# anyone with experiences with T3 pills????????



## neil16377 (Jul 3, 2012)

Hi guys, just wondering if any of you have/are ever taken T3 tabs for cutting, just after some info if your willing to share...cheers...neil


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## Ben_Dover (Apr 12, 2012)

I have taken 100mcg every day and lost loads of weight with a good diet and moderate cardio. How much of that was muscle I don't know as I didn't care at the time.

They definitely work let's put it that way


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## neil16377 (Jul 3, 2012)

BJ said:


> I have taken 100mcg every day and lost loads of weight with a good diet and moderate cardio. How much of that was muscle I don't know as I didn't care at the time.
> 
> They definitely work let's put it that way


cool,, ive read you have to wean off this stuff?? how you taking it ie morning??? and are there any symptoms your feeling?" someone told me it feels like your speeding" Dont want that s**t!!


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## Neil R (Oct 29, 2006)

100mcg is way too much T3.

You're body produces approx 150mcg a day, and if you screw it up, it doesn't come back, like you get with test suppression.

If you intend on running thyroid prep, go with T4, its safer as its almost entirely dependant on your body converting it to the active T3, and (generally) it will only convert what it needs.

I know a few people (mainly women TBH) who overdid T3 and are fat as a fookin' whale in the offseason, when they're not on the stuff.

IF (big if!) you are going to run T3, stick to a moderate 25mcg dose. If you feel you need more than that then your diet and cardio is Sh1T, and you need to sort out the basics first!


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## renshaw (Jun 5, 2012)

Yes t4 it safer. Levothyroxine (t4) your actually advised / perception dosage is 1.6-1.7 mcg per 1kg lean body mass.

Obviously your going to want to use more. But going on safe amount compared to your amount.

Say you are 100kg so times by 1.6 = 160mcg

You was saying you was going to take 100 mg covert that too MCG and your 100 mg equals 100*000mcg

This above is based for safe use... So your going to want to work out how much your body makes it self and maybe add 10% working up about 30% extra.

Probably give you simlar number to what Neil suggested.

Sent from my GT-I9100 using Tapatalk 2


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## 3752 (Jan 7, 2005)

Neil R said:


> 100mcg is way too much T3.
> 
> You're body produces approx 150mcg a day, and if you screw it up, it doesn't come back, like you get with test suppression.
> 
> ...


it is very hard to screw up your natural thyroid output, there are plenty of studies to show this....

this is a write up along with data from studies on the subject......notice the parts in bold.

Thyroid Hormone for Weight Loss:

Physiologic and Metabolic Effects

by Nandi

Introduction

It has been over 100 years since the discovery by Magnus-Levy that thyroid hormones play a central role in energy homeostasis, and 75 years since the hormones were first used for weight loss. Despite this great length of time, the precise mechanisms by which thyroid hormones exert their calorigenic effect are not completely characterized, and still actively debated. Despite numerous clinical studies having shown that the administration of thyroid hormone induces weight loss, it is not currently indicated as a weight loss agent. This is probably due to the number of side effects observed during thyroid hormone use at the relatively high doses used in the majority of obesity treatment studies. These deleterious effects include cardiac problems such as tachycardia and atrial arrhythmias, loss of muscle mass as well as fat, increased bone resorption and muscle weakness. Nevertheless, thyroid hormones, particularly triiodothyronine (T3) are a mainstay in the ****nal of drugs used by bodybuilders for fat loss. The widespread underground use of T3 warrants an understanding of its mechanism of action, as well as a knowledge of how it is most effectively and safely used, with an eye to minimizing side effects.

Thyroid Function and Physiology

Before jumping right into a discussion of the use of thyroid hormone for fat loss, a little review of thyroid function and physiology might be in order. The thyroid gland secretes two hormones of interest to us, thyroxine (T4) and triiodothyronine (T3). T3 is considered the physiologically active hormone, and T4 is converted peripherally into T3 by the action of the enzyme deiodinase. The bulk of the body's T3 (about 80%) comes from this conversion. 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 the hypothalamus. This is analogous to testosterone production, where GnRH from the hypothalamus causes the pituitary to release LH, which in turn stimulates the testes to produce testosterone.

In addition to T3, it has recently been recognized that there exist two additional active metabolites of T3: 3,5 and 3,3' diiodothyronines, which we will collectively call T2. Studies have shown that 3,3'-T2 may be more effective in raising resting metabolic rate when hypothyroid subjects are treated with T3, than when normal (euthyroid) subjects are given T3. Therefore in normal subjects 3,5-T2 may be the principal active metabolite of T3 (1)

Like the hypothalamic-pituitary-gonadal axis, the thyroid gland is under negative feedback control. When T3 levels go up, TSH secretion is suppressed. This is the mechanism whereby exogenous thyroid hormone suppresses natural thyroid hormone production. There is a difference though between the way anabolic steroids suppress natural testosterone production and the way T3 suppresses the thyroid. With steroids, the longer and heavier the cycle is, the longer your natural testosterone is suppressed. This is not the case with exogenous thyroid hormone.

*An early study that looked at thyroid function and recovery under the influence of exogenous thyroid hormone was undertaken by Greer (2). He looked at patients who were misdiagnosed as being hypothyroid and put on thyroid hormone replacement for as long as 30 years. When the medication was withdrawn, their thyroids quickly returned to normal.*

Here is a remark about Greer's classic paper from a later author:

*"In 1951, Greer reported the pattern of recovery of thyroid function after stopping suppressive treatment with thyroid hormone in euthyroid [normal] subjects based on sequential measurements of their thyroidal uptake of radioiodine. He observed that after withdrawal of exogenous thyroidthyroid function, in terms of radioiodine uptake, returned to normal in most subjects within two weeks. He further observed that thyroidthyroid medication as it did in those whose gland had been depressed for only a few days" (3) *

*These results have been subsequently verified in several studies.(3)(4) So contrary to what has been stated in the bodybuilding literature, there is no evidence that long term thyroid supplementation will somehow damage your thyroid gland.* therapy, function returned as rapidly in those subjects whose glands had been depressed by several years of Nevertheless, most bodybuilders will choose to cycle their T3 (or T4 which in most cases works just as well) as part of a cutting strategy, since T3 is catabolic with respect to muscle just as it is with fat. As previously mentioned, long term T3 induced hyperthyroidism is also catabolic to bone as well as muscle.

The proviso about T4 vs T3 for weight loss alluded to above needs some elaboration. There have been a number of studies that have shown that during starvation, or when carbohydrate intake is reduced to approximately 25 to 50 grams per day, levels of deiodinase decline, hindering the conversion of T4 to the physiologically active T3.(5) From an evolutionary standpoint this makes sense: during periods of starvation the body, teleologically speaking, would like to reduce its basal metabolic rate to preserve fat and especially muscle stores. However, a recent study demonstrating the effectiveness and safety of the ketogenic diet for weight loss recorded no change in circulating T3 levels.(6) So this issue not completely settled. Nevertheless, persons contemplating thyroid supplementation during ketogenic dieting might prefer T3 over T4 since the bulk of the research does suggest a decline in the peripheral conversion of T4 to T3 during low carb dieting.

Now that we have reviewed a little about thyroid function, let's consider just how it is that thyroid hormone exerts its fat burning effects.

Increased Oxidative Energy Metabolism

Thyroid hormone has long been recognized as a major regulator of the oxidative metabolism of energy producing substrates (food or stored substrates like fat, muscle, and glycogen) by the mitochondria. The mitochondria are often called the "cell's powerhouses" because this is where foodstuffs are turned into useful energy in the form of ATP. T3 and T2 increase the flux of nutrients into the mitochondria as well as the rate at which they are oxidized, by increasing the activities of the enzymes involved in the oxidative metabolic pathway. The increased rate of oxidation is reflected by an increase in oxygen consumption by the body.

T3 and T2 appear to act by different mechanisms to produce different results. T2 is believed to act on the mitochondria directly, increasing the rate of mitochondrial respiration, with a consequent increase in ATP production. T3 on the other hand acts at the nuclear level, inducing the transcription of genes controlling energy metabolism, primarily the genes for so-called uncoupling proteins, or UCP (see below). The time course of these two actions is quite different. T2 begins to increase mitochondrial respiration and metabolic rate immediately. T3 on the other hand requires a day or longer to increase RMR since the synthesis of new proteins, the UCP, is required (1).

There are a number of putative mechanisms whereby T2 is believed to increase mitochondrial energy production rates, resulting in increased ATP levels. These include an increased influx of Ca++ into the mitochondria, with a resulting increase in mitochondrial dehydrogenases. This in turn would lead to an increase in reduced substrates available for oxidation. An increase in cytochrome oxidase activity has also been observed. This would hasten the reduction of O2, speeding up respiration. These and a number of other proposed mechanisms for the action of T2 are reviewed by Lannie et al.(7)

What is the fate of the extra ATP produced during hyperthyroidism? There are a number of ways by which the increased ATP promotes an increase in metabolic activity, including the following:

Increased Na+/K+ATPase. This is the enzyme responsible for controlling the Na/K pump, which regulates the relative intracellular and extracellular concentrations of these ions, maintaining the normal transmembrane ion gradient. Sestoft(7) has estimated this effect may account for up to to 10% of the increased ATP usage.

Increased Ca++-dependent ATPase. The intracellular concentration of calcium must be kept lower than the extracellular concentration to maintain normal cellular function. ATP is required to pump out excess calcium. It has been estimated that 10% of a cell's energy expenditure is used just to maintain Ca++ homeostasis. (1)

Substrate cycling. Hyperthyroidism induces a futile cycle of lipogenesis/lipolysis in fat cells. The stored triglycerides are broken down into free fatty acids and glycerol, then reformed back into triglycerides again. This is an energy dependent process that utilizes some of the excess ATP produced in the hyperthyroid state (8). Futile cycling has been estimated to use approximately 15% of the excess ATP created during hyperthyroidism (8)

Increased Heart Work. This puts perhaps the greatest single demand on ATP usage, with increased heart rate and force of contraction accounting for up to 30% to 40% of ATP usage in hyperthyroidism (9)

Mitochondrial Uncoupling

As mentioned, the mitochondria are often characterized as the cell's powerhouse. They convert foodstuffs into ATP, which is used to fuel all the body's metabolic processes. Much research suggests that T3, like another much more potent agent DNP, has the ability to uncouple oxidation of substrates from ATP production. T3 is believed to increase the production of so called uncoupling proteins. Uncoupling protein (UCP) is a transporter family that is present in the mitochondrial inner membrane, and as its name suggests, it uncouples respiration from ATP synthesis by dissipating the transmembrane proton gradient as heat. Instead of useful ATP being produced from energy substrates, heat is generated instead. There are conflicting studies about the importance of T3 induced uncoupling. Animal studies have demonstrated an actual increase in ATP production commensurate with increased oxygen consumption as we discussed above. Other studies in humans have shown that in fact uncoupling in skeletal muscle does occur. This would contribute to T3 induced thermogenesis, with a resulting increase in basal metabolic rate.(10)

To make up for the deficit in ATP production (as well as provide fuel for the extra ATP production discussed above) more substrates must be burned for fuel, resulting in fat loss. Unfortunately, along with the fat that is burned, some protein from muscle is also catabolized for energy. This is the downside of T3 use, and the reason many people choose to use an anabolic steroid or prohormone during a T3 cycle to help preserve muscle mass. Studies have shown this to be an effective strategy (11). (Muscle glycogen is also more rapidly depleted, and less efficiently stored during hyperthyroidism. This may account for some of the muscle weakness generally associated with T3 use.)

Countering T3 induced muscle loss with AAS or prohormones makes sense from a physiological viewpoint as well. Thyroid hormone muscle protein breakdown is mainly mediated via the so-called ubiquitin-proteasome pathway. (12). (There are several independent metabolic pathways of protein breakdown in the body. For instance, another pathway, the lysosomal pathway, is responsible for the accelerated rate of muscle protein breakdown during and after exercise.) Testosterone administration has been shown to decrease ubiquitin-proteasome activity. (13) So AAS specifically target the muscle protein breakdown process stimulated by T3.

What may not be an effective strategy to maintain muscle mass during a T3 cycle is the use of exogenous growth hormone (GH). Studies have shown that when GH and T3 are administered concurrently, the increased nitrogen retention normally associated with GH use is abolished. This has been attributed to the observation that T3 increases levels of insulin like growth factor binding protein, reducing the bioavailability of igf-1 (14). Nevertheless, GH has fat burning properties independent of igf-1, so using GH with T3 would act additively to speed fat burning, but with little if any preservation of lean body mass. So again, if GH is used in conjunction with T3, anabolic steroid/prohormone use would be indicated.

Andregenic Receptor Modulation

Administration of T3 has been shown to upregulate the so-called beta 2 adrenergic receptor in fat tissue. What is the significance of this effect for fat loss? Before fat can be used as fuel, it must be mobilized from the fat cells where it is stored. An enzyme called Hormone Sensitive Lipase (HSL) is the rate-controlling enzyme in lipolysis, or fat mobilization. The body produces two catecholamines, epinephrine and norepinephrine, which bind to the beta 2 receptor and activate HSL. The upregulation of the beta 2 receptor due to T3 results in an increased ability of catecholamines to activate HSL, leading to increased lipolysis.

Bodybuilders often use drugs like clenbuterol, which bind to the beta 2 receptors and activate them in the same way as the body's endogenous catecholamines. The use of clenbuterol along with T3 can produce an additive lipolytic effect: T3 increases the number of receptors, while clenbuterol binds to the receptors activating HSL and increasing lipolysis. Since clenbuterol itself downregulates the beta 2 receptor, most bodybuilders use clenbuterol in a two week on/ two week off cycle, the rationale being that this minimizes downregulation and allows receptor recovery. Another option is to use the antihistamine Ketotifen concurrently with the clenbuterol. Studies have shown that Ketotifen attenuates the beta 2 receptor downregulation caused by clenbuterol (15). Moreover, research in AIDS patients has shown that Ketotifen blocks the production of the proinflammatory and catabolic cytokine TNF-alpha (16). This may be of relevance to bodybuilders since there is evidence showing TNF lowers both testosterone and IGF-1 levels quite significantly (17) (18), while strenuous exercise elevates TNF levels. (19)

Besides increasing beta 2 receptor density in adipose tissue, T3 upregulates this receptor in human skeletal muscle (12). This has some very intriguing if somewhat speculative implications for the combined use of clenbuterol and T3. Animal studies have shown that catecholamines, particularly clenbuterol, inhibit Ca++ dependent skeletal muscle proteolysis (20). Like the lysosomal and ubiquitin-proteasome pathways discussed above, Ca++ regulated proteolysis is yet another way for the body to degrade muscle protein. Again the implications are enticing: Increased beta 2 receptor density from T3 use, coupled with the beta 2 agonist clenbuterol, could slow this pathway of muscle catabolism.

Another adrenergic receptor important to lipolysis is the alpha 2 receptor, which impedes fat mobilization by counteracting the effects of the beta 2 receptor. There are some conflicting studies about the effects of T3 on the alpha 2 receptor, with studies showing either a downregulation (21) or no effect (22). If T3 does in fact downregulate alpha 2 receptors, this would further aid lipolysis.

Studies in rats have shown that inducing hyperthyroidism increases the lipolytic beta 3 receptor density in white adipose tissue by 70% (23). Beta 3 receptors are abundant in human white adipose tissue as well, and if T3 administration has the same effect in humans, this could could contribute significantly to T3 induced fat loss. This might also argue for taking a currently available beta 3 agonist such as octopamine along with T3 and perhaps clenbuterol.

Decreased Phosphodiesterase Expression

In hyperthyroid patients as well as in normal subjects given T3, levels of the enzyme phosphodiesterase are lowered in fat cells (20). When lipolytic hormones like epinephrine (adrenaline) bind to the beta 2 receptor described above, they initiate a signaling cascade mediated by the so called "second messenger" cyclic AMP (cAMP). cAMP in turn acts on other cellular enzymes to initiate and maintain lipolysis. The original signal is terminated when cAMP is degraded by the enzyme phosphodiesterase. Clearly, maintaining elevated cAMP levels, by lowering phosphodiesterase concentrations with T3, will prolong lipolysis.

As an aside, caffeine is thought to exert at least a portion of its lipolytic action by lowering phosphodiesterase in fat cells. Interestingly, Viagra and cialis are also phosphodiesterase inhibitors but their action seems to be limited to relaxing vascular smooth muscles.

Increased Growth Hormone Secretion

In vitro, animal, and human studies have all demonstrated that T3 administration increases growth hormone production. (24)(25) Since GH is calorigenic aside from any increase in igf-1, elevated GH may contribute to some of the fat burning associated with T3 administration. This effect may obviate the need for the use of expensive recombinant HGH, as mentioned above.

Decreased Insulin Secretion

Insulin is well known as a lipogenic hormone. It promotes fat storage by facilitating the uptake of fatty acids by adipocytes, and reducing lipid oxidation in muscle tissue. Several studies have shown that thyroid hormone is associated with glucose intolerance resulting from decreased glucose stimulated insulin secretion (26).

This defect in insulin secretion is believed to result from an increase in the rate of apoptosis (programmed cell death) of pancreatic beta cells as a direct effect of thyroid hormone excess.(27) This process is reversible, since when thyroid hormone is withdrawn the rate of beta cell replication increases until homeostasis returns. However, there are conflicting studies regarding the effects of T3 on insulin. For example, Dimitriadis et al (28) showed a decrease in glucose stimulated insulin secretion, consistent with (25), but an increase in basal insulin. They also observed increased insulin clearance, with a compensatory increase in basal insulin secretion.

So if in fact the hyperthyroid state is associated with lower insulin levels, this could explain a portion of hyperthyroid stimulated lipolysis. The obvious downside here is that insulin is also an anabolic hormone. Basal insulin concentration is thought to limit the action of the ubiquitin-proteasome degradative pathway of muscle protein breakdown (29). Of course supplementing with insulin during T3 use would be counterproductive. However, as mentioned above, anabolic steroids inhibit ubiquitin-proteasome activity, so their use could counter any loss in muscle anabolism resulting from a drop insulin levels.

The Future

As mentioned at the beginning of this article, a major roadblock in the adoption of T3 by the medical community as an antiobesity agent is its deleterious effect on the heart. Recent research has identified two isoforms of the thyroid hormone receptor, TRalpha and TRbeta. The TRalpha-form may preferentially regulate the heart rate, and an experimental agent, GC-1, has been developed that selectively binds the TRbeta receptor, with minimal effects on the heart (30). The distribution and actions of TRalpha and TRbeta throughout the body are not yet well characterized. However should it turn out that TRalpha is specific to the heart, then drugs like GC-1 may turn out to be effective fat burning agents with a much safer profile that T3 or T4.

One alleged "futuristic" agent that is here now is T2, or 3,5-Di-iodo-L-thyronine, the T3 metabolite discussed above. Unfortunately, this product does not live up to its hype. It has been claimed to be as or more effective that T3 for fat burning with minimal suppression of endogenous thyroid production. Regarding the relative effectiveness of T2 as a lipolytic agent, and its effect on TSH, this topic was thoroughly covered in a recent article by Bryan Hay**** in Muscle Monthly:

All of my research into this subject has led me to the same conclusion reached by Mr. Hay****. That is, T2 is only slightly less suppressive of TSH than is T3, and only packs a portion of the lipolytic punch of T3, with no ability to increase the expression of the UCPs, which is a major determinant of the action of thyroid hormone.

Summary

We have discussed a number of ways by which T3, and its active metabolite T2 act to increase resting energy expenditure. Also discussed were some drawbacks of T3 use, such as cardiac stress, as well as the potential loss of muscle mass. It is ironic that the latter may be of more concern to many bodybuilders that the other more serious potential impacts on health. Nevertheless, used moderately and for short periods (a couple of months or less) in people with no preexisting cardiovascular disease T3 has a relatively safe medical profile, compared to other lipolytic agents like DNP. *Perhaps most importantly we have presented substantial evidence that even the long-term use of supraphysiological levels of T3 does not damage the thyroid gland.*


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## Neil R (Oct 29, 2006)

And yet, the pharmaceutical companies that produce it state one of its primary uses is for TSH Suppression??



> Pharmacology
> 
> Increases metabolic rate of body tissues; is needed for normal growth and maturation.
> 
> ...


How, then, would you account for someone displaying significant weight gain (35lbs) upon cessation of T3 'supplementation' , inspite of having a clean, low card diet and still doing daily cardio?

They also, have had bloods done by the local hospital that show T3,T4 & TSH levels all below the minimum range?

I've gotta say, if its not T3 induced then its got me completely stumped!?!


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## 3752 (Jan 7, 2005)

Neil R said:


> And yet, the pharmaceutical companies that produce it state one of its primary uses is for TSH Suppression??
> 
> How, then, would you account for someone displaying significant weight gain (35lbs) upon cessation of T3 'supplementation' , inspite of having a clean, low card diet and still doing daily cardio?
> 
> ...


it is used for that but it does not say that suppression is caused by high T3 use? i am working with a guy now who has TSH suppression and uses 125mcg per day but this was not caused by using T3........

when any one uses a drug once they stop that drug there will be a rebound effect how this is handled depends on the severity of this rebound, iodine is a great addition to help the thyroid back to normal.

when any synthetic drug is used there is a suppression of the natural output until this synthetic is removed this will cause a rebound until levels are back in normal range, so whereas i agree there will be some initial suppression recovery is faster than many think and i disagree with the claims that it will permanently screw your thyroid up.

you mention above that these ladies had bloods done was it the Free T3 and T4 levels? what was there TSH levels as the normal range is pretty large plus how long after stopping T3 did they have this carried out?

i took T3 from January to November last year had my bloods taken before the prep started and TSH was in the middle to upper normal range (0.3-3.0) my level was 1.8 (the higher the number the slower the thyroid) i had all my bloods retaken on the 27th of december and my TSH was 1.6 this was 7 weeks after stopping the T3, my recent bloods taken 3 weeks ago when i was in hospital for a different matter my TSH was 1.5......


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## Neil R (Oct 29, 2006)

PScarb said:


> you mention above that these ladies had bloods done was it the Free T3 and T4 levels? what was there TSH levels as the normal range is pretty large plus how long after stopping T3 did they have this carried out?...


As far as I know it was free T3/T4, (unfortunately, they're not the brightest). However, the one in question had her bloods done in January which is 7 months after stopping the T3. (I'm confident she hasn't lied to me about this).

I can't think of anything else that might cause such suppression, although I'm not going to count out other potential environmental causes, if I knew of any, as being the cause.

The other ladies, I am slightly less trusting of, and have a feeling they've been 'out on the piss' on a weekly basis and they're GP's are saying they've a slow thyroid as a "fob 'em off" diagnosis (not unheard of in the medical profession, unfortunately!)


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## 3752 (Jan 7, 2005)

it could've been the T3 to say it was not would be a guess but many claim it screws them up and like you have said other influences come into play.....what were the TSH levels?


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