Premier HGH
The New 3rd Generation Human Growth Hormone (HGH) Releaser Product
That Works Best To Restore Your Youthful Vitality
Premier HGH
The New 3rd Generation Human Growth Hormone (HGH) Releaser Product
That Works Best To Restore Your Youthful Vitality
When You Consistently Use Premier HGH You Can Be Absolutely Sure
You Will Experience Exciting And Life Changing Results!
As you age your body produces less and less of it's own Human Growth Hormone or HGH. Your pituitary gland ages like a prune, shrivels and signals your body less often for HGH production and release. This fact is the major cause of aging and the associated annoying problems that come with it such as:
- Impaired sexual response
- Lack of libido
- Impaired sleep
- Belly fat
- Wrinkles, sagging skin, age spots
- Poor skin, nails, and hair
- Poor circulation
- Impaired memory
- Less energy and physical stamina
And much, much more.
From: The desk of Paul Miller
Dear Friend,
This is a lengthy page but I want you to be absolutely sure of my integrity. I want you to know that when I say something it is based on the fact that I have actually done my due diligence and have thoroughly researched a subject and have taken the product, Premier HGH, to see if I personally experienced great results by achieving increased Human Growth Hormone levels.
All people are different. One person may receive more or less benefit than someone else and some may see results faster than others; however; my own personal experience ( Premier HGH will turn you into a sexual Tyrannosaurus) along with the research files you'll read below strongly indicate you will soon experience very happy times with the results you receive from Premier HGH.
In the following research articles from PubMed.Com you'll see that the Key ingredients found in Premier HGH definitely do stimulate GH (Growth Hormone) release. Premier HGH contains these ingredients to help stimulate your pituitary to release more of your own Human Growth Hormone.
Arginine:
L-Glutamine and Glycine:
Broad Bean = Natural L-Dopa = GH Release
Erectile dysfunction, ED, or a lack of sexual stamina can cause all sorts of problems including self esteem issues. Erectile dysfuction can be caused by disease, not just low HGH levels, so it is always prudent to see your doctor to rule out things such as blockages in your coronary arteries and also other occlusions within your vascular system or diabetes.
The following research gives some strong suggestion, even proof, that increasing your HGH levels could bring the pleasure of sexual gratification back into your life if you currently suffer from ED.
You should now possess enough clinical research evidence to make an informed choice. Are you ready to change your life and enjoy the viatilty you deserve? You can have renewed youthful vitality in a few short weeks by stimulating your pituitary to release more of your own hGH.
Grow young with Premier HGH!
Kind regards,
P.S. Why go through life missing out on the vitality you once had? Make the decision right now to enjoy life again by using Premier HGH to safely increase your own HGH levels! By taking the next step you'll soon experience results that will re-affirm that you've made the best decision of your entire life.
P.P.S. Remember - Premier HGH comes with a 60 day 100% satisfaction retail purchase guarantee. You have nothing to lose and everything to gain. Order your supply of Premier HGH right now.
Scientific Research On The Primary Human Growth Hormone (HGH) Releasing Ingredients In Premier HGH
Growth Horm IGF Res. 2005 Apr;15(2):136-9. Epub 2005 Jan 26.
Growth hormone responses to varying doses of oral arginine.
Collier SR, Casey DP, Kanaley JA.
Department of Exercise Science, Syracuse University, 820 Comstock Avenue, Room 201, Syracuse, NY 13244, USA.
Intravenous (IV) arginine invokes an increase in growth hormone (GH) concentrations, however, little is known about the impact of oral arginine ingestion on the GH response.
OBJECTIVE: The purpose of this study was to determine the dose of oral arginine that elicits an optimal GH response and to determine the time course of the response.
DESIGN: Eight healthy males (18-33 years - 24.8+/-1.2 years) were studied on 4 separate occasions. Following an overnight fast at 0700 h, a catheter was placed in a forearm vein. Blood samples were taken every 10 min for 5 h. Thirty minutes after sampling was initiated, the subject ingested a dose of arginine (5, 9 or 13 g) or placebo (randomly assigned).
RESULTS: Mean resting GH values for the placebo, 5, 9 and 13 g day were 0.76, 0.67, 2.0 and 0.79 microg/L (n=6), respectively. Integrated area under the curve was not different with 13 g (197.8+/-65.7 min microg/L), yet it increased with 5 and 9 g compared with the placebo (301.5+/-74.6, 524.28+/-82.9 and 186.04+/-47.8 min microg/L, respectively, P<0.05). Mean peak GH levels were 2.9+/-0.69, 3.9+/-0.85, 6.4+/-1.3 and 4.73+/-1.27 microg/L on each day for the placebo, 5, 9 and 13 g days.
CONCLUSION: In conclusion, 5 and 9 g of oral arginine caused a significant GH response. A 13 g dose of arginine resulted in considerable gastrointestinal distress in most subjects without augmentation in the GH response. The rise in GH concentration started approximately 30 min after ingestion and peaked approximately 60 min post ingestion.
PMID: 15809017 [PubMed - indexed for MEDLINE]
Am J Physiol Endocrinol Metab. 2002 Oct; 283(4):E702-10.
IGF-I does not affect the net increase in GH release in response to arginine.
Nass R, Pezzoli SS, Chapman IM, Patrie J, Hintz RL, Hartman ML, Thorner MO.
Division of Endocrinology and Metabolism, Department of Medicine, University of Virginia, Charlottesville, Virginia 22908, USA.
Arginine stimulates growth hormone (GH) secretion, possibly by inhibiting hypothalamic somatostatin (SS) release. Insulin-like growth factor I (IGF-I) inhibits GH secretion via effects at the pituitary and/or hypothalamus. We hypothesized that if the dominant action of IGF-I is to suppress GH release at the level of the pituitary, then the arginine-induced net increase in GH concentration would be unaffected by an IGF-I infusion. Eight healthy young adults (3 women, 5 men) were studied on day 2 of a 47-h fast for 12 h (35th-47th h) on four occasions. Saline (Sal) or 10 microg. kg(-1). h(-1) recombinant human IGF-I was infused intravenously for 5 h from 37 to 42 h of the 47-h fast. Arginine (Arg) (30 g iv) or Sal was infused over 30 min during the IGF-I or Sal infusion from 40 to 40.5 h of the fast. Subjects received the following combinations of treatments in random order: 1) Sal + Sal; 2) Sal + Arg; 3) IGF-I + Sal; 4) IGF-I + Arg. Peak GH concentration on the IGF-I + Arg day was ~45% of that on the Sal + Arg day. The effect of arginine on net GH release was calculated as [(Sal + Arg) - (Sal + Sal)] - [(IGF-I + Arg) - (IGF-I + Sal)]. There was no significant effect of IGF-I on net arginine-induced GH release over control conditions. These findings suggest that the negative feedback effect of IGF-I on GH secretion is primarily mediated at the pituitary level and/or at the hypothalamus through a mechanism different from the stimulatory effect of arginine.
Publication Types:
Clinical Trial
PMID: 12217887 [PubMed - indexed for MEDLINE]
Nutr Neurosci. 2003 Oct;6(5):269-75.
Effects of an oral mixture containing glycine, glutamine and niacin on memory, GH and IGF-I secretion in middle-aged and elderly subjects.
Arwert LI, Deijen JB, Drent ML.
Department of Endocrinology, VU University Medical Center, de Boelelaan 1117, 1081 HVAmsterdam, The Netherlands.
Aging is associated with declining activity of the growth hormone-insulin-like growth factor-I (GH-IGF-I) axis and with a decrease in cognitive function. The stimulatory effect of an orally administered nutritional supplement, mainly containing glycine, glutamine and niacin on the GH-IGF-I axis and on mood and cognition was investigated. Forty-two healthy subjects (14 men and 28 women, aged 40-76 years) were enrolled in a randomised, double blind, placebo-controlled trial. They received 5 g of a nutritional supplement or placebo, twice daily orally for a period of 3 weeks. At baseline and after 3 weeks, blood was collected for measurement of serum GH and IGF-I levels and mood and cognitive function were tested. The nutritional supplement ingestion for 3 weeks was found to increase serum GH levels with 70% relatively to placebo, whereas circulating IGF-I levels did not change. Mean GH (+/- SD) increased in this group from 3.23 (+/- 4.78) to 4.67 mU/l (+/- 5.27) (p = 0.03). GH increase was not associated with improvement in mood or memory. Correlation analyses, however, revealed that individual increases in IGF-I, but not GH, were associated with improved memory and vigour. It is concluded that an oral mixture of glycine, glutamine and niacin can enhance GH secretion in healthy middle-aged and elderly subjects.
Publication Types:
Clinical Trial
Randomized Controlled Trial
PMID: 14609312 [PubMed - indexed for MEDLINE]
1: Nippon Naibunpi Gakkai Zasshi. 1987 Aug 20;63(8):934-46.
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
[Article in Japanese]
Mitsuhashi S, Yamasaki R, Miyazaki S, Saito H, Saito S.
First Department of Internal Medicine, School of Medicine, University of Tokushima, Japan.
The responses of plasma growth hormone-releasing hormone (GHRH) and growth hormone (GH) to oral administration of L-dopa were studied in normal subjects and patients with various endocrine and metabolic diseases to clarify the pathophysiological role of the GHRH-GH axis. In normal subjects, the plasma GHRH concentration was increased from the basal value of 9.8 +/- 1.4 pg/ml (mean +/- SE) to 34.8 +/- 3.1 pg/ml at 30 approximately 90 min after oral administration of 500 mg L-dopa, followed by a rise of GH release (plasma GH level from less than 1 ng/ml to 21.7 +/- 4.7 ng/ml) in most cases, indicating that L-dopa stimulates GH secretion via hypothalamic GHRH. On L-dopa administration, no apparent increases in both plasma GHRH and GH concentrations were observed in patients with hypothalamic hypopituitarism, whereas GHRH administration induced almost normal GH response. In patients with acromegaly, the plasma levels of GHRH remained stationary after the L-dopa administration and did not correlate with plasma GH levels. In subjects with simple obesity, the responses of plasma GHRH (peak 13.2 +/- 1.2 pg/ml) and GH (peak 4.3 +/- 1.7 ng/ml) to L-dopa were significantly lower than those in normal subjects (p less than 0.01). In patients with primary hypothyroidism, peak levels of plasma GHRH (12.6 +/- 1.3 pg/ml) and GH (2.4 +/- 0.6 ng/ml) were significantly lower than those in normal subjects (p less than 0.01). In patients with non-insulin dependent diabetes mellitus (NIDDM), the responses of GHRH and GH were divided into 2 groups; in the responder the peak values of GHRH and GH were 19.4 +/- 8.6 pg/ml and 12.2 +/- 1.4 ng/ml and in the low or non responder 14.7 +/- 1.5 pg/ml and 2.0 +/- 0.6 ng/ml, respectively. Between both groups, there was a significant difference in the values of fasting blood sugar and HbA1 and mean suffering period. These findings suggest that GH secretion evoked by the L-dopa administration is induced by GHRH released from the hypothalamus, and impairment of GH secretion associated with simple obesity, primary hypothyroidism, or NIDDM may be in part attributed to insufficiency of GHRH release from the hypothalamus, and indicate that L-dopa test is clinically useful for evaluating the ability of intrinsic GHRH release in such diseased states.
PMID: 3123283 [PubMed - indexed for MEDLINE]
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1: J Clin Endocrinol Metab. 1986 Mar;62(3):466-73.
L-dopa stimulates release of hypothalamic growth hormone-releasing hormone in humans.
Chihara K, Kashio Y, Kita T, Okimura Y, Kaji H, Abe H, Fujita T.
A sensitive RIA for human GH-releasing hormone-(1-44)-NH2 [hGHRH-(1-44)-NH2] was developed which allows its measurement in human plasma extracts. The assay did not detect hGHRH-(1-37)-OH or hGHRH-(1-40)-OH. A method to extract hGHRH from plasma was developed using silicic acid and acid-acetone, by which recovery of synthetic hGHRH-(1-44)-NH2 from plasma averaged 74.3%. Serial dilutions of plasma extracts gave an inhibition curve parallel with that of synthetic hGHRH-(1-44)-NH2 in the RIA system. On Sephadex G-50 columns, hGHRH-like immunoreactivity (hGHRH-LI) in plasma extracts eluted as a single peak corresponding to hGHRH-(1-44)-NH2. This hGHRH-LI peak, when subjected to reverse phase HPLC, emerged at the position where hGHRH-(1-44)-NH2 was eluted. hGHRH-LI was detectable in the peripherally circulating plasma of all subjects tested. The mean basal level of plasma hGHRH-LI in normal subjects was 9.4 +/- 0.7 (+/- SE) pg/ml (n = 22; range, 2.8-18.1 pg/ml), comparable to the basal plasma hGHRH-LI concentration in patients with hypothalamic lesions (11.3 +/- 1.1 pg/ml; n = 7). Oral administration of L-dopa (0.5 g) caused a significant increase in both plasma hGHRH-LI and GH levels in normal subjects, and the plasma hGHRH-LI peak slightly preceded or coincided with that of plasma GH in individual subjects. There was also a significant correlation between plasma hGHRH-LI and the GH rises after L-dopa administration when their net increments were compared. All of the patients with hypothalamic lesions had significant increases in plasma GH after hGHRH-(1-44)-NH2 injection (1 microgram/kg BW, iv), indicating the presence of functioning somatotrophs in their pituitaries. When L-dopa was orally administered to these patients, neither plasma hGHRH-LI nor GH concentration changed throughout a 120-min observation period. These findings suggest that 1) hGHRH, immunologically and chromatographically indistinguishable from synthetic hGHRH-(1-44)-NH2, is detectable in peripheral plasma in humans; 2) L-dopa stimulates the release of hypothalamic hGHRH, alterations of which are reflected in changes in peripheral levels; and 3) the source of circulating hGHRH is not restricted to the hypothalamus, since hGHRH-LI is present in the peripheral plasma of patients with hypothalamic lesions in amounts similar to those found in normal subjects.
PMID: 3080462 [PubMed - indexed for MEDLINE]
Will Increases In Growth Hormone Help ED?
1: Zhonghua Nan Ke Xue. 2004 Nov;10(11):867-9.
[Growth hormone deficiency and age-related erectile dysfunction]
[Article in Chinese]
Huang X, Li S, Hu L.
Research Center of Urology & Andrology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, China.
The incidence of erectile dysfunction (ED) significantly increases in aging men, which may be associated with the decrease of the serum growth hormone (GH) level. GH may play an important role in the maintenance of penile erectile function, perhaps by promotion of the NO-cGMP pathway, stimulation of the regeneration of NOS-containing nerve fibers and the augmentation of androgenic action.
PMID: 15595694 [PubMed - in process]
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Urology. 2002 Apr;59(4):609-14.
Serum levels of human growth hormone during different penile conditions in the cavernous and systemic blood of healthy men and patients with erectile dysfunction.
Becker AJ, Uckert S, Stief CG, Scheller F, Knapp WH, Hartmann U, Brabant G, Jonas U.
Department of Urology, Hannover Medical School, Hannover, Germany.
OBJECTIVES: To detect changes in growth hormone (GH) serum levels during different penile conditions in the cavernous and systemic blood of patients with erectile dysfunction and compare them with the course of GH registered in healthy men. It has been suggested that human GH is involved in sexual maturation and plays a regulatory role in male reproductive function. Deficiency may result in fatigability, loss of sexual desire and erection, or oligospermia or azoospermia. It is assumed that the biologic effects of GH include insulin-like growth factor 1-mediated stimulation of endothelial nitric oxide formation. It has recently been demonstrated that GH serum levels in the systemic and cavernous blood of healthy men increases during developing penile erection.
METHODS: Thirty-five healthy adult men and 45 patients with erectile dysfunction of either organogenic or psychogenic etiology were exposed to visual and tactile erotic stimuli to elicit penile tumescence and, in the group of healthy subjects, rigidity. Whole blood was simultaneously aspirated from the corpus cavernosum and the cubital vein during the different functional conditions of the penis. Serum levels of GH were determined by means of an immunoradiometric assay.
RESULTS: In the healthy subjects, systemic GH serum levels significantly increased during penile tumescence, followed by a transient decline from tumescence to rigidity and detumescence. In the unselected patients, the mean GH levels during penile flaccidity were determined to be about sevenfold lower than those registered in the blood of the healthy men. During penile tumescence, the mean increase in the GH levels in the systemic and cavernous blood of psychogenic patients was comparable to that seen in healthy men, but, in the group of organogenic patients, this increase was found to be negligible.
CONCLUSIONS: We believe our data provide strong evidence that GH may be of major importance in the maintenance of male erectile capability-probably through a stimulating effect on cyclic guanosine monophosphate generation in human cavernous smooth muscle-and that a decline in GH release may contribute to the manifestation of erectile dysfunction.
PMID: 11927337 [PubMed - indexed for MEDLINE]
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Paul Miller
