Roids, tema único

Thyroid Hormone + Growth Hormone
(If You Aren’t Using T4 with Your GH, You’re Not Doing It Right)

by Anthony Roberts with James Daemon, Ph.D.

Discussio n of pharmaceu tical agents below is presented for informati on only. Nothing here is meant to take the place of advice from a licensed health care practitio ner. Consult a physician before taking any medicatio n.

Quite some time ago, I wrote a book on Anabolics, and since then, I’ve received quite a bit of feedback on it. Some of the informati on contained in the book is based on the 50-60 profiles I completed for Steroid.c om’s main page. As a result, I get feedback on certain portions of the book from people who have read them online.

When someone takes the time to send an e-mail to Steroid.c om or AnabolicB ooks LLC, they’re screened, and eventuall y some of them make their way to my e-mail account. AnabolicB ooks LLC is publisher- a little known fact is that my book is actually wasn’t edited by me, nor do I own the rights to any of it. When they forward an e-mail to me, I typically consider it very care.y, and reply to the original sender. If amendment s or additions are useful for anything I’ve previousl y written (readers frequentl y send me recently published studies), I typically reply and thank the person for their help.

This time, something odd happened. I was forwarded an e-mail from AnabolicB ooks, and the reader seemed to know what he was talking about, but (I thought) mistaken about interacti ons between Growth Hormone and Thyroid medicatio n. I took a look at the e-mail, and knew that I could quickly find a study that I had saved previousl y, to send to the reader, to verify that the claims in my work on GH were sound.

In this particula r case- James Daemon, PhD- was the reader, and was correct in his assessmen t of the interacti on between thyroid hormone and Growth Hormone. And, in direct contradic tion, so was I. Thyroid medicatio n decreases the anabolic effect of Growth Hormone. And it increases it.

Huh?

There’re some leaps here, because research in some of the necessary areas is sketchy (or not done yet), but if you read the entirety of this article, you’ll learn how to get a significa ntly more gains from Growth Hormone, for pennies a day, by the addition of a readily available (and cheap) addition to it. And yeah, it’s a drug you can get anywhere on the ‘net, very easily. And no, it’s not a steroid.

In fact, I’ll go so far as to say you’re throwing away a substanti al portion of your gains from growth hormone if you are not using this drug with it.

Ok…I’ll explain things a bit further. First, a brief explanati on of Thyroid Hormone as well as Growth Hormone may be necessary .

Your thyroid gland secretes two hormones that are going to be of primary importanc e in understan ding Thyroid/GH interacti on. The first is thyroxine (T4) and the second is triiodoth yronine (T3). T3 is frequentl y considere d the physiolog ically active hormone, and consequen tly the one on which most athletes and bodybuild ers focus their energies on. T4, on the other hand, is converted in periphera l tissue into T3 by the enzymes in the deiodinas e group, of which there are three types- the three iodothyro nine deiodinas e either catalyze the initiatio n (D1, D2) or terminati on (D3) of thyroid hormone effects. The majority of the body's T3 (about 80%) comes from this conversio n via the first two types of deiodinas e, while conversio n to an inactive state is accomplis hed by the third type.

It’s important to note that not all of the body’s T4 is converted to T3, however- some remains unconvert ed. The secretion of T4 is under the control of Thyroid Stimulati ng Hormone (TSH) which is produced by the pituitary gland. TSH secretion is in turn controlle d through release of Thyrotrop in Releasing Hormone which is produced in your hypothala mus. So, when T3 levels go up, TSH secretion is suppresse d, due to the body’s self regulator y system known as the "negative feedback loop" . This is also the mechanism whereby exogenous thyroid hormone suppresse s natural thyroid hormone productio n. However, it should be noted that thyroid stimulati ng hormone (like all other hormones) can not work in a vacuum. TSH also requires the presence of Insulin or Insulin-like Growth Factor to stimulate thyroid function (1) When thyroid hormone is present without either insulin or IGF-1, it has no physiolog ical effect (ibid).

Most people think that T3 is just a physiolog ically active hormone that regulates bodyfat setpoint and has some minor anabolic effects, but in actuality, in some cases of delayed growth in children, T3 is actually too low, while GH levels are normal, and this has a growth limiting effect on several tissues (2) This could be due to T3’s ability to stimulate the prolifera tion of IGF-1 mRNA in many tissues (which would, of course, be anabolic), or it could be due to the synergist ic effect T3 has on GH, specifica lly on regulatio n of the growth hormone gene. Although it is largely overlooke d in the world of performan ce enhanceme nt, regulatio n of the growth hormone response is predomina ntly determine d by positive control of growth hormone gene transcrip tion which is proportio nal to the concentra tion of thyroid hormone-receptor complexes, which are influence d by T3 levels. (3)

At this point, just to give you a better understan ding of what’s going on, I think it’s prudent to also give a brief explanati on of Growth Hormone (GH) as well.

Your body’s GH is regulated by many internal factors, such as hormones and enzymes. hormones. A change in the level of your body’s GH output begins in the hypothala mus with somatosta tin (SS) and growth hormone-releasing hormone (GHRH). Somatosta tin exerts its effect at the pituitary to decrease GH output, while GHRH acts at the pituitary to increase GH output. Together these hormones regulate the level of GH you have in your body. In many cases, GH deficienc y presents with a low level of T3, and normal T4(4). This is of course because conversio n of T4-T3 is partially dependant on GH (and to some degree GH stimulate d IGF-1), and it’s ability to stimulate that conversio n process of T4 into T3.

Interesti ngly, the hypothala mus isn’t the only place where SS is contained; the thyroid gland also contains Somatosta tin-producing cells. This is of interest to us, because in the case of the thyroid, it’s been noted that certain hormones which were previousl y thought only to govern GH secretion can also influence thyroid hormone output as well. SS can directly act to inhibit TSH secretion or it may act on the hypothala mus to inhibit TRH secretion . So when you add GH into your body from an outside source, you are triggerin g the body into releasing SS, because your body no longer needs to produce its own supply of GH…and unfortuna tely, the release of SS can also inhibit TSH, and therefore limit the amount of T4 your body produces.

But that’s not the only interacti on we see between the thyroid and Growth Hormone.

As we learned in high-school Biology class, the body likes to maintain homeostas is, or "normal" operating condition s. This is the body’s version of the status quo, and it fights like hell to maintain the comfort of the status quo (much like moderator s on most steroid discussio n boards). What we see with thyroid/GH interplay is that physiolog ical levels of circulati ng thyroid hormones are necessary to maintain normal pituitary GH secretion, due to their directly stimulato ry actions. However, when serum concentra tions of thyroid hormone increase above the normal range we see an increase in hypothala mic somatosta tin action, which suppresse s pituitary GH secretion and overrides any stimulato ry effects that the thyroid hormone may have had on GH. The suppressi on of GH secretion by thyroid hormones is probably mediated at the hypothala mic level by a decrease in GHRH release(5).

In addition, as IGF-I productio n is increased in the hypothala mus after T3 administr ation and T3 may participa te in IGF-1 mediated negative feedback of GH by triggerin g either increased somatosta tin tone and/or decreased GHRH productio n (6). IGF, interesti ngly, has the ability to mediate some of T3’s effects independe nt of GH, but not to the same degree GH can (7.) In fact, IGF-I productio n is increased in the hypothala mus after T3, administr ation it may plausibly participa te in negative feedback by triggerin g either increased somatosta tin tone and/or decreased GHRH productio n. So we know that GH lowers T4 (more about this in a sec), but an increase in T3 upregulat es GH receptors ( as well as IGF-1 receptors (9,10).

As can be previousl y stated, and due to the ability of GH to convert inactive T4 into active T3, GH administr ation in healthy athletes shows us an entirely predicatb le increase in mean free T3 (fT3), and a decrease in mean free T4 (fT4) levels.(11)

So, with the use of GH, what we see is an increased conversio n of T4-T3, and possible inhibitio n of Thyroid Releasing Hormone by Somatosta tin, and therefore even though T3 levels may rise, there is no increase in T4 (logically, we see a decrease). Now, as we’ve seen, GH is HIGHLY synergist ic with T3 in the body, and as a mater of fact, if you’ve been paying any attention up until this point, you’ll note that the limiting factor on GH’s ability to exert many of it’s effects, is mediated by the amount of T3 in the body.

As noted before, T3 enhances many effects of GH by several mechanism s, including (but not limited to): increasin g IGF-1 levels, IGF-1 mRNA levels, and finally by actually mediating the control of the growth hormone gene transcrip tion process as seen below:

Compariso n of the kinetics of L-T3-receptor binding abundance to changes in the rate of transcrip tion of the GH gene.(3)

As you can see, T3 levels are directly correlati ve to GH gene transcrip tion. The scientist s who conducted the study which provided the graph above concluded that the amount of T3 present is a regulator y factor on how much GH gene transcrip tion actually occurs. And gene transcrip tion is what actually gives us the effects from GH. This last fact really seems to shed some light on why we need T3 levels to be supraphys iological if we’re going to be using supraphys iological levels of GH, right? Otherwise, the GH we’re using is going to be limited by the amount of T3 our body produces. However, since we’re taking GH, and it is convertin g more T4 into T3, T4 levels are lowered substanti ally, and this is the problem with GH. and may actually be THE limiting factor on GH…if we assume that at least some of GH’s effects are enhanced by thyroid hormone, and specifica lly T3, then what we are looking at is the GH that has been injected is being limited by a lack of T3. But that doesn’t make sense, because if we use T3 + GH, we get a decrease in the anabolic effect of GH.

This is where Mr. Daemon, who had contacted me via an e-mail to my publisher, about Thyroid + GH interacti on, was able to shed some light on things. You see, I knew that it couldn’t just be the actual presence of enough T3 along with the GH that was limiting GH’s anabolic effect, because, simply adding T3 to a GH cycle will reduce the anabolic effect of the GH (12.).

Originall y, he had said to me that T3 was synergist ic with GH, wheras I said that T3 actually reduced the anabolic effects of GH- now I realize we were both correct. Logically this presents a bit of a problem, which I believe can be solved. This came from reading several studies provided to me by Dr.Daemon . the trend I was seeing was that even when Growth Hormone therapy was used, T3 levels needed to be elevated in order to treat several condition s caused by a lack of natural growth hormone. And even if the patient was on GH, T3 levels still needed to be elevated. And what I noticed was that those levels were elevated success.y by using supplemen tal T4 but not T3.

Here’s why I think this is:

Additiona l T3 is not all that’s needed here. What’s needed is the actual conversio n process of T4-T3, and the deiodinas e presence and activity that it involves. This is because Local 5'-deiodination of l-thyroxine (T4) to active the thyroid hormone 3,3',5-tri-iodothyronine (T3) is catalyzed by the two 5'-deiodinase enzymes (D1 and D2). These enzymes not only "create" T3 out of T4, but actually regulates various T(3)-dependent functions in many tissues including the anterior pituitary and liver. So when there is an excess of T3 in the body, but normal levels of T4, the body’s thyroid axis sends a negative feedback signal., and produces less (D1 and D2) deiodinas e, but more of the D3 type, which signals the cessation of the T4-T3 conversio n process, and is inhibitor y of many of the synergist ic effects that T3 has! Remember, Type 3 iodothyro nine deiodinas e (D3) is the physiolog ic INACTIVAT OR of thyroid hormones and their effects (13) and is well known to have independe nt interacti on with growth factors (which is what GH and IGF-1 are).(14) This is because with adequate T4 and excess T3, (D1 and D2) deiodinas e is no longer needed for conversio n of T4 into T3, but levels of D3 deiodinas e will be elevated. When there is less of the first two types of deidinase, it would seem that the T3 which has been converted to T4 can not exert it’s protein sparing (anabolic effects), as those first two types are responsib le for mediation of many of the effects T3 has on the body. This seems to be one of the ways deiodinas e contribut es to anabolism in the presence of other hormones.

All of this would explain why anecdotal ly we see bodybuild ers who use T3 lose a lot of muscle if they aren’t using anabolics along with it- they’re not utilizing the enzyme that would regulate some of T3’s ability to stimulate protein synthesis, while they are simultane ously signaling the body to produce an inhibitor y enzyme (D3). And remember, for decades bodybuild ers who were dieting for a contest have been convinced that you lose less muscle with T4 use, but that it’s less effective for losing fat when compared with T3? Well, as we’ve seen, without something (GH in this case) to aid in the conversio n process, it would clearly be less effective! Since the deiodinas e enzyme is also located in the liver, and we see decreased hepatic nitrogen clearance with GH + T3, it would seem that the D3 enzyme is exerting it’s inhibitor y effects, but in the absence of the effects of the first two deiodinas e enzymes, it remains unchecked and therefore not only limits the GH’s nitrogen retention capabilit y.

In other words, if we have enough to GH in our body aid in supraphys iological conversio n of T4 into T3, but we already have the too much (exogenous) T3, the GH is not going to be convertin g any excess T4 into T3 after a certain point- which would be a limiting factor in GH’s anabolic effects, when coupled with the act that we’ve allowed the D3 enzyme to inhibit the T3/GH synergy that is necessary .

As further evidence, when we look at certain types of cellular growth (the cartilage cell in this case) we see that GH induced rises in IGF-I stimulate s prolifera tion, whereas T3 is responsib le for hypertrop hic different iation. So it would seem that in some tissues, IGF-1 stimulate s the synthesis of new cells, while T3 makes them larger. In this particula r case, The fact that T4 and (D1) deiodinas e is am active component in this system is noted by the authors. They clearly state (paraphras ing) that: "T4 is is converted to T3 by deiodinas e (5'-DI type 1) in periphera l tissues

Cytomel

(Liothyrin e Sodium )

This drug 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. (

Natural T3 is a regulator of the oxidative metabolis m of energy producing substrate s (food or stored substrate s like fat, muscle, and glycogen) by the mitochond ria. The mitochond ria, as you will recall from your high school biology class, are usually referred to as the "cell's powerhous es" because they produce ATP. Taking Cytomel (supplemen tal T3) greatly increases the uptake of nutrients into the mitochond ria and also their oxidation rate (i.e. the rate at which they are burned for energy), by increasin g the activitie s of the enzymes involved in the oxidative metabolic pathway. Everythin g is working harder, in other words, and more fuel is needed to supplemen t this increased work rate. Therefore, as you can guess, taking supplemen tal Cytomel will increase your body’s energy demands. And if you are in a hypocalor ic state, you will begin burning even more fat primarily due to an increase in ATP. This increased ATP causes an increase in overall metabolic activity. ( (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 mitochond ria/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 functioni ng…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, especiall y while dieting.

Thus we can see that there are many advantage s to using Cytomel to optimize our metabolic rate. It will also increase your body’s ability to synthesiz e protein, but from what I’ve seen personall y, it acts as a catabolic when it isn’t administe red with anabolic steroids. It is often the last thing added into a precontes t diet, as it has a reputatio n for getting rid of the last few percentag es of bodyfat…the “sticky fat” as it’s called in bodybuild ing…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 restricti on has diminishe d your thyroid output and you are adding it in simply to replace what was lost.

Unfortuna tely, in all of the studies I’ve seen, T3 also increased growth hormone productio n. (5)(6) As we all know, GH is also a strongly lipolytic compound, and this is another mechanism by which T3 may exert it’s effects, although I suspect this would only be a small percentag e of it’s overall effects. This being the case, it has always been somewhat problemat ic 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 previousl y, 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, administr ation of T3 has been shown to upregulat e the beta 2 receptors in fat tissue. As you know clenbuter ol and similar compounds downregul ate this receptor, so using T3 with your clen will help stave off or reverse this downregul ation. (1)(2)(3)(4). I would still recommend taking your benadryl every third week, though.

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 replaceme nt just aren’t true. I remember a few years ago, the rumor was circulati ng that the current Ms.Fitnes s had permanent ly shut off her thyroid gland, and was now fat and on thyroid hormone permanent ly. This is just another horror story based in nothing but conjectur e and rumour…the studies I’ve looked at have shown people recoverin g their thyroid hormone relativel y quickly (within months, at most) after going off of several YEARS (!) of thyroid replaceme nt 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 aggressiv e? Yes. Unsafe? NO.

Reference s:

1. Catechola mines inhibit Ca(2+)-dependent proteolys is in rat skeletal muscle through beta(2)-adrenoceptors and cAMP. Navegante s LC, Resano NM, Migliorin i RH, Kettelhut IC Am J Physiol Endocrino l Metab 2001 Sep;281(3):E449-54
2. Regulatio n of human adipocyte gene expressio n by thyroid hormone J Clin Endocrino l 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 adipocyte s from patients with hypothyro idism and hyperthyr oidism Metabolis m 1987 Nov;36(11):1031-9 Richelsen B, Sorensen NS
4. Regulatio n of beta 1- and beta 3-adrenergic agonist-stimulated lipolytic response in hyperthyr oid and hypothyro id rat white adipocyte s 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 expressio n 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 weightles sness in men and women. Am J Physiol 1999 Aug;277(2 Pt 1):E370-9 Lovejoy JC, Smith SR, Zachwieja JJ, Bray GA, Windhause r MM, Wickersha m PJ, Veldhuis JD, Tulley R, de la Bretonne JA.
7. Effects of long-term growth hormone (GH) and triiodoth yronine (T3) administr ation on functiona l hepatic nitrogen clearance in normal man. Wolthers T, Grofte T, Moller N, Vilstrup H, Jorgensen JO.
   J Hepatol 1996 Mar;24(3):313-9
8. Human Anatomy and Physiolog y, 6th Edition. John w. Hole jr.
9. Physician s Desk Reference
10. Recovery of pituitary thyrotrop ic function after withdrawa l 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 hypothala mic-pituitary-thyroid axis in patients taken of chronic thyroid therapy. J Clin Endocrino l Metab 1975 Jul;41(1):70-80 Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, Chua Teco GN

Synthroid

(Levothyro xine Sodium)

Synthroid is the less powerful of the two most popular thyroid replaceme nt drugs on the market. It is synthetic T4, and is actually the more prescribe d thyroid medicatio n in America, but the lesser used of the thyroid drugs which are popular with bodybuild ers. If you have naturally low T3 levels, then you may be able to supplemen t with T4, and have it convert to T3 via your body’s natural metabolic pathways, which involves the deiodinas e enzyme. However, There have been a number of studies that have shown that during reduced caloric intake, and/or when carbohydr ate intake is reduced dramatica lly, levels of deiodinas e decline, hindering the conversio n of T4 to the physiolog ically active T3(1). So, if you are dieting (which would necessari ly mean you have a reduced caloric intake and/or reduced carbohydr ate levels), then you have less deiodinas e enzyme (still with me?) and thus, that T4 you are taking in hopes of getting it to convert to T3, is not getting converted . This is not what we want, clearly, and is why most pre-contest dieters include Cytomel in their drug regimen instead of Synthroid . In fact, Synthroid may be particula rly bad for dieters on Cyclic Ketogenic Diets.

When you earn your living off of your body, as many fitness models, models, and bodybuild ers do, it’s just too haphazard to trust Synthroid . This is especiall y true if you are not monitorin g your Basal Body Temperatu re or (preferabl y) shelling out the money for a thyroid function test every month.

As compared to Cytomel, Synthroid requires significa ntly higher doses to be effective . Most bodybuild ers don’t exceed 100mcgs of Cytomel during a precontes t phase of dieting, but with Synthroid the doses climb significa ntly higher to achieve the same results. From interview s I’ve done with bodybuild ers who have used Synthroid, I’ve heard of it being used at up to 300mcgs/day. When you compare that to the mere 25-100mcgs/day of Cytomel that bodybuild ers are typically using, we have another strike against Synthroid . It isn’t really economica lly feasible to do that much Synthroid and remain cost effective, at least when compared with Cytomel. To give you a fair estimate, you could run an effective dose of both Cytomel and Clenbuter ol for the same price as an effective dose of Synthroid .

My advice? Use it if you have to, but only if that’s the case, and you can’t get Cytomel or Tricana. It works, and will eventuall y get you to the desired body temperatu re for optimal fat burning, but it just isn’t as elegant as the less suppressi ve Tricana, or the more effective Cytomel.

Reference s:

1. The effect of a low-calorie diet alone and in combinati on with triiodoth yronine therapy on weight loss and hypophyse al thyroid function in obesity. Koppescha ar HP, Meinders AE, Schwarz F.
   Int J Obes 1983;7(2):123-31