Anabolic Member
Wow is all i can say, i been using T3 for about 5 weeks now, the first two weeks normal moderate weight loss but after week 3 wow it started dropping fast.
I modified my diet after coming back from Mexico i was 242 and could not get below 234-230 i tought i was done at 40 years old forget it i will never be able to drop below 230.
I am now 218 and the T3 helped a lot. I have now hope of dropping below 190.
New Member
Congrats Yannick...are you doing anything special in your diet? How much are you running? Are you adding any anabolics? I find that as I lean out I get a bit weaker in deads and squats but start looking better nakedThe other problem is none of my clothes fit well any more....
Anabolic Member
I take between 50 and 75mcg per day, i am going to stay on this for 10 months, because i really want to get down to 190 for that damn back pain and better with prolotherapy treatments. My weights have gone down i do not squat nor deadlift anymore i injured myself that way to much compression on the spine.
Yes of course diet changes are a must i wont be on T3 all my life and i really really really dont want to gain anything back afterward. I cut out most sugar, i eat more protein, and limit carbs but not too much because T3 works well with carbs. I am taking GH at 1iu 5/2 this is just to get the benefits for anti aging and hairgrowht a bit of fat loss. I am also doing IF fasting 15 hours per day.
I am not taking any gear, i did lose some mass but i don't care the lighter i am the better i feel. Last year an idiot doctor put me on TRT and i ballooned up from 217 to 261 in 3 months. That idiot never gave me an AI and told me to keep using 200mg of testosterone enhantate every 7 days.
New Member
I would like to have my doc give me 200 mg a week, but I don't have water rention until i get over 500 mg a week. Are you going to cycle the t3 over the 10 months?
Anabolic Member
I now a few people who did 50mcg to 70mcg for 10 months and everything came back to normal in 2 weeks, i will not cycle. My plan is going well with diet and fasting and T3 if i get to 190 before i will not go the whole 10 months i am just god damn tired of being overweight fat having a gut and all i just wanna lose weight and then rebuild.Originally Posted by O40
I will not lie to you i am very honest, i lost a lot of muscle mass, but i have no choice if i want to reach 190 that is the way its gotta be.
My bones are not made to support 230-240 pounds even 220, i have a small frame.
Getting a presc for testosterone was very easy that medical doctor was an idiot, i filled a complaint against him because he give large doses and no AI, they are investigating him right now.
Even then buying testosterone on the black market is very cheap if you do a TRT type of thing a bottle will last you a very long time.
Delatestryl at 10ML bottle with 200mg per ML its gonna last you 20 weeks if you inject 100mg per week.
New Member
Hey Yannick, well good luck to you, sure you will get there. I have used up to 150 mcg but I I started at 25 for a week, 50 for a week 75, etc and when I hit 150 stayed there for 2 weeks and cycled back down. I ran it with clen and had that melting effect you mentioned. The clen gave me some head aches as I recall. I still have a bottle of T4 and some T3 in my gear box. My thyroid tests alway came back normal. I am going to start a tren/test prop/Mast cutting cycle shortly. I am in the US? My doc won't prescribe anything but straight test asked about HCG, he won't do it. Probably blow his moid asking for an AI.
New Member
Hi Yannick, I was reading your post and very impressed with the information you provided. Our stats are very similiar in that I am over 40 and although tall, with a large frame am probably 50+ lbs overweight. I am currently running 1iu daily of HGH. I workout intensely five Xs a week and try to get in at least 30 minutes of cardio daily. In the near future, I will be adding an additional cardio routine. Although, my diet is strict, the weight loss is so slow, it gets very discouraging. Since my Doc refuses to prescribe Testosterone, I also want to add that to my protocol. My test level was recently tested at 434, but I want to increase that to 800. My thyroid is normal almost bordering a low thyroid level. My Doc thinks this level is perfectly fine. However, I am not convinced. I am also interested in the Clen and the T3 or T4. Keep up the good work, bro! Dano
Anabolic Member
Clen is very bad, i cannot use any stimulate at 40, i used a lot when i was in my 20. 434 man this is low T your medical doctor is an a$$hole, you need testosterone, i am at 640 and sometimes around 700. I also take GH at 5/2 1IU per day.
Diet is the key no matter what, T3 is amazing and will give you an edge on weightloss.
Anabolic Member
I did clen then albuterol they are both terrible, they gave me the worst jitters and yes headacks. Medical doctors know nothing about hormone therapy they will never prescribe anything like T3 or Testosterone and GH. I would probably be stuck at 240 pounds i not for the T3.
New Member
Hi Yannick, I have to agree with you that my Doc is an A__hole! However, I would not expect anything more out of an HMO! I consider a 434 test level a low level. It did go up +10 when I started larger doses of DHEA. The only good thing about my Doc, is that I can talk him into running any lab test I need. I did not know that Clen is a stimulant. I agree totally with you and because of that will not be using the Clen. What do you mean when you are taking 5/2 1iu. Thanks dude for clarifying that. So, it looks like T3 is the answer along with the HGH. I was looking at the T3 from AR-R???
Anyway, keep up the great results and thank you for the assistance! Dano
Anabolic Member
I have yet to try T3, but have been considering it for awhile.
I've always understood T3 to simply increase BMR. But i've been hearing that it not only takes out bf%, but LBM as well. What I"m curious about is that if eating clean, and hitting the gym 4 or 5x a week, will there really be a noticeable loss of lbm?
see, it doesn't make any sense to me if all T3 does is increase BMR. Something else must be going on?
Disappointment* Known SCAMMER - Do Not Trust *
T3 is expressed in 381 genes - many found in muscle. I dont know what else it is thats going on but your right..there is def something else at work here TR.
I do know that the increase in bmr will increase not only the anabolic processes in the body but the catabolic ones also. Great topic for discussion.
Nandi wrote that t3 dramatically decrease ATP and the body turns to itself for fuel and not only fat but muscle becomes a source. He was pretty f ing smart so maybe it is that simple.
Female Member
Congrats Yannick on your great loss so far. I am on T3 as well I am only using 25 mg I lost 14 so far.
ARs TOP DOG ~ MONITOR ~
Good job bro
Anabolic Member
Mr. Jimmy,
Do you have a link you can share?
Disappointment* Known SCAMMER - Do Not Trust *
One better buddy:
Introduction
It has been over 100 years since the discovery by Magnus-Levy that thyroid hormones play a central role in energy homeostasis, and 75 years since the hormones were first used for weight loss. Despite this great length of time, the precise mechanisms by which thyroid hormones exert their calorigenic effect are not completely characterized, and still actively debated. Despite numerous clinical studies having shown that the administration of thyroid hormone induces weight loss, it is not currently indicated as a weight loss agent. This is probably due to the number of side effects observed during thyroid hormone use at the relatively high doses used in the majority of obesity treatment studies. These deleterious effects include cardiac problems such as tachycardia and atrial arrhythmias, loss of muscle mass as well as fat, increased bone resorption and muscle weakness. Nevertheless, thyroid hormones, particularly triiodothyronine (T3) are a mainstay in the 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 totestosterone 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 ofinsulin 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.
Summary
We have discussed a number of ways by which T3, and its active metabolite T2 act to increase resting energy expenditure. Also discussed were some drawbacks of T3 use, such as cardiac stress, as well as the potential loss of muscle mass. It is ironic that the latter may be of more concern to many bodybuilders that the other more serious potential impacts on health. Nevertheless, used moderately and for short periods (a couple of months or less) in people with no preexisting cardiovascular disease T3 has a relatively safe medical profile, compared to other lipolytic agents like DNP. Perhaps most importantly we have presented substantial evidence that even the long-term use of supraphysiological levels of T3 does not damage the thyroid gland.
Karl Hoffman aka Nandi
Anabolic Member
I lost 2 inches on my arms and lots more on my legs. This is all true T3 eats away fat and muscles too.
Great article, right now doing very light training during prolotherapy.
Usually most people will take T3 with testosterone or part of a steroid cycle to minimize the muscle loss.
Knowledgeable Member
Would you have the muscle loss if you used T4 instead of T3 since the T4 is converted into T3?
Disappointment* Known SCAMMER - Do Not Trust *
Im not exactly sure how efficient the body is at converting t4 to t3. I know 100mcg t4 = 25mcg t3 BUT- over that amount , much like other precursors in the body if you will, there are limiting factors. I would have to think t4 would not be as catabolic.
HRT
By any chance have you noticed an improvement in erection quality since administering T3?
Knowledgeable Member
Sorry for the hijack.
But is there any preference to which cutting course you would add T3 too? I often see Tren/Test/Mast/T3. Would you throw T4 in as well? Clen or Albuterol? Just curious on people's thoughts on stacking these, and stacking with AAS.
-Krugerr
Senior Member
I am considering a 3 month T3 plan with Anavar...
But reading this, I may do a T3 w/ Test
People who have done T3 / T4 - how many pounds per week did you loose? How long did it take before you started noticing it?
Female Member
You're probably going to get better answers to your questions if you start your own thread.... This one is quite old.
Anabolic Member
I got a new source for my T3 i will not post it here i think i am not allowed to post links but that thing was freaken powerful. I sort of got a bursite on the elbow and am sure it was due to taking this. I am off T3 for good now taking kelp instead and changing my diet in a big way.
New Member
Hi everyone - i have an injury that means gym time is out at least for another 4-5 more months. Have gained 25 pounds since this injury happened last year as was depressed that could not exercise which i love. Started eating garbage and junk food and let myself go. Finally seeing the light at the end of tunnel as know soon I can start working out again. So exercise for now is out.
I am eating pretty clean but since gym time is out, losing weight is hard. I started taking T3 to help speed along the fat burning process.
I DONT WANT TO HEAR PEOPLE TELL ME THIS IS DANGEROUS SH*T. Ive been in this game for years and know that and had never taken t3 before but without exercise I saw it as a way to kick start the process until my injury was healed.
Noticed I got pretty lean around the waist and hips after taking 30mcg for about 2 weeks. I want to keep this going so need some help on best way to cycle this.
Im a female - 5 6" , weighing around 160 now. I know will lose muscle mass too but I'm fine with that. Will hit the weights hard when back to hitting the weights. As I cannot do cardio etc, what is best advice to keep this weight loss going until i hit my target weight again?
New Member
Hi - love to hear your feedback on my post. Thank you
Banned
Do you normally ask for advice and turn around and dictate the answers you expect to hear? How well has that worked out for you in the past?
So you're ok with losing the muscle mass you worked so hard for so long as the fat comes off? If so drop the T3 and start fasting for extended periods of time. You'll lose both fat and muscle that way and it'll be cheaper than running the T3.
New Member
Thanks for the condescension. This is why our world is a mess. Cannot post on a forum without someone starting off with attitude
Take it elsewhere please Im looking to communicate with positive well meaning people .
enjoy your day
Banned
Condescension would imply I have a sense of superiority which I don't. My tone is raw I admit but like I asked you, do you normally ask for advice and dictate the answers you expect to hear? How about I ask you to come up with a training program for me but I tell you I don't do squats or dead lifts, or any difficult lift for that matter, I don't workout Fridays to Mondays, and every 3rd Wednesday of the month is cheat day but my goal is to be jacked and ripped.Thanks for the condescension. This is why our world is a mess. Cannot post on a forum without someone starting off with attitude
Take it elsewhere please Im looking to communicate with positive well meaning people .
enjoy your day
The world is a mess bc when ppl are given the correct info they refuse to accept it or disregard it and do whatever they want anyway, which our situation here is a classic example of. Don't blame it on condescension when you're coming in the thread with a holier than thou attitude and "I DONT WANT TO HEAR PEOPLE TELL ME THIS IS DANGEROUS SH*T." Etc
You want positive and well meaning, get off the T3 and work on your diet and training. If you're able to sit and type at a keyboard you're able to do some sort of athletic activities and at the very least increase your energy expenditure which will help you lose weight. You ask for advice to keep weight loss going...that advice is focus on your diet. A poor diet will elicit poor results. If you can't lose weight with your diet than whatever weight you lose with T3 will only come back when you get off.
You may not think you care about losing muscle but when you become a smaller version of yourself now you will. You won't have changed your body composition since you'd lose both muscle and fat (T3 isn't preferential, it will take the calories from wherever it can).
Beach Bodybuilder ~Elite-Hall of Fame~
You should start your own thread rather than piggyback somebody else's.Thanks for the condescension. This is why our world is a mess. Cannot post on a forum without someone starting off with attitude
Take it elsewhere please Im looking to communicate with positive well meaning people .
enjoy your day
NO SOURCES GIVEN
Knowledgeable Member
You must run test along side t3 to preserve muscle. I would not run lower then 500mg test for 50 mcg t3.
There are currently 13 users browsing this thread. (0 members and 13 guests)
Posting Permissions
Reply With Quote