A Great Overview of T3...and to a lesser degree, T2 and T4

  1. A Great Overview of T3...and to a lesser degree, T2 and T4

    I got this from a board, where it was posted from another board, so I'm bringing it to you 3rd hand :bruce1:

    I don't usually copy/paste, but I think there is a lack of T3 info here, so this should be a good resource. If any mods can think of a better place to put it, please do. It doesn't really fit into the other subforums.

    Highlights are mine to emphasize key points.
    Originally posted in beyond mass forums by chemical evelution.


    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.
    Last edited by Beowulf; 07-06-2006 at 10:04 AM.

  2. 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 anabolic steroids 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.

  3. 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)

    *[Note: this should also apply to albuterol]

    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.
    Last edited by Beowulf; 07-06-2006 at 10:11 AM.

  4. 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.


    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.
    Last edited by Beowulf; 07-06-2006 at 10:14 AM.

  5. Great read Beowulf,

    Do you know if there is a recommended jump-starter for the thyroid? I've heard different herbals would help but wondered what you thought.

    Again, great read.
    My The 1 LOG: http://anabolicminds.com/forum/steroids/254164-my-one-log.html

  6. I do not know of any herbals except guggls, but l-tyrosine does wonders in the range of 2-4grams. Reps to you big bad Beo...

  7. Ask and ye shall receive I assume by jumpstart you mean thyroid PCT.

    This is from a different board, and credit is due to a guy named Mallet

    Thyroid Post Cycle Therapy

    Here is a list of supplements and recommendations I have compiled for your thyroid post cycle therapy.

    Several nutrients are critical for the proper functioning of the thyroid gland. In order for the thyroid gland to produce the hormone thyroxine, it needs the trace elements iodine and selenium, and the amino acid Tyrosine. Without sufficient supply of the nutrients in the diet, thyroid function is diminished. A typical regimn of dietary supplements I recommend in support of thyroid function are listed below.

    BLADDERWRACK (fucus vesiculosus)
    Bladderwrack, or fucus, consists of the marine plant fucus vesiculosus. Marine algae have been used in Europe and Asia as medicinal agents for thousands of years. Bladderwrack is a rich source of iodine and is traditionally used for weight loss and hypothyroidism. Bladderwrack is thought to stimulate the thyroid gland, thus increasing basal metabolism. Bladderwrack also contains potassium, magnesium, calcium, iron, zinc, and other minerals.

    RECOMMENDED DOSE. 300-600 mgs, standardized to contain not more than 150mcg of iodine daily, one to three times a day.

    COLEUS (coleus forskolii)
    Coleus has been extensively researched in India over the last twenty years as a medicinal agent useful for thyroid support and for conditions such as high blood pressure, asthma, and weight loss, among others.
    Coleus is also thought to activate the enzyme adenylate cyclase. In doing so, it increases the level of cyclic adenosine monophosphate (cAMP) within cells ( cAMP, as you may recall, is important in the activation of several biochemical pathways). This catalyst is formed when neurotransmitters bind to the cell membrane and stimulate the formation of adenylate cyclase. Specific hormonal messengers bind to receptor cites to create the release of cAMP. Therefore, while Coleus is involved in hormonal regulation, it doesn't increase hormone levels. Instead it helps improve the effeciency of binding to target receptor cites. The stimulation of cAMP has an impact on the body chemistry in several ways. It stimulates thyroid function, increases insulin secretion, inhibits histamine release (involved in allergic reactions), and increases the burning of fats as fuels. Coleus is claimed to inhibit platelet activating factor (PAF)--that si, the formation of blood clots--by possibly directly binding to PAF receptor cites.

    RECOMMENDED DOSE. 250mgs of a 1 percent extract of coleus, twice a day. CAUTION: people with ulcers or who are taking blood pressure medication and anticoagulant medications should check with your healthcare professional before taking Coleus.

    CORDYCEPS (cordyceps sinesis)
    Cordyceps Is important for people with improperly functioning thyroid glands because people with low thyroid function have reduced oxygen utilization and increased oxidative stress. Cordyceps acts as an antioxidant, improves oxygen utilization by 15%, improves stamina, and reduces fatigue--all critical issues for people with poor thyroid regulation.

    RECOMMENDED DOSE. 525mgs of cordyceps, standardized to contain .14 to .18 percent adenosine and 5 percent mannitol, two to three times a day.

    Low thyroid function leads to poor conversion and utilization of essential fatty acids (EFA's). Without quality sources of dietary fat, particularily the Omega-3 fatty acid alpha-linoleic acid (ALA) and the Omeaga-6 fatty acid gamma-linolenic acid (GLA), the body is unable to regulate hormonal influence over certain cells. EFA's are the building blocks of eicosanoids, a group of "super hormones" that act as hormonal gatekeepers of the cells. EFA defficiencies and overproduction of inflammatory prostaglandins are associated with a variety of illnesses, including slowed metabolism and increased storage of body fat.

    RECOMMENDED DOSE. The best sources of GLA are borage and evening primrose oils. Sources of Omega-3 fatty acids are cold water fish ( salmon, mackerel, tuna trout, haddock), flaxseeds and flax oil. Although both EFA's are essential to our health, the ratio of omega-3 to Omega-6 oils in our diet should be 1:3. Udo's oil contains 3,6, and 9 fatty acids.

    GUGGUL (commiphora mukul)
    Guggul has been described in Indian medical literature as an agent for treating obesity and other eating disorders. Guggul was marketed as a lipid lowering agent in 1980, Guggul has been reported to stimulate thyroid function, which may lead to blood lipid lowering and weight loss, as well as improved thyroid function in hypothyroidism.

    RECOMMENDED DOSE. 500mgs, three times a day, standardized to contain 5 percent gugglesterones. CAUTION: people taking prescription medications for cardiovascular disease such as calcium channel blockers or beta blockers, as well as those with hyperthyroidism, should check with there physician before taking Guggul.

    If you can't get your hands on the bladderwrack, then sources of iodine include sea vegatables (nori, hijiki, wakame, kombu, and kelp), sea salt, and all seafood and saltwater fish. Iodized salt is another source, but contains to much aluminum, Iodized sea salt, however supplies iodine without unwanted aluminum.

    RECOMMENDED DOSE. 225-1000mcg of iodine daily

    Without sufficient available tyrosine, the adrenal glands have a sluggish or inadequate response to stress: heart rate, blood pressure, airway, and metabolism are diminished. And when the tyrosine pool is drained to make stress hormones, there is less available to make adequate levels of thyroid hormones. Tyrosine supplements have been used as nutritional or adjunctive support for the treatment of depression, anxiety, sleep disorders, and weight gain, all of which are associated with hypothyroidism.

    RECOMMENDED DOSE. 250-750mg of L-Tyrosine daily. Most body builders and athletes eat plenty of amino acids throughout the day, so supplementing with tyrosine isn't as important unless your under significant stress your body temp is low, and you have other symptoms of low thyroid effeciency.

    Thyroid glandular is a bovine-derived thyroid substance that may boost the human thyroid system when the gland is not functioning optimally. Glandular supplements are carefully processed animal gland tissue; thyroid glandulars contain extremely low levels of thyroid hormone. It is theorized that glandular tissues contain proteins that help the thyroid gland to rebuild itself. This has been very effective with people who have subclinical hypothyroid function...it has also been used in place of thyroid meds with great success.

    RECOMMENDED DOSE. T-100X...Is a good source of not only thyroid glandular, but also contains: Thyroid glandular ( thyroxine free) 100mg...Adrenal gladular 50mg...pituitary glandular 15mg...spleen glandular 5mg...thymus glandular 5mg...and It also contains bladderwrack 15mg...along with a few supportive herbs. Made by "Advanced Orthomolecular Research" (AOR) check out their website for more info " www.aor.ca". So as you can see T-100X is good for more than just thyroid support, it's quite effective at stimulating your total immune system...this baby is a must!!!

    DOSE. 1 tab (630mg) twice a day for post cycle or if you already have a low Resting Temp.

    Chromium depletion may influence thyroid function. Chromium is a necessary mineral for the conversion of carbohydrates to energy, and helps maintain a stable blood sugar level. It is also an essential component to enzyme function that supports the conversion of T4 to T3. So chromium can indirectly impact your basal metabolic rate and how you are going to burn fat, use nutrients, and generate energy. Selenium has also been linked to subclinical hypothyroid symptoms. Selenium is found in selenoproteins, many of which have known roles in the prevention of cellular oxidative damage and thyroid hormone regulation. Selenium is an essential component of the enzyme iodothyronine deiodinase, the enzyme that converts thyroxine (T4) to the active triiodothyronine (T3). As with Zinc, selenium supplementation has been reported to improve thyroid function and regulate symptoms of hypothyroidism. Other nutrients important for optimum thyroid function include zinc and copper. These trace minerals are also required for the synthesis of iodothyronine deioinase. Studies have concluded that that zinc supplementation can restore normal thyroid function among people with low serum zinc, and signs of subclinical hypothyroidism. Zinc is required for the activity of more than 200 different enzymes in the body. Supplementing with extra zinc requires the addition of copper to maintain healthy zinc to copper ratio. Since the two elements antagonize one another, supplementing with one can kead to a deficciency of the other.

    RECOMMENDED DOSE 200mcg of chromium daily as part of a multivitamin/mineral supplement; 200mcg of selenium daily; anf 15 parts zinc to 1 part copper, or approx 20-50 mg of zinc to 2 mg of copper.


    Many physician now recognize the problems with thyroid regulation. In fact, the window for acceptable TSH levels has just recently been changed by the American Society of Endocrinologists so that millions more people may get diagnosed with hypothyroidism and get the help they need. Hopefully the use of t3 and t4 as drug therapy will become more popular, and in addition, the various influencers of thyroid metabolism such as stress and nutrient abnormalities will begin to become more recognized in the coming decade. Healthy thyroid function is crucial to graceful and vital aging. So whether you try Armour thyroid, nutritional approaches, get compounded thyroid therapy, or use traditional drugs, keep one thing in mind: If there's no relief of low-thyroid symptoms, you are probably still missing a piece of the metabolic puzzle.


    With all that said you can pick from the list provided above to determine your needs, or what's available to you...this is what I do with great success, I mean my temp is usually bang on every morning, the only time my temp drops or raises, is when I want it too!

    Coleus forskolii (acti-cyclase) 250mg twice daily when taking T3, 3 times daily when i'm not.

    T-100X. 630mg twice daily for post cycle (As mentioned above this is the glandular form) This ones a must!!!

    Life extension mix (powder) This baby is pricey but contains everything you need to sustain life. But for thyroid purposes : 200mcg selenium: 200mcg chromium: 75mcg iodine: 35mg zinc: 2mg copper

    Udo's oil contains omega 3,6, and 9 fatty acids...I use 2 tablespoons in my protein drinks, 2 tablespoons per can of tuna in place of mayo. I cook with it, you can even poor it on popcorn in place of butter...I say this because my GF is a popcorn freak.

    Backing off on training is a plus when doing long thyroid cycles. If your training 5 days a week, then try 4 days a week for the first 2 weeks when coming off t3, remember your adrenals will rob you of tyrosine to make cortisol. And since training and rest are 2 big factors of stress, lets give your body the extra edge for regulating your thyroid function with as little hinderance as possible. Try to make sure you get adequate rest when coming of thyroids also, this will help with the return of normal thyroid function as well.

    Also NOW Foods - discount nutritional vitamins and mineral supplements and health-related products has a good product called Thryoid energy that has a few of these elements in them.

  8. I just updated a bit, highlighting some key points to make this overview more applicable. Key points are italicized and/or bolded and/or underlined according to importance.

    Interestingly, for all the research that went into that piece, there is minimal discussion of potential cardiac sides. If I get a chance, I'll try to dig up some more on that.

  9. Beowulf,

    Have you known anyone to use T4 or T3 in off-season due to the increase in mitochondria activation and the "driver" action of T3/T4 of nutritients into the cells?

  10. Beowulf,

    Did you ever come up with any more information on the cardiac side effects of T3 use?

    I have heart palpitations and once ran a very short low dose (2 weeks ~50mcg of T3) cycle of T3 and I am wondering if it contributed in some way. The timing of my problem didn't exactly coincide perfectly with it or anything but it does give me suspicion. I'll personally never use it again.

    A lot of people with heart rhythm abnormalities have them because of messed up thyroid levels. Women especially have problems with it and it can be tough to correct. Even under proper medical supervision supplementing with T3 can be a bit risky imo.

    I can certainly add T3 to the list of things I will never use including insulin, dnp and other drugs that just don't make any sense for me to take.

  11. lotta good info

  12. Great info Here!

  13. Any new studies recently?

  14. good read op

  15. Great info


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