View Full Version : T3~Cytomel~liothyronine sodium

12-23-2010, 08:57 AM

(liothyronine sodium)

Cytomel is a synthetic T3 hormone. As you may already know, most natural T3 is not produced directly by your thyroid gland, but rather is converted from the T4 thyroid hormone. (8)

Cytomel T3 Weight Loss

Natural T3 is a regulator of the oxidative metabolism of energy producing substrates (food or stored substrates like fat, muscle, and glycogen) by the mitochondria. The mitochondria, as you will recall from your high school biology class, are usually referred to as the "cell´s powerhouses" because they produce ATP. Taking Cytomel (supplemental T3) greatly increases the uptake of nutrients into the mitochondria and also their oxidation rate (i.e. the rate at which they are burned for energy), by increasing the activities of the enzymes involved in the oxidative metabolic pathway. Everything is working harder, in other words, and more fuel is needed to supplement this increased work rate. Therefore, as you can guess, taking supplemental Cytomel will increase your body´s energy demands. And if you are in a hypocaloric state, you will begin burning even fatter primarily due to an increase in ATP. This increased ATP causes an increase in overall metabolic activity. (8)(9)This is exactly what we want, and is why we would be taking thyroid hormones like Cytomel in the first place. If you aren´t taking anabolic steroids with your Cytomel, however, your body may start to eat away muscle to provide energy for you to function. Remember mitochondria/ATP aren´t very picky, but they are very efficient. What I mean by this is that they will use whatever is on hand to generate energy for your body to continue functioning, fat, protein, glucose; it doesn´t matter to ATP, as long as there´s something to give them energy. Taking this drug will increase their need to find something to burn to create this energy. Ergo, if we aren´t taking anabolic steroids while taking our T3, we may lose too much muscle, especially while dieting.

Thus we can see that there are many advantages to using Cytomel to optimize our metabolic rate. It will also increase your body´s ability to synthesize protein, but from what I´ve seen personally, it acts as a catabolic when it isn´t administered with anabolic steroids. It is often the last thing added into a precontest diet, as it has a reputation for getting rid of the last few percentages of bodyfat& the "sticky fat" as it´s called in bodybuilding, the fat that just doesn´t want to leave you in the last few weeks of dieting. I think this is a poor use for this drug, and that it should be the first thing added into a diet to lose fat, as it will optimize your metabolic rate, which should be done at the outset of a diet, not after the calorie restriction has diminished your thyroid output and you are adding it in simply to replace what was lost.

Cytomel Side Effects

Unfortunately, in all of the studies I´ve seen, T3 also increased growth hormone production. (5)(6) As we all know, GH is also a strongly lipolytic compound, and this is another mechanism by which T3 may exert its effects, although I suspect this would only be a small percentage of its overall effects. This being the case, it has always been somewhat problematic to me to note that when GH and T3 are used together, the increased nitrogen retention normally found with GH use is negated. (7). If you were only using T3 and GH this may be a problem, but as I´ve already stated, you are going to need some anabolic agents if you are using T3. And as you have read previously, I recommend the veritable anabolic/lipolytic orgy of Insulin, T3, Anabolic Steroids, GH, and insulin, for 100% maximum results in minimal time.

On the brighter side, and of special note to dieters, administration of T3 has been shown to upregulate the beta 2 receptors in fat tissue. As you know clenbuterol and similar compounds downregulate this receptor, so using T3 with your clen will help stave off or reverse this downregulation. (1)(2)(3)(4). I would still recommend taking your benadryl every third week, though.

Going off cytomel

Finally, I would like to address the issue of recovery of your natural thyroid function after you stop taking cytomel. The horror stories of people on permanent thyroid replacement just aren´t true. I remember a few years ago, the rumor was circulating that the current Ms.Fitness had permanently shut off her thyroid gland, and was now fat and on thyroid hormone permanently. This is just another horror story based in nothing but conjecture and rumor, the studies I´ve looked at have shown people recovering their thyroid hormone relatively quickly (within months, at most) after going off of several YEARS (!) of thyroid replacement therapy (10)(11). I speculate that you can optimize your metabolic rate with Cytomel for 9-10 months a year, and just normalize yourself for 2-3 months (perhaps the winter, when you are mostly covered up), and then go right back on. Some people in the studies I read were on T3 for 30 years and recovered their natural thyroid function within short order. I think we can safely spend an athletic career using Cytomel 9-10 months out of the year, and just taking those few months off to normalize ourselves. Is this aggressive? Yes. Is this unsafe? NO.


1. Catecholamines inhibit Ca(2+)-dependent proteolysis in rat skeletal muscle through beta(2)-adrenoceptors and cAMP. Navegantes LC, Resano NM, Migliorini RH, Kettelhut IC Am J Physiol Endocrinol Metab 2001 Sep;281(3):E449-54

2. Regulation of human adipocyte gene expression by thyroid hormone J Clin Endocrinol Metab 2002 Feb;87(2):630-4 Viguerie N, Millet L, Avizou S, Vidal H, Larrouy D, Langin D.

3. Alpha 2- and beta-adrenergic receptor binding and action in gluteal adipocytes from patients with hypothyroidism and hyperthyroidism Metabolism 1987 Nov;36(11):1031-9 Richelsen B, Sorensen NS

4. Regulation of beta 1- and beta 3-adrenergic agonist-stimulated lipolytic response in hyperthyroid and hypothyroid rat white adipocytes Br J Pharmacol 2000 Feb;129(3):448-56. Germack R, Starzec A, Perret GY

5. Role of thyroid hormone in the control of growth hormone gene expression Braz J Med Biol Res 1994 May;27(5):1269-72. Volpato CB, Nunes MT.

6. Low-dose T(3) improves the bed rest model of simulated weightlessness in men and women. Am J Physiol 1999 Aug;277(2 Pt 1):E370-9 Lovejoy JC, Smith SR, Zachwieja JJ, Bray GA, Windhauser MM, Wickersham PJ, Veldhuis JD, Tulley R, de la Bretonne JA.

7. 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. J Hepatol 1996 Mar;24(3):313-9

8. Human Anatomy and Physiology, 6th Edition. John w. Hole jr.

9. Physicians Desk Reference

10. Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy. N Engl J Med 1975 Oct 2;293(14):681-4 Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH.

11. Patterns off recovery of the hypothalamic-pituitary-thyroid axis in patients taken of chronic thyroid therapy. J Clin Endocrinol Metab 1975 Jul;41(1):70-80 Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, Chua Teco GN

12-23-2010, 08:57 AM
What I found interesting about this profile of T3 was the fact that recovery after years of use happened within a few weeks of cessation of T3. On the net there are tons of people saying you may permanentaly shut down your thyroid with prolonged use of T3 but science says the opposite.

Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy.

Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH.

The pattern of thyrotropin secretion was analyzed in seven euthyroid women, before and after withdrawal of long-term thyroid hormone, by serial measurements of thyroid 131l uptake, serum thyroxine, tri-iodothyronine, and thyrotropin concentrations, and the response to thyrotropin-releasing hormone. During exogenous hormone administration, 131l uptake was suppressed, and serum thyrotropin concentrations before and after administration of thyrotropin-releasing hormone were undetectable. After withdrawal of exogenous hormone, thyrotropin secretory function was transiently impaired, as indicated by undetectable basal thyrotropin concentrations together with absence of response to thyrotropin-releasing hormone, and subsequently by normal values of basal thyrotropin concentration and normal responses to releasing hormone while serum thyroxine and tri-iodothyronine concentrations were subnormal. Decreased thyrotropin reserve persisted for two to five weeks. Detectable values of serum thyrotropin (less than 1.2 muU per milliliter) and a normal 131l uptake usually occurred concurrently in two to three weeks. Serum thyroxine concentration returned to normal at least four weeks after hormone withdrawal.

PMID: 808728 [PubMed - indexed for MEDLINE]

Patterns off recovery of the hypothalamic-pituitary-thyroid axis in patients taken of chronic thyroid therapy.

Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, Chua Teco GN.

To determine the patterns of recovery of the hypothalamic-pituitary-thyroid axis following long-term thyroid hormone therapy, TRH tests were performed on 8 euthyroid nongoitrous patients, 5 euthyroid goitrous patients, and 5 hypothyroid patients while they were taking full doses of thyroid hormone and 3, 7, 10, 14, 17, 21, 28, 35, 42, 49, and 56 days after stopping it. Serum TSH, T3, and T4 were measured before and at multiple intervals over a 4-h period after giving 500 mug TRH iv. In euthyroid non-goitrous patients, the mean duration of suppressed TSH response to TRH (maximum deltaTSH less than 8 muU/ml) was 12 +/- 4 (SE) days after stopping thyroid hormone and the mean time to recovery of normal TSH response to TRH (maximum deltaTSH greater than 8 muU/ml) was 16 +/- 5 days. None of the euthyroid nongoitrous patients ever hyperresponded to TRH; their average maximal deltaTSH was 24.5 +/- 2.2 muU/ml. Serum T4 fell below normal in 4 euthyroid non-goitrous patients, reaching lowest values at 4 to 28 days. While serum T4 was low, deltaTSH was subnormal. Normal increments of T4 and T3 after TRH occurred at 19 +/- 5 and 22 +/- 6 days, respectively. In the 5 goitrous patients, patterns of recovery of pituitary and thyroid function assessed by the same parameters were much less consistent. In the 5 hypothyroid patients, the mean duration of suppressed basal TSH and suppressed deltaTSH was 13 +/- 3 days; mean time to attain a supranormal basal TSH (greater than 8 muU/ml) was 16 +/- 4 days and to reach a supranormal deltaTSH (greater than 38 muU/ml) after TRH was 29 +/- 8 days. Following prolonged thyroid therapy in euthyroid patients, recovery of normal TSH responsiveness to TRH preceded recovery of the normal T3 and T4 response to TRH by 3 to 6 days. Basal serum TSH may be used to differentiate euthyroid from hypothyroid patients 35 days after withdrawal of thyroid therapy; the response to TRH does not improve this differentiation.

PMID: 807596 [PubMed - indexed for MEDLINE]

12-23-2010, 08:59 AM
Thyroid Hormone for Weight Loss:
Physiologic and Metabolic Effects
by Nandi


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 arsenal 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 thyroid therapy, thyroid function, in terms of radioiodine uptake, returned to normal in most subjects within two weeks. He further observed that thyroid function returned as rapidly in those subjects whose glands had been depressed by several years of thyroid 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. 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 Haycock in Muscle Monthly:

All of my research into this subject has led me to the same conclusion reached by Mr. Haycock. 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.


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.


(1) Endocrinology 2002 Feb;143(2):504-10 Are the effects of t3 on resting metabolic rate in euthyroid rats entirely caused by t3 itself? Moreno M, Lombardi A, Beneduce L, Silvestri E, Pinna G, Goglia F, Lanni A.

(2)(Greer,M. N Engl J Med 244:385, 1951)

(3)N Engl J Med 1975 Oct 2;293(14):681-4 Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy. Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH.

(4) J Clin Endocrinol Metab 1975 Jul;41(1):70-80 Patterns off recovery of the hypothalamic-pituitary-thyroid axis in patients taken of chronic thyroid therapy. Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, Chua Teco GN

(5) Int J Obes 1983;7(2):123-31 The effect of a low-calorie diet alone and in combination with triiodothyronine therapy on weight loss and hypophyseal thyroid function in obesity. Koppeschaar HP, Meinders AE, Schwarz F.

(6) Am J Med 2002 Jul;113(1):30-6 Effect of 6-month adherence to a very low carbohydrate diet program. Westman EC, Yancy WS, Edman JS, Tomlin KF, Perkins CE.

(7) J Endocrinol Invest 2001 Dec;24(11):897-913 Control of energy metabolism by iodothyronines.
Lanni A, Moreno M, Lombardi A, de Lange P, Goglia F

(8) Clin Endocrinol (Oxf) 1980 Nov;13(5):489-506 Metabolic aspects of the calorigenic effect of thyroid hormone in mammals. Sestoft L.

(9)Annu Rev Nutr 1995;15:263-91 Thermogenesis and thyroid function. Freake HC, Oppenheimer JH.

(10) J Clin Invest 2001 Sep;108(5):733-7 Effect of triiodothyronine on mitochondrial energy coupling in human skeletal muscle. Lebon V, Dufour S, Petersen KF, Ren J, Jucker BM, Slezak LA, Cline GW, Rothman DL, Shulman GI.

(11)J Clin Endocrinol Metab 1999 Jan;84(1):207-12 Testosterone administration preserves protein balance but not muscle strength during 28 days of bed rest. Zachwieja JJ, Smith SR, Lovejoy JC, Rood JC, Windhauser MM, Bray GA.

(12) Genome Res 2002 Feb;12(2):281-91 In vivo regulation of human skeletal muscle gene expression by thyroid hormone. Clement K, Viguerie N, Diehn M, Alizadeh A, Barbe P, Thalamas C, Storey JD, Brown PO, Barsh GS, Langin D.

(13) J Clin Endocrinol Metab 2003 Jan;88(1):358-62 Related articles, Links Differential anabolic effects of testosterone and amino Acid feeding in older men. Ferrando AA, Sheffield-Moore M, Paddon-Jones D, Wolfe RR, Urban RJ.

(14) 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.

(15) Cardiovasc Res 1998 Oct;40(1):211-22 Terbutaline-induced desensitization of human cardiac beta 2-adrenoceptor-mediated positive inotropic effects: attenuation by ketotifen. Poller U, Fuchs B, Gorf A, Jakubetz J, Radke J, Ponicke K, Brodde OE.

(16) Eur J Clin Pharmacol 1996;50(3):167-70 Ketotifen in HIV-infected patients: effects on body weight and release of TNF-alpha. Ockenga J, Rohde F, Suttmann U, Herbarth L, Ballmaier M, Schedel I.

(17)Endocrinology 1998 Jun;139(6):2863-8 Tumor necrosis factor-alpha inhibits leydig cell steroidogenesis through a decrease in steroidogenic acute regulatory protein expression. Mauduit C, Gasnier F, Rey C, Chauvin MA, Stocco DM, Louisot P, Benahmed M.

(18) Growth Horm IGF Res 2001 Aug;11(4):250-60 Tissue-specific regulation of IGF-I and IGF-binding proteins in response to TNFalpha. Lang CH, Nystrom GJ, Frost RA.

(19) Exerc Immunol Rev 2001;7:18-31 Exercise and cytokines with particular focus on muscle-derived IL-6. Pedersen BK, Steensberg A, Fischer C, Keller C, Ostrowski K, Schjerling P.

(20) Am J Physiol Endocrinol Metab 2001 Sep;281(3):E449-54 Catecholamines inhibit Ca(2+)-dependent proteolysis in rat skeletal muscle through beta(2)-adrenoceptors and cAMP. Navegantes LC, Resano NM, Migliorini RH, Kettelhut IC

(21) J Clin Endocrinol Metab 2002 Feb;87(2):630-4 Regulation of human adipocyte gene expression by thyroid hormone Viguerie N, Millet L, Avizou S, Vidal H, Larrouy D, Langin D.

(22) Metabolism 1987 Nov;36(11):1031-9 Alpha 2- and beta-adrenergic receptor binding and action in gluteal adipocytes from patients with hypothyroidism and hyperthyroidism. Richelsen B, Sorensen NS

(23) Br J Pharmacol 2000 Feb;129(3):448-56 Regulation of beta 1- and beta 3-adrenergic agonist-stimulated lipolytic response in hyperthyroid and hypothyroid rat white adipocytes. Germack R, Starzec A, Perret GY

(24) Braz J Med Biol Res 1994 May;27(5):1269-72 Role of thyroid hormone in the control of growth hormone gene expression. Volpato CB, Nunes MT.

(25) Am J Physiol 1999 Aug;277(2 Pt 1):E370-9 Related articles, Links Low-dose T(3) improves the bed rest model of simulated weightlessness in men and women. Lovejoy JC, Smith SR, Zachwieja JJ, Bray GA, Windhauser MM, Wickersham PJ, Veldhuis JD, Tulley R, de la Bretonne JA.

(26) Life Sci 2002 Jul 19;71(9):1059-70 Evidence for a deficient pancreatic beta-cell response in a rat model of hyperthyroidism. Fukuchi M, Shimabukuro M, Shimajiri Y, Oshiro Y, Higa M, Akamine H, Komiya I, Takasu N.

(27) Diabetologia 2002 Jun;45(6):851-5 Thyroxine induces pancreatic beta cell apoptosis in rats.
Jorns A, Tiedge M, Lenzen S.

(28) Am J Physiol 1985 May;248(5 Pt 1):E593-601 Effect of thyroid hormone excess on action, secretion, and metabolism of insulin in humans.= Dimitriadis G, Baker B, Marsh H, Mandarino L, Rizza R, Bergman R, Haymond M, Gerich J

(29) Curr Opin Clin Nutr Metab Care 2000 Jan;3(1):67-71 Effects of insulin on muscle tissue.
Wolfe RR.

(30) J Steroid Biochem Mol Biol 2001 Jan-Mar;76(1-5):31-42 Selective modulation of thyroid hormone receptor action. Baxter JD, Dillmann WH, West BL, Huber R, Furlow JD, Fletterick RJ, Webb P, Apriletti JW, Scanlan TS.

12-23-2010, 09:00 AM
The following abstract showed a higher leucine turnover in women than men but weightloss was similar in the men and women who used 50 MCG's T3 daily.

Low-dose T3 improves the bed rest model of simulated weightlessness in men and women

Jennifer C. Lovejoy1, Steven R. Smith1, Jeffrey J. Zachwieja1, George A. Bray1, Marlene M. Windhauser1, Peter J. Wickersham1, Johannes D. Veldhuis3, Richard Tulley1, and Jacques A. de la Bretonne2
1 Pennington Biomedical Research Center, Louisiana State University, 2 Baton Rouge General Health Center, Baton Rouge, Louisiana 70808; and 3 University of Virginia Health Sciences Center and National Science Foundation Center for Biological Timing, Charlottesville, Virginia 22908


This study tested the hypothesis that low-dose 3,5,3'-triiodothyronine (T3) administration during prolonged bed rest improves the ground-based model of spaceflight. Nine men (36.4 ± 1.3 yr) and five women (34.2 ± 2.1 yr) were studied. After a 5-day inpatient baseline period, subjects were placed at total bed rest with 6° head-down tilt for 28 days followed by 5-day recovery. Fifty micrograms per day of T3 (n = 8) or placebo (n = 6) were given during bed rest. Serum T3 concentrations increased twofold, whereas thyroid-stimulating hormone was suppressed in treated subjects. T3-treated subjects showed significantly greater negative nitrogen balance and lost more weight (P = 0.02) and lean mass (P < 0.0001) than placebo subjects. Protein breakdown (whole body [13C]leucine kinetics) increased 31% in the T3 group but only 8% in the placebo group. T3-treated women experienced greater changes in leucine turnover than men, despite equivalent weight loss. Insulin sensitivity fell by 50% during bed rest in all subjects (P = 0.005), but growth hormone release and insulin release were largely unaffected. In conclusion, addition of low-dose T3 to the bed rest model of muscle unloading improves the ground-based simulation of spaceflight and unmasks several important gender differences.

03-09-2011, 10:38 AM
Testosterone protects muscle loss while on T3

Testosterone Administration Preserves Protein Balance But Not Muscle Strength during 28 Days of Bed Rest
Jeffrey J. Zachwieja, Steven R. Smith, Jennifer C. Lovejoy, Jennifer C. Rood, Marlene M. Windhauser and George A. Bray

They gave one group of subjects 50 mcg/day of T3 plus placebo (P), or 50 mcg/day of T3 plus 200 mg/week of testosterone enanthate (T). As you can see, the T group gained LBM despite the T3, whereas the T3 group lost muscle mass:

"After 28 days of bed rest, the men in the P group lost an average of 3.9 kg of body weight (i.e. from 82.0 ± 7.1 to 78.1 ± 7.1 kg). Body weight in the T-treated subjects declined by only 1.0 kg (78.9 ± 4.9 to 77.9 ± 4.9 kg). This treatment x time interaction was statistically significant (P = 0.002). Lean body mass declined by 1.5 kg in the P group, whereas the T-treated subjects experienced nearly a 2-kg increase in lean mass (i.e. 1.7 ± 0.9 kg); again, the treatment x time interaction was statistically significant (P = 0.04)."

http://jcem.endojournals.org/cgi/content/full/84/1/207 (http://jcem.endojournals.org/cgi/content/full/84/1/207)

09-19-2012, 01:25 PM
Looked for dosing protocol that I liked. took a while. Found this article. Feel free to delete if you guys disagree for you know more than I. but seemed legit

T3 and the Modern Athlete.

T3 and the Modern Athlete
By: TJ

* The following article is for educational purposes and not meant to replace a doctor's advice, the author in no way means to encourage the use of any medicine without a prescription from your doctor. As always this article is the property of the author (TJ) and permission should be requested from him and Anabolex before using elsewhere.

So you've decided to use T3 to help you shed fat now that you've read up on it and gotten past the nay sayers who expound the ills of shutting down your body?s own production of natural thyroid. Wonderful, T3 when used correctly can be a great addition to any diet and cardio plan. Read that again boys and girls, IN ADDITION TO ANY DIET AND CARDIO PLAN!!! If you've turned to T3 because you think it's a magic pill that will allow you to eat like crap and still lose weight you've been listening to the wrong advice. Can you lose weight/fat while using T3 and still eating junk food, unfortunately yes to a degree. I say unfortunately because this fact often leads people to do just that, it starts with a cheat meal that turns to a cheat day, which eventually has the athlete eating whatever and whenever they want and still they lose some weight. So what's wrong with this if the eventual out come, weight loss that is, is reached? The first problem is the weight you are losing may not be fat if your eating like crap, the second is what happens when you stop the T3 cycle and your metabolism is suppressed temporarily, if you were eating sloppy during the T3 usage your most likely to keep following that pattern and the combination of a slow metabolism combined with sloppy eating results in rebound weight gain. So in the end what have you really accomplished outside of being able to eat what you want with out getting any fatter for a month or so? And that's if you?re lucky and the rebound weight gain doesn't push you past your starting weight!!!

Now that I have your attention and you know what NOT to do, let's concentrate on what TO do. Just like any other chemical we find in our arsenal, T3 can and is used in a variety of ways when it comes to dosage and length of cycle, both for cutting and bulking. This article will deal with cutting use only. There are some who prefer to "hit it hard" and go high dosage with a quick taper down at the end losing a great amount of weight in a short time, but this way tends to eat as much muscle as fat in my experience and you end up looking basically the same as when you began, except that you weigh less and are smaller. There are those who like to use the same dosage throughout the cycle with no taper up or down figuring if your metabolism is going to be sluggish anyhow why waste the days using it at a low dosage when you could be burning more fat on those days. Then there are those who slowly taper up, maintain the highest dosage for a set time and then slowly taper down. It's the last group I'll concentrate on here, as this is the system that has shown it's best overall results with those I've worked with.

Let's start with the dosage, T3 is a very individual drug, when it comes to dosage I've seen guys use as high as 250-300mcg/day and others as low as 25mcg/day where both athletes lost fat and reached their goals. As a rule I start everyone (and for now I'm dealing with men I'll pen an article on women?s usage in the future) at 25mcg/day. I usually base the time of the cycle on their individual weight loss goals, if it's a smaller amount I'll go 3 weeks tops, if it's a lot of weight to lose we'll go 4, 5 and sometimes 6 weeks. I generally don?t go over 6 weeks with anyone, as T3 tends to stop working in most people after that amount of time. I?d rather they run 4 weeks cycles with 2 weeks off where they use an ECA stack or Clen (http://www.anabolex.com/forums/autolink.php?id=6&script=showthread&forumid=2) during the break to continue to lose fat, then run another 4 week cycle. So the 1st 3 days in this cycle would be 25mcg/day, then the 2nd 3-day period is 50mcg/day, etc. The typical 21-day cycle will look like this:

Days 1-3.................. 25mcg/day
Days 4-6...................50mcg/day
Days 7-9...................75mcg/day
Days 10-12................100mcg/day
Days 13-15................75mcg/day
Days 16-18................50mcg/day
Days 19-21................25mcg/day

As you can see the dosage is increased by 25mcg/day every 4th day until the maximum dosage is reached for the subject, in this case 100mcg/day, then lowered the by the same 25mcg/day increments every 4th day until the end of the cycle. Given that most of the people I've worked with have tried everything else and are still considerably overweight when they start, the full 4-week cycle is often used instead of the 21-day cycle. The one I've used lately with the most success is as follow, remember the jumps are still 25mcg/day but this time you increase/decrease the dosage every 4 days:

Days 1-4...................25mcg/day
Days 5-8...................50 "
Days 9-12.................75 "
Days 13-16...............100 "
Days 17-20...............75 "
Days 21-24...............50 "
Days 25-28...............25 "

Note: You could also do the 3-day increase/decrease and hold the maximum dosage of 100mcg/day for days 10-19, but some find 100mcg/day makes them too uncomfortably warm and they sweat too much, especially during the warmer months.

There you have it, simple yet effective. If you remember to supplement your diet with plenty of protein (which every lifter should anyhow), eat a clean calorie controlled diet, drink 1-2 gallons of water per day and to take a mild steroid cycle to minimize muscle loss you should be able to see rapid fat loss with this cycle. I should also mention that some people like to stack T3 with Clenbuterol (http://www.anabolex.com/forums/autolink.php?id=6&script=showthread&forumid=2) for even better results. I?ve purposely left this out as I will be including Clen (http://www.anabolex.com/forums/autolink.php?id=6&script=showthread&forumid=2) in Part 2 of this series. Good luck and may you all reach your cutting goals!!!

T3 basic dosage protocal? - MuscleChemistry.com (http://www.musclechemistry.com/upload/musclechemistry-discussion/42171-t3-basic-dosage-protocal.html)

12-08-2012, 06:54 AM
Ingestion of androgenic-anabolic steroids induces mild thyroidal impairment in male body builders.


Deyssig R,et al. Show all (http://www.ironmagazineforums.com/#)Deyssig R, Weissel M.


J Clin Endocrinol Metab. 1993 Apr;76(4):1069-71.

Third Medical University Clinic, Vienna, Austria.


Self-administration of very high doses of androgenic anabolic steroids is common use in power athletes because of their favorable effect on performance. Since androgenic steroids decrease serum T4-binding globulin (TBG) concentrations dramatically, we were interested in the effects of this procedure on thyroid function: we performed TRH tests (200 micrograms Relefact, i.v.), with blood withdrawal before and for 180 min after injection, for determination, using RIA kits, of serum concentrations of total and free T4, total T3, TSH, and TBG in 13 young (20-29 yr old) male body builders with clinically normal thyroid glands, who were all in the same state of training. Five of these athletes admitted taking androgenic anabolic steroids at an average total dose of 1.2 g/week for at least 6 weeks before the tests. TBG, total T4, and total T3 were significantly (P < 0.001) decreased, whereas basal TSH and free T4 were not significantly different from the values of the other 8 without androgenic steroids. The maximum TSH increase after TRH administration (mean +/- SE, 16 -/+ 6 vs. 9 -/+ 4 mU/L; P < 0.05) was relatively increased, whereas the T3 response to TRH (0.61 -/+ 0.10 vs. 1.13 -/+ 0.13 nmol/L; P < 0.05) was relatively decreased in the group receiving androgens. The 5 patients taking androgens had significantly greater weight (114 vs. 90 kg; P < 0.01) and higher total cholesterol levels (6.3 -/+ 1.3 vs. 3.8 -/+ 0.3 mmol/L; P < 0.05) together with very low high density lipoprotein cholesterol levels (0.20 -/+ 0.03 vs. 1.03 -/+ 0.10; P < 0.001) than the controls. PRL levels were normal and similar in both groups. We conclude from our results that high dose androgenic anabolic steroid administration leads to a relative impairment (within the normal range) of thyroid function. Whether this is due to a direct thyroid hormone release (or synthesis?)-blocking effect of these steroids needs further investigation.


8473383 [PubMed - indexed for MEDLINE]

12-16-2012, 11:45 AM
Interesting studies...aas use is shown to effect thyroid function but didnt show to.lower free t4..so i would think.there isnt a real negative impact.from aas use??