other hormones. 

All of this would explain why anecdotally we see bodybuilders who use T3 lose a lot of muscle if they aren’t using anabolics along with it- they’re not utilizing the enzyme that would regulate some of T3’s ability to stimulate protein synthesis, while they are simultaneously signaling the body to produce an inhibitory enzyme (D3). And remember, for decades bodybuilders who were dieting for a contest have been convinced that you lose less muscle with T4 use, but that it’s less effective for losing fat when compared with T3? Well, as we’ve seen, without something (GH in this case) to aid in the conversion process, it would clearly be less effective! Since the deiodinase enzyme is also located in the liver, and we see decreased hepatic nitrogen clearance with GH + T3, it would seem that the D3 enzyme is exerting it’s inhibitory effects, but in the absence of the effects of the first two deiodinase enzymes, it remains unchecked and therefore not only limits the GH’s nitrogen retention capability. 

In other words, if we have enough to GH in our body aid in supraphysiological conversion of T4 into T3, but we already have the too much (exogenous) T3, the GH is not going to be converting any excess T4 into T3 after a certain point- which would be a limiting factor in GH’s anabolic effects, when coupled with the act that we’ve allowed the D3 enzyme to inhibit the T3/GH synergy that is necessary. 

As further evidence, when we look at certain types of cellular growth (the cartilage cell in this case) we see that GH induced rises in IGF-I stimulates proliferation, whereas T3 is responsible for hypertrophic differentiation. So it would seem that in some tissues, IGF-1 stimulates the synthesis of new cells, while T3 makes them larger. In this particular case, The fact that T4 and (D1) deiodinase is am active component in this system is noted by the authors. They clearly state (paraphrasing) that: "T4 is is converted to T3 by deiodinase (5'-DI type 1) in peripheral tissues…[furthermore]GH stimulates conversion of T4 to T3 , suggesting that some effects of GH may involve this pathway." The thing I want you to notice is that the authors of this paper state that the that the conversion PATHWAY is probably involved, and not the simple presence of T3. (15 )

Also, that same study notes that T3 has the ability to stimulates IGF-I and expression in tissues that whereas GH has no such effect (ibid).

So what are we doing when we add T3 to GH? We’re effectively shutting down the conversion pathway that is responsible for some of GH’s effects! And what would we be doing if we added in T4 instead of T3? You got it- we’d be enhancing the pathway by allowing the GH we’re using to have more T4 to convert to T3, thus giving us more of an effect from the GH we’re taking. Adding T4 into our GH cycles will actually allow more of the GH to be used effectively! 

Remember, the thing that catalyzes the conversion process is the deiodinase enzyme. This is also why using low amounts of T3 would seem (again, anecdotally in bodybuilders) to be able to slightly increase protein synthesis and have an anabolic effect – they aren’t using enough to tell the body to stop or slow down production of the deiodinase enzyme, and hence .Although this analogy isn’t perfect, think of GH as a supercharger you have attached to your car…if you don’t provide enough fuel for it to burn at it’s increased output level, you aren’t going to derive the full effects. Thyroid status also may influence IGF-I expression in tissues other than the liver.So what we have here is a problem. When we take GH, it lowers T3 levels…but we need T3 to keep our GH receptor levels optimally upregulated. In addition, it’s suspected that many of GH’s anabolic effects are engendered as a result of production of IGF-1, so keeping our IGF receptors upregulated by maintaining adequate levels of T3 seems prudent. But as we’ve just seen, supplementing T3 with our GH will abolish Growth Hormone’s functional hepatic nitrogen clearance, possibly through the effect of reducing the bioavailability of insulin-like growth factor-I (12.) 

So 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 without enough T3. And now we know that not only do we need the additional T3, but we actually want the CONVERSION process of T4 into T3 to take place, because it’s the presence of those mediator enzymes that will allow the T3 to be synergistic with GH, instead of being inhibitory as is seen when T3 is simply added to a GH cycle. And remember, we don’t only want T3 levels high, but we want types 1 and 2 deiodinase to get us there- and when we take supplemental T3, that just doesn’t happen…all that happens is the type 3 deiodinase enzyme shows up and negates the beneficial effects of the T3 when we combine it with GH.

And that’s where myself and Dr. Daemon ended up, after a week of e-mails, researching studies, and gathering clues. 

If you’ve been using GH without T4, you’ve been wasting half your money – and if you’ve been using it with T3, you’ve been wasting your time. Start using T4 with your GH, and you’ll finally be getting the full results from your investment.

References:

Growth Factors. 1990;2(2-3):99-109.Interaction of TSH, insulin and insulin-like growth factors in regulating thyroid growth and function. Eggo MC, Bachrach LK, Burrow GN.

F, Rumpler M, Klaushofer K 1994 Thyroid hormones increase insulin-like growth factor mRNA levels in the clonal osteoblastic cell line MC3T3- E1. FEBS Lett 345: 67–70

Relationship of the rate of transcription to the level of nuclear thyroid hormone-receptor complexes.J Biol Chem. 1984 May 25;259(10):6284-91. Yaffe BM, Samuels HH.

Thyroid morphology and function in adults with untreated isolated growth hormone deficiency. J Clin Endocrinol Metab. 2006 Mar;91(3):860-4. Epub 2006 Jan 4. 

Eur J Endocrinol.1995 Dec;133(6):646-53.Influence of thyroid hormones on the regulation of growth hormone secretion. Giustina A, Wehrenberg WB.

Binoux M, Faivre-Bauman A, Lassarre C, Tixier-Vidal A 1985 Triiodothyronine stimulates the production of insulin-like growth factor I (IGF-I) by fetal hypothalamus cells cultured in serum free medium. Dev Brain Res 21:319–323

Eur J Endocrinol. 1996 May;134(5):563-7.Insulin-like growth factor I alters peripheral thyroid hormone metabolism in humans: comparison with growth hormone.Hussain MA, Schmitz O, Jorgensen JO, Christiansen JS, Weeke J, Schmid C, Froesch ER

Harakawa S, Yamashita S, Tobinaga T, Matsuo K, Hirayu H, Izumi M, Nagataki S, Melmed S. In vivo regulation of hepatic insulin-like growth factor-1 messenger ribonucleic acids with thyroid hormone. Endocrinol Jpn 37(2):205-11, 1990

Hochberg Z, Bick T, Harel Z Alterations of human growth hormone binding by rat liver membranes during hypo- and hyperthyroidism. Endocrinology 126(1):325-9, 1990

Matsuo K, Yamashita S, Niwa M, Kurihara M, Harakawa S, Izumi M, Nagataki S, Melmed S Thyroid hormone regulates rat pituitary insulin-like growth factor-I receptors. Endocrinology 126(1):550-4, 1990

The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 11 5221-5226, 2003. High Dose Growth Hormone Exerts an Anabolic Effect at Rest and during Exercise in Endurance-Trained Athletes M. L. Healy, J. Gibney, D. L. Russell-Jones, C. Pentecost, P. Croos, P. H. Sönksen and A. M. Umpleby

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

Huang, SA. Physiology and pathophysiology of type 3 deiodinase in humans. Thyroid. 2005 Aug;15(8):875-81. Review.

Hernandez. A. Structure and function of the type 3 deiodinase gene.Thyroid. 2005 Aug;15(8):865-74. Review.

F, Rumpler M, Klaushofer K 1994 Thyroid hormones increase insulin-like growth factor mRNA levels in the clonal osteoblastic cell line MC3T3- E1. FEBS Lett 345: 67–70


any commets on this recent article


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## SHRUGS (Sep 20, 2012)

I would love to hear GETSOME's opinion on this


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## NbleSavage (Sep 20, 2012)

Interesting angle...in for more input.


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## Curiosity (Sep 20, 2012)

yes, bump for expert opinions


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## robot lord (Sep 21, 2012)

So I just read this very informative and lengthy article. It was building and building toward something very exciting for me. Then fizzled out like fireworks landing in my pool. This is great news for us GH users but where's the how to for the t4? I have used t3,t4 and clenbuterol for weight loss and remember pyramiding up and down/2 weeks on and 2 weeks off if I am not mistaken. The idea was to not disturb or damage thyroid permanently. So how can I use the t4 to effectively get more bang for the buck from my GH and be safe as well? This is the golden question! Can't wait to get this puzzle solved. Someone please chime in here.


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## beasto (Sep 21, 2012)

I mean from what I take from this article say...100MCG daily of T4 is golden so the conversion of T4 to T3 can take place.


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## SHRUGS (Sep 22, 2012)

I'm not buyin it. Would really like GETSOMEs input on this. He must be busy lately. Very interesting thread though. Lookin forward to a knowledgeable bros opinion....


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## Supra (Sep 23, 2012)

robot lord said:


> So I just read this very informative and lengthy article. It was building and building toward something very exciting for me. Then fizzled out like fireworks landing in my pool. This is great news for us GH users but where's the how to for the t4? I have used t3,t4 and clenbuterol for weight loss and remember pyramiding up and down/2 weeks on and 2 weeks off if I am not mistaken. The idea was to not disturb or damage thyroid permanently. So how can I use the t4 to effectively get more bang for the buck from my GH and be safe as well? This is the golden question! Can't wait to get this puzzle solved. Someone please chime in here.



T3 is much harder and more potent than t4. I have gone on and off T4 with zero problems. If you have a healthy functioning thyroid, they are highly resilient gland.  
As for proper dosing, I do 50mcg per 2.5iu's of GH everyday. But 100mcg ED pretty much seems to be the gold standard.


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## robot lord (Sep 26, 2012)

Thanks supra. Is there a time frame for t4 use. A mandatory cut off point if u will. If I were to run GH for 8 months can I use the t4 for that amount of time safely?


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## Supra (Sep 26, 2012)

Yes you can run t4 the entire time and then get off, I have gotten on and off t4 many times, no problems, as I said T3 is much harsher on the thyroid then t4. I would never take T3, only T4 for cutting and with GH, its superior IMO.


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## grind4it (Sep 29, 2012)

Damn fine post right here. I am adding T4 ASAP. Anybody have a source that's ligit; preferably tested?
Hit me with a pm if you can help.

Thanks, grind


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## Azog (Sep 29, 2012)

grind4it said:


> Damn fine post right here. I am adding T4 ASAP. Anybody have a source that's ligit; preferably tested?
> Hit me with a pm if you can help.
> 
> Thanks, grind



Pretty sure manpower carries it.


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## LeanHerm (Sep 29, 2012)

Fuck t3. I've seen guys with thyroid issues and its a mess. No need to run compounds to fuck it up


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## NbleSavage (Sep 29, 2012)

BigHerm said:


> Fuck t3. I've seen guys with thyroid issues and its a mess. No need to run compounds to fuck it up



Leaning this way myself, BigHerm.


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## amore169 (Sep 30, 2012)

I would never mess with my thyroid, my wife suffers from low thyroid and she needs to be taking syntroid for life, that's disease is hereditary, we went to so many different doctors so they could find her the right dosage. After seeing first hand all the suffering that my wife has endure, personally I would never mess with it.


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## Supra (Oct 2, 2012)

BigHerm said:


> Fuck t3. I've seen guys with thyroid issues and its a mess. No need to run compounds to fuck it up



Whether you believe it or not GH will lower your thyroid levels. This is one of the reasons why people get tiredness from GH, some can even get so tired they dont want to go to the gym or do much of anything. I have experienced this and it sucks. Like I said I have gone on and off T4 many times without any issues. 

t3 is a differente story and as this article suggests to not use it with gh.


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## robot lord (Oct 2, 2012)

Supra I think you just answered a question I didn't even ask you yet. I have dropped from 5iu to 4iu to 3iu because I am so god damn tired. I have tried morning pins, split doses and ultimately prior to bed pins. Still my motivation is slipping away. I was just thinking to myself that I started TRT/cycling and GH to recapture some youth at 40 but I feel 60 at the moment as far as energy goes. I look great but feel lethargic. So if there is truth to GH lowering thyroid hormones then bumping it back up with T4 shoulkd theoretically give me a boost in energy correct? I sure hope so!!!


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## Supra (Oct 2, 2012)

Also if you look up what the Gen-Tech and Bio-Tech companies say about GH, the all suggest using it with T4 because it will lower your thyroid lvls. There is no reason one should not take it when it infact makes GH more effective, gets rid of the tiredness and possible depression due to lack of energy of GH,


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## Azog (Oct 4, 2012)

Supra said:


> Also if you look up what the Gen-Tech and Bio-Tech companies say about GH, the all suggest using it with T4 because it will lower your thyroid lvls. There is no reason one should not take it when it infact makes GH more effective, gets rid of the tiredness and possible depression due to lack of energy of GH,



I'd like to get to the bottom of whether this is really safe long term. I really don't want to be fucking up my thyroid. Do you know if a 100mcg dose of t4 would suppress natural production? What about 50mcg? Maybe if the dose is low enough, it won't suppress the thyroid, but supplement it? I think I read that on some other forum...


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## Supra (Oct 4, 2012)

Azog said:


> I'd like to get to the bottom of whether this is really safe long term. I really don't want to be fucking up my thyroid. Do you know if a 100mcg dose of t4 would suppress natural production? What about 50mcg? Maybe if the dose is low enough, it won't suppress the thyroid, but supplement it? I think I read that on some other forum...



I think your confusing the potency of T3 with T4, they are completely different animals.


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## Azog (Oct 4, 2012)

No, I'm not. I understand t4 is weak by comparison. I was just hoping you had some knowledge on it's effects on thyroid function. 

This article is nice and all, but it's all theoretical. He hasn't tested these theories in animals or humans, or has he? I'd like to see some real world data.


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## transcend2007 (Oct 4, 2012)

I have been on gh since 01/11 and tried both T3 and T4.  I noticed no difference.  This article has been out for some time.  I also deal with gh fatigue and I have talked to many other on 12 months or more.  Very few escape this side effect.


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## Supra (Oct 4, 2012)

Azog said:


> No, I'm not. I understand t4 is weak by comparison. I was just hoping you had some knowledge on it's effects on thyroid function.
> 
> This article is nice and all, but it's all theoretical. He hasn't tested these theories in animals or humans, or has he? I'd like to see some real world data.



I can only speak from exp and I literally could not get out of bed at 5iu. I was tired fatigued and sleep all the time, once I started t4 all that went away and I noticed more fat buring. I posted this article for more informative reasons feel free to use the advice or do not, it is your choosing. I have been on other boards where the group think is always pair GH with T4, maybe this board has a difference of opinion. All of which is ok.
Cheers friend.


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## Azog (Oct 4, 2012)

I appreciate the knowledge bro! I'm just struggling to satisfy my safety concerns and was hoping for some more insight. I'll keep searching and post anything I find over here.


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## Curiosity (Oct 4, 2012)

It would be amazing if this worked, gh fatigue has been killing me! Maybe ill try it.


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## Azog (Oct 4, 2012)

I'm gonna get my thyroid tested before and when on gh. See what happens. If I need t4 I'll get it tested again.


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## robot lord (Oct 8, 2012)

Just ordered some t4 tabs from manpower along with my caber(getting on the tren train)tonight. Does dose time make any differance? Hour or so prior to GH pin(bedtime for me) or should I just take it with other supps PO? How about us 5 on 2 off guys? T4 on off days or no?


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## PFM (Oct 8, 2012)

I am genuinely concerned how much some of you guys are fucking with with your bodies.


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## robot lord (Oct 8, 2012)

Too much CFM? Cycle,rips,t4,hcg,adex and caber. Yeah the list seems a little long doesn't it.


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## 63Vette (Oct 8, 2012)

I am taking T3 and T4 at the moment...I will be dropping the T3 after one week and keeping the T4 (dosed at 112mcg ed). It took two days to knock the fatigue from the GH out...thank God.

I am taking 3iu of Rips/ed, split dose. Was running 5 and then 4 but the sides were too much on this batch.

For what it's worth,
Vette


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## Azog (Oct 8, 2012)

Crazy F Mike said:


> I am genuinely concerned how much some of you guys are fucking with with your bodies.



Agreed. I am concerned as well. I am really trying to figure out if this is necessary or safe.


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## robot lord (Oct 18, 2012)

Added the T4 at 25mcg per IU(75mcg at 3iu). I do not use GH on weekends and will reserve the t4 for Mon-Fri. I can say that the lethargy has dropped to little or none at this point. Also the addition of caber for the tren along side the t4 has me feeling great. My motivation was slipping, so much so that I considered dropping GH all together. There was no way I could have continued feeling so down with no spark to speak of. I am back to life again and even quit smoking 3 days ago. Me+caber+T4-smoking= awesome.


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## NbleSavage (Oct 18, 2012)

Props on ditching the smokes, RobotLord!!


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## Supra (Oct 29, 2012)

robot lord said:


> Added the T4 at 25mcg per IU(75mcg at 3iu). I do not use GH on weekends and will reserve the t4 for Mon-Fri. I can say that the lethargy has dropped to little or none at this point. Also the addition of caber for the tren along side the t4 has me feeling great. My motivation was slipping, so much so that I considered dropping GH all together. There was no way I could have continued feeling so down with no spark to speak of. I am back to life again and even quit smoking 3 days ago. Me+caber+T4-smoking= awesome.



Glad this could help you man!


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## csully8080 (Nov 6, 2012)

transcend2007 said:


> I have been on gh since 01/11 and tried both T3 and T4.  I noticed no difference.  This article has been out for some time.  I also deal with gh fatigue and I have talked to many other on 12 months or more.  Very few escape this side effect.



does the t4 help you with the fatigue?


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## robot lord (Nov 9, 2012)

Speaking only for myself, in my case the t4 removed the fatigue and also seems to have accelerated the fat loss associated with GH. I am also running tren a and mast p on top my test. So could be the tren, the GH/t4 or all the above. Keep in mind we are all different to some capacity. From what I have read some people don't even respond to GH. So to say this is the cure all(t4) would be untrue.


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## username1 (Mar 22, 2013)

Would like to hear any updates from people that started the t4 with their GH. I'm also considering it since I've been on GH. I did notice in here that it said it's good for cutting. I just started bulking NPP/TPP will start dbol next week. Can I still run the t4 to accelerate the effects of GH? Or should I not do it since I'm bulking? If it's only going to help burn fat quicker then should it be ok?


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## username1 (Mar 23, 2013)

no updates?


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## robot lord (Mar 27, 2013)

User I ran out of GH around Christmas and discontinued the T4. I ran it on cycle and was feeling much better than the GH alone. GH fatigued me so much so I was ready to drop it at only 3iu a day 5 on 2 off. Rips are strong and speculated to be overdosed at 12-13 IU a vial instead of 10. Too many variables for me to say T4 alone was resposible for fat loss. Was also on Test,Tren, Mast,dieting and up to speed with cardio. It was a synergistic combo that worked well for me. I will reup on GH soon and I can say without a doubt T4 will be part of my GH/TRT protocol. In concept, T4 should multiply the output of your GH, however we are all different and respond accordingly. I would wait and see how you feel on the GH. Useing so many compounds and not knowing if its needed, doing anything or potentially harmfull is cause for concern. I personally can not tolerate GH without T4. Many can and even more feel there is not enough data on prolonged T4 use to consider it. I will add that I dropped several pounds coming off the GH as good GH will cause some bloat/water retention. Hope I helped and not confused you further. LOL!


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## username1 (Mar 27, 2013)

Appreciate the update! I've already been on gh since December. I never noticed fatigue even when I got to about 4.5 - 5iu but I'm pre diabetic and it was making my sugar go up too high but brought it down to 3iu and sugar is on the high end of normal so not terrible. 

I would like to see if I can enhance the fat burning capabilities of gh with the t4. It does look like I'm leaning out a bit. I started npp/tpp about a month ago and since then on/off I go through periods of just feeling really tired and not wanting to do anything but just lay in bed. Last week my e2 was 92 so I increased ai while I'm not as lethargic still just not feeling any energy or motivation. One night last week I went to sleep at like 6pm yesterday I seemed fine at 7 pm as soon as I sat down to eat. I just lost all my energy so ate about half my food and went to sleep at like 8pm. I'm laying in bed right now lol 

I wonder if its the npp or if its the gh it might be having a synergistic effect and maybe its the gh making me feel like this. The t4 is on the way might even be here already will start that soon. Hope it helps.


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## robot lord (Mar 28, 2013)

I believe the t4 should help, but with your e2 so high I can't help but think It too is a contributing factor. Crashed or high e2 will both produce similar shitty,tired and aching painful joints. I like to stay around 25-30. Have you given any thought to possibly adding caber 2-3 times a week? Last cycle I ran it along side my adex. It's a dopamine agonist so it makes you feel better, drops the e and can make you a porn star. Don't fall in love with it however. Long term use can cause issues so I'm told research suggests. Like any of this shit we use, get on get off and be safe. Thyroid,heart,kidney and liver problems for a few extra pounds of mass just don't seem worth it when your shriveled up like a polar bears nuts on a hospital bed. Talking about how big you used to be must suck after a doc red lights you on ever going back on again.


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## Supra (Mar 28, 2013)

Currently Running 100mcg of T4 with 3iu of GH ED. Dropping bodyfat rapidly!


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## username1 (Mar 28, 2013)

Yeah most likely was the E2, I'm feeling much better now after I increased my dose. It must take a few days for it to build up in your blood I suppose, since I increased it last Friday I think and really not feeling up to normal until yesterday and today. Going to get a blood test tomorrow just to see where I'm at. Also, I'm already taking caber, while I'm on the NPP and will discontinue once I'm off. Thanks for the tips.



robot lord said:


> I believe the t4 should help, but with your e2 so high I can't help but think It too is a contributing factor. Crashed or high e2 will both produce similar shitty,tired and aching painful joints. I like to stay around 25-30. Have you given any thought to possibly adding caber 2-3 times a week? Last cycle I ran it along side my adex. It's a dopamine agonist so it makes you feel better, drops the e and can make you a porn star. Don't fall in love with it however. Long term use can cause issues so I'm told research suggests. Like any of this shit we use, get on get off and be safe. Thyroid,heart,kidney and liver problems for a few extra pounds of mass just don't seem worth it when your shriveled up like a polar bears nuts on a hospital bed. Talking about how big you used to be must suck after a doc red lights you on ever going back on again.


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## robot lord (Apr 2, 2013)

Supra said:


> Currently Running 100mcg of T4 with 3iu of GH ED. Dropping bodyfat rapidly!



Hopefully the GH fairy will leave a couple kits under my pillow in a few weeks. Summer on it's way and I would like to shed about 10lbs of BF. Good stuff Supra. You respond very well to GH/T4.


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## Supra (Apr 5, 2013)

Thanks man!


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## username1 (Apr 16, 2013)

I started the T4, too soon for me to notice any difference but, there's something strange I noticed. When I first started GH I was getting night sweats every night in my sleep. I would keep a towel with me in bed, and since I started the T4, the first week I don't remember sweating at all but, now I'm noticing on some nights it's like my body wants to sweat but, it's holding it in, if that makes any sense. Whenever I was having night sweats before I would wake up because I feel nasty from it, and it's cold and so I immediately start wiping down with a towel but, lately I haven't even kept a towel in my bed, because it's like I'm about to sweat but, I don't, I'll wake up when I notice this happen but, just fall back to sleep since there's nothing to wipe etc. kind of strange but, glad the night sweats seem to be over.


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## Supra (Apr 16, 2013)

I'm at 3iu ed right now and 100mcg, feeling great.


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## NbleSavage (May 11, 2013)

Bump for updates on this topic.


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## Supra (May 11, 2013)

Im bumping up 1o 150mcg ED of T4. Still losing bodfat!


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## Supra (May 11, 2013)

NbleSavage said:


> Bump for updates on this topic.



Here is an interesting article its long but its a really good read

"TH exists in two major forms. Levothyroxine (T4), with four iodine atoms per molecule, is an inactive form that can be converted into T3, and is produced exclusively by the thyroid gland. Triiodothyronine (T3), with three iodine atoms per molecule, is eight times more effective than T4. It is converted from T4 in the thyroid, brain, liver, and bloodstream, and in various tissues of the body.

The Role of TH in the Body 
One important function of TH is helping the body convert food into energy and heat. T3 directly boosts energy metabolism in mitochondria, the powerhouses of cells. T3 triggers rapid protein synthesis and influences mitochondrial gene transcription, the reading of genes and synthesis of proteins from genetic information. These activities cause breakdown of proteins and an increase in free fatty acids, as well as increased oxygen use. TH elevates the heart rate to meet the increased oxygen needs.

TH also regulates body temperature. TSH, which stimulates the thyroid to produce TH, also stimulates brown adipose tissue, a mitochondria-rich tissue, to boost heat production in mammals without muscle activity. TH fluctuates in response to caloric intake and external temperature. During starvation, the body naturally lowers TH, not only to reduce caloric needs, but also to prevent ketone bodies from building up in the blood and kidneys. Ketone build-up, which can also happen in diabetes, can cause damage to the kidneys and other part of the body. Injury and illness lower TH levels, which rebound once the patient is healed.

TH is sensitive to the levels of other hormones besides TSH. Estrogen partially blocks the efficiency of TH, so women compensate by producing more TH than men. This may be why women have larger thyroids than men and are more prone to thyroid disease of all types. Women who take TH replacement pills must increase their TH dosage if they start taking birth control pills, to compensate for the higher levels of estrogen from birth control pills. Growth hormone also partially blocks TH, but it also complements TH in its effects on growth, development, and metabolism.

TH plays a major role in metamorphosis and development in all vertebrates. It affects development by binding to thyroid hormone receptors (TRs), molecules that then change their shape to an activated form. Once activated by TH, TRs can bind to responsive elements in the DNA, triggering gene transcription. The position of the TR attaching to the responsive elements facilitates the copying of some genes, and blocks others from being copied. Two major forms of thyroid hormone receptors exist: TRa and TRb.

TRs are nuclear receptors like retinoid A receptors, Vitamin D receptors, and steroid hormone receptors. TRs change configuration when attached to T3, and this changed configuration allows them to attach to responsive elements in the genome. Nuclear receptors are often dimerized (attached to another nuclear receptor of the same or different type), but they remain inactive until bonded by the usual trigger. For example, thyroid hormone receptors dimerized with retinoid X receptors will not activate until they are bonded with T3 or retinoids (derivatives of Vitamin A).

We still do not know all the genes that are regulated by TH. Some TR-responsive elements in the DNA are Alu elements, which are able to move around in the genome on occasion, creating even more Alu elements in the genome. This allows many different genes to come under the control of TH without the genes themselves mutating. Different species may have different genes under control of TH, especially these concerned with development. For instance, while most mammals show similar symptoms of hypothyroidism (fatigue, apathy, etc.), dogs show the additional symptom of seizures. Most chemicals that cause hypothyroidism do not block thyroid receptors in the genes; they only block the efficiency or synthesis of TH. Hence most of our information about which genes are regulated by TH comes from studying genetic disorders in which the TRs are non-functional.

Genetic Disorders Involving TH, TSH, or TRs 
Resistance to TH is a genetic disorder caused by mutations in the TRb gene. Patients with this disorder have high TH levels and TSH levels, goiter (enlarged thyroid gland), and mild hypothyroid metabolisms. Clinical effects are less severe than with congenital hypothyroidism and can include short stature, delayed bone maturation, hyperactivity, learning disabilities, and hearing defects, as well as mixed features of hyper- and hypothyroidism. This condition is usually inherited dominantly.

Pendred's Syndrome is caused by a genetic defect that limits the incorporation of iodine into thyroid hormone, which wrecks the structure of the hormone. Pendred's Syndrome can cause hypothyroidism with goiter. The body compensates by producing more TSH and working harder to make enough thyroid hormone that works. The syndrome can also cause more serious problems, such as profound deafness, or non-syndromal deafness alone. These symptoms are present from birth. People who develop hypothyroidism later in life may have ringing in their ears and dulled hearing, but these symptoms are usually correctable by TH therapy, while deafness caused by Pendred's Syndrome is not.

TSH receptor (thyrotropin receptor) gene mutations often cause hyperthyroidism, or TSH insensitivity, which leads to normal TH levels in the blood with elevated TSH levels. TSH has unknown effects on lymphocytes and brain cells; therefore imbalances affecting TSH levels may cause additional, unknown effects on the brain and immune system. One mutation was found in association with Graves' disease. Graves' disease is an autoimmune form of hyperthyroidism, and the genes that seem to increase risk of Graves' disease are associated with immunity.

In humans, thyroid hormone plays a notable role in brain development from the middle of pregnancy to the second year of life. Maternal or fetal hypothyroidism, whether caused by lack of iodine during the pregnancy, or by other problems, can cause a non-genetic condition called cretinism. Babies affected by cretinism can develop normal intelligence if the condition is remedied within a few months, but otherwise they suffer severe, irreversible mental retardation. One severe type of cretinism can also be caused by mutations in the TRa gene, and may be untreatable.

Effects of TH Imbalance: Hypothyroidism 
Some of the most profound effects of TH imbalance are in the mental arena. Hypothyroid people sleep easily and do not get full refreshment from their sleep. During waking hours, they experience fatigue, apathy, and "brain fog" (short-term memory problems and attention deficits). These problems may affect their daily functioning and cause increased stress and depression.

TH acts as a neurotransmitter. TH imbalance can mimic psychiatric disease because T3 influences levels of serotonin, a neurotransmitter integral to moods and behavior. Low levels of T3 can cause depression. Some anti-depressants make hypothyroid patients feel even worse because the medications depress T3 levels. Paradoxically, some substances labelled depressants such as alcohol or opiates can increase T3 levels by impairing the breakdown of T3 in the brain, thus lifting mood. This may be one reason why these substances are so addictive.

Severe hypothyroidism can cause symptoms similar to Alzheimer's disease: memory loss, confusion, slowness, paranoid depression, and in extreme stages, hallucinations. Thyroid disease is one of the many treatable diseases that must be ruled out before arriving at the diagnosis of Alzheimer's, which is incurable and cannot be definitely diagnosed until after death. Risk of hypothyroidism increases with age; by age 60, 17% of women and 9% of men have symptoms of thyroid disease1 .

Low TH levels also produce fatigue, slight hypoglycemia (low blood sugar), slowed digestion of food, and constipation. Infertility is common. These symptoms can indicate that other diseases are present, particularly because TH levels tend to go down during prolonged illness in an effort to conserve energy. Chronic disease, such as Lyme disease, can mimic (or cause) hypothyroidism. Hypothyroidism is not difficult to diagnose by symptoms, if the patient reports enough symptoms to the doctor and if the doctor thinks of it. Diagnosis can be confirmed by blood tests, but the cause is less easy to discern.

TH imbalance has a profound effect on cardiovascular fitness because TH helps control heart rate and blood pressure. Under hypothyroid conditions, the heart can slow to 30 heart beats a minute and develop arrhythmia. Blood pressure may fall from normal levels of 120/90 to 70/50. Hypothyroidism also weakens muscles, including the diaphragm. As a result, breathing can become less efficient. A goiter impairs breathing even more. Snoring may start or become worse. Fatigue sets in easily; in fact it never quite leaves a person with symptomatic hypothyroidism. Muscles and joints often ache. With respiration impaired and oxygen in short supply, exercise takes a heavy toll on the body, and muscles do not strengthen in response to exercise; nor does stamina improve.

Low thyroid levels actually trigger muscle fibers to change their type, from fast-twitch fibers to slow-twitch fibers. This may be an adaptive strategy for coping with starvation, since blood sugar is low under hypothyroid conditions and fast-twitch muscle fibers require high levels of glucose to operate. Fatty acid levels in the blood are elevated to provide fuel for the fat-burning slow-twitch muscles. However, low oxygen in the blood due to slow heart rate and respiratory problems limits the slow-twitch muscles' effectiveness.

Even after receiving treatment for hypothyroidism, many people find that their caloric needs and ability to handle exercise have changed permanently. Strength training can help restore their fitness, but only after thyroid hormone levels have normalized. Therefore, hypothyroidism affects the ability of people to undergo both aerobic and anaerobic exercise.

Hypothyroidism is the second leading cause of high cholesterol, after diet. When TH levels drop, the liver no longer functions properly and produces excess cholesterol, fatty acids, and triglycerides, which increase the risk of heart disease. High cholesterol may also contribute to the risk of Alzheimer's disease. Hypothyroid patients may develop yellowed skin due to carotenoid (Vitamin A precursors) deposits in the skin when the liver no longer can store enough. Vitamin A usage and synthesis drops as thyroid hormone levels drop.

Effects of TH Imbalance: Hyperthyroidism 
Hyperthyroidism is associated with a different set of symptoms. People with this disorder sleep with difficulty and sleep much less than normal. Unlike hypothyroid patients, they exhibit manic-depressive behavior as the TH levels drive their energy levels beyond their physical limits. In fact, thyroid hormone testing is routine at psychiatric admission for suspected manic-depressive patients. Lithium, a common treatment for manic-depression, is known to depress T3 in the brain back to normal levels.

Hyperthyroidism causes accelerated heart rate and fatigue, even when patients are at rest. It produces lower exercise tolerance because protein and fat catabolism are accelerated, resulting in build-up of ketones. Hyperthyroid people often show a fine tremor in their hands. They have higher resting heart rates, but not higher maximum heart rates for exercise, in comparison to normal subjects. Some experience thyroid storms--high overloads of thyroid hormones that accelerate their heart rate to as high as 300 beats a minute. This is a very life-endangering condition and can result in arrhythmia or heart attack.

Some drugs cause a temporary TH imbalance. Caffeine and other stimulants interfere with T3 and adrenal hormone metabolism while in the body. Smoking depresses TH levels and produces an chronic underlying hypothyroidism as well as low adrenal hormone levels. The hormonal imbalances due to smoking may contribute to the severity of withdrawal symptoms in smokers trying to quit. Research shows that nicotine increases the synthesis of T3 from T4 in the brain, while alcohol and opiates block the breakdown of T3 in the brain2. Research into thyroid hormone's role in addiction might lead to better treatment and prevention of drug addiction3.

Causes of Thyroid Disease 
The most common causes of acquired thyroid disorders are iodine deficiency and autoimmune thyroid disease. Iodine deficiency is the major cause of hypothyroidism for much of the world, due to absence of iodine in the diet and/or high consumption of soy, corn, and brassica plants (cabbage, broccoli, brussel sprouts, etc.). These plants produce natural goitrogens. Goitrogens can be largely abolished through proper cooking. In the U.S., salt is iodized to ensure people get enough iodine. Iodine overdose rarely is a problem, as the thyroid gland stores iodine until it is necessary, and releases TH in the less active T4 form, and TH is also bound up by transport proteins in the blood until it is needed. Some experts believe that continual iodine overdoses leads to autoimmune thyroid disease, because it seems to be the major cause of thyroid disorder in developed countries.

Two autoimmune thyroid diseases, Graves' disease and Hashimoto's thyroiditis, are thought to be inherited, but have not been linked positively to any genes. Autoimmune thyroid disease is identified by detecting antibodies in the blood. In the case of Graves' disease, antibodies latch onto an enzyme essential for making T4, and keep it active and continually turned on. Graves' disease is treated by suppressing or killing (removing) the thyroid and then stabilizing the patient on thyroid hormone replacements. In Hashimoto's thyroiditis, antibodies latch onto the same enzyme, but block its function, and help trigger destruction of the thyroid. In the early stages of Hashimoto's thyroiditis, the thyroid may produce too much TH, but as the thyroid is slowly destroyed, the patients TH levels drop. Hashimoto's thyroiditis is treated with thyroid hormone replacements.

Some experts have suggested that autoimmune thyroid disease develops as a result of iodine overconsumption. Both the U.S. and Japan have high levels of iodine consumption and of autoimmune thyroid disease. Japanese people consume iodine because seafood makes up a large proportion of the diet, and Americans do because salt is iodinated and the food industry uses iodine as a machine wash. Other experts believe that pollutants are a more important factor. Pollutant chemicals like polychlorinated biphenyls (PCBs) and dioxins have been shown to interfere with thyroid function and are more prevalent in industrialized countries where thyroid disease levels are high. Autoimmune thyroid disease, either hyperthyroidism or hypothyroidism, is also linked to post-traumatic stress disorder and is often first observed clinically after periods of prolonged stress.

Conclusion 
Research on the treatment of thyroid disease is proceeding in promising directions. Autoimmune thyroid disease is being intensively studied, and synthetic antibodies have been produced that neutralize Graves' antibodies in mice. Other studies are uncovering the role of TH in the brain, and finding new genetic causes of thyroid hormone metabolism disorders. TH function is being studied in various vertebrates, and environmental chemicals are undergoing examination as possible TH disruptors. Such research provides hope that autoimmune thyroid disease can one day be attacked at its source.

However, adequate information has not spread into the medical field. Labs performing blood work use overly broad normal ranges of TSH levels. Published research indicates 1-3 �g/ml in the blood (micrograms per milliliter of blood) is the best range of normal4, but most doctors work under the assumption that values as high as 5.5 are normal, which results in underdiagnosis and undertreatment of many cases of hypothyroidism.

A worse problem is the lack of testing. Though an estimated 200 million people worldwide have thyroid disorders5, thyroid function tests are rarely given unless the doctor suspects a thyroid disorder, and most doctors do not suspect hypothyroidism in their patients because the symptoms are subtle. Of the estimated 13 million Americans affected by thyroid disease, more than half are unaware of their condition6. Thyroid disease affects 8 times as many women as men, possibly because women need higher levels of TH than men do, but it has no age, gender, or ethnic barriers. Patients may have some or all the obvious symptoms: fatigue, lack of focus, depression, constipation, anxiety attacks, dry hair, dry skin, edema (swelling), lack of exercise tolerance, weight gain (especially in the stomach), muscle and joint pains, problems swallowing (due to enlarged thyroid), goiter, facial puffiness, unusual new headaches, loss of eyebrows, lack of sex drive, lowered body temperature, low or high blood pressure, and slowed heart rate. Yet patients may not be diagnosed for years.

The link between high cholesterol and underlying hypothyroidism is vastly overlooked, even though cholesterol's role in heart disease is heavily publicized. People have their cholesterol tested more regularly than their thyroid hormone levels. The result is prescriptions for expensive cholesterol-lowering drugs that don't address the real problem. People diagnosed with high cholesterol, especially those with low body temperature, should have their thyroid function tested before they begin taking such drugs. Also, smokers and other substance abusers should be watched for hypothyroidism (and urged to quit), as stimulants and depressants both can affect TH metabolism.

The under-diagnosis of thyroid disease handicaps research as well as the lives of affected patients. Researchers need to understand the proper function of thyroid hormone and the pathology of thyroid disease to fully understand how our bodies, brains, and immune systems develop and work, in health and in illness. It is impossible to know the prevalence of thyroid disease and figure out all the causes if patients take years on average to be diagnosed. We still do not know what causes the high prevalence of autoimmune thyroid disease in developed countries. Until researchers turn up strong and clear evidence on the cause, more cases of autoimmune thyroid disease will occur every year.

© Copyright 2001, All Rights Reserved, C SA
Synthroid, Knoll Pharmaceutical Company (http://www.synthroid.com/consumer/1310.htm)
Examination of antithyroid effects of smoking products in cultured thyroid follicles: only thiocyanate is a potent antithyroid agent (Acta Endocrinol (Copenh), 1992 Dec, 127(6):520-5)
Thyrotropin releasing hormone decreases alcohol intake and preference in rats (Alcohol, 2000 Jan, 20(1):87-91)
Weetman AP. Fortnightly review: Hypothyroidism: screening and subclinical disease. BMJ 1997;314:1175 (19 April) (http://www.bmj.com/cgi/content/full/314/7088/1175)
back to article
American Association of Clinical Endocrinologists (http://www.aace.com/pub/spec/tam2001/presstam2001.
Source
http://www.csa.com/discoveryguides/thyroid/overview.php


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## SHRUGS (May 12, 2013)

PFM said:


> I am genuinely concerned how much some of you guys are fucking with with your bodies.



I'm still over here with this... ^^^^^^^^^
!SHRUGS!


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## Supra (May 12, 2013)

SHRUGS said:


> I'm still over here with this... ^^^^^^^^^
> !SHRUGS!




Whats all the gear you are running?


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## SHRUGS (May 13, 2013)

2ius of GH daily. Thats it bro.
!SHRUGS!


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## Supra (May 13, 2013)

SHRUGS said:


> 2ius of GH daily. Thats it bro.
> !SHRUGS!



You thinking adding in some t4 is really gonna mess you up? My thing is if you need take it, if you dont.then dont't


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