MuscleMeds Phenbuterol 30ct
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PHENBUTEROL: UCP-1 Activator PHENBUTEROL introduces a new development in advanced fat burning technology through the activation of Uncoupling Protein 1 (UCP-1). UCP-1 enhances fat burning in brown adipose tissue (BAT) by shuttling fatty acids from stored body fat into the mitochondria to generate heat and trigger thermogenesis. Utilizing fatty acids from stored body fat, rather than ATP from muscle tissue, is a unique fat burning mechanism of UCP-1 and brown adipose tissue – and one of the key fat burning actions and benefits of PHENBUTEROL. To optimize the fat burning potential of UCP-1 and BAT, in the development of PHENBUTEROL MuscleMeds researchers explored the key mechanisms of action and identified some newly discovered highly standardized natural compounds. One of their key finding was a potent clinically researched compound called 6-Paradol. This compound is derived from a plant native to West Africa called Grains of Paradise, and it has been show in clinical studies to upregulate UCP-1. Other naturally derived compounds such as hordenine, octopamine, synepherine, llex paraguariensis and Rouwolfia serpentia provide synergistic fat burning effects. In addition, these select active ingredients in PHENBUTEROL also exert powerful energizing and mood enhancing effects to take the edge off dieting. PHENBUTEROL is a potent fat burning catalyst for serious athletes looking to lose excess body fat quickly and effectively. NOTE: PHENBUTEROL is a trade name and is not intended to depict any comparison to any pharmaceutical or other product or any particular benefit thereof. PHENBUTEROL: This is the first fat burning supplement targeting the activation of UCP-1 and BAT from MuscleMeds. Since BAT tissue is activated through Beta 1, 2 and 3 (and to some extent Alpha) adrenergic receptors and is highly activated by norepinephrine, a unique combination of ingredients was assembled to maximize the fat burning potential of BAT by activating several receptors. In addition, ingredients were chosen for their potential to stimulate norepinephrine, which acts on Beta-3 and is by far the most potent activator of BAT. THE SCIENCE OF UCP-1 THERMOGENESIS Uncoupling Protein 1: Uncoupling Protein 1 (aka UCP-1) is a protein known to be required for a specific fat cell’s heat-generating capabilities. Originally coined “Thermogenin,” UCP-1 is used by specific tissues to generate heat via non-shivering thermogenesis, which is the primary means of heat generation in certain mammals (hibernating mammals for example) and in human infants. The name was originally used to describe an oxidative process for energy generation not coupled to ATP synthesis. 15 UCP-1 is a mitochondrial transport protein found within the inner membrane of mitochondria in all mammals and in plants. Mitochondria themselves are organelles within cells where respiration occurs. In this case, respiration refers to the process by which a cell obtains energy from organic compounds. In other words, the burning of a fuel source to generate heat. Or more simply put, thermogenesis.1 The citric acid cycle, fatty acid oxidation and gluconeogenesis are other actions that also take place within mitochondria. The energy produced by respiration within the mitochondria is used for ATP synthesis via oxidative phosphorylation. What is unique about UCP-1 is that it can cause a rapid, uncoupled respiration that does not rely upon ATP synthesis, rather it shuttles fatty acids into the cell to burn with an end result of heat generation. In other words, UCP-1 is the equivalent of a “regulated uncoupler” that can control heat production. 1 UCP-1 works by decreasing the proton gradient thereby increasing the permeability of the inner mitochondrial membrane. It is thought that with this reduced gradient/increased permeability; protons can grab fatty acids and pour them into the cell to burn. Not all cells contain UCP-1. In fact, it is unique to a specific tissue, sometimes referred to as an organ, called Brown Adipose Tissue (BAT). The rate of metabolism in all tissues, other than BAT, is determined by utilization of ATP. UCPI and BAT are unique in that they do not follow this same metabolic pathway. The physiological action of UCP-1 on BAT can be called “unrestrained oxidation of fuels with the sole byproduct being the generation of heat.” 12 Brown Adipose Tissue (BAT): We have at least two functionally different types of adipose tissue in our bodies. Brown Adipose Tissue and White Adipose Tissue (WAT). WAT is the primary place in the body where energy is stored. It is also involved in the release of hormones and cytokines that are involved in both metabolism and modulation of insulin resistance. The simplest way to describe the difference between these two types of fat is to describe the difference between gaining and losing weight as it is well known at this point that excess WAT = overweight! BAT, although a fat cell as well, is functionally very different. BAT is important for basal body temperature, the temperature you essentially wake up at before moving or eating. In addition BAT is important for thermogenesis mediated by UCP-1.2,15 BAT is the mechanism by which the sympathetic nervous system produces heat during non-shivering thermogenesis. 11,15 Brown adipocytes are smaller than white adipocytes, contain less fat, are highly vascular, have an abundance of nerves and can contain high concentrations of triiodothyronine (T3), an endogenous thyroid hormone. Further, Beta-3 Adrenergic Receptors are highly abundant in this tissue while being markedly absent in WAT. 12 When you picture “fat” in a human, most people immediately think of large protruding bellies, round thighs and “chicken wings.” BAT is very different in that these deposits are not found in any of these areas. Rather they are found in supraclavicular deposits in the neck area.3 Older studies have “estimated a prevalence of BAT as low as 5% in adult humans” however testing methodologies, sensitivity and reproducibility have been difficult leading most researchers to believe this number to be greater. Lee et al., looked at this and concluded a universal prevalence of BAT in human adults, which far exceeds 5% 3 and Chen et al., concluded via nuclear medicine that BAT is clearly present in adult humans. 10 Why Scientists Are Studying BAT In Overweight People: BAT is an efficient heat generating “organ” within the body. Under different conditions, such as exposure to cold, UCP-1 will activate BAT and start to burn the fatty acids that are shuttled into the cell. In other words, BAT burns fat to generate heat! BAT is regulated by the sympathetic nervous system and can be stimulated by the Beta-Adrenergic system. 3 This means that noradrenaline, for example, can stimulate BAT to generate heat by burning fat. Further, BAT can be activated by diet5 and a single meal can activate BAT. 15 Where WAT stores lipids for energy to be used at a future point, BAT has evolved to ensure mammals maintain a core body temperature by burning lipids.13 The heat generating capability of BAT has been talked about for decades and researched extensively in animals.4 It is only in recent years that scientists have been able to determine the purpose and use of BAT within the human body.3 It is thought that BAT serves two primary purposes – to maintain body temperature during exposure to cold and to waste food energy.5 This leads one to inquire about overweight people and how BAT is affected. It is understood that BAT can grow when stimulated or it can atrophy. In most models within animals, BAT is usually atrophied.5 Also, in most models BAT is low or absent and so it is hypothesized that lifestyle and body composition can create differences in the amount and in the activity of BAT. 11 Atrophied BAT may even be associated with insulin resistance. Scientific discovery that BAT uses fat and not ATP for fuel is a major breakthrough for weight loss and extremely beneficial for athletes and bodybuilders. The principal fuel for BAT that has been stimulated is fatty acids in the form of endogenously stored lipids. BAT has “a huge capacity to remove lipids from the circulatory system to fuel thermogenesis” and when “thermogenically active, the high rates of oxidative phosphorylation mean it requires large quantities of lipids.”13 BAT is capable of obtaining fatty acids from four basic sources. The first of four endogenous stores is fat, the second is from plasma lipoproteins, the third is from free fatty acids in the blood and the fourth is from glucose, as BAT can synthesis fatty acids to burn from glucose although glucose is not the major fuel source for BAT.5 For UCP-1 to stimulate BAT, fatty acids are necessary in furthering the knowledge that BAT is a built in and potent fat burning organ in the human body.11 All of the thermogenic activation changes that take place in BAT are mediated through adrenergic receptors, either Alpha or Beta. 15 An increased rate of lipolysis is observed when norepinephrine is acting on Beta-adrenergic receptors. Other related compounds that have been shown to stimulate BAT include nicotine, ephedrine, caffeine and theophylline as well as the drug fenfluramine.5† BAT “reactivation” and its potential use in combating overweight has garnered the attention of the medical and nutritional industries for some time now.6 Some of the research has even looked at increases in oxygen consumption via BAT activation in animal models. Various substances with Beta-Andrenoceptor mechanisms have been looked at for their potential as a potential BAT activator, 8,9 particularly since BAT has such a high density of Beta-adrenoceptors. It has been hypothesized that ephedrine’s ability to reduce weight via its fat burning mechanism was due to its Beta-receptor stimulation of BAT, although at the time limited methods to look at BAT were available. Exactly how ephedrine worked remains unknown, but new data from rats show that part of its affect is by BAT activation. 14 Of the beta-receptors, beta-3 may be the most significant mediator of thermogenesis. However alpha, beta-1 and 2 receptors are also found within BAT.11 Potential targets to activate BAT continue to be identified and include cold exposure, insulin, thyroid hormone, beta-agonists11 and even exercise13. Perhaps the most interesting compound shown to activate BAT is 6-paradol found in PHENBUTEROL – in particular the highly standardized 6-paradol contained in Aframomum melegueta, a plant with the common name Grains of Paradise (GOP) that is a member of the ginger family. GOP has been shown in both animal and humans studies to activate BAT and increase whole-body energy expenditure. 17,18 However, its important to mention that not just any form of GOP will provide the necessary levels of standardized 6-paradol needed to be effective. In fact, very few manufacturers are capable of providing the potency used in PHENBUTEROL. Activating UCP-1 may help dieters breakthrough plateaus and reach their weight loss goals. Attempts have been made to summarize the fat burning potential of activated BAT14. Whittle suggests that just a few grams of BAT might increase daily energy expenditure by 20%.13 Cypress, et al., postulates that 50 grams could account for 20% daily energy expenditure.2 The overall point is that where many adults in the U.S. carry kilograms of extra WAT, very small amounts of BAT may help burn some of that excess off. The first question that comes to mind is what has happened to BAT in overweight people? UCP-1 has been shown to decrease in models of fasting and food restriction.15 Decreased UCP-1 leads to decreased activity of BAT leading to the hypothesis that Western dieting techniques only serve to deactivate BAT. This may help explain why dieters often plateau and find it more difficult to lose weight after only a few weeks of dieting and caloric restriction. PHENBUTEROL may actually be able to reduce the diet induced down-regulation of UCP-1 and help dieters break through those plateaus. PHENBUTEROL ACTIVE INGREDIENTS: Aframomum melegueta (Grains of Paradise) Grains of Paradise, also known as Aframomum melagueta, is a spice native to West Africa that has been shown to activate brown adipose tissue (BAT) while increasing whole-body energy expenditure. 18 Therefore, Aframomum melagueta may increase the reduction of body fat through activation of BAT and subsequent thermogenesis. 49,50,51,52,53 Brown adipose tissue is one of two types of fats in the body, with the other being white adipose tissue (WAT). BAT has thermogenic properties, as its primary function is to generate body heat, while WAT stores triglycerides into fat cells, causing us to store fat. The problem being is that WAT is more predominant in the human body and BAT is only highly active when we are infants. While there are still small amounts in our body, as we get older, studies have shown that there are higher amounts of BAT in people with a lower body weight. 17 However, BAT may continue to decrease as we get older 54, increasing the importance of finding ways to activate it to help reduce body fat. When the human body is exposed to a cold environment, BAT functions as a non-shivering thermogenesis. It acts as a heater organ to raise the internal body temperature to keep the body warm. Stimulating the sympathetic nerve system will increase norepinephrine, which can activate the thermogenesis effects of BAT. Phenbuterol, through the administration of Aframomum melagueta, supports the natural increase of norepinephrine. Besides the warming properties of Aframomum melagueta, the spice is a strong antioxidant that has beneficial digestive properties. 55,56 Antioxidants are vital for overall health because they support all the functions of your organs and they fight free radical cells in your body that support the decrease in fat storage and an increase in the use of fat to be burned as energy. Caffeine Caffeine is a central nervous system and metabolic stimulant.28 Caffeine has been shown to increase energy, reduce fatigue and improve clarity and mental focus. 29,30 Caffeine also contributes to increasing the lipolysis process, therefore helping to mobilize fatty acids to aid in fat loss. This mechanism can at least in part be explained by not only increased metabolism by raising resting energy expenditure, but by activation of BAT. Rauwolfia serpenia Rauwolfia serpenia acts primarily as an alpha-2 antagonist. 45 Alpha-2 receptors hinder the release of norepinephrine and are highly anti-lipolytic. This means that it is harder for the fat to break down in stubborn fat areas when alpha-2 receptors are present. Rauwolfia acts to help suppress alpha-2 receptors, thus allowing the release of norepinephrine. The blocking of the alpha-2 receptors in turn helps maximize powerful thermogenic effects and, as discussed earlier, when norepinephrine is released, BAT can be activated. It is through the above mechanism that Rauwolfia acts as a CNS stimulant. Therefore, this compound promotes lipolysis and may actually help you burn fat in problem areas such as the abdomen and glutes. 46,47 This is made possible by allowing the fat burning beta-receptors to work more freely. Rauwolfia contains another very important benefit: It has nitric oxide benefits that help blood flow into the muscle that can result in greater muscle pumps. While Rauwolfia naturally contains small amounts of yohimbine, it does not carry the same side effects associated with high doses of this herb. It only contains enough yohimbine to help assist Rauwolfia serpenia in alpha-2 receptor suppression. 48 † Phenbuterol contains no ephedrine, fenfluramine or any synthetic drug. For informational and educational purposes only. REFERENCES: Rousset et al., The Biology of Mitochondrial Uncoupling Proteins. Diabetes 2004, 53:Supp 1 Cypress et al., Identification and Importance of Brown Adipose Tissue in Adult Humans. The New England Journal of Medicine 2013, 360:15 Lee et al., High Prevalence of Brown Adipose Tissue in Adult Humans. J ClinEndocrinMetab. 2011, 96:8 Garrow J. S. British Medical Journal 1983, 286 Himms-Hagen J., Brown adipose tissue thermogenesis: interdisciplinary studies. FASEB J. 1990, 4:2890-2898 Holloway, Brian. Reactivation of brown adipose tissue. Proceedings of the Nutrition Society 1989, 48:225-230 Holloway, Brian et al., ICI D7114 a novel selective beta-adrenoceptor agonist selectively stimulates brown fat and increases whole-body oxygen consumption. 1991, 104:97-104 Choo, J.J. et al., Am. J. Physiol. 1992, E50-E56 Rothwell, Nancy et al. Changes in tissue blood flow and Beta-Receptor density of skeletal muscle in rats, Br. J. Pharmacol. 1987, 90:601-607 Chen, Zheng. Nuclear Medicine Contributes to the Identification of Brown Adipose Tissue in Adult Human. J Nucl Med RadiatTher. 2012, 3:5 Vigen, Guy and Lichtenbelt, Wouter. Brown Adipose Tissue: clinical impact of a re-discovered thermogenic organ. Frontiers in Bioscience. 2013, E5:823-833 Lowell B.B. and Flier J. S. Brown Adipose Tissue, B3-Adrenergic receptors. Annu Rev Med 1997, 48:307-16 Whittle, Andrew. Searching for ways to switch on brown fat: are we getting warmer? Journal of Molecular Endocrinology. 2012, 49:R79-R87 Cypess A. and Kahn C.R.. CurrOpinEndocrinolDiabetestObes. 2010, 17(2):143-149 Cannon B. and Nedergaard J. Brown Adipose Tissue: Function and Physiological Significance. Physiol Rev. 2004, 84:277-359 Puigserver, P. et al., Induction and degradation of the uncoupling protein thermogenin in brown adipocytes in vitro and in vivo.Biochem J. 1992, 284:393-398 Iwami, M et al. Extract of grains of paradise and its active principle 6-paradol trigger thermogenesis of brown adipose tissue in rats. Automonic Neuroscience: Basic and Clinical. 2011, 161:63-67 Sugita, J. et al., Grains of Paradise (Aframomummelegueta) extract activates brown adipose tissue and increases whole-body energy expenditure in men. British Journal of Nutrition. 2012, 110(4):733-8 Yang, L.; Wang, Z.; Xu, L. Simultaneous determination of phenols (bibenzyl, phenanthrene, and fluorenone) in Dendrobiumspecies by high-performance liquid chromatography with diode array detection. J. Chromatogr. A. 2006, 1104, 230–237. Chen & Chen (1935). The pharmacological action of dendrobine. The Alkaloid of Chin-Shih-Hu. JPET, 55: 319-25. Sabelli, HC, Javaid, JI. Phenylethylamine modulation of affect: therapeutic and diagnostic implications. J Neuropsychiatry ClinNeurosci. 1995, 7(1): 6-14. Szabo, A, Billett, E, Turner, J. Phenylethylamine Br J Sports Med 2001; 35: 342-3. Bailey, BA, Phillips, SR, Boulton, AA. In vivo release of endogenous dopamine, 5-hydroxytryptamine and some of their metabolites from rat caudate nucleus by phenylethylamine. Neurochem Res. 1987, 12: 173-178. Janssen, PA, Leysen, JE, Megens, AA, Awouters, FH. Int J Neuropsychopharmcol1999; 2: 229-240. Knoll, J. Enhancer regulation/Endogenous and Synthetic Enhancer Compounds: A Neurochemical Concept of the Innate and Acquired Drives. Neurochem Res 2003, 28:1187-1209. Shannon, HE, Thompson, WA. Behavior maintained under fixed interval and second-order schedules by intravenous injections of endogenous noncatecholicphenylethylamines in dogs. J PharmacolExpTher 1984; 228: 691-5. Fuxe, K, Grobecker, H, Jonsson, J. The effect of β-phenylethylamine on central and peripheral monoamine-containing neurons. Eur J Pharmacol 1967; 2: 202-7. Bolton, Sanford (1981). “Caffeine: Psychological Effects, Use and Abuse”. OrthomolecularPsychiatry 10 (3): 202–211. Kaplan GB, Greenblatt DJ, Ehrenberg BL, et al., Dose-dependent pharmacokinetics and psychomotor effects of caffeine in humans. J ClinPharmacol. 1997 Aug;37(8):693-703 Smith A. Effects of caffeine on human behavior. Food ChemToxicol. 2002 Sep;40(9):1243-1255 Ryu S, Choi SK, Joung SS, Suh H, Cha YS, Lee S, Lim K. “Caffeine as a lipolytic food component increases endurance performance in rats and athletes.” J NutrSciVitaminol 2001 Apr: 47(2): 139-46. Yao, X., et al., Coupling ligand structure to specific conformational switches in the beta2-andenoceptor. Nat ChemBiol, 2006. 2(8): p. 417-22. Davis, C.B. and B.J. Camp, The vasoactive potential of halostachine, an alkaloid of tall fescue (Festucaarundinaceae, Schreb) in cattle. Vet Hum Toxicol, 1983. 25(6): p. 408-11 Shannon, H.E., E.J. Cone, and D. Yousefnejad, Physiologic effects and plasma kintetics of phenylethanolamine and its N-methyl homolog in the dog. J PharmacolExpTher. 1981. 217(2): p. 379-85.K. K. Chen, C.-K. Wu and E. Henriksen (1929). “Relationship between the pharmacological action and the chemical constitution and configuration of the optical isomers of ephedrine and related compounds.” J. Pharmacol. Exp. Ther. 36 363-400. Tsukiyama, M; Ueki, T; Yasuda, Y; Kikuchi, H; Akaishi, T; Okumura, H; Abe, K (2009). “Beta2-adrenoceptor-mediated tracheal relaxation induced by higenamine from Nandinadomestica Thunberg”. Plantamedica 75 (13): 1393–9. Kimura, I; Makino, M; Takamura, Y; Islam, MA., Kimura, M. Positive chronotropic and inotropic effects of higenamine, Jpn J Pharmacol. 1994 Sep; 66(1): 75-80 Bai, G; Yang, Y; Shi, Q; Liu, Z; Zhang, Q; Zhu, YY., Identification of higenamine in Radix AconitiLateralisPreparata as a beta2-andrenergic receptor agonist1. ActaPharmacol Sin. 2008 Oct; 29(10): 1187-94. Tsukiyama, M., et al., Beta2-adrenoceptor-mediated tracheal relaxation induced by higenamine from Nandinadomestica Thunberg. Planta Med, 2009. 75(13): p. 1393-9. Kang, Y.J., et al., Inhibition of activation of nuclear factor kappaB is responsible for inhibition of inducible nitric oxide synthase expression by higenamine, an active component of aconite root. J PharmacolExpTher, 1999. 291(1): p. 314-20. T.A. Wheaton and I. Stewart (1970) Lloydia33 244-254. T.A. Smith (1977). “Phenethylamine and related compounds in plants.” Phytochem. 16 9-18 J. Lundstrom (1989). “B-Phenethylamines and ephedrines of plant origin. “In The Alkaloids, Vol. 35” A. Brossi, Ed. pp. 77-154. H.J. Hapke and W. Strathmann (1995). “Pharmacological effects of hordenine.” Dtsch. Tierarztl. Wochenschr. 102 228-232 Wainscott DB, Sasso DA, Kursar JD, Baez M, Lucaites VL, Nelson DL (January 1998). “Rauwolscine: an antagonist radioligand for the cloned human 5-hydroxtryptamine2b (5-HT2B) receptor.” Naunyn-Schmiedeberg’s Archives of Pharmacology 357(1): 17-24. Berlan M, Galitzky J, Riviere D, et al., Plasma catecholamine levels and lipid mobilization induced by yohimbine . . . .. Int J Obes. 1991 May: 15(5): 305-315 Galitzky J, Taouls M, Berian M, et al., Alpha 2-antagonist compounds and lipid mobilization: evidence for a lipid mobilizing effect of oral yohimbine in healthy male volunteers. Eur J Clin Invest. 1988 Dec: 18(6): 587-594 Perry BD, U’Prichard DC. [3H]rauwolscine (alpha-yohimbine): a specific antagonist radioligand for brain alpha 2-adrenergic receptors. Eur J Pharmacol. 1981 Dec 17: 76(4): 461-464 Kawada T, Watanabe T, Takaishi T, et al., (1986) Capsaicininduced beta-adrenergic action on energy metabolism in rats: influence of capsaicin on oxygen consumption, the respiratory quotient, and substrate utilization. ProcSocExpBiol Med 183, 250–256. Kawada T, Hagihara K & Iwai K (1986) Effects of capsaicin on lipid metabolism in rats fed a high fat diet. J Nutr 183,1272–1278. Yoshioka M, Lim K, Kikuzato S, et al., (1995) Effects of red-pepper diet on the energy metabolism in men. J NutrSciVitaminol 41, 647–656. Lejeune MP, Kovacs EM &Westerterp-Plantenga MS (2003) Effects of capsaicin on substrate oxidation and weight maintenance after modest body-weight loss in human subjects. Br J Nutr 90, 651–659. Ludy MJ, MooreGE&MattesRD(2012) The effects of capsaicin and capsiate on energy balance: critical review and metaanalyses of studies in humans. Chem Senses 37, 103–121. Yoneshiro T, Aita S, Matsushita M, et al., (2011) Age-related decrease in cold-activated brown adipose tissue and accumulation of body fat in healthy humans. Obesity 19, 1755–1760. Gbolade A.. J Ethnopharmacol. 2012 Oct 31;144(1):1-10. Adefegha SA, Oboh G. Acetylcholinesterase (AChE) inhibitory activity, antioxidant properties and phenolic composition of two Aframomum species. J Basic ClinPhysiolPharmacol. 2012 Sep 26;0(0):1-9 NOTE: PHENBUTEROL is a trade name and is not intended to depict any comparison to any pharmaceutical or other product or any particular benefit thereof. *THESE STATEMENTS HAVE NOT BEEN EVALUATED BY THE FOOD AND DRUG ADMINISTRATION. MUSCLEMEDS PRODUCTS ARE NOT INTENDED TO DIAGNOSE, TREAT, CURE OR PREVENT ANY DISEASE.


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