Si te parece Kiko100 recopilo el articulo que has puesto antes sobre el tema y añado algo mas para ver si podemos tratar el tema que seguro tendra mucha miga.

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��

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

Despues de leer todo esto y ademas en ingles (no se si lo habre entendido todo) haremos dos distincio nes. La primera uso con GH, parece que al usar t3 con gh lo positivo de la gh en ralacion con el NO se anula por lo que resta su anabolism o, cosa que creo haber entendido que puede regularse con el uso simultane de clen, ya que la t3 se come todo grasa y musculo pudiendo entrar en un estado de catabolim o. Esto se puede evitar usando gh y T4 la relacion es 300 mcgrs de t4 para el equivalen te a 25 mcgrs de t3. De esta forma el cuerpo sigue producien do T3 de forma natural al convertir t4 en t3 por el proceso que luego posteare que ha traducido Kiko100, sin entrar en estado catabolic o.
Al margen de la gh la T3 no debe usarse sino es con roids ya que consume musculo.

Si algun alma caritativ a lo traduce podremos profundiz ar mas.

La secreción hormonal de la tiroides se produce mediante un proceso proteolít ico. La cantidad de T4 que se libera es superior a la de T3. Sin embargo, gran parte de la T4 se convierte en T3 debido a la acción de esa enzima que se encuentra en el tejido periféric o denominad a 5-deiodasa. De hecho, el 75% de la T3 que se encuentra en la corriente sanguínea procede de la conversió n de T4 en T3.
Más del 99% de la T3 y T4 que se halla en la corriente sanguínea está unida a proteínas plasmátic as y, por lo tanto, sólo hay disponibl e una pequeña cantidad de hormona tiroidea para producir efectos biológico s. (Si se encuentra unida a una proteína, queda inutiliza ble temporalm ente.) Las hormonas tiroideas se eliminan a través del metabolis mo hepático y, puesto que la mayoría está unida a proteínas plasmátic as, tienen una vida media larga: unos dos días la de la T3 y cerca de siete la de la T4.
Las hormonas tiroideas están reguladas por el eje hipotálam o-hipófiso-testicular. El íúpotálam o secreta la hormona liberador a de rirotropi na (TRH), que actúa sobre la glándula pituitari a anterior, lo que causa la secreción de la hormona estimulad ora de la tiroides (TSH). La TSH actúa entonces sobre la glándula tiroides y estimula todos los aspectos relaciona dos con la secreción de hormonas tiroideas . Si tomo sustancia s tiroideas sintética s, mi nivel de T3 y T4 en plasma aumentará . El hipotálam o detectará este increment o y reducirá la producció n de TRH y. por consiguie nte, el nivel endógeno de hormonas tiroideas descender á.


UN PACTO CON EL DIABLO


Si sois inteligen tes, comprende réis las consecuen cias que el consumo de hormonas tiroideas puede acarrear a un culturist a. En el caso de que no seáis tan inteligen tes, os las explicaré . Los culturist as utilizan las hormonas tiroideas para aumentar su ritmo metabólic o y poder, así, quemar más calorías (con la esperanza de que sea tejido adiposo, aunque no siempre es así). Este método es potencial mente útil en las ocasiones en las que el culturist a debe desprende rse de una gran cantidad de grasa en un espacio de tiempo breve a fin de presentar se a esa competici ón tan important e.
No me gustan las hormonas tiroideas por un par de razones. No cabe duda de que a corto plazo estas hormonas os harán perder grasa a una velocidad supersóni ca. No obstante, utilizarl as es como hacer un pacto con el diablo. Lo pagaréis más tarde, y con intereses . A diferenci a del eje hormonal que controla la producció n de andrógeno s. el eje que controla la producció n de hormonas tiroideas no es tan piadoso. Por lo tanto, si una persona utiliza una cantidad excesiva de sustancia s tiroideas durante un espacio prolongad o de tiempo, su cuerpo reducirá o detendrá de manera definitiv a su producció n. Deberá seguir tratamien to médico el resto de su vida.
Los culturist as que utilizan hormonas tiroideas suelen tener un aspecto fantástic o el día de la competici ón, pero al cabo de un mes ganan entré 10 y 15 kilos de grasa. Tenedlo presente: el exceso de hormonas tiroideas aumenta el ritmo metabólic o basal, pero también ocurre lo contrario; el déficit de estas hormonas reducirá en gran medida el ritmo metabólic o. Cuando los culturist as abandonen los preparado s tiroideos, sufrirán hipotiroi dismo de manera temporal (con un poco de suerte). Su glándula tiroides no secretará la suficient e cantidad de hormonas para mantener un ritmo metabólic o elevado. Tienen dos opciones: comer de manera normal y ponerse como un elefante o morirse de hambre y no engordar.


Manteneos alejados de estas sustancia s y eliminad el exceso de grasa mediante la dieta y el entrenami ento adecuados .
¿Recordáis que he mencionad o que las hormonas tiroideas causan cambios en la función cardiaca? Bueno, un exceso de este tipo de hormonas puede provocar una enfermeda d denominad a tormenta tiroidea, que puede ser fatal si no se trata de inmediato . Entre los efectos secundari os que se derivan del consumo de estas sustancia s destacan la taquicard ia, dolor anginoso, temblores, nerviosis mo, insomnio, hiperterm ia, intoleran cia al calor y sudor profuso. Si una persona necesita estar fantástic a una o dos semanas al año y no le importa el aspecto que pueda tener el resto del tiempo, las hormonas tiroideas podrían constitui r una opción aceptable . Si yo deseara tener buen aspecto todo el año, no tocaría esos fármacos.
Existe todo tipo de mediación tiroidea. La que se utiliza con más frecuenci a en Estados Unidos son Cytomel (liotironi na que se presenta en comprimid os de 5 y 25 microgram os), Synthroid (comprimid os de 50 a 500 microgram os de levotirox ina) y Thyolar (liotrix presentad o en comprimid os de 60 microgram os en una proporció n de T4 y T3 de 4:1). Existe un fármaco en Europa denominad o Triacana que es casi una sustancia tiroidea, un derivado de la liotironi na con algunas diferenci as en los aminoácid os que lo distingue n del resto de preparado s tiroideos y que, en principio, no es tan perjudici al para el eje hormonal. No he visto nunca Triacana, así que supongo que su disponibi lidad es bastante reducida.
Si me decidiera a utilizar un fármaco tiroideo para perder grasa, lo más probable es que optara por Cytomel (comprimid os de liotironi na), pues es el que posee una acción más breve. Seguramen te no tomaría más de entre 15 y 25 microgram os diarios y no durante largo tiempo —como mucho, 21 días—. Es posible que muchos culturist as se mofen de mi precaució n. He oído decir que algunos insensato s toman la friolera de 400 microgram os de Cytomel diarios durante varias semanas. Todos ellos, sin excepcion es, han experimen tado efectos secundari os graves. Otros culturist as os dirán que no podréis perder grasa a menos que toméis más de 50 microgram os diarios, pero muchos de ellos han estado tomando estas sustancia s de manera ininterru mpida durante varios años. Observad lo que les ocurrirá cuando las abandonen, si es que las abandonan . Conozco a una mujer que fue reina del fitness y que decidió dejar de utilizar estas sustancia s. En poco menos de tres meses pasó de pesar unos esbeltos 55 kilos a unos fofos 82. Estaba horrorosa . Os garantizo que no volveréis a ver en un escenario a una estrella que era conocida en todo este país. Su eje hormonal sufrió tal alteració n que ni siquiera logró perder la grasa que había ganado recurrien do de nuevo a los preparado s tiroideos .
He aquí otros hechos que no deben olvidarse . Los fármacos tiroideos elevan el ritmo metabólic o basal y, por lo tanto, la temperatu ra corporal. Cualquier persona que utilice estas sustancia s tendrá un aspecto sudoroso y sentirá calor. Por cada grado Fahrenhei t que se eleve la temperatu ra corporal normal, quemaréis un 7% más de calorías de lo habitual a fin de producir este exceso de energía calorífic a. Si seguís una dieta de 3.000 calorías diarias, sólo quemaréis 210 calorías más cada día (o poco menos de 225 gramos de grasa por semana). Si creéis que podéis elevar hasta ese punto vuestra temperatu ra corporal mediante los fármacos tiroideos, estáis equivocad os. Necesitái s una cantidad significa tiva para experimen tar un ascenso de apenas uno o dos grados. Aumentad la cantidad de estas sustancia s y sufriréis unos efectos secundari os que no os gustarán. Y ese aumento de la temperatu ra os hará sentir fatal, como si tuvierais la gripe. Probablem ente, lo mejor es que os mantengái s alejados de estas sustancia s y eliminéis el exceso de grasa mediante la dieta y el entrenami ento adecuados . El riesgo que represent a utilizar hormonas tiroideas (junto con otras sustancia s para perder peso, como la dexfenflu ramina, la fentermin a, la fenilprop anolamina , el dinitrofe nol y el clenbuter ol) no compensa los resultado s. Hacer un pacto con el diablo tiroideo os podría costar vuestra alma culturist a.

Como apunte indicar que el clenbuter ol puede ser util en el primer caso mencionad o porque regula los niveles de T3 a la baja, cosa que suele soluciona rse con taurina.

Yo en principio el tiroides ni tocarlo.

Te has mirado la tiroides y esta todo en orden? a mi me da miedo tocarmela . Me viene grande el jugar con hormonas tiroideas .

Si esta todo OK.

Yo he leido articulos que hablan de esto, de usar GH, insulina y hormona tiroidea, por lo que he leido se ve que es la mejor combinaci on posible en lo que a ciclos se refiere, la T4 se usa para evitar coger el poco de grasa que te da la insulina.


saludos