T-3 with IGF-1/MGF

  1. T-3 with IGF-1/MGF


    I have read many threads on the controversy between T-3 and T-4....it seems that it is better off to use t-3. I'm looking for a good stack to run between my anabolic cycles.

    T-3 seems to be superior to clen as it burns fat and helps build muscle

    If taking IGF (3x per week 40/40 pwo) and MGF (2x per week 100mcg) for 4 week intervals with 8+ weeks off...what would a good T-3 dosing schedule look like?

    I don't want to go above 50mcg...

    And how long is an effective run compared to clen which is only good for about 2 weeks...


  2. how about neither.

    i have done t3 and t4 and don't understand why everyone thinks they are so important when using igf or gh. honestly, without alot of gear you really risk burning muscle and feeling lethargic.

    i thought t4 diminished the effects of igf when i used it. this thyroid stuff is over-hyped.

    you can take ketotifen at night and keep on using clen for several weeks. albuterol works good to.

    i found that mgf made me cut up, so you might not need to even mess with those. i'm not gonna rave about mgf, but one thing it did do was get me ripped when i was not eating super clean or doing alot of cardio. i dunno through what mechanism it did this, but it did rip me up.
    •   
       


  3. Quote Originally Posted by NattyNow
    how about neither.

    i have done t3 and t4 and don't understand why everyone thinks they are so important when using igf or gh. honestly, without alot of gear you really risk burning muscle and feeling lethargic.

    i thought t4 diminished the effects of igf when i used it. this thyroid stuff is over-hyped.

    you can take ketotifen at night and keep on using clen for several weeks. albuterol works good to.

    i found that mgf made me cut up, so you might not need to even mess with those. i'm not gonna rave about mgf, but one thing it did do was get me ripped when i was not eating super clean or doing alot of cardio. i dunno through what mechanism it did this, but it did rip me up.
    well what i would really like to do is run a long winter bulker with igf/mgf right before the cycle and then again in pct and then in that 15-20 week layoff take some t-3 like 3 weeks on/3 weeks off

  4. t3/t4 are needed more for GH than IGF.

  5. Quote Originally Posted by parttimer
    t3/t4 are needed more for GH than IGF.
    yea i figured that...i wasnt looking for a synergistic thing...i have a good cheap source for t-3 so i wanted to add it to my arsenal if it could bring a lot of positive effects....aka fat loss and muscle gain....
    •   
       


  6. Maybe some fatloss but probably not as good at clen or clen/t3 combo.

  7. your saying that clen is better for fatloss than t-3? I've always heard the opposite

    Plus many people claim T-3 can be anabolic...unlike clen...

  8. t3 will increase muscle turnover. if you are in alot of gear then it might help your body utilize more of the gear. your post seems to indicate you want to use it at a time when you are going clean. i think that is a terrible idea. i am not repeating what i've read or anything... i've done t3 in different situations, and never felt it did any good when i was on very little assistance or totally clean.

  9. Quote Originally Posted by NattyNow
    t3 will increase muscle turnover. if you are in alot of gear then it might help your body utilize more of the gear. your post seems to indicate you want to use it at a time when you are going clean. i think that is a terrible idea. i am not repeating what i've read or anything... i've done t3 in different situations, and never felt it did any good when i was on very little assistance or totally clean.
    ok so i'll try it in the last few weeks of my upcoming cycle..thanks!

  10. How T3 works and its negative effects on Muscle

    --------------------------------------------------------------------------------

    The Problem with T3

    For a long time we have known that thyroid hormones played a role in gene transcription during myoblast proliferation and differentiation. The regulation of gene expression by thyroid hormone (T3) involves binding of the hormone to nuclear receptors [thyroid hormone receptor (TR)] acting as T3-dependent transcription factors encoded by TRalpha (NR1A1) and TRbeta (NR1A2) genes. This in turn leads to the desired increase in the SERCA1 and SERCA2a mRNA proteins we all want because these cod for the Ca++ pumps on the muscle cell that cause use to burn extra calories through increased active Ca++ transport. However new research in spring 2006 revealed an regulatory mechanism that might not make you so happy. In this study, they identified another transcript, TRalpha-DeltaE6, produced by alternative splicing with microexon 6b instead of exon 6. This splicing leads to the synthesis of a protein devoid of a hinge domain. And what this new factor was found to be responsible for was that although TRalpha-DeltaE6 did not bind DNA, its expression induced a TRalpha1 sequestration in the cytoplasm. Functional studies demonstrated that TRalpha-DeltaE6 inhibits the transcriptional activity of TRalpha1 and retinoic X receptor-alpha, but not of retinoic acid receptor-alpha. We also found that TRalpha-DeltaE6 efficiently decreased the ability of TRalpha to inhibit MyoD transcriptional activity during myoblast proliferation. Consequently, when overexpressed (like when people take synthetic T3) in myoblasts, it stimulated terminal differentiation. This suggest that TRalpha-DeltaE6 may act as down regulator of overall T3 receptor activity, including its ability to repress MyoD transcriptional activity during myoblast proliferation.

    OK what did I just say????
    By taking T3 you basically up regulate a regulatory mechanism that regulates the effect of T3 not by effecting the adult muscle cells, but it actually kills off you muscle stem cells before they have a chance to join with the adult muscle cell. These are the same cells that MGF and IGF and anabolic steroids increase, and are the same cells that your body recruits for growth and repair.

    In addition say you take MGF, and IGF, and anabolic steroids with your T3 to try and combat this effect. (btw I have no research to suggest these would significantly help the situation and people that say they lose less by using them may be an alternative mechanism etc. so you still might be losing the effect of recruitment of muscle stem cells)
    T3 up regulates these SERCA1 proteins right. Here is a question that always bothered me, because these proteins have a long half life and t3 itself isn’t increasing your metabolism like a stimulant… you shouldn’t need to slowly come off it. It should be that the slow loss of the CA++ pumps would serve as a slow decline on its own. Here in lies the other problem. Your body responds to up regulated SERCA1 proteins with another group of hormones to catabolize them. Corticosteroids!!! Like the all famous cortisol.
    This is done in part by the corticosteroids causing an increase in sarcolipin mRNA which decrease the activity of the SERCA1 pumps. So not only are you losing the energy burning pumps after you come off t3, you are decreasing the effectiveness and levels of the ones you naturally would have and your increasing corticosteroid levels. That makes for a hell of a rebound effects….

    So how do I cut then???
    Here is an idea.
    If you use T4 you are going to have a small conversion to T3, and reduce the negative effects. If you use HGH in with your T4 they will synergistically benefit you and HGH will help reduce the increase in cortisol through negative feedback. Then after you or towards the end of you T4 cycle you should add IGF. This increases the half-life of the SERCA1 proteins making them last longer so there is no fall off effect. If you are going to use T3 I recommend all the above and staying at a low dose as well as adding a cortisol blocker at the end. T3 with a cortisol blocker should have a synergistic effect due to increased SERCA1 activity which means more energy burning.

    To be safe you are best not using T3 if you are competitive athlete who depends on performance and can not afford loss of strength or increased risk of injury.

    But I will add some more information for those still considering the compound.

    How does T3 actually work, here is the non science definition

    T3 increases you metabolism by causing your muscle to use more atp to maintain proper calcium levels. It does this by increasing the number of calcium pumps on the surface of your muscle cells. Because of the change in Calcium levels in the muscle it actually puts your muscles in a more relaxed state. This may atribute to the sudden loss of strength some users see while taking T3.
    There are no current studies that indicate long term use of T3 results in the permant shut down of the thyroid. However long term use is deterimental for the muscle tissue. T3 can cause protein loss and decreases myotuble formation. Long term use can also result in a rebound effect where a user gains more fat afterwards because it take the body longer to return to its normal basal metabolic rate.

    T3 with IGF-I not only increases these effects but prolongs the effect.

    The in dept process
    Thyroid hormone (L-tri-iodothyronine; T3) has major effects
    on Ca2l homeostasis in heart and skeletal muscle [1,2]. One of the
    most striking effects is the increased speed of muscle relaxation
    in hyperthyroidism and the decreased relaxation rate in
    hypothyroidism [3-6]. In the last decade it has become clear
    through work by ourselves and others that T3-dependent changes
    in the sarcoplasmic reticulum (SR) underlie these phenomena. T3
    administration in vivo causes an increase of the amounts of Ca21
    pumps (Ca2+-ATPase) and SR, thereby increasing the rate of
    Ca2+ removal from the sarcoplasma as well as the capacity for
    Ca2+ storage [7-11]. As a consequence of the increased Ca2+
    release and re-uptake (Ca2+ cycling) the metabolic rate is
    stimulated in skeletal muscle by consuming more ATP, which
    contributes to the well known thermogenic effect of thyroid
    hormone
    This process works continuously because the cell has Ca++ channels that operate solely on the concetratoin gradient. There fore the result is a faster cycleing of Ca++ in and out of the cell.
    Thyroid hormone (T3) is a major determinant of the fast-type
    sarcoplasmic-reticulum Ca2+-ATPase (SERCAl) level in skeletal
    muscle [1-4]. This Ca2+-transporting protein is responsible for
    the removal of Ca2+ from the cytosol during a contractionrelaxation
    cycle. The T3-induced increase in SERCAl expression
    is mainly responsible for the enhanced muscle relaxation rate
    which is characteristic of the hyperthyroid status [5-7]. Evidence
    that T3 regulates SERCAI expression in vivo at least partly at a
    pre-translational level was provided in one of our previous
    studies, in which it was shown that T3increases SERCAI mRNA
    levels in rat soleus and extensor digitorum longus muscle


    More in depth on the IGF synergy
    T3 administration in vivo causes an increase of the amounts of Ca21
    pumps (Ca2+-ATPase) and SR (sarcoplasimic reticulum), thereby increasing the rate of Ca2+ removal from the sarcoplasma as well as the capacity for Ca2+ storage. The muscle cell has natural calcium channels that Ca2+ can flow through according to the gradient requiring no energy expenditure. As a consequence of the increased Ca2+ release and re-uptake (Ca2+ cycling) the metabolic rate is stimulated in skeletal muscle by consuming more ATP to run the pumps, which contributes to the well known thermogenic effect of thyroid hormone. T3’s mechanism of action occurs at the nuclear level upregulating the transcription of the mRNA’s for these [email protected]= ATPase’s. IGF-I assist in the maturation of the SR where these pumps are located on the cell. It has alsop been reported that through an insulin like mechanism the IGF actually increases the stability of the mRNA. A quote from research:
    “The SERCAI mRNA (the discussed above) half-life was twice as long in IGF-I + T3-treated cultures
    compared with T3-treated cultures, which is in reasonable agreement
    with the 1.6-fold greater increase in the SERCAI mRNA
    levels by IGF-I + T3 compared with T3. T3 or IGF-I alone did not
    affect the SERCAI mRNA half-life, which indicates that both T3
    and IGF-I are involved in the process leading to the T3 + IGF-I
    induced increase in SERCA1 mRNA stability

  11. Great post. rep points for you of course.

    i don't want to ever take HGH...and now from reading i guess i should steer clear of T-3..

    However, Do you suggest I take T-4 for 3 weeks followed by the IGF/MGF stack? I'm not sure if i read this correctly..

  12. Quote Originally Posted by Tom 185
    Great post. rep points for you of course.

    i don't want to ever take HGH...and now from reading i guess i should steer clear of T-3..

    However, Do you suggest I take T-4 for 3 weeks followed by the IGF/MGF stack? I'm not sure if i read this correctly..
    YES

  13. What is a good dosage and length for T-4?

  14. Quote Originally Posted by Tom 185
    What is a good dosage and length for T-4?
    well 200mcg of t4 =50mcg of t3 and your body makes about 25mcg naturaly a day[t3]

  15. Quote Originally Posted by skull
    well 200mcg of t4 =50mcg of t3 and your body makes about 25mcg naturaly a day[t3]
    how is this?

    week 1: 100mcg
    week 2: 150mcg
    week 3: 200mcg
    week 4: 150mcg
    week 5: 100mcg

    5 weeks too much?

  16. From what I have read, T4 can be used for longer periods. I do believe that the half life is somewhat longer than that of T3. I think the best thing for you to do would be to get in touch with Dr. D. He has been using synthetic T4 for over a decade if I remember correctly.

  17. Quote Originally Posted by Jared
    From what I have read, T4 can be used for longer periods. I do believe that the half life is somewhat longer than that of T3. I think the best thing for you to do would be to get in touch with Dr. D. He has been using synthetic T4 for over a decade if I remember correctly.
    I agree

  18. i can't PM so i dont know how i will get in touch...hope he sees this....?

  19. He does frequent another board where he has his own sub-forum to answer questions. This board has a lot of thyroid drug information as well. IBE is the name of the company operating this board.

  20. Quote Originally Posted by Jared
    He does frequent another board where he has his own sub-forum to answer questions. This board has a lot of thyroid drug information as well. IBE is the name of the company operating this board.
    gotcha thanks...i check there every once in a while as i am a member there too...
  •   

      
     

Similar Forum Threads

  1. Interesting finds with IGF-lr3 & peg-MGF.....my take
    By Distilled Water in forum IGF-1/GH
    Replies: 6
    Last Post: 03-22-2009, 04:05 PM
  2. Replies: 48
    Last Post: 04-18-2008, 08:57 PM
  3. Should i go with IGF or MGF?
    By NPCout in forum IGF-1/GH
    Replies: 6
    Last Post: 05-11-2007, 04:35 PM
  4. Replies: 6
    Last Post: 11-27-2006, 12:45 AM
  5. Cutting with IGF?
    By Kitchen Chemist in forum IGF-1/GH
    Replies: 11
    Last Post: 03-16-2004, 01:19 PM
Log in
Log in