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Chicago — June 1st, 2011 — Nutrigenomics Research Company has announced the release of its innovative, new supplement- Cabergolean.
Cabergolean is the most powerful HGH Booster, Prolactin Inhibitor, and Nutraceutical Nootropic ever to be sold as a nutritional supplement. Cabergolean also acts as a powerful Nitric Oxide (NO) Releaser, and Sleep Enhancer. Cabergolean naturally increases endogenous production of HGH through a clinically proven increase in GHRH (Growth Hormone Releasing Hormone) and through the suppression of GHIH (Growth Hormone Inhibiting Hormone or Somatostatin).
Cabergolean is a clinically proven, proprietary formula that you will not find in any other HGH Booster.
Here is what the science behind Cabergolean clearly communicates:
Cabergolean improves memory and the ability to focus
Cabergolean improves memory and the ability to focus by increasing the amount of the neurotransmitter Acetylcholine and Dopamine. Acetylcholine is involved with synaptic plasticity, specifically in learning, short-term memory and the ability to sustain attention and focus. Studies involving Dopamine's effects on cognitive performance clearly illustrate the link between enhanced cognitive performance and Dopamine production(28,29).
Huperzine A, N-Acetyl-L-Carnitine, Pantothenic Acid, and dimethylethanolamine (DMAE) either facilitate the release and synthesis of Acetylcholine or inhibit Acetylcholinesterase (an enzyme that degrades Acetylcholine)(4,5,15).
Cabergolean also employs the use of N-Acetyl-L-Carnitine. N-Acetyl-L-Carnitine has been shown to improve memory, increase energy and allow the energy-producing organelles in our cells (mitochondria) to work more effectively by protecting them from free radicals(20,21). Cabergolean also employs NADH as a scavenger of free radicals. NADH is also referred to as Coenzyme 1. NADH (or Coenzyme 1) executes the scavenging of free radicals better than any other biological substance known to the body.
Cabergolean improves HGH output
Cabergolean significantly improves growth hormone production, and it does so in a two-fold process. The this two-fold process is critical! You can increase the production of growth hormone with many supplements; however, if Somatostatin is present than there will be no release or "pulse" of HGH. Somatostatin acts as a gate for your endocrine system so that HGH is not released from your Anterior Pituitary Gland.
1. Cabergolean produces a significant rise in plasma growth hormone via the production of L-Dopa which is found in Mucuna Pruriens and synthesized from the amino acid N-Acetyl-L-Tyrosine(3,6,7,33) and the coenzyme beta-nicotinamide adeninedinucleotide (NADH)(26). As a matter of fact, one University study showed that 90 minutes after oral administration of 500mg L-Dopa, plasma GH levels increased from less than 1 ng/ml to 21.7 +/- 4.7 ng/ml in "most normal subjects"(34) (meaning those individuals without endocrine disease of any sort). That is over a 2000% increase in plasma GH.
2. Cabergolean inhibits the production of Somatostatin via the increase in the neurotransmitter Acetylcholine(22). Huperzine A, N-Acetyl-L-Carnitine, Pantothenic Acid, and dimethylethanolamine (DMAE) either facilitate the release and synthesis of Acetylcholine or inhibit Acetylcholinesterase (an enzyme that degrades Acetylcholine)(4,5,15).
Let us further elucidate the importance of utilizing a dietary supplement that both increases HGH output and inhibits Somatostatin:
As you can see in the diagram below both Somatostatin and GHRH (Growth Hormone Releasing Hormone) are released from the Hypothalamus. You also see that once the HGH is synthesized by the Pituitary Gland it goes into a "waiting area" or pool to be released.
Invalid Link Removed
Somatostatin inhibits the "flood gates" from being opened and a subsequent release of GHRH to the Pituitary Gland. Somatostatin also inhibits the "flood gates" from being opened and a subsequent release of HGH by the Pituitary Gland. So the key here is to "flood the pool" via the production of L-Dopa, which stimulates the Hypothalamus to produce GHRH and deliver it to the Pituitary Gland(6,7,8,33), and then to open the "flood gates", by inhibiting Somatostatin, via the production of Acetylcholine(25). Cabergolean inhibits Somatostatin by increasing the synthesis of Acetylcholine and inhibiting Acetylcholinesterase (an enzyme that degrades Acetylcholine). So now that the pool is full and Somatostatin is inhibited, the "flood gates" are opened and we have a SIGNIFICANT release of HGH.
One last note on efficacy of Cabergolean as a L-Dopa producer. Many supplement enthusists are familiar Mucuna Pruriens as a compound to increase L-Dopa; however, there is a powerful coenzyme that is not included in any other HGH boosters (that we could find) that is significantly more efficacious than Mucuna Pruriens in increasing L-Dopa levels. That coenzyme is beta-nicotinamide adeninedinucleotide or NADH- and you will only find it in Nutrigenomic Research Company's HGH Booster.
Here is how NADH works:
NADH triggers the activation of tyrosine-hydroxylase. Tyrosine hydroxylase or tyrosine 3-monooxygenase is the enzyme responsible for catalyzing the conversion of the amino acid L-Tyrosine (an ingredient in Cabergolean) to L-Dopa(31,32).
Cabergolean reduces prolactin levels
Prolactin is a hormone produced by the Anterior Pituitary Gland primarily associated with lactation and plays a vital role in breast development during pregnancy. Now if you are a pregnant female or you plan on becoming a pregnant female in the near future, then Cabergolean is NOT for you; however, if you are a casual fitness enthusiast or any type of athlete then excess Prolactin may not be for you! Prolactin also acts as an inhibitor of Gonadotropin Hormone Releasing Hormone (GnRH) neurons, which indirectly stimulates the production of LH (Luteinizing Hormone) and Testosterone(9).
For years athletes consumed aromatase inhibitor supplements to reduce signs of gynecomastia and improve their libido. The reality is that these products did work well for some individuals, but they certainly did not work well for all! Estrogen is a very essential hormone for both males and females and lowering circulating estrogen levels was not the panacea that supplement companies claimed it would be.
Why might your prolactin levels be elevated?
Prolactin levels increase as we age and if you are under any doctor supervised HRT that includes Testosterone or HGH then your Prolactin levels are most likely elevated. Also, any OTC supplement that increase DHEA or HGH will most certainly increase Prolactin levels significantly.
Research communicates that lowering clinically high Prolactin levels can improve libido significantly! Eliminate or reduce the signs of gynecomastia! Improve sperm motility! And increase Testosterone(9,30)! The decrease in Prolactin levels come via the increase in Dopamine from the compounds Mucuna Pruriens Extract, N-Acetyl-L-Tyrosine, and NADH (beta-nicotinamide adeninedinucleotid).
Cabergolean Increases Nitric Oxide (NO) bioavailability
Cabergolean Increases Nitric Oxide (NO) bioavailability via NADH (beta-nicotinamide adeninedinucleotid)(27). The Coenzyme of the enzyme NO-Synthase is NAHD. The more NADH available, the more NO can be produced. NO mediates vasodilation (an expansion of the internal diameter of blood vessels), which in turn leads to increased blood flow, oxygen transport, delivery of nutrients to skeletal muscle and a reduction in blood pressure. One of the leading experts on NO research, investigated the effect of NADH on NO production and said "NADH stimulates NO production ten times more than any other substance I have tested so far(35).“
Cabergolean improves sleep
Improved sleep quality comes via the increase in delta wave sleep (stage 3 sleep) and REM sleep (stage 4 sleep). There is a direct correlation between the increase of HGH and IGF-1 (which is produced by the liver as a result of HGH production) and delta wave sleep (stage 3 sleep)(23). The improvement in the quality of REM sleep (stage 4 sleep) comes via the increase in acetylcholine(24). Cabergolean increases both delta wave sleep and REM sleep!
In conclusion, Cabergolean is the most effective orally administered HGH Releaser, Nutraceutical Nootropic, Nitric Oxide (NO) Enhancer, Sleep Enhancer and Prolactin Inhibitor EVER offered in the history of sports nutrition.
For more information, you can contact Nutrigenomics Research Company at [email protected]
Studies and Clinical Info:
(1) Ohtsuka S, Oyake Y, Seo Y, Eda K, Yamaguchi I. Magnesium sulphate infusion suppresses the cardiac release of noradrenaline during a handgrip stress test.Can J Cardiol. 2002 Feb;18(2):133-40.
(2) International Journal of Pharmaceutical Compounding. Nicotinamide-Adenine Dinucleotide (NADH) in Parkinson's Disease and Alzheimer's Disease. Author(s): Glasnapp Andrew, Schaefer Erin. Issue: Jul/Aug 2000 - Compounding for Hospice and Cancer Patients
(3) Niesko Pras, Paul G. M. Hesselink, Jan ten Tusscher, Theo M. Malingré. Biotechnology and Bioengineering. Volume 34. pages 214–222, 20 June 1989. Kinetic aspects of the bioconversion of L-tyrosine into L-DOPA by cells of Mucuna pruriens L. Entrapped in different matrices
(4) Br J Pharmacol, 1988 September; 95(1):77. Effects of ethanol and pantothenic acid on brain acetylcholine synthesis. L. Rivera-Calimlim, D. Hartley, and D. Osterhout. Department of Pharmacology, University of Rochester, School of Medicine and Dentistry, NY 14642.
(5) Eur J Med Res. 2003 May 30;8(5):183-91. Dimpfel W, Wedekind W, Keplinger I. Efficacy of dimethylaminoethanol (DMAE) containing vitamin-mineral drug combination on EEG patterns in the presence of different emotional states. Pro Science, Private Research Clinic GmbH - med. Forschung und Entwicklung -, Kurt-Schumacher-Str. 9, D-35440 Linden, Germany. [email protected]
(6) N Engl J Med 1970; 283:1425-1429December 24, 1970. Hanes, K., Tanaka, A, and Utsumi, A. Plasma GH responses to GHRH, arginine, L-dopa, pyridostigmine, sequential administration of GHRH and combined administration of PD and GHRH in Turner’s syndrome. J. Endocrinol. Invest. 1998. Feb.; 21(2): 72-77.
(7) Fevang FO, Stoa RF, Thorsen T, Aarskog D. The Effect of L-dopa with and without decarboxylase inhibitor on growth hormone secretion in children with short stature. Acta Paediatr Scand. 1977 Jan; 66(1):81-84
(8) Gordon M, Markham J, Hartlein JM, Koller JM, Loftin S, Black KJ. Intravenous levodopa administration in humans based on a two-compartment kinetic model. J. Neurosci Methods, 2007 Jan 30:159(2):300-307. Epub 2006 Aug 24
(9) Proc. Nati. Acad. Sci. USA Vol. 91, pp. 1244-1247, February 1994. Inhibition of gonadotropin hormone-releasing hormone release by prolactin from GT1 neuronal cell lines through prolactin receptors. JILJANA MILENKOVI*, GISELA D'ANGELO*, PAUL A. KELLY, AND RICHARD I. WEINER*. *Reproductive Endocrinology Center, University of California School of Medicine, San Francisco, CA 94143; and Unit Endocrinologie Molculaire Facult de Medecine Necker-Enfants Malades, Paris 75743, France
(10) Modi KP, Patel NM, Goyal RK. Estimation of L-dopa from Mucuna pruriens LINN and formulations containing M. pruriens by HPTLC method. Chem Pharm Bull (Tokyo). 2008 Mar: 56(3): 357-359.
(11) Ahmad MK, Mahdi AA, Shukla KK, Islam N, Jaiswar SP, Ahmad S. Effect of Mucuna pruriens on semen profile and biochemical parameters in seminal plasma of infertile men. Fertil Steril. 2008 Sep;90(3):627-35. Epub 2007 Nov 14.
(12) Shukla KK, Mahdi AA, Ahmad MK, Shankhwar SN, Rajender S, Jaiswar SP. Mucuna pruriens improves male fertility by its action on the hypothalamus-pituitary-gonadal axis. Fertil Steril. 2008 Oct 28. [Epub ahead of print]
(13) Vaidya RA, Aloorkar SD, Sheth AR, Pandya SK. Activity of bromoergocryptine, Mucuna pruriens and L-dopa in the control of hyperprolactinaemia. Neurol India. 1978 Dec;26(4):179-82.
(14) Vaidya RA, Sheth AR, Aloorkar SD, Rege NR, Bagadia VN, Devi PK, Shah LP. The inhibitory effect of the cowhage plant- mucuna pruriens-and L-dopa on chloropromazine-induced hyperprolactinemia. Neurol India. 1978 Dec;26(4):177-8.
(15) Wang R, Yan H, Tang XC. Progress in studies of huperzine A, a natural cholinesterase inhibitor from Chinese herbal medicine. Acta Pharmacol Sin. 2006 Jan;27(1):1-26
(16) Liang YQ, Tang XC. Comparative studies of huperzine A, donepezil, and rivastigmine on brain acetylcholine, dopamine, norepinephrine, and 5-hydroxytryptamine levels in freely-moving rats. Acta Pharmacol Sin. 2006 Sep;27(9):1127-36
(17) Li YX, Zhang RQ, Li CR, Jiang XH. Pharmacokinetics of huperzine A following oral administration to human volunteers. Eur J Drug Metab Pharmacokinet. 2007 Oct-Dec;32(4):183-7.
(18) DI MARZIO L.; MORETTI S. ; D'ALO S. ; ZAZZERONI F. ; MARCELLINI S. ; SMACCHIA C. ; ALESSE E. ; CIFONE M. G. ; DE SIMONE C. Clin Immunol. 1999 Jul;92(1):103-10. Acetyl-l-carnitine administration increases insulin-like growth factor 1 levels in asymptomatic HIV-1-infected subjects : Correlation with its suppressive effect on lymphocyte apoptosis and ceramide generation.
(19) Kraemer WJ, Spiering BA, Volek JS, Ratamess NA, Sharman MJ,Rubin MR, French DN, Silvestre R, Hatfield DL, Van Heest JL, Vingren JL, Judelson DA, Deschenes MR, Maresh CM. Androgenic responses to resistance exercise: effects of feeding and L-carnitine. Med Sci Sports Exer., 2006 Jul: 38(7): 1288-96.
(20) Ann N Y Acad Sci. 2004 Nov;1033:108-16. Delaying the mitochondrial decay of aging with acetylcarnitine. Ames BN, Liu J. Nutritional Genomics Center, Children's Hospital Oakland Research Institute, Oakland, CA 94609, USA. [email protected].
(21) Memory loss in old rats is associated with brain mitochondrial decay and RNA/ DNA oxidation: Partial reversal by feeding acetyl-L-carnitine and or alpha lipoic acid. Jiankang Liu, Elizabeth Head, Afshin M. Gharib, Wenjun Yuan, Russell T. Ingersoll, Tory M. Hagen, Carl W. Cotman, and Bruce N. Ames. Division of Biochemistry and Molecular Biology, University of California, Berkeley, CA 94720; Children’s Hospital Oakland Research Institute, 5700 Martin Luther King, Jr., Way, Oakland, CA 94609; Institute for Brain Aging and Dementia, University of California, Irvine, CA 92697-4540; and Department of Biochemistry and Biophysics, Linus Pauling Institute, Oregon State University, Corvallis, OR 97331
(22) Int J Dev Neurosci. 1998 Nov-Dec;16(7-8):795-802. delta 1-Opioid receptor-mediated control of acetylcholine (ACh) release in human neocortex slices. Feuerstein TJ, Albrecht C, Wessler I, Zentner J, Jackisch R.
(23) J Gerontol A Biol Sci Med Sci. 1995 Jul;50(4):M222-6. Higher plasma IGF-1 levels are associated with increased delta sleep in healthy older men. Prinz PN, Moe KE, Dulberg EM, Larsen LH, Vitiello MV, Toivola B, Merriam GR.
(24) Annu Rev Pharmacol Toxicol. 1987;27:137-56. Acetylcholine and the regulation of REM sleep: basic mechanisms and clinical implications for affective illness and narcolepsy. Shiromani PJ, Gillin JC, Henriksen SJ.
(25) Journal of Neuroendocrinology. Volume 2, Issue 4, pages 429–432, August 1990. Pyridostigmine, an Acetylcholinesterase Inhibitor, Stimulates Growth Hormone Release, but has no Effect on Basal Thyrotrophin or Adrenocorticotrophin Levels, or the Thyrotrophin Response to Thyrotrophin-Releasing Hormone. Emma Freeman, Rick Touzel, Ashley Grossman, Michael Besser, Richard Ross
(26) Stimulation of endogenous L-dopa biosynthesis — a new principle for the therapy of Parkinson's disease. The clinical effect of nicotinamide adenine dinucleotide (NADH) and nicotinamide adenine dinucleotidephosphate (NADPH). G.J.D. Birkmayer, W. Birkmayer. Acta Neurologica Scandinavica. Volume 80, Issue Supplements 126, pages 183–187,November 1989
(27) Acta Biochim Pol. 2004;51(2):459-69. Endothelial NADH/NADPH-dependent enzymatic sources of superoxide production: relationship to endothelial dysfunction. Kalinowski L, Malinski T. Department of Clinical Chemistry and Laboratory of Cellular and Molecular Nephrology, Medical Research Centre of the Polish Academy of Science, Medical University of Gdańsk, Poland.
[28] Nieoullon A. Dopamine and the regulation of cognition and attention. Prog Neurobiol 2002;67:53–83.
[29] Kulisevsky J. Role of dopamine in learning and memory: implications for the treatment of cognitive dysfunction in patients with Parkinson's disease. Drugs Aging 2001;16:65-7
(30) European Journal of Endocrinology (2003) 148 325–33. Gender differences in the prevalence, clinical features and response to cabergoline in hyperprolactinemia. Annamaria Colao, Antonella Di Sarno, Paolo Cappabianca, Francesco Briganti, Rosario Pivonello, Carolina Di Somma, Antongiulio ***giano, Bernadette Biondi and Gaetano Lombardi. Departments of Molecular and Clinical Endocrinology and Oncology, Section of Endocrinology and Neurological Sciences, Section of Neurosurgery and Section of Neuroradiology, ‘Federico II’ University of Naples, via S. Pansini 5, 80131 Naples, Italy
(31) Kaufman S (1995). "Tyrosine hydroxylase". Adv. Enzymol. Relat. Areas Mol. Biol. 70: 103–220.
(32) Nagatsu T (1995). "Tyrosine hydroxylase: human isoforms, structure and regulation in physiology and pathology". Essays Biochem. 30: 15–35.
(33) Dopaminergic Regulation of Gonadotropin and Thyrotropin Hormone Secretion Is Altered with Age. Susan L. Greenspan, David Sparrow, John W. Rowe. Horm Res 1991;36:41-46 (DOI: 10.1159/000182105).
(34) Effect of oral administration of L-dopa on the plasma levels of growth hormone-releasing hormone (GHRH) in normal subjects and patients with various endocrine and metabolic diseases. Mitsuhashi S, Yamasaki R, Miyazaki S, Saito H, Saito S. First Department of Internal Medicine, School of Medicine, University of Tokushima, Japan. Nippon Naibunpi Gakkai Zasshi. 1987 Aug 20;63(8):934-46.
(35) NADH: The Biological Hydrogen: The Secret of Our Life Energy, George D. Birkmayer, Basic Health Publications, Inc., 2009
Chicago — June 1st, 2011 — Nutrigenomics Research Company has announced the release of its innovative, new supplement- Cabergolean.
Cabergolean is the most powerful HGH Booster, Prolactin Inhibitor, and Nutraceutical Nootropic ever to be sold as a nutritional supplement. Cabergolean also acts as a powerful Nitric Oxide (NO) Releaser, and Sleep Enhancer. Cabergolean naturally increases endogenous production of HGH through a clinically proven increase in GHRH (Growth Hormone Releasing Hormone) and through the suppression of GHIH (Growth Hormone Inhibiting Hormone or Somatostatin).
Cabergolean is a clinically proven, proprietary formula that you will not find in any other HGH Booster.
Here is what the science behind Cabergolean clearly communicates:
Cabergolean improves memory and the ability to focus
Cabergolean improves memory and the ability to focus by increasing the amount of the neurotransmitter Acetylcholine and Dopamine. Acetylcholine is involved with synaptic plasticity, specifically in learning, short-term memory and the ability to sustain attention and focus. Studies involving Dopamine's effects on cognitive performance clearly illustrate the link between enhanced cognitive performance and Dopamine production(28,29).
Huperzine A, N-Acetyl-L-Carnitine, Pantothenic Acid, and dimethylethanolamine (DMAE) either facilitate the release and synthesis of Acetylcholine or inhibit Acetylcholinesterase (an enzyme that degrades Acetylcholine)(4,5,15).
Cabergolean also employs the use of N-Acetyl-L-Carnitine. N-Acetyl-L-Carnitine has been shown to improve memory, increase energy and allow the energy-producing organelles in our cells (mitochondria) to work more effectively by protecting them from free radicals(20,21). Cabergolean also employs NADH as a scavenger of free radicals. NADH is also referred to as Coenzyme 1. NADH (or Coenzyme 1) executes the scavenging of free radicals better than any other biological substance known to the body.
Cabergolean improves HGH output
Cabergolean significantly improves growth hormone production, and it does so in a two-fold process. The this two-fold process is critical! You can increase the production of growth hormone with many supplements; however, if Somatostatin is present than there will be no release or "pulse" of HGH. Somatostatin acts as a gate for your endocrine system so that HGH is not released from your Anterior Pituitary Gland.
1. Cabergolean produces a significant rise in plasma growth hormone via the production of L-Dopa which is found in Mucuna Pruriens and synthesized from the amino acid N-Acetyl-L-Tyrosine(3,6,7,33) and the coenzyme beta-nicotinamide adeninedinucleotide (NADH)(26). As a matter of fact, one University study showed that 90 minutes after oral administration of 500mg L-Dopa, plasma GH levels increased from less than 1 ng/ml to 21.7 +/- 4.7 ng/ml in "most normal subjects"(34) (meaning those individuals without endocrine disease of any sort). That is over a 2000% increase in plasma GH.
2. Cabergolean inhibits the production of Somatostatin via the increase in the neurotransmitter Acetylcholine(22). Huperzine A, N-Acetyl-L-Carnitine, Pantothenic Acid, and dimethylethanolamine (DMAE) either facilitate the release and synthesis of Acetylcholine or inhibit Acetylcholinesterase (an enzyme that degrades Acetylcholine)(4,5,15).
Let us further elucidate the importance of utilizing a dietary supplement that both increases HGH output and inhibits Somatostatin:
As you can see in the diagram below both Somatostatin and GHRH (Growth Hormone Releasing Hormone) are released from the Hypothalamus. You also see that once the HGH is synthesized by the Pituitary Gland it goes into a "waiting area" or pool to be released.
Invalid Link Removed
Somatostatin inhibits the "flood gates" from being opened and a subsequent release of GHRH to the Pituitary Gland. Somatostatin also inhibits the "flood gates" from being opened and a subsequent release of HGH by the Pituitary Gland. So the key here is to "flood the pool" via the production of L-Dopa, which stimulates the Hypothalamus to produce GHRH and deliver it to the Pituitary Gland(6,7,8,33), and then to open the "flood gates", by inhibiting Somatostatin, via the production of Acetylcholine(25). Cabergolean inhibits Somatostatin by increasing the synthesis of Acetylcholine and inhibiting Acetylcholinesterase (an enzyme that degrades Acetylcholine). So now that the pool is full and Somatostatin is inhibited, the "flood gates" are opened and we have a SIGNIFICANT release of HGH.
One last note on efficacy of Cabergolean as a L-Dopa producer. Many supplement enthusists are familiar Mucuna Pruriens as a compound to increase L-Dopa; however, there is a powerful coenzyme that is not included in any other HGH boosters (that we could find) that is significantly more efficacious than Mucuna Pruriens in increasing L-Dopa levels. That coenzyme is beta-nicotinamide adeninedinucleotide or NADH- and you will only find it in Nutrigenomic Research Company's HGH Booster.
Here is how NADH works:
NADH triggers the activation of tyrosine-hydroxylase. Tyrosine hydroxylase or tyrosine 3-monooxygenase is the enzyme responsible for catalyzing the conversion of the amino acid L-Tyrosine (an ingredient in Cabergolean) to L-Dopa(31,32).
Cabergolean reduces prolactin levels
Prolactin is a hormone produced by the Anterior Pituitary Gland primarily associated with lactation and plays a vital role in breast development during pregnancy. Now if you are a pregnant female or you plan on becoming a pregnant female in the near future, then Cabergolean is NOT for you; however, if you are a casual fitness enthusiast or any type of athlete then excess Prolactin may not be for you! Prolactin also acts as an inhibitor of Gonadotropin Hormone Releasing Hormone (GnRH) neurons, which indirectly stimulates the production of LH (Luteinizing Hormone) and Testosterone(9).
For years athletes consumed aromatase inhibitor supplements to reduce signs of gynecomastia and improve their libido. The reality is that these products did work well for some individuals, but they certainly did not work well for all! Estrogen is a very essential hormone for both males and females and lowering circulating estrogen levels was not the panacea that supplement companies claimed it would be.
Why might your prolactin levels be elevated?
Prolactin levels increase as we age and if you are under any doctor supervised HRT that includes Testosterone or HGH then your Prolactin levels are most likely elevated. Also, any OTC supplement that increase DHEA or HGH will most certainly increase Prolactin levels significantly.
Research communicates that lowering clinically high Prolactin levels can improve libido significantly! Eliminate or reduce the signs of gynecomastia! Improve sperm motility! And increase Testosterone(9,30)! The decrease in Prolactin levels come via the increase in Dopamine from the compounds Mucuna Pruriens Extract, N-Acetyl-L-Tyrosine, and NADH (beta-nicotinamide adeninedinucleotid).
Cabergolean Increases Nitric Oxide (NO) bioavailability
Cabergolean Increases Nitric Oxide (NO) bioavailability via NADH (beta-nicotinamide adeninedinucleotid)(27). The Coenzyme of the enzyme NO-Synthase is NAHD. The more NADH available, the more NO can be produced. NO mediates vasodilation (an expansion of the internal diameter of blood vessels), which in turn leads to increased blood flow, oxygen transport, delivery of nutrients to skeletal muscle and a reduction in blood pressure. One of the leading experts on NO research, investigated the effect of NADH on NO production and said "NADH stimulates NO production ten times more than any other substance I have tested so far(35).“
Cabergolean improves sleep
Improved sleep quality comes via the increase in delta wave sleep (stage 3 sleep) and REM sleep (stage 4 sleep). There is a direct correlation between the increase of HGH and IGF-1 (which is produced by the liver as a result of HGH production) and delta wave sleep (stage 3 sleep)(23). The improvement in the quality of REM sleep (stage 4 sleep) comes via the increase in acetylcholine(24). Cabergolean increases both delta wave sleep and REM sleep!
In conclusion, Cabergolean is the most effective orally administered HGH Releaser, Nutraceutical Nootropic, Nitric Oxide (NO) Enhancer, Sleep Enhancer and Prolactin Inhibitor EVER offered in the history of sports nutrition.
For more information, you can contact Nutrigenomics Research Company at [email protected]
Studies and Clinical Info:
(1) Ohtsuka S, Oyake Y, Seo Y, Eda K, Yamaguchi I. Magnesium sulphate infusion suppresses the cardiac release of noradrenaline during a handgrip stress test.Can J Cardiol. 2002 Feb;18(2):133-40.
(2) International Journal of Pharmaceutical Compounding. Nicotinamide-Adenine Dinucleotide (NADH) in Parkinson's Disease and Alzheimer's Disease. Author(s): Glasnapp Andrew, Schaefer Erin. Issue: Jul/Aug 2000 - Compounding for Hospice and Cancer Patients
(3) Niesko Pras, Paul G. M. Hesselink, Jan ten Tusscher, Theo M. Malingré. Biotechnology and Bioengineering. Volume 34. pages 214–222, 20 June 1989. Kinetic aspects of the bioconversion of L-tyrosine into L-DOPA by cells of Mucuna pruriens L. Entrapped in different matrices
(4) Br J Pharmacol, 1988 September; 95(1):77. Effects of ethanol and pantothenic acid on brain acetylcholine synthesis. L. Rivera-Calimlim, D. Hartley, and D. Osterhout. Department of Pharmacology, University of Rochester, School of Medicine and Dentistry, NY 14642.
(5) Eur J Med Res. 2003 May 30;8(5):183-91. Dimpfel W, Wedekind W, Keplinger I. Efficacy of dimethylaminoethanol (DMAE) containing vitamin-mineral drug combination on EEG patterns in the presence of different emotional states. Pro Science, Private Research Clinic GmbH - med. Forschung und Entwicklung -, Kurt-Schumacher-Str. 9, D-35440 Linden, Germany. [email protected]
(6) N Engl J Med 1970; 283:1425-1429December 24, 1970. Hanes, K., Tanaka, A, and Utsumi, A. Plasma GH responses to GHRH, arginine, L-dopa, pyridostigmine, sequential administration of GHRH and combined administration of PD and GHRH in Turner’s syndrome. J. Endocrinol. Invest. 1998. Feb.; 21(2): 72-77.
(7) Fevang FO, Stoa RF, Thorsen T, Aarskog D. The Effect of L-dopa with and without decarboxylase inhibitor on growth hormone secretion in children with short stature. Acta Paediatr Scand. 1977 Jan; 66(1):81-84
(8) Gordon M, Markham J, Hartlein JM, Koller JM, Loftin S, Black KJ. Intravenous levodopa administration in humans based on a two-compartment kinetic model. J. Neurosci Methods, 2007 Jan 30:159(2):300-307. Epub 2006 Aug 24
(9) Proc. Nati. Acad. Sci. USA Vol. 91, pp. 1244-1247, February 1994. Inhibition of gonadotropin hormone-releasing hormone release by prolactin from GT1 neuronal cell lines through prolactin receptors. JILJANA MILENKOVI*, GISELA D'ANGELO*, PAUL A. KELLY, AND RICHARD I. WEINER*. *Reproductive Endocrinology Center, University of California School of Medicine, San Francisco, CA 94143; and Unit Endocrinologie Molculaire Facult de Medecine Necker-Enfants Malades, Paris 75743, France
(10) Modi KP, Patel NM, Goyal RK. Estimation of L-dopa from Mucuna pruriens LINN and formulations containing M. pruriens by HPTLC method. Chem Pharm Bull (Tokyo). 2008 Mar: 56(3): 357-359.
(11) Ahmad MK, Mahdi AA, Shukla KK, Islam N, Jaiswar SP, Ahmad S. Effect of Mucuna pruriens on semen profile and biochemical parameters in seminal plasma of infertile men. Fertil Steril. 2008 Sep;90(3):627-35. Epub 2007 Nov 14.
(12) Shukla KK, Mahdi AA, Ahmad MK, Shankhwar SN, Rajender S, Jaiswar SP. Mucuna pruriens improves male fertility by its action on the hypothalamus-pituitary-gonadal axis. Fertil Steril. 2008 Oct 28. [Epub ahead of print]
(13) Vaidya RA, Aloorkar SD, Sheth AR, Pandya SK. Activity of bromoergocryptine, Mucuna pruriens and L-dopa in the control of hyperprolactinaemia. Neurol India. 1978 Dec;26(4):179-82.
(14) Vaidya RA, Sheth AR, Aloorkar SD, Rege NR, Bagadia VN, Devi PK, Shah LP. The inhibitory effect of the cowhage plant- mucuna pruriens-and L-dopa on chloropromazine-induced hyperprolactinemia. Neurol India. 1978 Dec;26(4):177-8.
(15) Wang R, Yan H, Tang XC. Progress in studies of huperzine A, a natural cholinesterase inhibitor from Chinese herbal medicine. Acta Pharmacol Sin. 2006 Jan;27(1):1-26
(16) Liang YQ, Tang XC. Comparative studies of huperzine A, donepezil, and rivastigmine on brain acetylcholine, dopamine, norepinephrine, and 5-hydroxytryptamine levels in freely-moving rats. Acta Pharmacol Sin. 2006 Sep;27(9):1127-36
(17) Li YX, Zhang RQ, Li CR, Jiang XH. Pharmacokinetics of huperzine A following oral administration to human volunteers. Eur J Drug Metab Pharmacokinet. 2007 Oct-Dec;32(4):183-7.
(18) DI MARZIO L.; MORETTI S. ; D'ALO S. ; ZAZZERONI F. ; MARCELLINI S. ; SMACCHIA C. ; ALESSE E. ; CIFONE M. G. ; DE SIMONE C. Clin Immunol. 1999 Jul;92(1):103-10. Acetyl-l-carnitine administration increases insulin-like growth factor 1 levels in asymptomatic HIV-1-infected subjects : Correlation with its suppressive effect on lymphocyte apoptosis and ceramide generation.
(19) Kraemer WJ, Spiering BA, Volek JS, Ratamess NA, Sharman MJ,Rubin MR, French DN, Silvestre R, Hatfield DL, Van Heest JL, Vingren JL, Judelson DA, Deschenes MR, Maresh CM. Androgenic responses to resistance exercise: effects of feeding and L-carnitine. Med Sci Sports Exer., 2006 Jul: 38(7): 1288-96.
(20) Ann N Y Acad Sci. 2004 Nov;1033:108-16. Delaying the mitochondrial decay of aging with acetylcarnitine. Ames BN, Liu J. Nutritional Genomics Center, Children's Hospital Oakland Research Institute, Oakland, CA 94609, USA. [email protected].
(21) Memory loss in old rats is associated with brain mitochondrial decay and RNA/ DNA oxidation: Partial reversal by feeding acetyl-L-carnitine and or alpha lipoic acid. Jiankang Liu, Elizabeth Head, Afshin M. Gharib, Wenjun Yuan, Russell T. Ingersoll, Tory M. Hagen, Carl W. Cotman, and Bruce N. Ames. Division of Biochemistry and Molecular Biology, University of California, Berkeley, CA 94720; Children’s Hospital Oakland Research Institute, 5700 Martin Luther King, Jr., Way, Oakland, CA 94609; Institute for Brain Aging and Dementia, University of California, Irvine, CA 92697-4540; and Department of Biochemistry and Biophysics, Linus Pauling Institute, Oregon State University, Corvallis, OR 97331
(22) Int J Dev Neurosci. 1998 Nov-Dec;16(7-8):795-802. delta 1-Opioid receptor-mediated control of acetylcholine (ACh) release in human neocortex slices. Feuerstein TJ, Albrecht C, Wessler I, Zentner J, Jackisch R.
(23) J Gerontol A Biol Sci Med Sci. 1995 Jul;50(4):M222-6. Higher plasma IGF-1 levels are associated with increased delta sleep in healthy older men. Prinz PN, Moe KE, Dulberg EM, Larsen LH, Vitiello MV, Toivola B, Merriam GR.
(24) Annu Rev Pharmacol Toxicol. 1987;27:137-56. Acetylcholine and the regulation of REM sleep: basic mechanisms and clinical implications for affective illness and narcolepsy. Shiromani PJ, Gillin JC, Henriksen SJ.
(25) Journal of Neuroendocrinology. Volume 2, Issue 4, pages 429–432, August 1990. Pyridostigmine, an Acetylcholinesterase Inhibitor, Stimulates Growth Hormone Release, but has no Effect on Basal Thyrotrophin or Adrenocorticotrophin Levels, or the Thyrotrophin Response to Thyrotrophin-Releasing Hormone. Emma Freeman, Rick Touzel, Ashley Grossman, Michael Besser, Richard Ross
(26) Stimulation of endogenous L-dopa biosynthesis — a new principle for the therapy of Parkinson's disease. The clinical effect of nicotinamide adenine dinucleotide (NADH) and nicotinamide adenine dinucleotidephosphate (NADPH). G.J.D. Birkmayer, W. Birkmayer. Acta Neurologica Scandinavica. Volume 80, Issue Supplements 126, pages 183–187,November 1989
(27) Acta Biochim Pol. 2004;51(2):459-69. Endothelial NADH/NADPH-dependent enzymatic sources of superoxide production: relationship to endothelial dysfunction. Kalinowski L, Malinski T. Department of Clinical Chemistry and Laboratory of Cellular and Molecular Nephrology, Medical Research Centre of the Polish Academy of Science, Medical University of Gdańsk, Poland.
[28] Nieoullon A. Dopamine and the regulation of cognition and attention. Prog Neurobiol 2002;67:53–83.
[29] Kulisevsky J. Role of dopamine in learning and memory: implications for the treatment of cognitive dysfunction in patients with Parkinson's disease. Drugs Aging 2001;16:65-7
(30) European Journal of Endocrinology (2003) 148 325–33. Gender differences in the prevalence, clinical features and response to cabergoline in hyperprolactinemia. Annamaria Colao, Antonella Di Sarno, Paolo Cappabianca, Francesco Briganti, Rosario Pivonello, Carolina Di Somma, Antongiulio ***giano, Bernadette Biondi and Gaetano Lombardi. Departments of Molecular and Clinical Endocrinology and Oncology, Section of Endocrinology and Neurological Sciences, Section of Neurosurgery and Section of Neuroradiology, ‘Federico II’ University of Naples, via S. Pansini 5, 80131 Naples, Italy
(31) Kaufman S (1995). "Tyrosine hydroxylase". Adv. Enzymol. Relat. Areas Mol. Biol. 70: 103–220.
(32) Nagatsu T (1995). "Tyrosine hydroxylase: human isoforms, structure and regulation in physiology and pathology". Essays Biochem. 30: 15–35.
(33) Dopaminergic Regulation of Gonadotropin and Thyrotropin Hormone Secretion Is Altered with Age. Susan L. Greenspan, David Sparrow, John W. Rowe. Horm Res 1991;36:41-46 (DOI: 10.1159/000182105).
(34) Effect of oral administration of L-dopa on the plasma levels of growth hormone-releasing hormone (GHRH) in normal subjects and patients with various endocrine and metabolic diseases. Mitsuhashi S, Yamasaki R, Miyazaki S, Saito H, Saito S. First Department of Internal Medicine, School of Medicine, University of Tokushima, Japan. Nippon Naibunpi Gakkai Zasshi. 1987 Aug 20;63(8):934-46.
(35) NADH: The Biological Hydrogen: The Secret of Our Life Energy, George D. Birkmayer, Basic Health Publications, Inc., 2009