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8-10 iu GH a day

If your referring ME having a Rep status as holding an agenda here, as to advocating to use test with HGH than your wrong. Far as inexperienced or having used poor quality HGH too, well that's a bit sassy to say the least!
Sassy, not really. I am just confident with my knowledge and trying to help the OP as much as i can.
I am going to post what i dont agree with, and if u can provide a study or u know what, if any of the respected and known members here agree with what u wrote, then i will shut up, apologize and do MORE research.
WE GOOD?!

Now IMO, HGH has poor properties far as skeletal muscle mass when taken by itself, and it's definitely not worth the large price if you are taking it solely for gaining muscle, and by itself it's really only going to provide fat loss or “sculpting” if you will.
Keep in mine that lean body mass does not necessarily mean muscle,People who lean out on HGH only, and yet gain 8-10 lbs, at the same time of losing fat don't consider that HGH will increase skeletal "bone" density, and tissue growth ( not necessarily muscle ).
When used with Test The only real use in gaining muscle may be as a synergistic effects. Now far as tissue repair that's different. Testosterone is a must with HGH to gain quality muscle mass.
 
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Sassy, not really. I am just confident with my knowledge and trying to help the OP as much as i can.
I am going to post what i dont agree with, and if u can provide a study or u what, if any of the respected and known members here agree with what u wrote, then i am willing to apologize, shut up and do MORE research.
WE GOOD?!
Really,Your telling me to do more research and to shut up?
I guess my experience with/how my body reacts is insufficient.

Here, take a look at some of these reads and tell me how you feel.

1) So, your going to speculate that I have an agenda, and also speculate that I am inexperienced, and then make the claim that I haven't ran quality HGH
2) You need to hear from the community to back what you said, before you admit your not partially wrong? But, with your confidence and your inflated Ego why bother with what the consensus has to say? I mean with the arrogance that you carry you should not need the point of views from others.

So with that being said, here is some reads for you.

These read I will post even have references from individuals that have PHD's,
I think that's a little more sufficient than Bro-science, don't you think?


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Growth Hormone vs. Testosterone

A Retrospective Based on the Latest Research

by Karlis Ullis, M.D. and Joshua Shackman, Ph.D.


I was one of the first private practitioners in the country to dispense growth hormone as part of an overall anti-program hormone replacement program for adults that fit the criteria of the "Adult Onset Growth Hormone Deficiency Syndrome". Like many other anti-aging physicians, I was extremely impressed by the initial research on growth hormone showing dramatic improvements in body composition, kidney function, skin, mood, well being, etc. I have been a member of the Growth Hormone Research Society for many years and have closely followed all the latest research on growth hormone and other adult hormone replacement therapies. As the number of studies on growth hormone as well as testosterone has piled up since I first began prescribing testosterone, I believe now is the time to look back at the research and see if growth hormone and testosterone have lived up to their promises.

It is well established in bodybuilding circles that testosterone is superior to growth hormone for gaining muscle. However, growth hormone still is enormously popular and generally has a better reputation than testosterone both in bodybuilding and in anti-aging circles. The general impression is that testosterone will make you big, but at the price of acne, puffiness, temper tantrums, prostate enlargement, and possibly "gyno". Well it is acknowledged that growth hormone is not as anabolic as testosterone, people still think of growth hormone as a hormone that will make you lean and toned with almost no side effects. Growth hormone also has a reputation as being the "fountain of youth" among anti-aging enthusiasts, whereas testosterone is still considered somewhat dangerous. The purpose of this article is to see how the research on testosterone and growth hormone from the last few years has supported or disputed the public’s view of these two hormones.

Which is Better for Body Composition?

New research has shed some light on the anabolic effects of growth hormone. Several studies in the past have shown an increase in lean body mass in subjects taking growth hormone. However, lean body mass does not necessarily mean muscle, but anything that is not fat and this includes water, organ tissue growth, bone mass, and connective tissue growth. My friend Michael Mooney (author of Built to Survive and editor of the Medibolics Newsletter) has helped publicize the fact that not much, if any, of the lean mass gained while on growth hormone is actually muscle. One recent study on HIV positive test subjects showed no significant change in skeletal muscle mass after taking six milligrams (about 18 units) per day of growth hormone for 12 weeks.(1) Another study, also on HIV positive test subjects, also showed a lack of muscle growth when doses of nine milligrams (roughly 27 units) per day were given.(2) Keep in mind that HIV positive individuals are often suffering from muscle wasting conditions, which should make them more responsive to any possible anabolic effects of growth hormone. Growth hormone is probably equally ineffective in healthy individuals.

One study on young (aged 22-33), highly trained athletes did show a significant increase in lean mass after six weeks of taking 2.67 milligrams (about 8 units) per day.(3) However this increase was only 4%, and may have not included any muscle mass at all. It seems overwhelming clear that growth hormone is either non-anabolic or very weakly anabolic for skeletal muscle when taken by itself, and it definitely not worth the large price if you are taking it solely for gaining muscle. The only real use in gaining muscle may be as a synergistic agent with testosterone. A synergistic effect of taking growth hormone with testosterone has been reported for increases in lean mass, but further research needs to be done to see if this synergistic effects holds for skeletal muscle. Keep in mind that some increases in lean mass are not desirable. Growing some organs too big such as kidneys can produce some embarrassing effects seen in some professional bodybuilders. You do not want your "guts" sticking blatantly out of your body.

But enough on growth hormone for muscle gain. For information, see Bryan Haycock’s article in this issue or go to Michael Mooney’s web site. If you are going to spend the money on growth hormone to try to improve your body, your best bet is to use it as a fat loss or "sculpting" agent. The previously mentioned study with growth hormone on trained athletes did show an impressive 12% decrease in bodyfat. So well it is well established that testosterone is far, far better for building muscle than growth hormone, is growth hormone the better choice for fat loss? The research on this issue is mixed, and there is no easy answer to this question.

One recent study put growth hormone head to head with testosterone and measured its effects on fat loss. In this study, men on growth hormone lost an average of 13% of their bodyfat compared to 5.8% in the group taking testosterone.(4) But before you jump to conclusions, there are a couple of reasons why this study doesn’t settle the question. For one thing, this study was on very old individuals (aged 65 to 88) who had low IGF-1 and testosterone levels. Another problem is that the doses of the hormones haven’t been reported yet (the study is only in abstract form right now) which also makes the comparison difficult to make. Most interesting about this study was that a synergistic effect was found in a group taking both testosterone and growth hormone, as they lost an average of 21% of their bodyfat. This is more than the averages of the testosterone alone and growth hormone alone groups combined.

Not all studies have shown this dramatic of an effect on body fat. One study using fairly large doses (adjusted by weight, but roughly 5 mg per day) on obese women failed to show any significant effects on body fat.(5) The growth hormone group lost less than two pounds more than the placebo group over a one month period. The main significant result was that the growth hormone group lost much less lean mass (an average loss of 1.52 kg compared to 3.79 in the placebo). While this may seem impressive, the same results could be achieved with a caffeine/ephedrine formula at a fraction of the price. While there are a good number of studies showing growth hormone to be effective for fat loss, testosterone may be almost as good for this purpose.

Testosterone was recently found to be effective for fat loss in young men even in small doses. One recent study showed that men given only 100 milligrams per week of testosterone enanthate lost an average of six percent of their bodyfat after eight weeks.(6) 100 mg per week is generally considered a very low dose by bodybuilding standards. Most impressive about this study was that the result was obtained in young, normal healthy men (aged 18 to 45), not obese or testosterone deficient. Most of the studies showing positive effects with hormone replacement therapy are on subjects who are obese or hormone deficient – i.e. the very subjects most likely to respond. While the amount of muscle gain reported in this study was not reported (it is still just in abstract form), another study showed 100 mg per week of testosterone enanthate was not anabolic.(7) It appears that testosterone has a strong mechanism for fat loss other than increased metabolic rate from increased muscle. Considering how much cheaper testosterone is than growth hormone, it may well be the cost-effective choice for burning fat even if it is slightly less effective overall.

Safety of Growth Hormone and Testosterone

Testosterone is widely believed to be far more dangerous than growth hormone. However, recent research is rapidly showing that much of these dangers have been exaggerated. For instance, the hypothesis that testosterone causes prostate cancer has never been established. In fact, one study even showed a slight negative correlation between testosterone levels and prostate cancer! A study on young men given supraphysiologic doses of testosterone showed no change is prostate specific antigen (PSA), which is one measure of prostate cancer risk.(8)

Growth hormone may also be less dangerous to the prostate than previously believed. One study showed strong positive correlation with prostate cancer and IGF-1 levels.(9) Since growth hormone stimulates IGF-1 synthesis in the liver, this study and others bring up the possibility of a link of growth hormone and prostate and breast cancer. Keep in mind that statistical correlations do not necessarily prove causality, i.e. IGF-1 has not yet been proven to be a cancer-causing villain. Actually IGF-11 may be one of the culprits in the cancer story, and not IGF-1. At the Serano sponsored Symposia on the Endocrinology of Aging in October, 1999 and at the Endocrine Society Meeting in June, 1999 there was an informal consensus that patients on growth hormone did not increase their risk of breast or prostate cancer. Several other recent studies have also cast doubt on the role of growth hormone as a cancer-causing villain.

Testosterone may have also gotten a bad rap for its effects on blood lipids. Since testosterone and other anabolic steroids have been shown in some studies to lower HDL cholesterol levels, it was believed that testosterone may increase the risk for heart disease. This was refuted in one recent study on testosterone that showed some positive results. A study on 21 hypogonadal men (aged 36 to 57) showed a replacement dose of testosterone using the Androderm transdermal patch to reduce blood clotting.(9) While HDL levels did drop slightly, blood coagulability is believed to be the more important marker of heart disease risk. Another study showed a very strong negative correlation with testosterone levels and heart disease.

Growth hormone has shown mixed results on its effects on heart disease risk. One study on elderly men and women (aged 65-88) showed that growth hormone administration to lower LDL levels, but raised triglyceride levels.(10) Since high LDL and triglyceride levels are considered measures of heart disease risk, growth hormone’s effects on heart disease risk are ambiguous. However, long-term use of growth hormone as been shown to decrease the thickness of the carotid artery lining – i.e. increased room for blood flow.

While much more research needs to be done, I am convinced right now that testosterone replacement therapy in hypogonadal men may be safer than excessively large doses of growth hormone. The long-term studies have not yet been done to test the true long-term effects of these hormones, but the research seems quite clear at the moment. Michael Mooney has reported similar results on safety and side effects of these hormones:

While none of the studies on testosterone or anabolic steroids used for HIV have documented any significant health problems associated with their proper therapeutic use, Dr. Gabe Torres' data on his patients who experienced a reduction in symptoms of HIV-related lipodystrophy with Serostim growth hormone showed that at the standard 5 and 6 mg doses, 80 percent of his HIV patients experienced significant side effects, that included elevated glucose, elevated pancreatic enzymes, or carpal tunnel syndrome. (1)

Conclusion

Don’t get me wrong – I still use both growth hormone and testosterone as part of overall anti-aging programs in my patients. This article is not meant to say one hormone is "good" and another is "bad". It is just my opinion at the moment that the overall benefit/cost ratio for improving body composition is higher with testosterone than growth hormone. By cost, I mean both the monetary price – testosterone is far cheaper than growth hormone, and the side effect/safety profile – testosterone is safer than high-dose growth hormone use.

Since growth hormone is extremely expensive and perhaps riskier than testosterone, I screen patients very carefully and only recommend it to those who either have very low IGF-1 levels and fail growth hormone stimulation tests, or those who have failed to respond to testosterone or other therapies. The new research has also made me confident in encouraging more and more patients to go on testosterone. However, we must keep constant track of the new research to better refine both anti-aging and bodybuilding programs. The science of hormone supplementation is still in its infancy, and there is still a lot more questions that need to be answered.

References

1. Mooney, Michael, HIV Study Shows No Muscle Growth From Serostim Growth Hormone, Medibolics, July, 1999

2. Yarasheski KE; Campbell JA; Smith K; Rennie MJ; Holloszy JO; Bier DM. Am J Physiol Effect of growth hormone and resistance exercise on muscle growth in young men. Am J Physiol, 262(3 Pt 1):E261-7 1992 Mar

3. Crist DM, et al. Body composition response to exogenous GH during training in highly conditioned adults. J Appl Physiol. 1988 Aug;65(2):579-84.

4. Blackman, MR, et al. Effects of growth hormone and/or sex steroid administration on body composition in healthy elderly women and men, Presented at 1999 Endrocrine Society conference, San Diego, California

5. Tagliaferri M, et al. Metabolic effects of biosynthetic growth hormone treatment in severely energy-restricted obese women. Int J Obes Relat Metab Disord. 1998 Sep;22(9):836-41.

6. Anawalt, BD, et al. Testosterone administration to normal men decreases truncal and total body fat . Presented at 1999 Endrocrine Society conference, San Diego, California

7. Friedl KE, et al. Comparison of the effects of high dose testosterone and 19-nortestosterone to a replacement dose of testosterone on strength and body composition in normal men. J Steroid Biochem Mol Biol. 1991;40(4-6):607-12

8. Cooper, C.S., MacIndoe, J.H., Perry, P.J., Yates, W.R. and Williams, R.D.: The effect of exogenous testosterone on total and free prostate specific antigen levels in healthy young men. J Urol, 156:438, 1996.

9. Wallace, J., et. al (1998) Growth Hormone and IGF Res (abstract) 8(4): 329, 348

10. Christmas, C. et al, Effects of growth hormone and/or sex steroid administration on serum lipid profiles in healthy elderly women and men, Presented at 1999 Endrocrine Society conference, San Diego, California


 
One more for you, with some more references..
By the way, none told you to shut-up, so no need to tell others to...

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Growth hormone and testosterone interact positively to enhance protein and energy metabolism in men
James Gibney,1 Troels Wolthers,1 Gudmundur Johannsson,1 A. Margot Umpleby,2 and Ken K. Y. Ho1

1Pituitary Research Unit, Garvan Institute of Medical Research and Department of Endocrinology, St. Vincent’s Hospital, Sydney, Australia; and 2Dept. of Diabetes and Endocrinology, Guy’s, King’s and St. Thomas’ School of Medicine, St. Thomas' Hospital, London, United Kingdom

Submitted 11 October 2004 ; accepted in final form 18 February 2005

ABSTRACT

We investigated the impact of growth hormone (GH) alone, testosterone (T) alone, and combined GH and T on whole body protein metabolism. Twelve hypopituitary men participated in two studies. Study 1 compared the effects of GH alone with GH plus T, and study 2 compared the effects of T alone with GH plus T. IGF-I, resting energy expenditure (REE), and fat oxidation (Fox) and rates of whole body leucine appearance (Ra), oxidation (Lox), and nonoxidative leucine disposal (NOLD) were measured. In study 1, GH treatment increased mean plasma IGF-I (P < 0.001). GH did not change leucine Ra but reduced Lox (P < 0.02) and increased NOLD (P < 0.02). Addition of T resulted in an additional increase in IGF-I (P < 0.05), reduction in Lox (P < 0.002), and increase in NOLD (P < 0.002). In study 2, T alone did not alter IGF-I levels. T alone did not change leucine Ra but reduced Lox (P < 0.01) and increased NOLD (P < 0.01). Addition of GH further reduced Lox (P < 0.05) and increased NOLD (P < 0.05). In both studies, combined treatments on REE and Fox were greater than either alone. In summary, GH-induced increase of circulating IGF-I is augmented by T, which does not increase IGF-I in the absence of GH. T and GH exerted independent and additive effects on protein metabolism, Fox and REE. The anabolic effects of T are independent of circulating IGF-I.
insulin-like growth factor I; protein turnover

GROWTH HORMONE (GH) AND TESTOSTERONE are potent anabolic hormones. There is strong evidence in children that both hormones interact positively to enhance growth and body composition (2, 22, 35). The mechanistic basis of this interaction is poorly understood.

Testosterone enhances the growth of boys with hypogonadism and those with hypopituitarism during GH treatment (2, 35). However, the effect of testosterone on somatic growth is poor in boys with hypopituitarism without concomitant GH treatment (2, 35). In hypopituitary adults who are not receiving GH replacement, testosterone exerts no effect on circulating IGF-I (18). These collective observations suggest that the growth promoting and anabolic effects of testosterone may be dependent on GH and possibly mediated in part by IGF-I.

How GH and testosterone interact to regulate protein metabolism in adult life is also poorly understood. There is evidence that both hormones are necessary to exert an optimal effect. Even after adequate androgen replacement, lean body mass is reduced in GH-deficient men (15). The observation that the effects of GH replacement are more marked in men than in women (9) provides further evidence that testosterone might enhance the anabolic effects of GH. The anabolic effects of GH are mediated by IGF-I, but whether IGF-I also plays a role in mediating the anabolic effects of testosterone is unknown. The aim of the study was to investigate how GH and testosterone interact to regulate anabolism by studying the independent and combined effects of these two hormones on IGF-I and protein metabolism.

SUBJECTS AND METHODS

Subjects. Twelve hypopituitary men with GH deficiency and hypogonadotropic hypogonadism were recruited from the Endocrine Outpatient Clinic at St. Vincent’s Hospital, Sydney, Australia. The clinical characteristics of these patients are shown in Table 1. Two studies were undertaken; the first compared the effects of GH alone with GH plus testosterone, and the second compared the effects of testosterone alone with GH plus testosterone. A three-period crossover study design was originally planned to investigate the effects of GH, testosterone, and combined (GH plus testosterone) treatment. However, the demands and logistics precluded the adoption of such a design, as many of the subjects were frail and lived outside Sydney. Instead, a design comprising two interrelated studies was adopted. GH deficiency was confirmed by a peak GH response to insulin-induced hypoglycemia of <3 ng/ml (14), and hypogonadotropic hypogonadism was defined as serum testosterone measured in a morning sample <4 nmol/l, accompanied by low serum luteinizing hormone level. The duration of hypopituitarism was ≥1 yr. All subjects were receiving stable hormone replacement for other deficiencies throughout and during the study periods. The Research Ethics Committee of St. Vincent’s Hospital approved the studies. Written informed consent was obtained from all subjects.

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Table 1. Characteristics of hypogonadal GH-deficient patients

Study design. Both studies were of open-label randomized crossover design and together allowed comparison of the individual and combined effects of testosterone and GH while taking time-dependent effects into consideration. Before commencement of each study, subjects underwent a 6-wk run-in period, when testosterone and GH were withdrawn. During this time and throughout the studies, they were instructed to follow their usual diet and habitual activities. In both studies, GH (Humatrope, Lilly Australia) was administered at a dose of 0.5 mg daily by self-injection at 8 PM, and testosterone enanthate (Primoteston) was administered as 250 mg intramuscularly 2 wk before measurement. The dose and timing of the testosterone injection were based on known pharmacokinetics of testosterone enanthate and aimed to expose subjects to physiological plasma testosterone levels during the 2 wk preceding the metabolic studies.

In the first study (study 1), GH was administered daily for 6 wk. Testosterone was administered either at baseline (group A, n = 5) or week 4 (group B, n = 5) of the study. Investigations were carried out at baseline, after 2 wk and 6 wk so that the effects of testosterone were assessed 2 wk after administration. Thus studies were carried out when subjects were not receiving GH or testosterone replacement, during replacement with GH alone, and during GH plus testosterone replacement (Fig. 1).


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Fig. 1. Study 1 was designed to compare effects of growth hormone (GH) alone with combined treatment of GH + testosterone (T). Ten patients were randomized to either group A or group B. T was administered as 250 mg of testosterone enanthate im at week 0 in group A and week 4 in group B. GH was administered as daily bedtime sc injections of 1.5 IU/day for 6 wk. Study 2 was designed to compare T alone with combined treatment with T + GH. Nine patients were randomized to either group A or group B. The same doses of GH and T were administered as for study 1. T was administered at weeks 2 and 6 in both groups. GH was administered from week 0 to week 4 in group A and from week 4 to week 8 in group B. Arrows indicate time points of measurements.

In the second study (study 2), testosterone was administered at week 2 and week 6 of the study. GH was administered either during the first 4 wk (group A, n = 5) or the second 4 wk (group B, n = 4) of the study. Investigations were carried out at baseline, after 4 wk, and after 8 wk. Thus studies were carried out when subjects were not receiving GH or testosterone replacement, during replacement with testosterone alone, and during combined GH plus testosterone replacement (Fig. 1).

At each visit, all subjects underwent measurements of plasma IGF-I and whole body protein turnover using [1-13C]leucine tracer, as previously described (16, 34), and assessment of resting energy expenditure and fat and carbohydrate oxidation by use of indirect calorimetry (25). All subjects were studied at 8 AM after an overnight fast.

Study techniques. Whole body protein turnover was undertaken using a primed constant infusion of [1-13C]leucine. The technique has been extensively validated (1, 3, 10, 17, 27, 32) and has proved highly reproducible in our hands (12, 16, 28, 29, 34). NaH13CO3 (99%) was obtained from Cambridge Isotope Laboratories (Woburn, MA), and 99% [1-13C]leucine was obtained from MassTrace (Woburn, MA). Solutions of each were prepared under sterile conditions using 0.9% saline.

Subjects were studied in the Clinical Research Facility, Garvan Institute of Medical Research, after an overnight fast. At 0800, cannulae were inserted into both antecubital veins, one for isotope infusion and the other for blood sampling. A 0.1 mg/kg priming dose of NaH13CO3 was followed immediately by [1-13C]leucine (prime, 0.5 mg/kg; infusion, 0.5 mg·kg–1·h–1). Blood and breath samples were collected before (–10, 0 min) and at the end of a 3-h infusion (140, 160, and 180 min), at which time we and others have previously demonstrated a physiological and isotopic steady state (7, 12, 16, 21, 30, 34). Blood was placed on ice, and plasma was separated and stored at –80°C until analysis. O2 and CO2 production rates were undertaken with an open circuit, ventilated hood system (Deltatrac monitor, Datex Instrumentation, Helsinki, Finland). The monitor was calibrated against standard gases before each study. Measurements were averaged over 20–40 and 160–180 min. The coefficient of variation for energy expenditure was 4.2%, and for substrate oxidation was 4% (24).

Calculation of whole body protein turnover. Rates of appearance (Ra) of leucine, nonoxidative leucine disposal (NOLD), and leucine oxidation were calculated as previously described (16, 34). Isotopic enrichment of plasma α-ketoisocaproic acid (KIC), which is believed to reflect intracellular leucine enrichment more closely than the isotopic enrichment of plasma leucine, was measured. Because leucine represents 8% of total body protein, or 590 µmol of leucine represents 1 g of protein, rates of protein turnover may be estimated using these constants (21, 26).

Calculation of energy expenditure and substrate oxidation. Energy expenditure (EE) and substrate oxidation were calculated from the following equations: EE = 3.91 O2 + 1.10 CO2 – 0.53 protein oxidation; fat oxidation = 1.67 O2 – 1.67 CO2 – 0.31 protein oxidation; and carbohydrate oxidation = 4.55 CO2 – 3.21 O2 – 0.46 protein oxidation (11). Carbohydrate, lipid, and protein oxidation are expressed as grams per minute. O2 represents O2 consumption, and CO2 represents CO2 production in liters per minute.

Analytic methods. KIC was extracted by the method of Nissen et al. (23). As previously described (16, 34), KIC enrichment was measured as the butyldimethylsilyl derivative by gas chromatography (model 5890, Hewlett-Packard, Palo Alto, CA)-mass spectrometry (MSD 5971A, Hewlett-Packard), with selective monitoring of ions 302 and 303 (31). CO2 enrichment in breath was measured on a SIRA Series II isotope ratio mass spectrometer (VG Isotech, Cheshire, UK).

Statistics. Nonnormally distributed data were logarithmically transformed before analysis. Repeated measures ANOVA was used in each study to determine treatment effect, and paired t-tests were used to compare different time points. Results are expressed as means ± SE, and statistical significance was set at an α-level of 0.05.

RESULTS

There were no baseline differences between subjects who took part in the two studies. Both treatments alone and in combination were well tolerated, and no sequence effect was detected in either study.

IGF-I and testosterone. Mean IGF-I levels and testosterone concentrations in hypopituitary subjects from both study groups were subnormal (reference range for IGF-I: 15–35 nmol/l; testosterone: 12–30 nmol/l). In study 1, treatment with GH alone significantly increased IGF-I but did not alter plasma levels of testosterone, which remained in the hypogonadal range in all subjects (Table 2). Addition of testosterone to GH increased testosterone into the normal range in all subjects and resulted in a further uniform increase in plasma IGF-I levels (Table 2).

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Table 2. Plasma levels of IGF-I and testosterone in hypogonadal GH-deficient subjects at baseline and after treatment with GH alone and GH with testosterone (study 1) and at baseline and after treatment with testosterone alone and GH with testosterone (study 2)

In study 2, treatment with testosterone alone increased testosterone into the normal range but did not alter mean plasma levels of IGF-I (Table 2). Compared with testosterone alone, treatment with GH plus testosterone did not result in any further change in plasma testosterone but increased IGF-I into the normal range (Table 2).

In summary, treatment with testosterone plus GH normalized plasma levels of testosterone and IGF-I, respectively, but testosterone increased IGF-I only during concomitant administration of GH.

Leucine turnover. In study 1, leucine Ra at baseline (147 ± 11 µmol/min) was not significantly different from that observed during GH treatment (148 ± 8 µmol/min) or combined treatment with testosterone (145 ± 11 µmol/min; Fig. 2). GH alone significantly reduced (P < 0.05) leucine oxidation from 41 ± 3 to 35 ± 2 µmol/min, and the addition of testosterone reduced leucine oxidation further (P < 0.05) to 27 ± 2 µmol/min (Fig. 2, left). When expressed as percent Ra, this corresponded to a fall in leucine oxidation from 29.2 ± 2% at baseline to 24.2 ± 2% with GH and to 19 ± 1% with combined treatment (Fig. 2, right). There was a trend toward an increase of NOLD with GH treatment (106 ± 10 to 111 ± 8 µmol/min) and toward a further increase with combined treatment (118 ± 10 µmol/min), although the changes did not reach statistical significance. However, when expressed as a fraction of Ra, the changes for NOLD were significant (P < 0.05) for each intervention, increasing from 71 ± 2 to 76 ± 2% with GH and rising further to 81 ± 1% of Ra. These results did not differ when expressed in relation to body weight.


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Fig. 2. Absolute rates of appearance (Ra) and oxidation of leucine and nonoxidative leucine disposal (NOLD; left) and percentage rates of leucine oxidation and NOLD (right) in hypogonadal GH-deficient subjects at baseline, after treatment with GH alone, and after GH + T (study 1) and at baseline, after treatment with T alone, and after GH + T (study 2). *P < 0.05 vs. baseline; †P < 0.05 vs. baseline and vs. GH only; #P < 0.05 vs. baseline and vs. T only.

In study 2, leucine Ra during testosterone (172 ± 11 µmol/min) treatment alone or during combined treatment with GH (160 ± 8 µmol/min) was not significantly different from baseline (164 ± 11 µmol/min). Testosterone alone significantly reduced (P < 0.05) leucine oxidation from 43 ± 3 to 31 ± 3 µmol/min and the addition of GH reduced leucine oxidation further (P < 0.05) to 29 ± 2 µmol/min (Fig. 2, left). When expressed as percent Ra, this corresponded to a fall in leucine oxidation from 25 ± 1% at baseline to 19 ± 1% with GH and to 17 ± 1% with combined treatment (Fig. 2, right). The absolute values for NOLD at baseline (129 ± 6 µmol/min), with testosterone (128 ± 6 µmol/min), and with combined treatment (135 ± 10 µmol/min) were not significantly different. However, when expressed as a proportion of Ra, NOLD increased significantly (P < 0.05) from 75 ± 1 to 80 ± 1% with testosterone, rising further to 83 ± 1% of Ra (P < 0.05) with combined treatment. These results did not differ when expressed in relation to body weight.

Resting EE and substrate metabolism. In study 1, GH alone induced an increase in resting EE, which narrowly failed to reach statistical significance (P = 0.07), but the addition of testosterone resulted in a cumulative increase that was significant (P < 0.05; Table 3) compared with baseline. GH alone increased fat oxidation, although the change did not reach statistical significance, whereas the addition of testosterone resulted in a further increase that was significant compared with GH alone and to baseline (P < 0.05).

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Table 3. REE, PRox, Fox, and CHox in hypogonadal GH-deficient subjects at baseline, following treatment with GH alone and GH with testosterone (study 1), and at baseline and after treatment with testosterone alone and GH with testosterone (study 2)

In study 2, testosterone alone significantly increased REE (P < 0.05), whereas combined treatment with testosterone and GH induced a further rise in REE that was significant compared with baseline (P < 0.05). Testosterone alone significantly increased fat oxidation, whereas the addition of GH resulted in a further increase that was significant compared with GH alone and with baseline (P < 0.05). In summary, combined treatment induced the greatest changes in REE and fat oxidation, whereas the effects of GH plus testosterone alone were intermediate.

DISCUSSION

These two open-label, randomized crossover studies demonstrate that testosterone increases circulating IGF-I in hypopituitary men during GH treatment but has no effect on circulating IGF-I in the absence of GH. GH and testosterone independently and additively increased resting energy expenditure and fat oxidation. Neither hormone affected protein breakdown, but each exerted independent and additive effects in suppressing protein oxidation and in stimulating protein synthesis. These are the first data to demonstrate that testosterone and GH interact positively to regulate energy expenditure, fat metabolism, and protein anabolism. Taken together, the data provide a mechanistic explanation for recent observations that the effects of combined GH and testosterone supplementation on body composition and muscle strength in elderly men are greater than those of GH or testosterone alone (4, 8).

Studies in children have provided strong evidence for a positive interaction between GH and androgens in growth and development. Testosterone stimulates growth of prepubertal and hypogonadal children (35). As it is well established that testosterone increases GH release (33), greater GH secretion is one mechanism through which growth is augmented. However, the observation that androgens also accelerate growth in hypopituitary boys receiving a constant GH dose strongly suggests that these effects are independent of GH secretion (2). There is also evidence that in addition to its effects on growth and anabolism, GH augments other biological effects of testosterone. The development of secondary sexual characteristics in hypopituitary boys is modest unless GH is administered concurrently (35). In hypopituitary men, Blok et al. (5) observed that androgen-dependent hair growth is increased by GH in hypopituitary men receiving stable androgen replacement, despite unchanged or even reduced androgen levels.

In the present study, plasma levels of IGF-I were greater during combined treatment with GH and testosterone than during treatment with GH alone, indicating that testosterone enhances GH-induced IGF-I production. Because the liver is an androgen-responsive organ and is also the major source of circulating IGF-I (20), it is likely that testosterone increased hepatic production of IGF-I by GH. To our knowledge, this is the first study to address the effect of testosterone on IGF-I levels in hypogonadal GH-deficient subjects during GH replacement. Testosterone does not change IGF-I in hypogonadal GH-deficient subjects who are not receiving GH replacement (18) but increases plasma IGF-I levels in normal subjects (13, 33). This effect is at least partly due to increased pituitary GH secretion and is dependent on aromatization to estrogen (33). Interestingly, studies in which testosterone and GH have been administered together and in combination to healthy older subjects have shown no additional effect of combined testosterone and GH to increase IGF-I compared with GH alone (4, 8). Differences between these observations and those in the present study might reflect the difference between augmenting low-normal testosterone in healthy subjects and normalizing testosterone in profoundly hypogonadal subjects. Although plasma testosterone levels were at the lower end of the normal range at the time of the metabolic studies, in view of the known pharmacokinetic profile of intramuscular testosterone enanthate, it is likely that subjects were exposed to higher testosterone levels over the preceding 14 days.

The finding that testosterone alone exerted significant protein anabolic effects was surprising in view of the observation that the growth response of hypopituitary children to androgens is very poor unless GH is replaced (6). This observation suggests that the anabolic effects of androgens are dependent on the presence of GH. Testosterone alone also significantly stimulated resting energy expenditure and fat oxidation in our hypopituitary subjects. These findings have important clinical and physiological implications. The observation that the metabolic effects of GH are enhanced during concomitant testosterone administration explains why sex steroid-replaced hypopituitary men are more responsive to GH replacement than hypopituitary women (9). Testosterone is probably not the sole determinant of this effect, however, as there is also evidence that orally administered estrogen reduces the metabolic effects of GH (34). The observation that GH and testosterone exert additive effects on protein metabolism and fat oxidation implies that administration of testosterone or GH alone may not maximize these processes; thus, in hypopituitary men, treatment with GH or testosterone alone is unlikely to normalize body protein or fat mass. In addition to the clinical implications of this finding, there are also economic implications. GH replacement therapy is expensive, and the cost is directly dependent on the dose used. The findings of the current study indicate that the effect of GH to stimulate protein anabolism is approximately doubled when testosterone is coadministered, suggesting that optimizing of concurrent androgen replacement will reduce GH dose requirements, providing a significant cost saving.

The findings also have wider relevance in the context of normal human aging. The decline in endogenous GH and testosterone production rates with increasing age (19) might contribute to some of the effects of aging, including reduced muscle mass and increased body fat. However, studies in which testosterone or GH have been administered in isolation to elderly subjects have demonstrated little or no clinically significant effect. Because our findings show that the optimization of the effects of GH and testosterone requires administration of both hormones simultaneously, there is a rationale for future studies to address the effects GH and testosterone administered in combination as well as or instead of in isolation. Results from clinical trials of combined treatments are encouraging (4, 8).

In summary, testosterone replacement in hypopituitary adults increased circulating IGF-I only during concomitant administration of GH. Testosterone and GH exerted independent and additive effects to reduce irreversible oxidative protein loss and increase protein synthesis. These findings suggest that testosterone enhances the anabolic effects of GH through IGF-I but exerts protein anabolic effects that are independent of GH action. Concurrent administration of testosterone and GH in GHD subjects is likely to be both physiologically and economically important. Further studies are needed to delineate the molecular mechanisms by which these effects occur.

GRANTS

Eli Lilly and the National Health and Medical Research Council of Australia supported this work. The Swedish Society of Medicine and the Novo Nordisk Foundation supported Dr. Johannsson.

ACKNOWLEDGMENTS

We thank Dr. Andrea Attanasio for valuable input into the planning of these studies. We are most grateful to Maria Males, Bronwyn Heinrich, and Olivia Wong for clinical assistance, and Nicola Jackson and Nathan Doyle for excellent technical assistance. We also thank Dr. George Smythe and Anne Poljack, Bioanalytical Mass Spectroscopy Facility at the University of New South Wales for analytic GC-MS support.

FOOTNOTES


Address for correspondence: K. K. Y. Ho, Garvan Institute of Medical Research, 384 Victoria St., Darlinghurst, NSW 2010, Australia (e-mail: [email protected])

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

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Really,Your telling me to do more research and to shut up?
first of all before i comment on any of ur posts, i have to make one thing clear. no brother, we might disagree but i will never insult you.
i was sayin
"then i will 1.shut up, 2.apologize and 3.do MORE research."

i will comment on your research as soon as i read it


I NEVER INTEND TO INSULT YOU OR ANY MEMBER ON HERE, WE ARE ALL BROTHERS OF IRON
 
When you say it still works the same, what exactly are you referring to?
I'm not calling you out brother, not in the least, I'm just curious on what you mean.

Now IMO, HGH has poor properties far as skeletal muscle mass when taken by itself, and it's definitely not worth the large price if you are taking it solely for gaining muscle, and by itself it's really only going to provide fat loss or “sculpting” if you will.
Keep in mine that lean body mass does not necessarily mean muscle,People who lean out on HGH only, and yet gain 8-10 lbs, at the same time of losing fat don't consider that HGH will increase skeletal "bone" density, and tissue growth ( not necessarily muscle ).
When used with Test The only real use in gaining muscle may be as a synergistic effects. Now far as tissue repair that's different. Testosterone is a must with HGH to gain quality muscle mass.

Testosterone is far superior for muscle growth over HGH any day....

With the cost of a lengthy intake of HGH at 8-10ius alone, one could spend that on other "compound's" that are anabolic, and gain better results and yield more quality muscle....

Spend the money on food and Test, and maybe some tbol/vars, and add some NPP to the mix, or even some mast or proviron....
And this all can be achieved with no where near as much that would be spent on HGH...
The results one can expect with HGH alone at the end of the day would fail to provide anyone with impressing results to consider spending the funds and doing it again.
Why would anyone not want to run other compounds with it, like it's counter part "Test"?

Just IMHO...:cool:

you are forgetting what gh converts to in supraphysiological diseases. he isn't looking from my understanding to gain the most muscle or most of anything. he asked is 8-10our of gh a waste. no it is not. I will go into more detail.tomm.

Sent from my SGH-T989 using Tapatalk
 
first of all before i comment on any of ur posts, i have to make one thing clear. no brother, we might disagree but i will never insult you.
i was sayin
"then i will 1.shut up, 2.apologize and 3.do MORE research."

i will comment on your research as soon as i read it


I NEVER INTEND TO INSULT YOU OR ANY MEMBER ON HERE, WE ARE ALL BROTHERS OF IRON

I don't mean to have all this come off as dramatic, or blow out of proportion.
But, when you made your post and stated ( inexperienced, never tried quality HGH on it's own or following a certain agenda.) we both know who that was aimed at. It wasn't necessary to make such speculations and then label someone as being one of these in particular type of individuals.
I see that you had a typo and edited it, thanks for clarifying that.

My original post wasn't baseless,as I too care about members and I wish to help where I can, and I'm sure many members could agree on that, and that I go out on a limb to help where I can.

Thank you for taking to time to clarify you intentions over all here!
 
you are forgetting what gh converts to in supraphysiological diseases. he isn't looking from my understanding to gain the most muscle or most of anything. he asked is 8-10our of gh a waste. no it is not. I will go into more detail.tomm.

Sent from my SGH-T989 using Tapatalk

I see that your on the phone, and composing a lengthy reply is rather difficult, so most definitely chime in tomorrow.

Real fast if I may add, if he was to take 8-10ius and not expect to gain the most of it and get the most results, then why waste the product on such a baseless goal when there is far better options to aid the 8-10ius with?To use it for sculpturing and shredding fat.. Evan at that, in conjunction with clens or t3s would yield greater results.. I agree that results can and still will be achieved at 8-10ius, no doubt about that. But his question is would it be a waste overall?

The best thing about these forums is the diversity among us and the ideals and theories we all have, and how we all can share/have peaceful debates.
 
Im taking 6ius right now along with some test prop &making incredible gains. My buddy istaking 8ius a day with no other compounds as of now & he has leaned out very well but has gained a bit of muscle nothing crazy tho. So yes adding test will help you grow a lot moreand quicker but if your looking to lean out put a bit of muscle slowly and some rejuvenation hgh is a good route to take but work up to your dose. If you have the money go for it!
 
Im taking 6ius right now along with some test prop &making incredible gains. My buddy istaking 8ius a day with no other compounds as of now & he has leaned out very well but has gained a bit of muscle nothing crazy tho. So yes adding test will help you grow a lot moreand quicker but if your looking to lean out put a bit of muscle slowly and some rejuvenation hgh is a good route to take but work up to your dose. If you have the money go for it!

what brand are you guys taking..
 
Well 10ius of good hgh isnt going to come with out a side effect price itself at 10ius can start experiencing pain in bones and joints. imo for your goals of looking good on the beach 5ius would offer pretty much the same as 10ius the 10iu level is more for a heavy steroid user using other drugs. 8 would proably be alright to I am no expert by no stretch osiris it but it seems like over kill and and that over kill would be in the price of around $200 dollars a month. ANd possible joint pains and swollen ankles and all sorts of shit 4-6 is prolly what your looking for. 10ius you can start seeing skull growth to possibly and such
 
Well 10ius of good hgh isnt going to come with out a side effect price itself at 10ius can start experiencing pain in bones and joints. imo for your goals of looking good on the beach 5ius would offer pretty much the same as 10ius the 10iu level is more for a heavy steroid user using other drugs. 8 would proably be alright to I am no expert by no stretch osiris it but it seems like over kill and and that over kill would be in the price of around $200 dollars a month. ANd possible joint pains and swollen ankles and all sorts of shit 4-6 is prolly what your looking for. 10ius you can start seeing skull growth to possibly and such

Understood thanks.. so maybe use 4-6 iu for a few months and see what i get out off it? and then decide .??
 
im no expert but that seems logical osirs is an expert the other guys where right to. They say when you have to debate its usually best to meet in the middle.
 
Understood thanks.. so maybe use 4-6 iu for a few months and see what i get out off it? and then decide .??

Buy like 3 kits and run at 4iu/day. That will last you 75 days, more than enough time to make your judgment, and without investing too much money, learning how something effects you personally is the best way to decide if it's something you want to continue
 
I'd much rather run gh by itself then nothing at all.
Benefits may not be as outstanting but there would still be benefits.
 
I just got finished reading the articles. There are some things that the studies do not mention that we all know of.

The igf-1 secretion from GH creates new cells within the muscle.
Testosterone in itself doesn't not create new muscle cells. It just causes whatever muscles cells that exist to grow. Once new muscle cells are created from GH they have to grow. Testosterone causes those cells to grow into adult cells at a much faster rate than just exercise alone.

Infact anything that raises testosterone levels whether naturally or unaturally will cause those muscle cells to grow.

But guess what. The gains you get from a natural testosterone booster combined with GH will be more permanent compared to the gains you get from injectable test with GH. Once you come of your inj Test you will lose some mass gains from the Test. during pct.

So for a quick noticable muclemass gains nothing beats Test. For long term permanent gains I think GH is better.

So 8-10 IU of GH will create a but load of new cells that will grow when you exercise with or without Test and they will be permanent.


The Beggar
 
Really,Your telling me to do more research and to shut up?
I guess my experience with/how my body reacts is insufficient.

Here, take a look at some of these reads and tell me how you feel.

1) So, your going to speculate that I have an agenda, and also speculate that I am inexperienced, and then make the claim that I haven't ran quality HGH
2) You need to hear from the community to back what you said, before you admit your not partially wrong? But, with your confidence and your inflated Ego why bother with what the consensus has to say? I mean with the arrogance that you carry you should not need the point of views from others.

So with that being said, here is some reads for you.

These read I will post even have references from individuals that have PHD's,
I think that's a little more sufficient than Bro-science, don't you think?


--------------------------------------------------------------------------

Growth Hormone vs. Testosterone

A Retrospective Based on the Latest Research

by Karlis Ullis, M.D. and Joshua Shackman, Ph.D.


I was one of the first private practitioners in the country to dispense growth hormone as part of an overall anti-program hormone ..........

[/I][/B]

A Retrospective Based on the Latest Research
 
Really,Your telling me to do more research and to shut up?
I guess my experience with/how my body reacts is insufficient.

Here, take a look at some of these reads and tell me how you feel.

1) So, your going to speculate that I have an agenda, and also speculate that I am inexperienced, and then make the claim that I haven't ran quality HGH
2) You need to hear from the community to back what you said, before you admit your not partially wrong? But, with your confidence and your inflated Ego why bother with what the consensus has to say? I mean with the arrogance that you carry you should not need the point of views from others.

So with that being said, here is some reads for you.

These read I will post even have references from individuals that have PHD's,
I think that's a little more sufficient than Bro-science, don't you think?


--------------------------------------------------------------------------

Growth Hormone vs. Testosterone

A Retrospective Based on the Latest Research

by Karlis Ullis, M.D. and Joshua Shackman, Ph.D.


I was one of the first private practitioners in the country to dispense growth hormone as part of an overall anti-program hormone ..........

[/I][/B]

A Retrospective Based on the Latest Research
 
One more for you, with some more references..
By the way, none told you to shut-up, so no need to tell others to...

--------------------------------------------------------------------------
Growth hormone and testosterone interact positively to enhance protein and energy metabolism in men
James Gibney,1 Troels Wolthers,1 Gudmundur Johannsson,1 A. Margot Umpleby,2 and Ken K. Y. Ho1

1Pituitary Research Unit, Garvan Institute of Medical Research and Department of Endocrinology, St. Vincent’s Hospital, Sydney, Australia; and 2Dept. of Diabetes and Endocrinology, Guy’s, King’s and St. Thomas’ School of Medicine, St. Thomas' Hospital, London, United Kingdom

Submitted 11 October 2004 ; accepted in final form 18 February 2005

ABSTRACT

We investigated the...............

doses of HGH are not even close to 8-10 iu, add to that the facts that beggar mentioned.
 
doses of HGH are not even close to 8-10 iu, add to that the facts that beggar mentioned.

So more is better, how about 20-40ius? I provided studies, and all you have to say is the ( add to that the facts that beggar mentioned ), once more your failing to provide and prove anything other than your opinion that is baseless and holds no weight!

Speaking of igf-1 secretion from GH , what do YOU know about igf-1, and it's properties? I want to see you come up with something, other then saying ( Look what he said )..

Provide me with some facts and studies here. If I can do it, than so can you.. Your confidant, but yet provide nothing with just a few uttered words.

I never said that HGH at these dosed will not work, I said that it would be a waste of product considering the better options to utilize the compound with test.
Can your ego just sit aside for one second and agree that HGH works hand in hand with the intake of test, on a scale that is much more pronounced then ran alone?
 
Last edited:

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