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T-X by ALR Industries for Anti-Catabolic Muscle Building

ALRI
Thyroid Stimulator
T-X ALRI Industries Anti-Catabolic 90 ct.
ALR Industries T-X fights fat so you don't have to. World Class Nutrition offers the best supplement to support proper thyroid production for optimal fat loss. T-X's unique Lipolytic properties destroys fat. T-X by ALR Industries is an anti-catabolic thyroidal essential lipolytic matrix designed to promote a physiological repartitioning affect that supports increased protein synthesis while utilizing fat stores as a primary energy supply. The key is a unique synergy between ALR Industries compounds to promote optimal natural thyroid function, while augmenting thyroid hormone levels with our 2 highly active naturally occurring thyroid hormone analogs. The result is obvious: More lean mass, way less fat for the same effort…and better over-all thyroid health. World Class Nutrition is hee to help you save money when you buy bodybuilder supplements. Consider the positive healthy benefits of optimal circulating levels of thyroid hormones:
  • Increased protein synthesis rate.
  • * Increased rate of fat oxidation.
  • * Increased receptor activity for androgens, Insulin, GH, IGF-1, PGE-1, PGF-2, creatine, (and other performance lean mass goodies your body makes)
  • * Increased metabolization of proteins, carbohydrates, fats and micronutrients.
  • * Increased metabolic rate and calories expenditure.
  • * Enhanced oxygen consumption by most body tissues
  • * Improved recovery time.
  • * Stimulation of HPTA In short, we feel and look healthier and leaner because our bodies are able to recover at an accelerated rate while promoting lean tissue regeneration and fat utilization. Why? (I was really hoping you would ask…) THYROID HORMONES Thyroid hormones govern the body's metabolic rate. This means that the metabolism of nutrients, and subsequent cellular utilization or storage rate, is dependent upon active blood circulatory thyroid hormone levels. Optimized levels result in elevated over-all metabolic rates. THYROID HORMONES AND CALORIE EXPENDITURE Those of you who stayed awake during High School Human Biology are aware of the term "oxidative phosphorylation".which is the process of regeneration of cellular energy. This is a process by which our cells/mitochondria convert ADP (Adenosine Diphosphate) into ATP (Adenosine Triphosphate). Basically this means adding another phosphate molecule to ADP so that it can be converted back into the body's energy/ATP. But the term keeps kids flunking biology anyway. As a rule the extra phosphate comes from creatine phosphate…but that is another biology lesson. Basically this process must occur to maintain cellular energy and that requires calories. Normally our bodys are pretty conservative (okay, lazy) and do not waste much energy when doing this process…which is why fat can accumulate due to fewer calories being burned. Optimized thyroid hormone levels and activity make cells waste calories and burn way-more fat by "uncoupling" the oxidative phosphorylation process and making it less efficient, even when at rest. So more calories are used as either energy to build lean tissue (anabolism) or burned off as heat (thermogenesis) Basically, you burn more calories and fat in a shorter period of time but recover and grow faster. THYROID HORMONES AND FAT OXIDATION Fat oxidation (thermogenesis) involves the conversion of fat calories into heat. In the case of thermogenesis caused by thyroid hormones, it is due to "special uncoupling proteins" found in fat, muscle, and organs called UCP-3. Two things before we continue here. First UCP-3 stands for uncoupling protein -3 (big deal) and "special" refers to "specific", not "special" like the weirdo we all dated once and tried to explain later. When UCP-3 is increased, the calorie expenditure through thermogenesis increases. But decreases will result in an increase in fat stores. As example some studies have shown that supraphysiological thyroid hormone T-3 levels can increase UCP-3 600%, and below normal levels results in a 300% decrease. This is why calorie restricted diets significantly decrease in results after 2-4 weeks. The body down-regulates thyroid hormone production to save calories and reduce calorie expenditure as heat. The result is less UCP-3 and slower metabolism…and your diet results suck while you lose muscle. THYROID HORMONES ARE HYPERTROPHIC Thyroid hormones trigger the release of fat stores so other cells can convert the long chain triglycerides (fat) into heat, energy, ATP. By increasing ATP, muscle cells are better able to regenerate, and do so at an increased rate due to increased rate of protein synthesis. Many are not aware of the fact that thyroid hormones are hypertrophic (anabolic) in nature. THYROID HORMONES STIMULATE HPTA FUNCTION Another important factor of thyroid hormone activity is their ability to stimulate the testes. So? Thyroid hormones have been shown to acutely stimulate testosterone production by the Leydig cells in vitro via stimulating the production of steroidogenic acute regulatory protein (StAR) and StAR mRNA in Leydig cells; StAR is associated with intracellular trafficking of cholesterol into the mitochondria during steroid hormone synthesis. Bottom line? Optimal thyroid activity results in stimulation of testosterone production by males, and better hormonal modulation in females. T-X™ contains two exciting naturally occurring thyroid hormone analogs called Diprop and Triprop. What makes them special? Everyone has heard of the powerful thyroid hormone T-3. And of course many have reported the benefits from the T-3 analog Triac. Triprop is a naturally occurring thyroid analog of T-3 similar to Triac in some positive regards. Well, according to animal studies, Triprop has a higher affinity for the thyroid hormone receptor-beta 1 (TR beta 1) than does T-3 by 1.8-fold. This means that it does not take much to do a lot. Diprop is similar to T-2 in that it has been attributed to have brown fat promoting properties. When you are first born, your body does not have much white fat to help insulate and retain body heat; although there are white fat cells, there is not much fat stored in them. A newborn baby produces heat (thermogenesis) primarily by breaking down fat molecules into fatty acids in brown fat cells. Instead of those fatty acids leaving the brown fat cell, as happens in white fat cells, they get further broken down in the mitochondria and their energy is released directly as heat. This same process occurs in hibernating animals, which have more brown fat than humans. Once the newborn baby starts eating more, developing layers of white fat, the brown fat goes away. Adult humans have little or no brown fat. More brown fat means way less white fat, a leaner body and better over-all body composition control. Diprop has also been shown to increase cellular metabolic rate in a synergistic manner with all other thyroid hormones and analogs. Yeah, I know, it would seem like all would be perfect if we simply mega dosed on thyroid hormone analogs and train. Unfortunately, there is always a reaction to every action and this is no different. Doing that would men thyroid gland shut-down in a very short period of time. Why? NATURAL THYROID HORMONE PRODUCTION IN HUMANS (Warning: Science Geek Stuff) The thyroid is a part of the endocrine system. The endocrine system monitors and manufactures/synthesizes many hormones and hormone-like substances. For this reason, the endocrine system and its sub-systems have many built in "checks and balances" to assure proper hormonal ratios and activity levels. 1) Endogenous thyroid hormone production begins when neuro-input tells the hypothalamus to synthesize and release Thyroptropin -Releasing -Hormone. (TRH) 2) TRH stimulates the anterior pituitary gland to release Thyroid-Stimulating-Hormone (TSH) (also referred to as Thyrotropin on some lab chem. Panels) 3) When TSH contacts its receptor-sites located throughout the thyroid gland, a series of enzymic reactions occur using tyrosine and iodine as raw materials to produce and/or release L-Thyroxine (T-4). T-4 is then released into the vascular system so it can circulate. 4) The active T-4 circulating in the vascular system merges with receptors and triggers metabolic “some” activity, but when it reaches the liver it is changed into the more active thyroid hormone L-Triiodothyronine (T-3) by an enzyme called 5-deiodinase. T-3 is about 5 times more active than T-4. The newly formed T-3 is released into the vascular system where it may contact and merge with cellular receptors which initiates all the metabolic activity discussed earlier. Simple so far? THYROID FEED-BACK MECHANISMS and FEED-BACK LOOPS Of course the thyroid does not simply mass produce thyroid hormones continuously. Actually it tries pretty hard to produce as little as possible. This is due to the "checks and balances" nature included in the action/reaction factors for the endocrine system called "feedback-mechanisms". In the case of thyroid function, the feedback-mechanism or loop involves the hypothalamus (secretes TRH), pituitary gland (secretes TSH), thyroid gland (secretes T-4), and the liver (converts T-4 into T-3). A feedback-mechanism or loop can trigger the release of another hormone (positive feed-back), or inhibit its release (negative feed-back) thus maintaining that balance. This means high levels of T-4 or T-3 initiate a negative feed-back loop that tells the hypothalamus to produce less TRH, and low levels of T-4 or T-3 initiate a positive feed-back loop that tells the hypothalamus to produce more TRH. So, simply supplementing with higher than normal levels of thyroid hormone analogs will result in a negative feed-back loop that tells the pituitary to stop producing TRH and the hypothalamus to get greedy with TSH…and natural thyroid hormone production goes in the toilet with you metabolism. Hmmm, picture what happens when you stop taking the extra thyroid analogs. The obvious effective goal therefore becomes to maximize total circulating thyroid hormone levels both supplementally…and provide synergistic support to natural thyroid hormone production by our bodies. One or the other simply is inefficient. So now that we have the powerful ALRI analogs Triprop and Diprop to add to total circulating levels, we need to inhibit the negative feed back-loop. Natural Thyroid Function Support Thyroid hormone production in the body begins with the amino acid tyrosine. Unfortunately free-form tyrosine really does not pass well into the circulatory system at a very high rate orally. Like most amino acids (but not all) a lipophylic carrier or such as an ethyl ester has the potential to increase oral bioavailability up to 400%...so yes, we created tyrosine ethyl ester for T-X™. Now that we have the raw material for natural thyroid hormone production, we need to maintain or even increase the natural production signals by triggering TRH and TSH release from the pituitary and hypothalamus. In rat studies freeze dried extract of Olea europaea (olive leaf extract) was shown to have a maintained stimulatory affect upon the pituitary-thyroid axis that resulted in increased thyroid gland activity. The study shows that this is not a result of pituitary stimulation but of hypothalamic stimulation thus supporting TSH activity. Which is pretty cool, huh? Clary sage is a rather interesting herbal goodie that can be standardized for many of its active compounds. In one study it was shown that, as an aroma therapy, it aids in improvingstress scores significantly. Okay, but the really cool effect it has is due to its cAMP stimulating value. There is a significant similarity between compounds in this interesting herb and Thyroid Stimulating Hormone (TSH). As most are aware, increased TSH means more fat burning anabolism promoting T-3 production (yes, it acts synergistically with the next goodie in this regard…but through different pathways). The connection here is that the TSH-like effect triggers an enzyme called adenylate cyclase in the thyroid that results in an increase in cAMP activity and subsequently lots of extra T-3 production…naturally. Since there is an increase in cAMP, there is an accompanying increase in nitrogen retention. There appears to be some research that supports the belief that increased cAMP results in greater LH release as well (you know, that stuff that tells “The Boy’s” to make more testosterone? Okay, the LH part affects only the guys, women don’t have testes…or shouldn’t). Think about the HPTA stimulating synergy between Clary sage extract and thyroid hormones explained prior. Hmmmm? Beta AET ECPE (beta-androstenetriol ECPE)? We have all heard, and in many cases experienced, the positive effects of DHEA and its even better metabolites. As example are the patented and effective products 7-OXO-DHEA and of course 7-Hydroxy-DHEA analogs. They are noted for their unique ability to avoid conversion into androgenic metabolites or affect androgen receptors while promoting fat loss, lean mass retention and even maximizing thyroid gland activity. Of course oral bio-availability is pretty poor with most of these analogs thus requiring higher dosages. Did I mention that bAET (b-androstenetriol) is between 100 and 100,000 times more active than its DHEA precursor metabolites? Okay, how about that bAET ECPE is nearly 100% orally bioavailable? Yup. It’s why we formulated it. Okay, let me explain a little about the fat loss and lean muscle side of things in regard to bAET ECPE… Glucocorticoids in humans are in two forms: Inactive cortisone and very active for eating muscle cortisol. There are two enzymes that are able to make each of these convert into the other. 11b-HSD-1: Converts inactive cortisone into cannibalistic cortisol. Studies have implicated this event in fat tissue as a pathway for increased fat storage. Part of the reason GH has a positive affect upon body composition is through its ability to inhibit 11b-HDS-1 11b-HSD-2: Converts nasty cortisol into cortisone. 11betaHSD2 debunks intracellular cortisol by 90%. (Let the 11b-HSD-2 rule the house) Hmmm, more 11b-HSD-1 means more cortisol which eats more muscle. And less means…Duh! Beta-AET ECPE inhibits the 11b-HSD-1 enzyme both locally and systemically. This means that there is less conversion of cortisone to cortisol in muscle as a result of training and everywhere else due to stress like dieting. Based upon the studies, it appears that in mediating this pathway, bAET ECPE increases immune function and recovery of cells as well. Add this to its stimulatory affect upon the thyroid gland to support natural thyroid hormone production? Yup, less cortisol, higher metabolic rate, inhibition of that nasty negative thyroid hormone production feed-back loop…less fat, more lean muscle and positive support to health. Not bad! T-X™ is the first multi-structured thyroid analog product that provides superior thyroid function support in an anti-catabolic environment to support your quest for the perfect physique. T-X™, the cutting edge you have been waiting for! T-X Ingredients Research References: 1) iodothyroacetic acid has unique potential for therapy of resistance to thyroid hormone. J Clin Endocrinol Metab. 1995 Jul;80(7):2033-40. 2) Use of triprop in the treatment of hypothyroidism. N Y State J Med. 1963 Aug 1;63:2204-10. 3) Structure-activity relation of thyroid hormone analogues and tissue epidermal growth factor concentrations in neonatal and adult mice. Am J Dis Child. 1984 Mar;138(3):251-3. 4) PRO-ANGIOGENESIS ACTION OF THE THYROID HORMONE ANALOG 3, 5-DIIODOTHYROPROPIONIC ACID (DITPA) IS INITIATED AT THE CELL SURFACE AND IS INTEGRIN-MEDIATED. Endocrinology. 2005 Dec 29; 5) Thyroid hormone analogs for treatment of hypercholesterolemia and heart failure: past, present and future prospects. J Mol Cell Cardiol. 2004 Dec;37(6):1137-46. 6) Role of sulfated tyrosines of thyroglobulin in thyroid hormonosynthesis. Endocrinology. 2005 Nov;146(11):4834-43. Epub 2005 Jul 21. 7) Transforming growth factor-beta promotes inactivation of extracellular thyroid hormones via transcriptional stimulation of type 3 iodothyronine deiodinase. Mol Endocrinol. 2005 Dec;19(12):3126-36. Epub 2005 Jul 21. 8) Effect of freeze dried extract of Olea europaea on the pituitary-thyroid axis in rats. Phytother Res. 2002 May;16(3):286-7. 9) Steroids. 2002 Nov;67(12):953-66. Immune up-regulation and tumor apoptosis by androstene steroids. Loria RM. Department of Microbiology, Immunology and Pathology, Medical College of Virginia, Virginia Commonwealth University, 1101 East Marshal Street, Richmond, VA 23298-0768, USA. loria@hsc.vcu.edu 10) Immunopharmacol Immunotoxicol. 2005;27(1):15-32. Molecular specificity of 5-androstenediol as a systemic radioprotectant in mice. Whitnall MH, Villa V, Seed TM, Benjack J, Miner V, Lewbart ML, Dowding CA, Jackson WE 11) Rinsho Byori. 1998 Jun;46(6):505-17. Control of the immune response by DHEA and its metabolites. Loria RM, Padgett DA. Department of Microbiology, Virginia Commonwealth University, Medical College of Virginia, Richmond 23298-09678, USA. 12) Ann N Y Acad Sci. 2000;917:860-7. Androstenetriol and androstenediol. Protection against lethal radiation and restoration of immunity after radiation injury. Loria RM, Conrad DH, Huff T, Carter H, Ben-Nathan D. 13) J Endocrinol. 2000 Feb;164(2):161-9. Conversion of dehydroepiandrosterone to downstream steroid hormones in macrophages. Schmidt M, Kreutz M, Loffler G, Scholmerich J, Straub RH. Institute of Biochemistry, Genetics and Microbiology, University of Regensburg, Germany. 14) J Neuroimmunol. 1998 Apr 1;84(1):61-8. Endocrine regulation of murine macrophage function: effects of dehydroepiandrosterone, androstenediol, and androstenetriol. Padgett DA, Loria RM. Department of Oral Biology, College of Dentistry, The Ohio State University, Columbus 43210, USA. padgett.11@osu.edu 15) Psychoneuroendocrinology. 1997;22 Suppl 1:S103-8. Antiglucocorticoid function of androstenetriol. Loria RM. Virginia Commonwealth University, Medical College of Virginia, Richmond 23298-0678, USA. Loria@gems.vcu.edu 16) Ann N Y Acad Sci. 1992 Apr 15;650:363-6. Mobilization of cutaneous immunity for systemic protection against infections. Loria RM, Padgett DA. Virginia Commonwealth University, School of Basic Health Sciences, Medical College of Virginia, Richmond 23298. 17) Obes Res. 2005 Jul;13(7):1157-66. Increased cortisol bioavailability, abdominal obesity, and the metabolic syndrome in obese women. Duclos M, Marquez Pereira P, Barat P, Gatta B, Roger P. 18) Laboratoire Neurogenetique et Stress, INSERM U471, Institut Francois Magendie, Universite Bordeaux II, rue C. Saint Saens, 33077 Bordeaux Cedex, France. duclos@pop.bordeaux.inserm.fr. 19) Horm Metab Res. 2005 Apr;37(4):193-7. Obesity and cortisol status. Salehi M, Ferenczi A, Zumoff B. Division of Endocrinology and Metabolism, Department of Medicine, Beth Israel Medical Center and Albert Einstein College of Medicine, New York, NY 10003, USA. 20) Heart Fail Rev. 2005 Jan;10(1):15-22. Mineralocorticoid receptors: distribution and activation. Funder JW. Prince Henry's Institute of Medical Research, Clayton 3168, Victoria, Australia. john.funder@phimr.monash.edu.au 21) Blood. 2005 Jun 7; Expression of 11{beta}-hydroxysteroid dehydrogenase type 1 permits regulation of glucocorticoid bioavailability by human dendritic cells. Freeman L, Hewison M, Hughes SV, Evans KN, Hardie D, Means TK, Chakraverty R. Department of Hematology, University of Birmingham, Birmingham, United Kingdom. 22) Clin Endocrinol (Oxf). 2003 May;58(5):601-11.The effect of growth hormone replacement therapy on adrenal androgen secretion in adult onset hypopituitarism. Isidori AM, Kaltsas GA, Perry L, Burrin JM, Besser GM, Monson JP. Department of Endocrinology, Barts and The London, Queen Mary's School of Medicine and Dentistry, London, UK. 23) Taehan Kanho Hakhoe Chi. 2004 Apr;34(2):344-51. [The effect of aroma inhalation method on stress responses of nursing students.] Park MK, Lee ES. Department of Nursing, Nambu University, Gwangsan-gu, Gwangju city, Korea. pmk0220@hanmail.net 24) Anonymous. Sclareolide Effect on cAMP in Two Cell Lines. Unpublished report by NovaScreen. 2003; 19 pp 25) Neurosci Lett. 2005 Aug 5;383(3):215-9. Epub 2005 Apr 26 Tyramine-immunoreactive neuronal structures in the rat brain: abundance in the median eminence of the mediobasal hypothalamus. Kitahama K, Araneda S, Geffard M, Sei H, Okamura H. CNRS UMR5123, Laboratoire de Physiologie Integrative Cellulaire et Moleculaire, Universite Claude Bernard, Villeurbanne, France. kitahama@sommeil-univ-lyon1.fr 26) Histol Histopathol. 2004 Jul;19(3):985-97. Effects of thyroid hormones on Leydig cells in the postnatal testis. Mendis-Handagama SM, Ariyaratne HB. Department of Comparative Medicine, The University of Tennessee College of Veterinary Medicine, Knoxville, TN 37996, USA. mendisc@utk.edu WARNING: NOT FOR USE BY INDIVIDUALS UNDER THE AGE OF 21 YEARS. DO NOT USE IF PREGNANT OR NURSING. KEEP OUT OF REACH OF CHILDREN. Do NOT consume this product if you have a medical condition and/or taking any prescription medication. Do not exceed recommended serving. Discontinue use and call a physician or licensed qualified health care professional immediately if you experience rapid heartbeat, dizziness, severe headache, or other similar symptoms. These statements have not been evaluated by the FDA. This product is not intended to diagnose, treat, or prevent any disease.
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    $27.99
  • T-X ALRI Industries Anti-Catabolic 90 ct.
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    Regular Price:$49.99
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    Product Description

    ALR Industries T-X fights fat so you don't have to. World Class Nutrition offers the best supplement to support proper thyroid production for optimal fat loss.

    T-X's unique Lipolytic properties destroys fat.

    T-X by ALR Industries is an anti-catabolic thyroidal essential lipolytic matrix designed to promote a physiological repartitioning affect that supports increased protein synthesis while utilizing fat stores as a primary energy supply. The key is a unique synergy between ALR Industries compounds to promote optimal natural thyroid function, while augmenting thyroid hormone levels with our 2 highly active naturally occurring thyroid hormone analogs. The result is obvious: More lean mass, way less fat for the same effort…and better over-all thyroid health. World Class Nutrition is hee to help you save money when you buy bodybuilder supplements.

    Consider the positive healthy benefits of optimal circulating levels of thyroid hormones:

  • Increased protein synthesis rate.
  • * Increased rate of fat oxidation.
  • * Increased receptor activity for androgens, Insulin, GH, IGF-1, PGE-1, PGF-2, creatine, (and other performance lean mass goodies your body makes)
  • * Increased metabolization of proteins, carbohydrates, fats and micronutrients.
  • * Increased metabolic rate and calories expenditure.
  • * Enhanced oxygen consumption by most body tissues
  • * Improved recovery time.
  • * Stimulation of HPTA

    In short, we feel and look healthier and leaner because our bodies are able to recover at an accelerated rate while promoting lean tissue regeneration and fat utilization. Why? (I was really hoping you would ask…) THYROID HORMONES

    Thyroid hormones govern the body's metabolic rate. This means that the metabolism of nutrients, and subsequent cellular utilization or storage rate, is dependent upon active blood circulatory thyroid hormone levels. Optimized levels result in elevated over-all metabolic rates.

    THYROID HORMONES AND CALORIE EXPENDITURE

    Those of you who stayed awake during High School Human Biology are aware of the term "oxidative phosphorylation".which is the process of regeneration of cellular energy. This is a process by which our cells/mitochondria convert ADP (Adenosine Diphosphate) into ATP (Adenosine Triphosphate). Basically this means adding another phosphate molecule to ADP so that it can be converted back into the body's energy/ATP. But the term keeps kids flunking biology anyway. As a rule the extra phosphate comes from creatine phosphate…but that is another biology lesson. Basically this process must occur to maintain cellular energy and that requires calories.

    Normally our bodys are pretty conservative (okay, lazy) and do not waste much energy when doing this process…which is why fat can accumulate due to fewer calories being burned. Optimized thyroid hormone levels and activity make cells waste calories and burn way-more fat by "uncoupling" the oxidative phosphorylation process and making it less efficient, even when at rest. So more calories are used as either energy to build lean tissue (anabolism) or burned off as heat (thermogenesis) Basically, you burn more calories and fat in a shorter period of time but recover and grow faster. THYROID HORMONES AND FAT OXIDATION

    Fat oxidation (thermogenesis) involves the conversion of fat calories into heat. In the case of thermogenesis caused by thyroid hormones, it is due to "special uncoupling proteins" found in fat, muscle, and organs called UCP-3. Two things before we continue here. First UCP-3 stands for uncoupling protein -3 (big deal) and "special" refers to "specific", not "special" like the weirdo we all dated once and tried to explain later. When UCP-3 is increased, the calorie expenditure through thermogenesis increases. But decreases will result in an increase in fat stores.

    As example some studies have shown that supraphysiological thyroid hormone T-3 levels can increase UCP-3 600%, and below normal levels results in a 300% decrease. This is why calorie restricted diets significantly decrease in results after 2-4 weeks. The body down-regulates thyroid hormone production to save calories and reduce calorie expenditure as heat. The result is less UCP-3 and slower metabolism…and your diet results suck while you lose muscle. THYROID HORMONES ARE HYPERTROPHIC

    Thyroid hormones trigger the release of fat stores so other cells can convert the long chain triglycerides (fat) into heat, energy, ATP. By increasing ATP, muscle cells are better able to regenerate, and do so at an increased rate due to increased rate of protein synthesis. Many are not aware of the fact that thyroid hormones are hypertrophic (anabolic) in nature.

    THYROID HORMONES STIMULATE HPTA FUNCTION

    Another important factor of thyroid hormone activity is their ability to stimulate the testes. So? Thyroid hormones have been shown to acutely stimulate testosterone production by the Leydig cells in vitro via stimulating the production of steroidogenic acute regulatory protein (StAR) and StAR mRNA in Leydig cells; StAR is associated with intracellular trafficking of cholesterol into the mitochondria during steroid hormone synthesis.

    Bottom line? Optimal thyroid activity results in stimulation of testosterone production by males, and better hormonal modulation in females.

    T-X™ contains two exciting naturally occurring thyroid hormone analogs called Diprop and Triprop. What makes them special?

    Everyone has heard of the powerful thyroid hormone T-3. And of course many have reported the benefits from the T-3 analog Triac. Triprop is a naturally occurring thyroid analog of T-3 similar to Triac in some positive regards. Well, according to animal studies, Triprop has a higher affinity for the thyroid hormone receptor-beta 1 (TR beta 1) than does T-3 by 1.8-fold. This means that it does not take much to do a lot.

    Diprop is similar to T-2 in that it has been attributed to have brown fat promoting properties. When you are first born, your body does not have much white fat to help insulate and retain body heat; although there are white fat cells, there is not much fat stored in them. A newborn baby produces heat (thermogenesis) primarily by breaking down fat molecules into fatty acids in brown fat cells. Instead of those fatty acids leaving the brown fat cell, as happens in white fat cells, they get further broken down in the mitochondria and their energy is released directly as heat. This same process occurs in hibernating animals, which have more brown fat than humans. Once the newborn baby starts eating more, developing layers of white fat, the brown fat goes away. Adult humans have little or no brown fat. More brown fat means way less white fat, a leaner body and better over-all body composition control.

    Diprop has also been shown to increase cellular metabolic rate in a synergistic manner with all other thyroid hormones and analogs.

    Yeah, I know, it would seem like all would be perfect if we simply mega dosed on thyroid hormone analogs and train. Unfortunately, there is always a reaction to every action and this is no different. Doing that would men thyroid gland shut-down in a very short period of time. Why?

    NATURAL THYROID HORMONE PRODUCTION IN HUMANS (Warning: Science Geek Stuff)

    The thyroid is a part of the endocrine system. The endocrine system monitors and manufactures/synthesizes many hormones and hormone-like substances. For this reason, the endocrine system and its sub-systems have many built in "checks and balances" to assure proper hormonal ratios and activity levels.

    1) Endogenous thyroid hormone production begins when neuro-input tells the hypothalamus to synthesize and release Thyroptropin -Releasing -Hormone. (TRH)

    2) TRH stimulates the anterior pituitary gland to release Thyroid-Stimulating-Hormone (TSH) (also referred to as Thyrotropin on some lab chem. Panels)

    3) When TSH contacts its receptor-sites located throughout the thyroid gland, a series of enzymic reactions occur using tyrosine and iodine as raw materials to produce and/or release L-Thyroxine (T-4). T-4 is then released into the vascular system so it can circulate.

    4) The active T-4 circulating in the vascular system merges with receptors and triggers metabolic “some” activity, but when it reaches the liver it is changed into the more active thyroid hormone L-Triiodothyronine (T-3) by an enzyme called 5-deiodinase. T-3 is about 5 times more active than T-4. The newly formed T-3 is released into the vascular system where it may contact and merge with cellular receptors which initiates all the metabolic activity discussed earlier. Simple so far?

    THYROID FEED-BACK MECHANISMS and FEED-BACK LOOPS

    Of course the thyroid does not simply mass produce thyroid hormones continuously. Actually it tries pretty hard to produce as little as possible. This is due to the "checks and balances" nature included in the action/reaction factors for the endocrine system called "feedback-mechanisms". In the case of thyroid function, the feedback-mechanism or loop involves the hypothalamus (secretes TRH), pituitary gland (secretes TSH), thyroid gland (secretes T-4), and the liver (converts T-4 into T-3).

    A feedback-mechanism or loop can trigger the release of another hormone (positive feed-back), or inhibit its release (negative feed-back) thus maintaining that balance. This means high levels of T-4 or T-3 initiate a negative feed-back loop that tells the hypothalamus to produce less TRH, and low levels of T-4 or T-3 initiate a positive feed-back loop that tells the hypothalamus to produce more TRH.

    So, simply supplementing with higher than normal levels of thyroid hormone analogs will result in a negative feed-back loop that tells the pituitary to stop producing TRH and the hypothalamus to get greedy with TSH…and natural thyroid hormone production goes in the toilet with you metabolism. Hmmm, picture what happens when you stop taking the extra thyroid analogs.

    The obvious effective goal therefore becomes to maximize total circulating thyroid hormone levels both supplementally…and provide synergistic support to natural thyroid hormone production by our bodies. One or the other simply is inefficient. So now that we have the powerful ALRI analogs Triprop and Diprop to add to total circulating levels, we need to inhibit the negative feed back-loop.

    Natural Thyroid Function Support

    Thyroid hormone production in the body begins with the amino acid tyrosine. Unfortunately free-form tyrosine really does not pass well into the circulatory system at a very high rate orally. Like most amino acids (but not all) a lipophylic carrier or such as an ethyl ester has the potential to increase oral bioavailability up to 400%...so yes, we created tyrosine ethyl ester for T-X™.

    Now that we have the raw material for natural thyroid hormone production, we need to maintain or even increase the natural production signals by triggering TRH and TSH release from the pituitary and hypothalamus.

    In rat studies freeze dried extract of Olea europaea (olive leaf extract) was shown to have a maintained stimulatory affect upon the pituitary-thyroid axis that resulted in increased thyroid gland activity. The study shows that this is not a result of pituitary stimulation but of hypothalamic stimulation thus supporting TSH activity. Which is pretty cool, huh?

    Clary sage is a rather interesting herbal goodie that can be standardized for many of its active compounds. In one study it was shown that, as an aroma therapy, it aids in improvingstress scores significantly.

    Okay, but the really cool effect it has is due to its cAMP stimulating value. There is a significant similarity between compounds in this interesting herb and Thyroid Stimulating Hormone (TSH). As most are aware, increased TSH means more fat burning anabolism promoting T-3 production (yes, it acts synergistically with the next goodie in this regard…but through different pathways).

    The connection here is that the TSH-like effect triggers an enzyme called adenylate cyclase in the thyroid that results in an increase in cAMP activity and subsequently lots of extra T-3 production…naturally. Since there is an increase in cAMP, there is an accompanying increase in nitrogen retention.

    There appears to be some research that supports the belief that increased cAMP results in greater LH release as well (you know, that stuff that tells “The Boy’s” to make more testosterone? Okay, the LH part affects only the guys, women don’t have testes…or shouldn’t). Think about the HPTA stimulating synergy between Clary sage extract and thyroid hormones explained prior. Hmmmm?

    Beta AET ECPE (beta-androstenetriol ECPE)? We have all heard, and in many cases experienced, the positive effects of DHEA and its even better metabolites. As example are the patented and effective products 7-OXO-DHEA and of course 7-Hydroxy-DHEA analogs. They are noted for their unique ability to avoid conversion into androgenic metabolites or affect androgen receptors while promoting fat loss, lean mass retention and even maximizing thyroid gland activity. Of course oral bio-availability is pretty poor with most of these analogs thus requiring higher dosages. Did I mention that bAET (b-androstenetriol) is between 100 and 100,000 times more active than its DHEA precursor metabolites? Okay, how about that bAET ECPE is nearly 100% orally bioavailable? Yup. It’s why we formulated it.

    Okay, let me explain a little about the fat loss and lean muscle side of things in regard to bAET ECPE…

    Glucocorticoids in humans are in two forms: Inactive cortisone and very active for eating muscle cortisol. There are two enzymes that are able to make each of these convert into the other.

    11b-HSD-1: Converts inactive cortisone into cannibalistic cortisol. Studies have implicated this event in fat tissue as a pathway for increased fat storage. Part of the reason GH has a positive affect upon body composition is through its ability to inhibit 11b-HDS-1

    11b-HSD-2: Converts nasty cortisol into cortisone. 11betaHSD2 debunks intracellular cortisol by 90%. (Let the 11b-HSD-2 rule the house)

    Hmmm, more 11b-HSD-1 means more cortisol which eats more muscle. And less means…Duh!

    Beta-AET ECPE inhibits the 11b-HSD-1 enzyme both locally and systemically. This means that there is less conversion of cortisone to cortisol in muscle as a result of training and everywhere else due to stress like dieting. Based upon the studies, it appears that in mediating this pathway, bAET ECPE increases immune function and recovery of cells as well. Add this to its stimulatory affect upon the thyroid gland to support natural thyroid hormone production? Yup, less cortisol, higher metabolic rate, inhibition of that nasty negative thyroid hormone production feed-back loop…less fat, more lean muscle and positive support to health. Not bad!

    T-X™ is the first multi-structured thyroid analog product that provides superior thyroid function support in an anti-catabolic environment to support your quest for the perfect physique. T-X™, the cutting edge you have been waiting for!

    T-X Ingredients

    Research References:

    1) iodothyroacetic acid has unique potential for therapy of resistance to thyroid hormone. J Clin Endocrinol Metab. 1995 Jul;80(7):2033-40.

    2) Use of triprop in the treatment of hypothyroidism. N Y State J Med. 1963 Aug 1;63:2204-10.

    3) Structure-activity relation of thyroid hormone analogues and tissue epidermal growth factor concentrations in neonatal and adult mice. Am J Dis Child. 1984 Mar;138(3):251-3.

    4) PRO-ANGIOGENESIS ACTION OF THE THYROID HORMONE ANALOG 3, 5-DIIODOTHYROPROPIONIC ACID (DITPA) IS INITIATED AT THE CELL SURFACE AND IS INTEGRIN-MEDIATED. Endocrinology. 2005 Dec 29;

    5) Thyroid hormone analogs for treatment of hypercholesterolemia and heart failure: past, present and future prospects. J Mol Cell Cardiol. 2004 Dec;37(6):1137-46.

    6) Role of sulfated tyrosines of thyroglobulin in thyroid hormonosynthesis. Endocrinology. 2005 Nov;146(11):4834-43. Epub 2005 Jul 21.

    7) Transforming growth factor-beta promotes inactivation of extracellular thyroid hormones via transcriptional stimulation of type 3 iodothyronine deiodinase. Mol Endocrinol. 2005 Dec;19(12):3126-36. Epub 2005 Jul 21.

    8) Effect of freeze dried extract of Olea europaea on the pituitary-thyroid axis in rats. Phytother Res. 2002 May;16(3):286-7.

    9) Steroids. 2002 Nov;67(12):953-66. Immune up-regulation and tumor apoptosis by androstene steroids. Loria RM. Department of Microbiology, Immunology and Pathology, Medical College of Virginia, Virginia Commonwealth University, 1101 East Marshal Street, Richmond, VA 23298-0768, USA. loria@hsc.vcu.edu

    10) Immunopharmacol Immunotoxicol. 2005;27(1):15-32. Molecular specificity of 5-androstenediol as a systemic radioprotectant in mice. Whitnall MH, Villa V, Seed TM, Benjack J, Miner V, Lewbart ML, Dowding CA, Jackson WE

    11) Rinsho Byori. 1998 Jun;46(6):505-17. Control of the immune response by DHEA and its metabolites. Loria RM, Padgett DA. Department of Microbiology, Virginia Commonwealth University, Medical College of Virginia, Richmond 23298-09678, USA.

    12) Ann N Y Acad Sci. 2000;917:860-7. Androstenetriol and androstenediol. Protection against lethal radiation and restoration of immunity after radiation injury. Loria RM, Conrad DH, Huff T, Carter H, Ben-Nathan D.

    13) J Endocrinol. 2000 Feb;164(2):161-9. Conversion of dehydroepiandrosterone to downstream steroid hormones in macrophages. Schmidt M, Kreutz M, Loffler G, Scholmerich J, Straub RH. Institute of Biochemistry, Genetics and Microbiology, University of Regensburg, Germany.

    14) J Neuroimmunol. 1998 Apr 1;84(1):61-8. Endocrine regulation of murine macrophage function: effects of dehydroepiandrosterone, androstenediol, and androstenetriol. Padgett DA, Loria RM. Department of Oral Biology, College of Dentistry, The Ohio State University, Columbus 43210, USA. padgett.11@osu.edu

    15) Psychoneuroendocrinology. 1997;22 Suppl 1:S103-8. Antiglucocorticoid function of androstenetriol. Loria RM. Virginia Commonwealth University, Medical College of Virginia, Richmond 23298-0678, USA. Loria@gems.vcu.edu

    16) Ann N Y Acad Sci. 1992 Apr 15;650:363-6. Mobilization of cutaneous immunity for systemic protection against infections. Loria RM, Padgett DA. Virginia Commonwealth University, School of Basic Health Sciences, Medical College of Virginia, Richmond 23298.

    17) Obes Res. 2005 Jul;13(7):1157-66. Increased cortisol bioavailability, abdominal obesity, and the metabolic syndrome in obese women. Duclos M, Marquez Pereira P, Barat P, Gatta B, Roger P. 18) Laboratoire Neurogenetique et Stress, INSERM U471, Institut Francois Magendie, Universite Bordeaux II, rue C. Saint Saens, 33077 Bordeaux Cedex, France. duclos@pop.bordeaux.inserm.fr.

    19) Horm Metab Res. 2005 Apr;37(4):193-7. Obesity and cortisol status. Salehi M, Ferenczi A, Zumoff B. Division of Endocrinology and Metabolism, Department of Medicine, Beth Israel Medical Center and Albert Einstein College of Medicine, New York, NY 10003, USA.

    20) Heart Fail Rev. 2005 Jan;10(1):15-22. Mineralocorticoid receptors: distribution and activation. Funder JW. Prince Henry's Institute of Medical Research, Clayton 3168, Victoria, Australia. john.funder@phimr.monash.edu.au

    21) Blood. 2005 Jun 7; Expression of 11{beta}-hydroxysteroid dehydrogenase type 1 permits regulation of glucocorticoid bioavailability by human dendritic cells. Freeman L, Hewison M, Hughes SV, Evans KN, Hardie D, Means TK, Chakraverty R. Department of Hematology, University of Birmingham, Birmingham, United Kingdom. 22) Clin Endocrinol (Oxf). 2003 May;58(5):601-11.The effect of growth hormone replacement therapy on adrenal androgen secretion in adult onset hypopituitarism. Isidori AM, Kaltsas GA, Perry L, Burrin JM, Besser GM, Monson JP. Department of Endocrinology, Barts and The London, Queen Mary's School of Medicine and Dentistry, London, UK.

    23) Taehan Kanho Hakhoe Chi. 2004 Apr;34(2):344-51. [The effect of aroma inhalation method on stress responses of nursing students.] Park MK, Lee ES. Department of Nursing, Nambu University, Gwangsan-gu, Gwangju city, Korea. pmk0220@hanmail.net 24) Anonymous. Sclareolide Effect on cAMP in Two Cell Lines. Unpublished report by NovaScreen. 2003; 19 pp

    25) Neurosci Lett. 2005 Aug 5;383(3):215-9. Epub 2005 Apr 26 Tyramine-immunoreactive neuronal structures in the rat brain: abundance in the median eminence of the mediobasal hypothalamus. Kitahama K, Araneda S, Geffard M, Sei H, Okamura H. CNRS UMR5123, Laboratoire de Physiologie Integrative Cellulaire et Moleculaire, Universite Claude Bernard, Villeurbanne, France. kitahama@sommeil-univ-lyon1.fr

    26) Histol Histopathol. 2004 Jul;19(3):985-97. Effects of thyroid hormones on Leydig cells in the postnatal testis. Mendis-Handagama SM, Ariyaratne HB. Department of Comparative Medicine, The University of Tennessee College of Veterinary Medicine, Knoxville, TN 37996, USA. mendisc@utk.edu

    WARNING: NOT FOR USE BY INDIVIDUALS UNDER THE AGE OF 21 YEARS. DO NOT USE IF PREGNANT OR NURSING. KEEP OUT OF REACH OF CHILDREN. Do NOT consume this product if you have a medical condition and/or taking any prescription medication. Do not exceed recommended serving. Discontinue use and call a physician or licensed qualified health care professional immediately if you experience rapid heartbeat, dizziness, severe headache, or other similar symptoms.

    These statements have not been evaluated by the FDA. This product is not intended to diagnose, treat, or prevent any disease.
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