# t3, how to use/risks?



## f.r.a.n.k.

So I've been looking into T3 a bit and curious how to use it, what dosages, and what risks are involved with T3 supplementation and the severity of these risks.

Any info is greatly appreciated! 

FrOnk


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## DocDePanda187123

Risks are relatively minimal compared to most other compounds we talk about. 

Do not use it without some sort of AAS being co-administered. 

How to use: anywhere from 50-200mcg depending on size and tolerance and goals. I'm taking ~125mcg daily while on cycle. Stared it at wk 2 to allow hormone levels to raise a bit before taking it


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## f.r.a.n.k.

Docd187123 said:


> Risks are relatively minimal compared to most other compounds we talk about.
> 
> Do not use it without some sort of AAS being co-administered.
> 
> How to use: anywhere from 50-200mcg depending on size and tolerance and goals. I'm taking ~125mcg daily while on cycle. Stared it at wk 2 to allow hormone levels to raise a bit before taking it



So do not take it unless running a cycle...

How many weeks would you suggest? Off and on or for an extended time? 
And I'm assuming start with the smallest recommended dose and work my way up.
Also split doses throughout the day or all at once every morning?

Thanks doc


Edit: also I'm 5'10" and roughly 205 to 210 depending on what carb intake day it is. Best guess is 15% bf


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## DocDePanda187123

f.r.a.n.k. said:


> So do not take it unless running a cycle...
> 
> How many weeks would you suggest? Off and on or for an extended time?
> And I'm assuming start with the smallest recommended dose and work my way up.
> Also split doses throughout the day or all at once every morning?
> 
> Thanks doc



Definitely don't take it without being on cycle. Proteolysis gets promoted more than protein synthesis which is why it gets a rep as being catabolic. It can definitely eat through muscle especially at the doses I recommended above. 

Start it at wk2 of a cycle or whenevery if on TRT/B&C so serum levels of hormones can raise before the T3 kicks in. How long is up to you. I'd say less than 3-4wks isnt worth it. I personally begin wk2 of a cycle and run it to the very end. No need for off and on, just take it ED for as long as you decide to take it. 

Naturally you make around 25mcg so anything less than that is a waste IMO unless thyroid down regulation occurs and you want to simply to to baseline. I find I tolerate 100-150mcg without issues so when I use it I go right back to that dose or higher if I want. Never hurts though to start low and titrate up. 

I forget it's half life and active life info but I'm actually experimenting now with taking a single daily dose and splitting it into 2. I also queried Austinite and an MD and waiting to hear what they say on the issue


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## f.r.a.n.k.

Docd187123 said:


> Definitely don't take it without being on cycle. Proteolysis gets promoted more than protein synthesis which is why it gets a rep as being catabolic. It can definitely eat through muscle especially at the doses I recommended above.
> 
> Start it at wk2 of a cycle or whenevery if on TRT/B&C so serum levels of hormones can raise before the T3 kicks in. How long is up to you. I'd say less than 3-4wks isnt worth it. I personally begin wk2 of a cycle and run it to the very end. No need for off and on, just take it ED for as long as you decide to take it.
> 
> Naturally you make around 25mcg so anything less than that is a waste IMO unless thyroid down regulation occurs and you want to simply to to baseline. I find I tolerate 100-150mcg without issues so when I use it I go right back to that dose or higher if I want. Never hurts though to start low and titrate up.
> 
> I forget it's half life and active life info but I'm actually experimenting now with taking a single daily dose and splitting it into 2. I also queried Austinite and an MD and waiting to hear what they say on the issue



Let me know what A and the MD say about it.

What do you find superior? T3 or T4? When it comes to fat loss while preserving lbm


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## Iron1

f.r.a.n.k. said:


> Let me know what A and the MD say about it.
> 
> What do you find superior? T3 or T4? When it comes to fat loss while preserving lbm



T3.

T4 is an inactive form of thyroid hormone and must be converted to T3 before it can be utilized.
That's why you don't see a lot of T4 in research chems.

Unfortunately, some people have conversion problems. i.e. their T4 levels are normal but their T3 is still low.

It's still not really great for preserving LBM since as doc pointed out its increased proteolysis out paces synthesis.

Is there a reason you're looking at T3 and not something like clen/keto?


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## f.r.a.n.k.

Oh also, what possible sides am I looking at? Similar sides to clen such as a higher resting heart rate? BP increase?


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## DocDePanda187123

Iron1 said:


> T3.
> 
> T4 is an inactive form of thyroid hormone and must be converted to T3 before it can be utilized.
> That's why you don't see a lot of T4 in research chems.
> 
> Unfortunately, some people have conversion problems. i.e. their T4 levels are normal but their T3 is still low.
> 
> It's still not really great for preserving LBM since as doc pointed out its increased proteolysis out paces synthesis.
> 
> Is there a reason you're looking at T3 and not something like clen/keto?



X2

Most notable sides are the catabolism (take alongside AAS), elevated body temps and heart rate, sweating, etc. The most serious side I've seen in the literature is allergic reactions.


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## f.r.a.n.k.

Iron1 said:


> T3.
> 
> T4 is an inactive form of thyroid hormone and must be converted to T3 before it can be utilized.
> That's why you don't see a lot of T4 in research chems.
> 
> Unfortunately, some people have conversion problems. i.e. their T4 levels are normal but their T3 is still low.
> 
> It's still not really great for preserving LBM since as doc pointed out its increased proteolysis out paces synthesis.
> 
> Is there a reason you're looking at T3 and not something like clen/keto?



I'm only looking at it because it's available. I'm looking into clen as well but already have info on clen.

Which would you say is more harsh on the heart? T3 or clen?
Also would you suggest I run albut over clen considering it is in fact less harsh on the heart? 

I may not run any of these...but being that I am young, compounds with the least risk are at the top of my list.


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## f.r.a.n.k.

Also from quite a few individuals that clen wasn't worth it...so led me into looking into t3


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## Iron1

f.r.a.n.k. said:


> Also from quite a few individuals that clen wasn't worth it...so led me into looking into t3



You'd hear the same stories about any compound that's supposed to aid weight loss.

Clen is harder on the heart since it shuttles taurine away from muscles causing them to cramp.
Your heart is a muscle and when it cramps, yea.


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## TheLupinator

Personally I hated T3. Never messed with my heart rate, but it made me heat intolerant. Now that I think about it, T3 was worse for me than DNP.


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## DocDePanda187123

Iron1 said:


> You'd hear the same stories about any compound that's supposed to aid weight loss.
> 
> Clen is harder on the heart since it shuttles taurine away from muscles causing them to cramp.
> Your heart is a muscle and when it cramps, yea.



X2 again. Clen is a stimulant when looked at acutely and can cause a number of heart related issues

http://www.medscape.com/viewarticle/549131


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## f.r.a.n.k.

So if I choose to use a stim, I'll probably go with albut.
And between the thyroid compounds, t3 over t4.

Thanks for the info gents


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## f.r.a.n.k.

Oh when it comes to the muscle cramps, would supplementing taurine help at all or would it just get shuttled out of the muscle as well?


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## NbleSavage

To stir the pot, the inevitable article from James Daemon advocating T4 over T3 when running with HGH...

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

--------------------------------------------------------------------------------
with James Daemon, Ph.D.

-----------------------------------------------------------
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


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## Maintenance Man

I ran T3 off cycle Frank, right before I went on. It was for a month at 100-140mcgs ED. The 140 was quite too much for me but 100-120 was good. My heart was always beating too fast. Heart murmurs or palpitations which always sound worse than they really are or can be. Breathing was slightly labored. No cramps or anything like that tho. I did enjoy the benefits as it helped me cut some fat and was very evident. Id would do it again on cycle tho


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## Crim Crim

Wow, what a great thread.  




Iron1 said:


> T3.
> 
> Is there a reason you're looking at T3 and not something like clen/keto?



Currently doing a Tren / Test cycle.  I have some clen on hand and was about to order some T3.  Don't want to derail this thread, but would keto be a better choice than T3 to add to clen?


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## DocDePanda187123

Crim Crim said:


> Wow, what a great thread.
> 
> 
> 
> 
> Currently doing a Tren / Test cycle.  I have some clen on hand and was about to order some T3.  Don't want to derail this thread, but would keto be a better choice than T3 to add to clen?



Keto is used to prevent down regulation of beta-2 receptors, the ones clen acts upon. It cannot be compared to T3 bc they do very different things and serve different purposes.


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## TheBlob

Something I dont see mentioned much,, but t3 atleast for me really revs up the appetite.... So dieting was nearly impossible.. But at 100mcg daily fat came off anyway. Sweaty, yes. Hungry, yes.Fatloss,yes. Muscle loss,, minimal even with only 250mg weekly of test.


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## 11Bravo

I'll be starting T3 shortly so I'll report back


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## f.r.a.n.k.

11Bravo said:


> I'll be starting T3 shortly so I'll report back



Badass! Let us know how it goes


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## NbleSavage

11Bravo said:


> I'll be starting T3 shortly so I'll report back



Rip it up, Brother.


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## Zeus

I use 50mcg year around. Great stuff. Keeps my metabolism at a very good level..


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## NbleSavage

Zeus said:


> I use 50mcg year around. Great stuff. Keeps my metabolism at a very good level..



Zeus, you finding this dose helpful to stay lean even when bulking / eating over maintenance?


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## italian1

I can't get into this shit. 20mcg and after five days I feel and look like I'm gonna die. WTF? Drop it and I feel like a million bucks again.


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## f.r.a.n.k.

italian1 said:


> I can't get into this shit. 20mcg and after five days I feel and look like I'm gonna die. WTF? Drop it and I feel like a million bucks again.



Only 20? Your body produces on average 25 daily. I'm using 75 right now and feel fine. Little warm but that's about it.


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## 850gator

Most of what I've read on T3 recommends a 2 weeks on 2 off cycle. Is that not accurate or necessary?


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## desertrock

T3 is definitely much more healthy than Clen. In fact, I've always found the side effects to be very minimal. With Clen I hate that it makes me so jittery and I get all kinds of cravings on it. None of that with T3, it just makes me feel nice and warm.

That being said, I think it's actually counter-productive while trying to cut, because the way it amps up your appetite counter-balances the increase in metabolism. If you can resist the hunger pangs, then sure you'll burn fat faster. Personally I'd only use it at a replacement dose while cutting to stop any possible slowdown in metabolism.

I'm actually going to experiment using it at 50mcg per day while bulking. Based on what I've read it's a good addition to a bulking cycle because it increases your rate of recovery as well as protein synthesis. Not to mention that you can eat more.


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## ToolSteel

Hey Doc. Do you taper off at the end? If so, at what rate?


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## DocDePanda187123

ToolSteel said:


> Hey Doc. Do you taper off at the end? If so, at what rate?



No need to with T3 and I don't do it.


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## GuerillaKilla

Farook, I have a serious question. 

Do you recommend T3/T4 combo tabs, like bitiron? These are 12.5mcg T3+50 mcg T4 each tab. 

Been running 2 a day and seeing pretty insane results alongside 5iu grey tops and my regular AAS run. 

Just wondering what your thoughts were.


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## GuerillaKilla

Dammit Doc, if I've told you once I've told you a thousand times. 

Answer me!!


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## GuerillaKilla

Why do you treat me like this


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## Seeker

Lmao.. .......you don't matter, GK.


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## GuerillaKilla

I know that, you know that, everyone knows that. 

But people have always had the good manners to at least pretend.


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## GuerillaKilla

Wow doc! Thanks for that quick response! You really helped me there.


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## Seeker

Still not mattering...


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## GuerillaKilla

Still not mattering is right. Maybe farook put me on his ignore list?


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## Seeker

He was too busy with the naked lady peep hole thread


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## DocDePanda187123

GuerillaKilla said:


> Farook, I have a serious question.
> 
> Do you recommend T3/T4 combo tabs, like bitiron? These are 12.5mcg T3+50 mcg T4 each tab.
> 
> Been running 2 a day and seeing pretty insane results alongside 5iu grey tops and my regular AAS run.
> 
> Just wondering what your thoughts were.





GuerillaKilla said:


> Dammit Doc, if I've told you once I've told you a thousand times.
> 
> Answer me!!



Lol!

Personally I prefer T3 alone. It's more bioactive and doesn't need to be converted but in the end it doesn't matter much if you don't have a T4 -> T3 conversion issue. I'd opt for whichever one saves your wallet more.


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## Beefcake

What is the half life of T-3?  Do you just take it once a day or multiple times?


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## DocDePanda187123

Beefcake said:


> What is the half life of T-3?  Do you just take it once a day or multiple times?



The biological half life of T3 is about 2.5 days. I take it once daily when I take it and it's what doctors prescribe.


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## Beefcake

Thanks Doc.  Do you ramp it up once your system gets used to it?  What's the half life for albuterol 6 hours?


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## DocDePanda187123

Beefcake said:


> Thanks Doc.  Do you ramp it up once your system gets used to it?  What's the half life for albuterol 6 hours?



You're welcome. 

No, there's no need to ramp up the dose. If you want to your first time ever running it to find the right dose you want you could but once you know your dose there's no need for it. 

Albuterol in inhaler form has roughly a 6hr half life while in oral/tablet/pill form it's about 5hrs.


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## Beefcake

Great thanks again Doc.


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## GuerillaKilla

Thank you Abdullah. I appreciate your quick response. Really grateful you found a ****ing minute and a half for me in the last week or so.


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