NEW: ALPHA-T2 (90 capsules)

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  1. Gotta bump the coupon code thread

    Who doesnt like coupons?
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  2. Quote Originally Posted by nattydisaster View Post
    Gotta bump the coupon code thread

    Who doesnt like coupons?
    Jenga...Jenga
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  3. Quote Originally Posted by ax1 View Post
    but this is a HCI version, is it more potent than alpha-burn?

    also alpha-burn is standardized, Rauwolfia Serpentina (standarized for 30% Rauwolscine) 30mg, so if i got this correct it should be 9mg of pure rauwolscine per cap. lets keep in mind it also has the black pepper extract which is supposed to enhance absorption i believe.

    is the one in alpha-t2 standardized in any way? whats with this HCI version?
    Alkaloids from Rauvolfia canescens
    Indole alkaloids


    ajmaline
    yohimbine
    a-yohimbine
    isoreserpine
    corynanthine
    deserpidine
    reserpiline
    isoreserpiline
    aricine
    lankanescine


    Bauhinia purpurea – An ornamental tree with orchid-like flowers, Bauhinia purpurea is native to India and Southeast Asia. It’s also called “butterfly tree” because of its twin lobed leaves. Bauhinia purpurea extract is made from the gum of the bark and is used for medicinal purposes. Animal studies have shown that when combined with Ashwaganda root extract, it supports the healthy regulation of the thyroid hormone.
    so i think OEP is really mighty

  4. Quote Originally Posted by nattydisaster View Post
    Yup! 3 perfect ingredients working together.

    An alpha-2-receptor inhibitor, beta 3 agonist, and the 3,3-T2. Very stackable as well
    Can you point me to the research that shows that methyl-syneprhine is a beta-3 agonist?

    And your write up lists two references that support 3,5-T2, not 3,3. 3,3-T2 has very little evidence of efficacy, unlike 3,5-T2.

  5. Quote Originally Posted by micro2000 View Post
    Can you point me to the research that shows that methyl-syneprhine is a beta-3 agonist?

    And your write up lists two references that support 3,5-T2, not 3,3. 3,3-T2 has very little evidence of efficacy, unlike 3,5-T2.
    The studies both talk about 3,3-T2 as well, and both state the effects of 3,3-T2 and the fact it does not shut down TSH.

    Here is a pharmacology report on MS

    Quote Originally Posted by quote View Post
    Methylsynephrine


    Methylsynephrine
    Methylsynephrine (Oxilofrine, Hydroxyephrine, Oxyephrine) is a mixed-adrenergic agonist with an ephedrine-like pharmacological profile. It is used as a dietary supplement in various products and is marketed as a weight-loss compound. Here, I will explore the nature of this compound in the literature.

    Synephrine
    Synephrine is an adrenergic agonist similar to phenylephrine [1] . Due to its secondary terminal-amine structure, it possesses a stronger affinity for alpha-receptors than norepinephrine and has been used clinically as a vasoconstrictor and pressor (Figure 1). Synephrine is a positional-isomer of phenylephrine and its metabolism is likely similar with extensive MAO elimination in the GI tract and in the liver. Synephrine may also play a role in vesicular exchange-diffusion within synapses with norepinephrine, although this appears weak at therapeutic concentrations.


    Figure 1.



    Physiological effects
    A study using a bitter orange extract standardized for 27 mg synephrine failed to induce any changes in hemodynamics [2]. Conversely, in another study using twice the amount, significant effects were observed for heart rate, systolic pressure, and diastolic pressures, in which all values increased [3]. This would indicate that the minimum threshold dose to elicit adrenergic activity to be somewhere between 27 mg and 54 mg for adult males.

    Pharmacodynamics
    Beta-receptor affinity for phenylethylamine derivatives increases as the nonpolar bulkiness on the terminal amine gets larger (Figure 2). Compared with phenylethylamine, norepinephrine, or other primary amines, synephrine should have greater affinity for beta-receptors due to its secondary amine structure. Similarly, beta-receptor affinity also increases with the addition of nonpolar substituents on the alpha-carbon, which synephrine does not possess. The fact that diastolic pressure also increased in the above study is evidence for very little beta-receptor activation. Although synephrine has demonstrated an ability to induce lipolysis by activating beta-3 receptors en vitro, its efficiency in doing so en vivo is greatly limited because of its inherent affinity for alpha receptors [4]. The dose required to sufficiently trigger lipolysis within adipocytes would be intolerable due to its effects on hemodynamics [5].

    Figure 2.



    Synephrines downsides
    Increasing peripheral vascular resistance is a negative characteristic of a lot of stimulants and is especially exacerbated in compounds which primarily activate alpha-receptors like synephrine. Not only is the incidence of stroke and hemorrhage higher with these agents, but the work-load put on the heart can trigger ventricular fibrillations or other arrhythmias [6, 7, 8]. Using caffeine in conjunction with synephrine will potentiate the peripheral vasoconstriction by synergizing with the transduction mechanism induced by alpha-adrenergic agonism [9, 10]. Adrenergic agonists with high affinity to alpha-receptors also have the unfortunate capacity to induce platelet aggregation by agonizing alpha-2 receptors on platelets which can lead to intravascular clotting [11, 12].

    Methylsynephrine vs. Synephrine
    The primary difference between synephrine and methylsynephrine is the addition of a methyl group on the alpha carbon (Figure 3). As mentioned previously, this has extensive pharmacodynamic implications as it increases the affinity of the compound for beta-receptors.


    Figure 3.



    Pharmacokinetics
    The half-life for phenylephrine is an adequate gauge for the half-life and elimination statistics for synephrine due to its similar structure and chemical characteristics. Similarly, ephedrine and pseudoephedrine can be used to make an educated guess regarding the pharmacokinetics of methylsynephrine. Phenylephrine, a positional isomer of synephrine, has a half-life of 2.1 -3 hours. The half-life of ephedrine is from 3-6 hours, depending on urine pH. Pseudoephedrine enjoys an even longer half-life due to increased steric-hindrance of MAO. The mean half-life of methylsynephrine, as compared to synephrine, would be roughly twice the duration. Neither synephrine, ephedrine, nor methylsynephrine, possess notable central effects due to the common beta-hydroxyl which prevents substantial blood-brain-barrier permeability (Appendix A).

    Pharmacodyamics
    Although the exact pharmacology of methylsynephrine has not been studied in great detail, its pharmacodynamics can be inferred through its effects on systolic blood pressure, diastolic blood pressure, and heart rate. Differing from synephrine, methylsynephrines effects on the heart are mostly beneficial in that it increases the pulse pressure and is a positive inotrope (Appendix B). Diastolic pressure is used clinically as a diagnostic marker for peripheral vascular resistance, especially in relation to the arterial system [13]. Activating beta-2 receptors in the periphery induces vasodilation in vascular beds in the liver and skeletal muscle, which decreases the work-load on the heart. Since it also has some alpha-adrenergic activity, reflexive tachycardia would be avoided. Similarly, activating beta-receptors would increase venous tone, which will increase the amount of blood returning to the heart, and subsequently increase cardiac output, as illustrated by Starling’s Law [14, 15]. The beta-3 receptor, as noted above, directly mediates lipolysis. The genetic homology of the ligand-binding-domain between the beta-3 receptor and the beta-2 receptor is greater than that of the beta-1 receptor. This explains why norepinephrine, which possesses a primary terminal amine, has sufficient affinity for beta-1 receptors, but very little beta-2 or beta-3 affinity, and therefore limited ability to induce lipolysis. This means that compounds which significantly activate beta-2 receptors will also have great predilection to also activate beta-3 receptors.

    Physiological effects
    Methylsynephrine has been used clinically for orthostatic hypotension due to its effects on stroke volume, ejection fraction, and cardiac index [16, 17]. It has been used in doses of up to 120mg in healthy adults with no adverse effects [18, 19]. Even at this dose, diastolic pressure decreased, which is evidence for very little alpha-adrenergic activity. Furthermore, it had no effect on heart rate or mean arterial pressure. Some of methylsynephrines therapeutic efficacy is mediated by acting as a norepinephrine-releasing agent, and also by inhibiting its uptake [20]. The majority of methylsynephrines pharmacological appeal resides in its ability to activate beta receptors, which is exemplified through its effects on the heart and haemodynamics as described above. This also implies significant beta-3 activity and an ability to induce lipolysis which is consistent with some of its marketing claims [21]. Another deviation from synephrine is methylsynephrines limited propensity to activate alpha-2 receptors on platelets. This would avoid the complications of intravascular clotting, which has resulted in myocardial infarction mortality associated with synephrine, although allow for the possibility of cerebral hemorrhage [22].

    Summary
    Methylsynephrine is a unique compound which has not been used frequently in clinical practice. Due to its ephedrine-like pharmacology, and its surprisingly clean safety record, it will likely become a more common ingredient in fat loss supplements in the future. It is currently uncontrolled in the United States [23].

    Appendix A:


    Appendix B:
    Pulse Pressure (Pp) = Systolic pressure – Diastolic pressure

    Relevant links:
    PubMed Compound: http://pubchem.ncbi.nlm.nih.gov/summ...701&loc=ec_rcs
    Methylsynephrine wikipedia entry: http://en.wikipedia.org/wiki/Oxilofrine
    Mirrored site: http://www.recomp.com/wiki/index.php...ne&redirect=no


    References:
    1. http://www.ncbi.nlm.nih.gov/pubmed/19721332
    2. http://www.ncbi.nlm.nih.gov/pubmed/16305290
    3. http://www.ncbi.nlm.nih.gov/pubmed/16317106
    4. http://www.springerlink.com/content/uemq7ml1lcee6a3c/
    5. http://www.ncbi.nlm.nih.gov/pubmed/15337824
    6. http://www.ncbi.nlm.nih.gov/pubmed/20055074
    7. http://www.ncbi.nlm.nih.gov/pubmed/18700609
    8. http://www.ncbi.nlm.nih.gov/pubmed/16610576
    9. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1175678/
    10. http://www.ncbi.nlm.nih.gov/pubmed/18341680
    11. http://www.ncbi.nlm.nih.gov/pubmed/18637307
    12. http://www.ncbi.nlm.nih.gov/pubmed/20069086
    13. http://www.ncbi.nlm.nih.gov/pubmed/3229871
    14. http://www.ncbi.nlm.nih.gov/pubmed/3119915
    15. http://www.springerlink.com/content/vmw352074216g871/
    16. http://www.ncbi.nlm.nih.gov/pubmed/1530677
    17. http://www.ncbi.nlm.nih.gov/pubmed/3119915
    18. http://www.ncbi.nlm.nih.gov/pubmed/3229871?ordinalpos=1&itool=Ent rezSystem2.PEntrez.Pubmed.Pubm ed_ResultsPanel.Pubmed_SingleI temSupl.Pubmed_Discovery_RA&li nkpos=2&log$=relatedarticles&l ogdbfrom=pubmed
    19. http://www.ncbi.nlm.nih.gov/pubmed/3403107?ordinalpos=1&itool=Ent rezSystem2.PEntrez.Pubmed.Pubm ed_ResultsPanel.Pubmed_SingleI temSupl.Pubmed_Discovery_RA&li nkpos=1&log$=relatedarticles&l ogdbfrom=pubmed
    20. http://www.ncbi.nlm.nih.gov/pubmed/7191269
    21. http://www.ncbi.nlm.nih.gov/pubmed/12439645
    22. http://www.ncbi.nlm.nih.gov/pubmed/20179577
    [23] Wikipedia contributors. "Oxilofrine." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 17 Feb. 2010. Web. 14 Mar. 2010.
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  6. Quote Originally Posted by nattydisaster View Post
    The studies both talk about 3,3-T2 as well, and both state the effects of 3,3-T2 and the fact it does not shut down TSH.

    Here is a pharmacology report on MS
    The studies show that 3,3-T2 doesn't have any thyromimetic activity, but that 3,5-T2 does. In fact, the second study, when discussing the ability to increase RMR, states "3,3-T2 was also tested, but its effects were much weaker and did not reach significance."

  7. Quote Originally Posted by micro2000 View Post
    The studies show that 3,3-T2 doesn't have any thyromimetic activity, but that 3,5-T2 does. In fact, the second study, when discussing the ability to increase RMR, states "3,3-T2 was also tested, but its effects were much weaker and did not reach significance."
    Thyromimetic activety relevent to TSH supression.Basically saying 3,5 causes TSH supression, and 3,3 does not. That is the thyromimetic activety in which they refer.

  8. Quote Originally Posted by nattydisaster View Post
    Gotta bump the coupon code thread

    Who doesnt like coupons?
    bump for the code bud!

  9. Unless my mind is playing tricks on me... I am definitely up a lb and looking leaner!

    Wooohooo for the AT2 part if my stack!

  10. Quote Originally Posted by FlawedGrunt View Post
    Unless my mind is playing tricks on me... I am definitely up a lb and looking leaner!

    Wooohooo for the AT2 part if my stack!
    Damn it man!

  11. I should mention I'm also feeling like a fxcking beast! Doing exercises I haven't done in awhile and my weights are all 5-10lbs heavier than my heaviest on theese

  12. Helllllll yea!

    "ALPHA-T2" is the code -- use it while it works
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  13. Hmmm coulda swore the alpha was for alpha-yohimbine... But I think its more like "Alpha MOTHERFXCKING Male" cause that's how I feel. Definitely great synergy with bioprene, quake from scivation, and xtend

  14. Quote Originally Posted by FlawedGrunt View Post
    Hmmm coulda swore the alpha was for alpha-yohimbine... But I think its more like "Alpha MOTHERFXCKING Male" cause that's how I feel. Definitely great synergy with bioprene, quake from scivation, and xtend
    hahaha NICE
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  15. natty,was wondering if you guys were going to run this as a promo or discounted price in the near future or maybe send out a few samples.if i try it and like it,i will buy it.

  16. Quote Originally Posted by willib View Post
    natty,was wondering if you guys were going to run this as a promo or discounted price in the near future or maybe send out a few samples.if i try it and like it,i will buy it.
    We are currently running a promo right now in this thread and in the promo section.

    Nutraplanet has ALPHA-T2 on sale right now, as well as offering a 15% of coupon code "ALPHA-T2".

    So if there's any time to snag one for cheap, nows the time!
    HIGH VOLUME - Supreme Stim-Free Nitric Oxide Matrix
    SELECT Protein
    - Ultra-Premium Blend
    ALPHAMINE - Thermogenics...Redefined

  17. thanks.i can see you guys are on top of your products and cs.

  18. I'm going to get a cort supp right now... Do you guys think lean xtreme, lean fx(retain2) or controlled labs blue up (had good results before)

  19. Quote Originally Posted by FlawedGrunt View Post
    I'm going to get a cort supp right now... Do you guys think lean xtreme, lean fx(retain2) or controlled labs blue up (had good results before)
    I would suggest Primordial Performances' Endo-Amp or IBE's X-Lean.

  20. just out of curiosity... is 7-keto a cort control? can i run this with the AT2 as well as after?

  21. Quote Originally Posted by FlawedGrunt View Post
    I'm going to get a cort supp right now... Do you guys think lean xtreme, lean fx(retain2) or controlled labs blue up (had good results before)
    I would go Lean Xtreme or EndoAmp

    Quote Originally Posted by FlawedGrunt View Post
    just out of curiosity... is 7-keto a cort control? can i run this with the AT2 as well as after?
    Yessir it is. You can run it both with, and after.
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  22. nice job natty my man, this stuff looks very nice.
    WELL DONE IS BETTER THAN WELL SAID

  23. Quote Originally Posted by nattydisaster View Post
    Yessir it is. You can run it both with, and after.
    So it would be all the better for me to run this with my stack? I was gonna wait till my AT2 runs out but maybe ill run it the whole way through

  24. Just bought a bottle cant wait to try it!

  25. Quote Originally Posted by thebigt View Post
    nice job natty my man, this stuff looks very nice.
    Thanks mate! PES is coming to the show with a bang

    Quote Originally Posted by FlawedGrunt View Post
    So it would be all the better for me to run this with my stack? I was gonna wait till my AT2 runs out but maybe ill run it the whole way through
    You can do either. If you have 1 bottle of LX, I would just wait until the AT2 is finished and then run that bottle after. If you have more than one, then stacking them is beneficial as well since they are synergistic with each other

    Quote Originally Posted by Deeerdre View Post
    Just bought a bottle cant wait to try it!
    Let us know how it goes!
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  26. natty, PES may be new. but if they have your name behind them then i trust they will be a stand up company.



    i appreciate all the help and advice you have given me, total test has increased a bunch since following your protocol. thanks and-good luck.
    WELL DONE IS BETTER THAN WELL SAID

  27. Message to Natty...."You must spread some Reputation around before giving it to nattydisaster again"

    Great job on the boards...along with a fantastic product!
    Nice Products, Nice Prices, Nice People, No Problems....NutraPlanet.com!....Welcome to our World!

  28. Quote Originally Posted by thebigt View Post
    natty, PES may be new. but if they have your name behind them then i trust they will be a stand up company.



    i appreciate all the help and advice you have given me, total test has increased a bunch since following your protocol. thanks and-good luck.
    Glad to here it man! That protocol is the bomb
    HIGH VOLUME - Supreme Stim-Free Nitric Oxide Matrix
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  29. Quote Originally Posted by nattydisaster View Post


    Let us know how it goes!
    Ya I will, should be here monday

  30. 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.

    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. 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"

    These results have been subsequently verified in several studies. 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.
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