Cycle Advice T3 T4 Clen

cryptonakias54

Greenlighter
Joined
Feb 9, 2019
Messages
12
What you believe is the best option to run t3
T3 only; t3 with t4 ;
Ofcource aas and clen together
Clen with eca same day or only 2 week on off ;
 
Last edited by a moderator:
T3 on its own with clen cycled 2 weeks on and 2 weeks of to upregulate receptors again unless you using ketotifen which will help with regards to receptor down regulations. And a aas is a must with t3 as it will burn fat and muscle for an energy source.
 
T3 jacks my appetite up so much I cant use it but damn it is a wonder drug. Last show I won my class on a 4 week prep thanks to T3 haha.

Now I just use T4 as it keeps things moving but not as much as T3.

Personally I think clen is a garbage fat burner and extremely overrated in that department. It is a phenomenal diuretic, however, so I just start it 3-5 days out and watch 3-5lbs of water drop off
 
What dosages are you looking at using bud. And what aas are you gonna use. You mind maybe giving us a breakdown of the cycle in mind
 
Clen makes me super anxious and doesn't work particularly well.

Never tried T3/T4.

Tren + var (assuming you get the real thing....) + low dose test work really well for me without many side effects. 600 mg + tren e (hate a because I feel like a pincushion while you can easily inject tren e e3d or 2 per week + the concentrations are higher so the total volume injected is lower + e and a cost about the same per vial but a usually comes as 100 mg/ml while e is 200 mg/ml ) pw (I assume you hit diminishing returns sooner or later but for me the limit was always price), 50-100 mg var ed (imo 150 mg is too much and will screw your lipids too much to be worth it) and ~ 200 mg test e/c/d (whichever is cheapest) pw. The test is there only to replace your natural test so 200 mg pw is plenty (and you could probably go even a bit lower). High test + high tren gives me too many side effects to be worth it (basically all the tren sides), low test + high tren just gives me slight insomnia, a slight loss in cv performance and makes me a bit more sensitive to bullshit. The only noticeable sides from the var are crazy calf pumps, but it does screw with your lipids so taking it too long/often/at too high doses is probably a bad idea. You probably won't need an ai or dopamine agonist, but having some on hand just in case is a good idea (although I admit I never had nor needed any dopamine agonists, and had some letro just in case and took ~ 1.5 mg pw (hard to split a 2.5 mg pill accurately enough to get exactly 1.5 mg). Test and tren for 12 weeks, var for the last 8 (I prefer taking orals after the injectables hit since this gives better strength gains).
 
What you believe is the best option to run t3
T3 only; t3 with t4 ;
Of course aas and clen together
Clen with eca same day or only 2 week on off ;


This is very individual but let's consider that The average person has basal levels of:
75mcg T4
25mcg T3
It's Very Important to Keep this Ratio to avoid countermeasures and also to experience maximized Anabolism..

Clen has always seemed pretty weak as opposed to just restricting calories or increasing metabolic rate... Where I've found it has a use is the last few weeks pre-comp when everything else is dialled in, it can just add that extra boost..

ECA has always seemed fine for a couple of days then effects wear off (at least they do for me)..
 
Something regards T3, T4, and also its interaction with hGH:

Your thyroid gland secretes two hormones that are going to be of primary importance in understanding Thyroid/GH interaction. The first is thyroxine (T4) and the second is triiodothyronine (T3). T3 is frequently considered the physiologically active hormone, and consequently the one on which most athletes and bodybuilders focus their energies on. T4, on the other hand, is converted in peripheral tissue into T3 by the enzymes in the deiodinase group, of which there are three types- the three iodothyronine deiodinase either catalyze the initiation (D1, D2) or termination (D3) of thyroid hormone effects. The majority of the body?s T3 (about 80%) comes from this conversion via the first two types of deiodinase, while conversion to an inactive state is accomplished by the third type.

It's important to note that not all of the body's T4 is converted to T3, however- some remains unconverted. 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 your hypothalamus. So, when T3 levels go up, TSH secretion is suppressed, due to the body's self regulatory system known as the negative feedback loop . This is also the mechanism whereby exogenous thyroid hormone suppresses natural thyroid hormone production. However, it should be noted that thyroid stimulating 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 physiological effect (ibid).

Most people think that T3 is just a physiologically active hormone that regulates body fat 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 proliferation of IGF-1 mRNA in many tissues (which would, of course, be anabolic), or it could be due to the synergistic effect T3 has on GH, specifically on regulation of the growth hormone gene. Although it is largely overlooked in the world of performance enhancement, regulation of the growth hormone response is predominantly determined by positive control of growth hormone gene transcription which is proportional to the concentration of thyroid hormone-receptor complexes, which are influenced by T3 levels. (3)


At this point, just to give you a better understanding of what's going on, I think it's prudent to also give a brief explanation 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 hypothalamus with somatostatin (SS) and growth hormone-releasing hormone (GHRH). Somatostatin 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 deficiency presents with a low level of T3, and normal T4(4). This is of course because conversion of T4-T3 is partially dependant on GH (and to some degree GH stimulated IGF-1), and it's ability to stimulate that conversion process of T4 into T3.

Interestingly, the hypothalamus isn't the only place where SS is contained; the thyroid gland also contains Somatostatin-producing cells. This is of interest to us, because in the case of the thyroid, it's been noted that certain hormones which were previously 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 hypothalamus to inhibit TRH secretion. So when you add GH into your body from an outside source, you are triggering the body into releasing SS, because your body no longer needs to produce its own supply of GH and unfortunately, the release of SS can also inhibit TSH, and therefore limit the amount of T4 your body produces.


But that's not the only interaction we see between the thyroid and Growth Hormone.

As we learned in high-school Biology class, the body likes to maintain homeostasis, or normal operating conditions. This is the body's version of the status quo, and it fights like hell to maintain the comfort of the status quo. What we see with thyroid/GH interplay is that physiological levels of circulating thyroid hormones are necessary to maintain normal pituitary GH secretion, due to their directly stimulatory actions. However, when serum concentrations of thyroid hormone increase above the normal range we see an increase in hypothalamic somatostatin action, which suppresses pituitary GH secretion and overrides any stimulatory effects that the thyroid hormone may have had on GH. The suppression of GH secretion by thyroid hormones is probably mediated at the hypothalamic level by a decrease in GHRH release (5).

In addition, as IGF-I production is increased in the hypothalamus after T3 administration and T3 may participate in IGF-1 mediated negative feedback of GH by triggering either increased somatostatin tone and/or decreased GHRH production (6). IGF, interestingly, has the ability to mediate some of T3's effects independent of GH, but not to the same degree GH can (7.) In fact, IGF-I production is increased in the hypothalamus after T3, administration it may plausibly participate in negative feedback by triggering either increased somatostatin tone and/or decreased GHRH production.So we know that GH lowers T4, but an increase in T3 upregulates GH receptors (8) as well as IGF-1 receptors (9,10).

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

hGH converts inactive T4 into active T3

Interaction between GH, IGF-I, T3, and GC. GH stimulates hepatic IGF-I secretion and local production of growth plate IGF-I, and exerts direct actions in the growth plate. Circulating T3 is derived from the thyroid gland and by enzymatic deiodination of T4 in liver and kidney.. The regulatory 5′-DI and 11-HSD type 2 enzymes may also be expressed in chondrocytes to control local supplies of intracellular T3 and GC. Receptors for each hormone (GHR, IGF-IR, TR, GR) are expressed in growth plate chondrocytes.

So, with the use of GH, what we see is an increased conversion of T4-T3, and possible inhibition of Thyroid Releasing Hormone by Somatostatin, 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 synergistic with T3 in the body, and as a mater of fact, 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 mechanisms, including (but not limited to): increasing IGF-1 levels, IGF-1 mRNA levels, and finally by actually mediating the control of the growth hormone gene transcription process as seen below:

Comparison of the kinetics of L-T3-receptor binding abundance to changes in the rate of transcription of the GH gene.(3)

As you can see, T3 levels are directly correlative to GH gene transcription. The scientists who conducted the study concluded that the amount of T3 present is a regulatory factor on how much GH gene transcription actually occurs. And gene transcription 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 supraphysiological if we're going to be using supraphysiological levels of GH.. 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 converting more T4 into T3, T4 levels are lowered substantially, 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 specifically 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.

You see, 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.).

Originally, it was thought that T3 was synergistic with GH, whereas it was also thought that T3 actually reduced the anabolic effects of GH- now both options were correct. Logically this presents a bit of a problem, which can be solved. This came from several studies: the trend was that even when Growth Hormone therapy was used, T3 levels needed to be elevated in order to treat several conditions 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 was noticed was that those levels were elevated successfully by using supplemental T4 but not T3.

Here's why:

Additional T3 is not all that's needed here. What's needed is the actual conversion process of T4-T3, and the deiodinase presence and activity that it involves. This is because Local 5′-deiodination of l-thyroxine (T4) to active the thyroid hormone 3,3′,5-triiodothyronine (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) deiodinase, but more of the D3 type, which signals the cessation of the T4-T3 conversion process, and is inhibitory of many of the synergistic effects that T3 has!

Remember, Type 3 iodothyronine deiodinase (D3) is the physiologic INACTIVATOR of thyroid hormones and their effects (13)and is well known to have independent interaction with growth factors (which is what GH and IGF-1 are).(14) This is because with adequate T4 and excess T3, (D1 and D2) deiodinase is no longer needed for conversion of T4 into T3, but levels of D3 deiodinase will be elevated. When there is less of the first two types of deiodinase, 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 responsible for mediation of many of the effects T3 has on the body. This seems to be one of the ways deiodinase contributes to anabolism in the presence of other hormones.

All of this would explain why anecdotally we see bodybuilders 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 simultaneously signaling the body to produce an inhibitory enzyme (D3). And remember, for decades bodybuilders 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 conversion process, it would clearly be less effective! Since the deiodinase 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 inhibitory effects, but in the absence of the effects of the first two deiodinase enzymes, it remains unchecked and therefore not only limits the GH's nitrogen retention capability.

In other words, if we have enough to GH in our body aid in supraphysiological conversion of T4 into T3, but we already have the too much (exogenous) T3, the GH is not going to be converting 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 stimulates proliferation, whereas T3 is responsible for hypertrophic differentiation. So it would seem that in some tissues, IGF-1 stimulates the synthesis of new cells, while T3 makes them larger. In this particular case, The fact that T4 and (D1) deiodinase is an active component in this system. T4 is is converted to T3 by deiodinase (5′-DI type 1) in peripheral tissues [furthermore] GH stimulates conversion of T4 to T3 , suggesting that some effects of GH may involve this pathway.? The thing to notice is that the authors of this paper state that the that the conversion PATHWAY is probably involved, and not the simple presence of T3. (15 )

Also, that same study notes that T3 has the ability to stimulates IGF-I and expression in tissues that whereas GH has no such effect (ibid).

So what are we doing when we add T3 to GH? We're effectively shutting down the conversion pathway that is responsible for some of GH's effects! And what would we be doing if we added in T4 instead of T3.. You got it- we'd be enhancing the pathway by allowing the GH we're using to have more T4 to convert to T3, thus giving us more of an effect from the GH we're taking. Adding T4 into our GH cycles will actually allow more of the GH to be used effectively!

Remember, the thing that catalyzes the conversion process is the deiodinase enzyme. This is also why using low amounts of T3 would seem (again, anecdotally in bodybuilders) to be able to slightly increase protein synthesis and have an anabolic effect ? they aren't using enough to tell the body to stop or slow down production of the deiodinase enzyme, and hence .Although this analogy isn?t perfect, think of GH as a supercharger you have attached to your car if you don't provide enough fuel for it to burn at it?s increased output level, you aren't going to derive the full effects. Thyroid status also may influence IGF-I expression in tissues other than the liver.So what we have here is a problem. When we take GH, it lowers T3 levels but we need T3 to keep our GH receptor levels optimally upregulated. In addition, it's suspected that many of GH's anabolic effects are engendered as a result of production of IGF-1, so keeping our IGF receptors upregulated by maintaining adequate levels of T3 seems prudent. But as we've just seen, supplementing T3 with our GH will abolish Growth Hormone?s functional hepatic nitrogen clearance, possibly through the effect of reducing the bioavailability of insulin-like growth factor-I (12.)

So we want elevated T3 levels when we take GH, or we won't be getting ANYWHERE NEAR the full anabolic effect of our injectable GH without enough T3. And now we know that not only do we need the additional T3, but we actually want the CONVERSION process of T4 into T3 to take place, because it's the presence of those mediator enzymes that will allow the T3 to be synergistic with GH, instead of being inhibitory as is seen when T3 is simply added to a GH cycle. And remember, we don't only want T3 levels high, but we want types 1 and 2 deiodinase to get us there- and when we take supplemental T3, that just doesn't happen all that happens is the type 3 deiodinase enzyme shows up and negates the beneficial effects of the T3 when we combine it with GH.



If you?ve been using GH without T4, you've been wasting half your money and if you've been using it with T3, you've been wasting your time. Start using T4 with your GH, and you'll finally be getting the full results from your investment.


References:

Growth Factors. 1990;2(2-3):99-109.Interaction of TSH, insulin and insulin-like growth factors in regulating thyroid growth and function. Eggo MC, Bachrach LK, Burrow GN.

F, Rumpler M, Klaushofer K 1994 Thyroid hormones increase insulin-like growth factor mRNA levels in the clonal osteoblastic cell line MC3T3- E1. FEBS Lett 345: 67?70

Relationship of the rate of transcription to the level of nuclear thyroid hormone-receptor complexes.J Biol Chem. 1984 May 25;259(10):6284-91. Yaffe BM, Samuels HH.

Thyroid morphology and function in adults with untreated isolated growth hormone deficiency. J Clin Endocrinol Metab. 2006 Mar;91(3):860-4. Epub 2006 Jan 4.

Eur J Endocrinol.1995 Dec;133(6):646-53.Influence of thyroid hormones on the regulation of growth hormone secretion. Giustina A, Wehrenberg WB.

Binoux M, Faivre-Bauman A, Lassarre C, Tixier-Vidal A 1985 Triiodothyronine stimulates the production of insulin-like growth factor I (IGF-I) by fetal hypothalamus cells cultured in serum free medium. Dev Brain Res 21:319?323

Eur J Endocrinol. 1996 May;134(5):563-7.Insulin-like growth factor I alters peripheral thyroid hormone metabolism in humans: comparison with growth hormone.Hussain MA, Schmitz O, Jorgensen JO, Christiansen JS, Weeke J, Schmid C, Froesch ER

Harakawa S, Yamashita S, Tobinaga T, Matsuo K, Hirayu H, Izumi M, Nagataki S, Melmed S. In vivo regulation of hepatic insulin-like growth factor-1 messenger ribonucleic acids with thyroid hormone. Endocrinol Jpn 37(2):205-11, 1990

Hochberg Z, Bick T, Harel Z Alterations of human growth hormone binding by rat liver membranes during hypo- and hyperthyroidism. Endocrinology 126(1):325-9, 1990

Matsuo K, Yamashita S, Niwa M, Kurihara M, Harakawa S, Izumi M, Nagataki S, Melmed S Thyroid hormone regulates rat pituitary insulin-like growth factor-I receptors. Endocrinology 126(1):550-4, 1990

The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 11 5221-5226, 2003. High Dose Growth Hormone Exerts an Anabolic Effect at Rest and during Exercise in Endurance-Trained Athletes M. L. Healy, J. Gibney, D. L. Russell-Jones, C. Pentecost, P. Croos, P. H. S?nksen and A. M. Umpleby

J Hepatol. 1996 Mar;24(3):313-9. Effects of long-term growth hormone (GH) and triiodothyronine (T3) administration on functional hepatic nitrogen clearance in normal man.Wolthers T, Grofte T, Moller N, Vilstrup H, Jorgensen JO

Huang, SA. Physiology and pathophysiology of type 3 deiodinase in humans. Thyroid. 2005 Aug;15(8):875-81. Review.

Hernandez. A. Structure and function of the type 3 deiodinase gene.Thyroid. 2005 Aug;15(8):865-74. Review.

F, Rumpler M, Klaushofer K 1994 Thyroid hormones increase insulin-like growth factor mRNA levels in the clonal osteoblastic cell line MC3T3- E1. FEBS Lett 345: 67?70
 
I just want to also add. If you have high thyroid levels you will get an enlarged spleen and a good RBC bump from it. so be careful not to over do it
 
Top