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T3 cytomel for weight loss

T3 (cytomel)

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 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 anabolic steroids 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.

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Clen – T3 Cutting Cycle for weight loss

This is a 6 week Clenbuterol – T3 Cutting Cycle for fat loss

Clen is taken 1 week on – one week off:

As in my experience it is more effective for weight loss if used this way:

A mild anabolic of 50mg of Winstrol ED, Anavar at 40mg ED or Test Prop at 50mg ED or 100mg EOD is recommended to preserve muscle lose and fight of a catabolic state that T3 can cause. You could also use longer ester testosterone, but they will take much longer to kick in to be effective.

Start T3 at 50mcg as any lower makes no sense since your body should be producing between 20mcg-25mcg daily naturally… Clen doses use as a guideline along with the T3 doses, everyone has different tolerances for both, but this is was very effective for me and I lost a lot of excess body fat …

You can use a simple ECA (Ephedrine/caffiene/asprin) stack during your off weeks in the place of Clenbuterol if you want to help with the fat burning progress… Your diet should be fairly high in protein, moderate carbs with no sugars and moderate fat intake… You may also want to add a source of EFA’s like a flax seen oil to your diet during this time… Also Clen is known to cause allot of muscle cramping… Also I start off week three at the same dose I finished with at the end of week one… Again all depends on your tolerance to the drug, you may want to start a little lower for a few days before going right back to your maximum dose.

Drink more water along with taking extra minerals and potassium and 2-3 grams ED of the amino acid L-Taurine is recommended if cramping is really a problem… Also take your Clen and T3 in two divided doses during the day… Also to give you an idea my daily calorie intake was probably about 1,000 to 1,200 lower then normal
for this entire time…

BTW when I ran this cycle I was running 900mg week of Test Cyp as my only anabolic right at the end of a bulking cycle… My results is I went from a chunky, but thick as a bull 240lbs to a fairly hard 212lbs or so in only 6 weeks… Again adjust the doses to fit your tolerance…

At these doses you will be sweating and hot all day long… Plan on losing some muscle mass even with the anabolics…

Buy your clen and t3 here

Day 1 Clen 60mcg — T3 50mcg
Day 2 Clen 60mcg — T3 50mcg
Day 3 Clen 80mcg — T3 75mcg
Day 4 Clen 100mcg – T3 75mcg
Day 5 Clen 100mcg – T3 75mcg
Day 6 Clen 120mcg – T3 100mcg
Day 7 Clen 120mcg – T3 100mcg
Day 8 Clen off – T3 125mcg
Day 9 Clen off – T3 125mcg
Day10 Clen off – T3 125mcg
Day11 Clen off – T3 125mcg
Day12 Clen off – T3 125mcg
Day13 Clen off – T3 125mcg
Day14 Clen off – T3 125mcg
Day15 Clen 120mcg – T3 125mcg
Day16 Clen 120mcg – T3 125mcg
Day17 Clen 120mcg – T3 125mcg
Day18 Clen 120mcg – T3 125mcg
Day19 Clen 120mcg – T3 125mcg
Day20 Clen 120mcg – T3 125mcg
Day21 Clen 120mcg – T3 125mcg
Day22 Clen off – T3 125mcg
Day23 Clen off – T3 125mcg
Day24 Clen off – T3 125mcg
Day25 Clen off – T3 125mcg
Day26 Clen off – T3 125mcg
Day27 Clen off – T3 125mcg
Day28 Clen off – T3 100mcg
Day29 Clen 120mcg – T3 100mcg
Day30 Clen 120mcg – T3 100mcg
Day31 Clen 120mcg – T3 75mcg
Day32 Clen 120mcg – T3 75mcg
Day33 Clen 120mcg – T3 75mcg
Day34 Clen 120mcg – T3 50mcg
Day35 Clen 120mcg – T3 50mcg
Day36 Clen off – T3 50mcg
Day37 Clen off – T3 50mcg
Day38 Clen off – T3 25mcg
Day39 Clen off – T3 25mcg
Day40 Clen off – T3 25mcg
Day41 Clen off – T3 25mcg
Day42 Clen off – T3 25mcg

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