My Thoughts on HGH...

I've used MK pretty consistently for 18+ months.

Recovery? Great
Sleep? Amazing
Hunger? Consistent (althought it tapers)

Not much in terms of lipolysis though (although I haven't actively tried to get leaner, but it is one of GH's upsides). I think theres a difference in the 20 vs 22 kilodalton GH; endogenous v.s exogenous. I also think what receptor each person's body is susceptible to (Scott Stevenson has a video series on this that was posted earlier on this board) also plays a role. I think fatloss might be better with exogenous, and maybe it's just my experience.

To add to this, I've been running 3-4 ius of GH for probably 10+ weeks, and noticed more fat loss than from MK.

I personally don't think a dose higher than 4iu is a good idea for those starting off with GH. Grow into your doses in my opinion. Your first year of GH use shouldn't warrant 8 ius of ED use. And it makes very little sense financially too.

Consistency > Quantity. You also need to be aware of certain genetic predispositions, especially diabetes in your genetic history. Most people are concerned with cancer due to GH being a direct function of various growth factors. If we look at a large data set of bodybuilders, we have not really heard many getting cancer. Diabetes from GH abuse/ genetic predisposition combined? Absolutely. There's quite a few pros who are diabetic due to GH abuse.

FYI, MK raised my resting glucose far higher than GH did. 90+ on MK, low 70s on 4iu of GH.

Sorry for the disorganized post, these are just my thoughts.

Sent from my SM-G900T using Tapatalk

Here are some interesting reads posted by an aussie ifbb pro done by some very knowledgeable people. Now you may not agree with everything that's stated (I don't) but they are good reads none the less and very well referenced. Would be good for Scott Stevenson or anyone with the knowledge for that matter to address them or rebuttal them. I'll have to post these separately so apologies if it looks like I'm spamming the thread but they're longish reads.

One of the most comprehensive arguments AGAINST using HGH and Bodybuilding thanks to Bradley Clarke.

Respect to Bradley for using a writing style that allows your average gym rat to understand too.

Brads qualifications include:
Master of Human Factors Engineering and Health Science
DipAppSci;AdvDipEnv;AdvDipBus;GradCertForensInv;MESH;MA; MSIA;MHFESA
Scientific Investigator and Performance Chemist
5thprinciple.info

What’s wrong with Growth Hormone?
Today I am going to explain why I think growth hormone may well represent everything that I think is wrong with bodybuilding today.
It would be fair to say that the physiques of the 1970s had better symmetry than many of today’s larger frames and might have been easier to achieve for a couple of reasons. It appears to me that as time has gone on from the 1990s, midsection thickness has become the mainstay of today’s shape. This may be, in most part, due to growth hormone supplementation.

I am not talking about growth hormone secretion within the athletes own body but the supraphysiological use of pharmaceutical grade material which is targeting every tissue in the body but skeletal muscle. This means that rather than having a 28 inch waist like Flex Wheeler did, some body builders are on stage with what easily appear to 40 inch waists. [1] A few pros have managed to rein it in but many have not.

We must begin with some overarching comments in that growth hormone is a controlled poison for which both Customs and the various state police forces take umbrage at the importation, possession and use. Because of the high desirability of growth hormone, the chance of purchasing fake material in plain vials or counterfeit labelled materials in vials, ampules and boxes is also high. Coupled with the fact that growth hormone is expensive, grows tissue other than skeletal muscle thus thickens your waist means that you need to significantly grow your upper body to increase the appearance of clavicle width. This might add years you your journey.

So what does growth hormone do and at what dose? I’m happy to be wrong but don’t argue with me brining anecdote. What I am about to report is peer reviewed studies controlled for variables and the compounds used were real and known. I might also say that all of these research papers are written by people smarter than me and some of the papers have more than 10 authors who are all smarter than me.

Firstly, growth hormone is not antiaging. That’s become a massive scam and to be blunt, growth hormone is both disease promoting and pro-aging. Growth hormone promotes proliferation and mitosis of various tissues including cancer lines. It upregulates cell turnover which in effect is like photocopying copies of photocopies. Rather than cells spending more time in rest and repair phase of the cell cycle, they are quickly pushed through the cycle proliferating errors.
Growth hormone increases circulating IGF-1 which in most populations is not desirable. While IGF-1 is a potent anabolic and the only means by which growth hormone has any influence over skeletal muscle, oestrogen rather has the effect of increasing IGF-1 in contracting muscle. That is where it is desirable, not in lung and brain tissue. In fact, mice with diminished capacity to produce and receive growth hormone live 30 to 70% longer than their full GH cousins. [2-7]
Growth hormone increases insulin resistance which may have long lasting effects beyond the gym and into middle life. [8-10] While normal growth hormone levels are desirable to maintain generalised health, the reduction in insulin sensitivity brought about by high levels of growth hormone needs to be considered in order to reduce the likelihood of accreting visceral body fat after administration has ceased. The effectiveness of co-administrated insulin is affected as is the uptake of amino acids which use the insulin system for cellular transport. This is also disease promoting including fatty liver disease, heart disease, tissue degradation and sexual health. [11-14]
Growth hormone administration increases the size of smooth muscle including the viscera and vascular system. This is one of my main contentions, that thicker midsections mean that greater upper body volume is required to maintain symmetry. There is not a lot of research into high dose growth hormone administration on smooth muscle but we can start with the symptoms of acromegaly (excess GH production and secretion). In smooth muscle tissue such as the heart in which constant exposure to high levels of growth hormone occurs, a heart may weigh as much as 1000g. [15] In normal persons a large heart may be 300g. Liver cells are a target tissue for growth hormone as is cells of the stomach and upper gastrointestinal tract as well as bone tissue such as feet, hands and jaw. [16,17]

One beneficial targets for growth hormone is fibroblasts which build connective tissue such as tendons and cartilage. I have no issue there although fibroblast growth factor and procollagen 1 are better growth factors in that regard.
Moreover, growth hormone administration has been associated with Creutzfeldt-Jakob disease from human sources as recent as 20 years ago. [18-21] There is no evidence that black market hGH has not come from cadavers.

Now there is always a trade-off between health and performance. The consumption of milk protein is associated with breast cancer and a diet high in leucine is a risk factor for melanoma. The benefit is growth of skeletal muscle so the risk to benefit ratio is balanced toward using the supplements. So we would want growth hormone to build muscle in order to offset the negative effects, right?

Let’s look at a range of studies in athletes and normal subjects using both growth hormone in isolation and with steroids. I have put an approximate value of each program based on period of trial and volume used, at $10 per IU.
A study of 16 untrained men, aged 18 to 28 years, administered growth hormone at 0.56 IU/kg/week (say 6.4iu per day at 80kg) or placebo over 12 weeks of heavy resistance training. [22] After 12 weeks there was a more pronounced increase in free fatty mass and total body water in the growth hormone group compared to placebo, but there was no difference in muscle strength or limb circumference. The quadriceps muscle protein synthesis rate showed no difference between the groups. $5376
Seven trained weight-lifters with a mean age of 23 years were administered 0.56 IU/kg/week (same as the previous trial) during 14 days of heavy training. There was no increase in fractional rate of muscle protein synthesis and no decrease in whole body protein breakdown after 2 weeks. [23] $896
In a study which used 22 male power athletes, aged 18 to 48, growth hormone was administered at 0.63 IU/kg/week (say 7.2iu for 80kg) or placebo during six weeks exercise. The researchers found no difference in maximal voluntary strength of biceps or quadriceps muscles. There was no change in body weight or body fat decrease between the groups. [24] $3024

In a study looking at elderly men over 14 weeks of initial progressive resistance training, followed by 0.28 IU/kg/week (say 3.2iu) of growth hormone or placebo, administered over 10 weeks. Biopsy of the vastus lateralis muscles was performed at baseline and after 14 and 24 weeks. There was no change in muscle strength, morphology or muscle GH/IGF-I mRNA expression between the growth hormone and placebo groups. [25] $2240

In one study of male sprinters (63) which combined 250mg of testosterone per week with 6iu of growth hormone per day (funded by WADA), sprint capacity increased however other parameters such as plyometric strength did not. Further, the increase in lean mass associated with growth hormone was attributed to water retention. Increased capacity to sprint decreased to baseline after a six week wash out period. [26] $2520 (GH alone)

In a 28 day study of 30 young men and women, receiving 16iu per day at the highest dose, found no improvement in power output or oxygen uptake.[27] $4480 for the highest dosed group.
In a study of seven young men receiving 7.5iu growth hormone per day or placebo, over 4 days found that there was a greater mobilisation of fat stores but no greater oxidation during exercise. [28] $300

In another study looking at 31 older men, growth hormone administration at 1.8iu per day over 12 weeks ($1512) found no change in quadriceps power or muscle fibre number. What the study did show however is that in the placebo group the fibre type 2a moved toward 2x characteristics where in the growth hormone group 2x moved toward type 2a characteristics. [29]

In a study which looked at endogenous hormone levels in trained athletes, neither growth hormone nor testosterone secretion increase led to greater hypertrophy or strength. While this was not a study on supraphysiological doses, it does add an interesting dimension to the argument. [30]

I conclude by saying that the pro-aging effects of growth hormone combined with increases in tissue other than skeletal muscle are not worth the investment even if you consider the beneficial albeit transient results seen in the WADA funded study. The health concerns and increased risk of side effects seen in the Berggren et al study at doses greater than 16iu per day (at say the 28 days) do not correlate with any potential gains even accounting for the addition of other anabolic augmentation usually undertaken by bodybuilders. That study saw an investment of $4480 over 28 days which could be equivalent to an additional dietary intake of 8kg of steak per day if the investment was redirected. Red meat is anabolic in its own right (and apparently manly). [31-34]

1 Krasniewicz, L., & Blitz, M. (2006). Arnold Schwarzenegger: a biography. Greenwood Publishing Group.
2 Vance, M. L. (2003). Can growth hormone prevent aging?. New England Journal of Medicine, 348(9), 779-780.
3 Cao, H., Wang, G., Meng, L., Shen, H., Feng, Z., Liu, Q., & Du, J. (2012). Association between circulating levels of IGF-1 and IGFBP-3 and lung cancer risk: a meta-analysis. PloS one, 7(11), e49884.
4 Bartke, A., Brown-Borg, H. M., Bode, A. M., Carlson, J., Hunter, W. S., & Bronson, R. T. (1998). Does growth hormone prevent or accelerate aging?. Experimental gerontology, 33(7), 675-687.
5 Bartke, A. (2005). Minireview: role of the growth hormone/insulin-like growth factor system in mammalian aging. Endocrinology, 146(9), 3718-3723.
6 Flurkey, K., Papaconstantinou, J., Miller, R. A., & Harrison, D. E. (2001). Lifespan extension and delayed immune and collagen aging in mutant mice with defects in growth hormone production. Proceedings of the National Academy of Sciences, 98(12), 6736-6741.
7 Flurkey, K., Papaconstantinou, J., Miller, R. A., & Harrison, D. E. (2001). Lifespan extension and delayed immune and collagen aging in mutant mice with defects in growth hormone production. Proceedings of the National Academy of Sciences, 98(12), 6736-6741.
8 Guevara-Aguirre, J., Balasubramanian, P., Guevara-Aguirre, M., Wei, M., Madia, F., Cheng, C. W., ... & de Cabo, R. (2011). Growth hormone receptor deficiency is associated with a major reduction in pro-aging signaling, cancer, and diabetes in humans. Science translational medicine, 3(70), 70ra13-70ra13.
9 Rizza, R. A., Mandarino, L. J., & Gerich, J. E. (1982). Effects of growth hormone on insulin action in man: mechanisms of insulin resistance, impaired suppression of glucose production, and impaired stimulation of glucose utilization. Diabetes, 31(8), 663-669.
10 Carroll, P. V., Christ the members of Growth Hormone Research Society Scientific Committee, E. R., Bengtsson, B. A., Carlsson, L., Christiansen, J. S., Clemmons, D., ... & Sonksen, P. H. (1998). Growth hormone deficiency in adulthood and the effects of growth hormone replacement: a review. The Journal of Clinical Endocrinology & Metabolism, 83(2), 382-395.
11 Marchesini, G., Brizi, M., Morselli-Labate, A. M., Bianchi, G., Bugianesi, E., McCullough, A. J., ... & Melchionda, N. (1999). Association of nonalcoholic fatty liver disease with insulin resistance. The American journal of medicine, 107(5), 450-455.
12 Reaven, G. M. (1988). Role of insulin resistance in human disease. Diabetes, 37(12), 1595-1607.
13 Ginsberg, H. N. (2000). Insulin resistance and cardiovascular disease. The Journal of clinical investigation, 106(4), 453-458.
14 Bansal, T. C., Guay, A. T., Jacobson, J., Woods, B. O., & Nesto, R. W. (2005). ORIGINAL RESEARCH—ENDOCRINOLOGY: Incidence of Metabolic Syndrome and Insulin Resistance in a Population with Organic Erectile Dysfunction. The journal of sexual medicine, 2(1), 96-103.
15 Colao, A., Marzullo, P., Di Somma, C., & Lombardi, G. (2001). Growth hormone and the heart. Clinical endocrinology, 54(2), 137-154.
16 Isaksson, O. G. P., Eden, S., & Jansson, J. (1985). Mode of action of pituitary growth hormone on target cells. Annual review of physiology, 47(1), 483-499.
17 Chang, P. J., Nino-Murcia, M., & Kosek, J. (1990). Polypoid Menetrier's disease associated with acromegaly. Gastrointestinal radiology, 15(1), 61-63.
18 Ehrnborg, C., Bengtsson, B. Å., & Rosén, T. (2000). Growth hormone abuse. Best Practice & Research Clinical Endocrinology & Metabolism, 14(1), 71-77.
19 Collinge, J., Palmer, M. S., & Dryden, A. J. (1991). Genetic predisposition to iatrogenic Creutzfeldt-Jakob disease. The Lancet, 337(8755), 1441-1442.
20 Goodbrand, I. A., Ironside, J. W., Nicolson, D., & Bell, J. E. (1995). Prion protein accumulation in the spinal cords of patients with sporadic and growth hormone associated Creutzfeldt-Jakob disease. Neuroscience letters, 183(1), 127-130.
21 Brandel, J. P., Preece, M., Brown, P., Croes, E., Laplanche, J. L., Agid, Y., ... & Alpérovitch, A. (2003). Distribution of codon 129 genotype in human growth hormone-treated CJD patients in France and the UK. The Lancet, 362(9378), 128-130.
22 Yarasheski KE, Campbell JA, Smith K et al. (1992) Effect of growth hormone and resistance exercise on muscle growth in young men. American Journal of Physiology 1992; 262: E261±E267.
23 Yarasheski KE, Zachweija JJ, Angelopoulos TJ et al. (1993) Short-term growth hormone treatment does not increase muscle protein synthesis in experienced weight lifters. Journal of Applied Physiology 1993; 74: 3073±3076.
24 Deyssig R, Frisch H, Blum WF et al. (1993) Effect of growth hormone treatment on hormonal parameters, body composition and strength in athletes. Acta Endocrinologica (Copenhagen) 1993; 128: 313±318.
25 Taaffe DR, Jin IH, Vu TH et al. (1996) Lack of effect of recombinant human growth hormone (GH) on muscle morphology and GH-insulin-like growth factor expression in resistance-trained elderly men. Journal of Clinical Endocrinology and Metabolism 1996; 81: 421±425.
26 Meinhardt, U., Nelson, A. E., Hansen, J. L., Birzniece, V., Clifford, D., Leung, K. C., ... & Ho, K. K. (2010). The Effects of Growth Hormone on Body Composition and Physical Performance in Recreational AthletesA Randomized Trial. Annals of internal medicine, 152(9), 568-577.
27 Berggren, A., Ehrnborg, C., Rosén, T., Ellegård, L., Bengtsson, B. A., & Caidahl, K. (2005). Short-term administration of supraphysiological recombinant human growth hormone (GH) does not increase maximum endurance exercise capacity in healthy, active young men and women with normal GH-insulin-like growth factor I axes. The Journal of Clinical Endocrinology & Metabolism, 90(6), 3268-3273.
28 Hansen, M., Morthorst, R., Larsson, B., Dall, R., Flyvbjerg, A., Rasmussen, M. H., ... & Lange, K. H. W. (2005). No effect of growth hormone administration on substrate oxidation during exercise in young, lean men. The Journal of physiology, 567(3), 1035-1045.
29 Lange, K. H. W., Andersen, J. L., Beyer, N., Isaksson, F., Larsson, B., Rasmussen, M. H., ... & Kjær, M. (2002). GH administration changes myosin heavy chain isoforms in skeletal muscle but does not augment muscle strength or hypertrophy, either alone or combined with resistance exercise training in healthy elderly men. The Journal of Clinical Endocrinology & Metabolism, 87(2), 513-523.
30 West, D. W., Burd, N. A., Tang, J. E., Moore, D. R., Staples, A. W., Holwerda, A. M., ... & Phillips, S. M. (2010). Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors. Journal of Applied Physiology, 108(1), 60-67.
31 Daly, R. M., O'Connell, S. L., Mundell, N. L., Grimes, C. A., Dunstan, D. W., & Nowson, C. A. (2014). Protein-enriched diet, with the use of lean red meat, combined with progressive resistance training enhances lean tissue mass and muscle strength and reduces circulating IL-6 concentrations in elderly women: a cluster randomized controlled trial. The American journal of clinical nutrition, 99(4), 899-910.
32 Waters, D. L., Baumgartner, R. N., Garry, P. J., & Vellas, B. (2010). Advantages of dietary, exercise-related, and therapeutic interventions to prevent and treat sarcopenia in adult patients: an update. Clin Interv Aging, 5, 259-270.
33 McNeill, S. H. (2014). Inclusion of red meat in healthful dietary patterns. Meat science, 98(3), 452-460.
34 Sobal, J. (2005). Men, meat, and marriage: Models of masculinity. Food and Foodways, 13(1-2), 135-158.

Furions Qualifications
MPharm MPS ND BScHlthSci (Comp Med & Nutr)

Furions Summary from James Dries

HGH is a peptide hormone produced and secreted in the brain and is expressed in 4 similar forms, acting on all tissues in the body to promote tissue repair. In response to exercise, one particular type is primarily attributed to enhancing muscle growth (it is this specific type that synthetic forms attempt to replicate). HGH produced in the brain stimulates the release of IGF-1 from the liver, which plays a significant role in signalling muscle growth. When produced naturally, both hormones may work by themselves, or together, amplifying the effects of each other. For this reason, people mistakenly believe that administering synthetic versions of HGH and IGF-1 will promote muscle growth.

The way in which HGH is produced in laboratories leads to a slightly different shape and stability of the synthetic HGH molecule. Therefore, its ability to communicate with muscle cells and signal muscle growth is altered (remember the lock and key analogy). Even if measures are taken to make the purest form of HGH, not all of the product will be effective in its intended role due to manufacturing constraints.
In relation to Brads post, this would make sense as synthetic HGH may be very effective at signalling heart and gut growth, but much less effective in enhancing muscle growth due to its reduced ability to signal IGF-1 release within muscles (less compatible). A lesser quality synthetic HGH will most likely compound this problem. As Brad also mentioned, high circulating levels of IGF-1 are not desirable and may have detrimental effects on brain and lung tissue. Therefore, it appears that the optimal levels of HGH and IGF-1 in relation to building muscle, occurs naturally and is optimally stimulated by resistance training (and diet).

Furions Report
I will follow on from Brads article- through a neutral perspective to dissect this contentious and quantitatively negative finding of myogenic/hypertrophic activity as it pertains to applicable pharmacological qualitative analyses.
I will preface this by indicating that it the information presented here is in fact casted through substantiated hypothetical molecular targeting and effector downstream cascades. It is thus collectively theorized- however does indeed form congruence with the comprehensive quantitative results Brad has described.

As a sort of add-on bonus to the topic- I will describe a potential reason for the widely noted (and consequently accepted) discrepancies of approved GH as somatotropin pharmaceuticals vs. unapproved generically labelled GH- as it pertains to the manufacturing processes.
*********************************************************************
To examine the pharmacological activity of supraphysiological growth hormone administration for the physique athlete- it would seem most suitable to establish the endogenous fluxes and bioactivity during resistance exercise and then model these against the (then deduced) molecular targets and downstream effectors that may be conducive to myogenesis when using a pharmaceutical.
In doing this, it is pertinent to stipulate that GH, as a pituitary hormone, occurs as a “superfamily” of (now currently identified) 4 different molecular isoforms, these categorized by the weight (20 kDa, non-22 kDa, 44 kDa, and 66 kDa (1). Each isoform appears to bear role in mediating physiological activity during recovery in response to exercise stress (1-4). The pharmaceutical preparations of GH (as somatotropin) occur as only the monomeric 22kDa peptide, hence it is important to make this distinction when scrutinizing the endogenous patterns against exogenous administrations in exercise models and to consider that the complexity is such that no finites or absolutes can yet be made as to the complete pharmacological myogenic activity.

In saying this, associated evidence does suggest that in non-aged, non-obese subjects the more rapid-response patterns and greatest fluxes of endogenous GH associated with anaerobic resistance exercise are actually related to this 22-kDa (immunoreactive GH) isoform (5-8) see figure 1. It is also worth noting that there does appear to be aged and body compositional implications to the magnitude of the responses (7,8).

It is now understood that the growth hormone receptor (GHR) is ubiquitious and through signal transduction can have effect on all tissues (9,10). From a broad analytical examinations, any likely anabolic activity associated with exogenous GH will be confounded by anabolic activity of GH stimulated, hepatic secreted systemically circulating IGF-1. It has been recently identified that the anabolic activities between these two hormones may be in fact independent of each other, potentially additive and in respect to the endogenous patterns; synergistic as it pertains to myogenesis and tissue repair (11). Henceforth for the purposes of distinguishing these two hormones as exogenous preparations, this report will focus on that unique to GH alone.

Cumulative data suggests that the molecular patterns specific with growth hormone administration (or secretion) in combination with resistant exercise are hallmarked by an up regulation of a tissue specific mechanosensitive isoforms of IGF-1 (12,13). These are IGF-1 isoforms literally produced by skeletal muscle, to act locally within the skeletal muscle; a paracrine response (13,14). Skeletal muscle induced IGF undergoes alternative splicing and generates 3 isoforms; IGF1Ea, IGF1Eb and IGF1Ec (15,16). The IGF1Ec isoform, colloquially known as mechano growth factor (MGF) appears the most active and also has recently been implicated as the likely main driver behind the paracrine activity that may have the terminal responsibility for the downstream myogenesis associated with resistance training and subjectively augmented by growth hormone (17,18).
MGF (as IGF-1Ec) has been shown to activate muscle satellite cells, promote myonuclei accumulation and expand myofiber diameter (17,19) whilst growth hormone has independently been shown to rapidly induce expression of MGF in muscle satellite cells in varying models, and may in fact do so in an additive manner with MGF when combined with resistance training (12,13,20).

So to apply this as a theoretical basis, it may be postulated that the MGF response, as induced by the combination of mechanical loading and exogenous GH administration, may activate muscle satellite cells and accrue extra myonuclei as a repair response in greater amplitude than what can occur in normal physiological conditions. This induced state may therefore somewhat override the negative regulators of satellite cells maturation, such as myostatin, that normally halt and shift the satellite cell activation back into the quiescient state and potentially remove a limitation to the mitotic and subsequent myogenesis (21-23).

**Working off this premise- there may be further pharmaceutical methods to exploit this mode of action when considering the systemic IGF-1 implications. This would include the use of insulin and other anabolic compounds- however may need a separate article in itself**
Although it may seem as though this could explain the anecdotally claimed skeletal muscle hypertrophic capacity of growth hormone, these actions alone may not account for any measurable degree of muscle strength increase or performance enhancement- hence may provide some degree of rationale for the consistently negative results observed in the quantitative analyses Brad has cited. This has certainly been comprehensively concluded in related qualitative research (24-26). Additionally as this molecular pathway has not been comprehensively researched so I am really at a stretch here to conclusively say that this is the unique pharmacological property of growth hormone that distinguishes it from all performance and image enhancing drugs.
*****************************************************************************
Peptide syntheses can be performed via two main methods. The distinction between the methods may account for the discrepancies of subjective quality of approved GH preparation against those unapproved generically labelled.
Peptide synthesis can be performed via amino acid binding- known simply as chemical synthesis. This is generally the cheapest and simplest method for peptide syntheses. It is usually performed with apparatus that literally link the individual amino acid together in a linear manner using catalytic enzymes and chemicals. This permits manufacture of perfectly functional short chain peptides (such as melanotan, GHRPs, ect). For synthesizing long chain peptides with 3 dimensional complex binding this method is limited in creating the tertiary and quaternary conformation patterns often associated with these.

So although the peptide sequence may be correct, it is likely that the shape formed by the extra-sequence binding might not be consistently present, if at all.
Recombinant peptide synthesis differs completely. This involves a live in-cell model usually using strains of bacterial or fungi, whereby the DNA and ribosomal transcriptional activity is stimulated so as to produce and then harvest the desired peptide. The peptide will therefore contain the bioidentical, 3 dimensional structure owing to the presence of the tertiary and quaternary peptide bonding. This is often necessary to the exploit the complete activity of the hormone and given research has not completely elucidated the binding properties of the GH receptor at the skeletal muscle, we must assume that the structural homogeneity is necessary for this binding. This therefore may serve as plausible explanation for the biological activity discrepancies between GH preparations.

As completed synthetic preparations, the stability of each peptide between these manufacturing procedures can also give reason as to the variance in the bioactivity. A peptide synthesized by chemical means tends to be more flexible and therefore more stable in shorter chains (i.e less than 100 residues). This decreases linearly in concert with the increasing number of residues. The reciprocal applies for recombinantly synthesized peptides. As the growth hormone isomer consists of 191 residues- it could be inferred that subsequent manufacturing procedures, including the lyophilisation (freeze drying), could pose detriment to the integrity of the peptide. A lyoprotectant should be used in GH manufacturing to maintain the structural integrity during this process. As result of the presence of tertiary and quaternary bonds, the recombinantly synthesized peptide is much more stable in the presence of a lyoprotectant. The same can be guaranteed for a chemically synthesized peptide, thus it could be well-assumed a percentage may become damaged as result this process.
Hence it may also seem plausible that a greater percentage of the peptide would be damaged using a chemical synthesis process.


(1) Baumann, G. (1999). Growth hormone heterogeneity in human pituitary and plasma. Hormone Research in Paediatrics, 51(Suppl. 1), 2-6.
(2) Baumann, G. (1991). Growth hormone heterogeneity: genes, isohormones, variants, and binding proteins. Endocrine Reviews, 12(4), 424-449.
(3) Kraemer, W. J., Nindl, B. C., Marx, J. O., Gotshalk, L. A., Bush, J. A., Welsch, J. R., ... & Hymer, W. C. (2006). Chronic resistance training in women potentiates growth hormone in vivo bioactivity: characterization of molecular mass variants. American Journal of Physiology-Endocrinology and Metabolism, 291(6), E1177-E1187.
(4) Wallace, J. D., Cuneo, R. C., Bidlingmaier, M., Lundberg, P. A., Carlsson, L., Boguszewski, C. L., ... & Rosén, T. (2001). The Response of Molecular Isoforms of Growth Hormone to Acute Exercise in Trained Adult Males 1. The Journal of Clinical Endocrinology & Metabolism, 86(1), 200-206.
(5) Thomas, G. A., Kraemer, W. J., Kennett, M. J., Comstock, B. A., Maresh, C. M., Denegar, C. R., ... & Hymer, W. C. (2011). Immunoreactive and bioactive growth hormone responses to resistance exercise in men who are lean or obese. Journal of Applied Physiology, 111(2), 465-472.
(6) Gordon, S. E., Kraemer, W. J., Vos, N. H., Lynch, J. M., & Knuttgen, H. G. (1994). Effect of acid-base balance on the growth hormone response to acute high-intensity cycle exercise. Journal of Applied Physiology, 76(2), 821-829.
(7) Kraemer, W. J., Fleck, S. J., Dziados, J. E., Harman, E. A., Marchitelli, L. J., Gordon, S. E., ... & Triplett, N. T. (1993). Changes in hormonal concentrations after different heavy-resistance exercise protocols in women. Journal of applied physiology, 75(2), 594-604.
(8) Kraemer, W. J., Marchitelli, L., Gordon, S. E., Harman, E., Dziados, J. E., Mello, R., ... & Fleck, S. J. (1990). Hormonal and growth factor responses to heavy resistance exercise protocols. Journal of Applied Physiology, 69(4), 1442-1450.
(9) Simard, M., Manthos, H., Giaid, A., Lefebvre, Y., & Goodyer, C. G. (1996). Ontogeny of growth hormone receptors in human tissues: an immunohistochemical study. The Journal of Clinical Endocrinology & Metabolism, 81(8), 3097-3102.
(10) List, E. O., Berryman, D. E., Ikeno, Y., Hubbard, G. B., Funk, K., Comisford, R., ... & Bartke, A. (2015). Removal of growth hormone receptor (GHR) in muscle of male mice replicates some of the health benefits seen in global GHR-/-mice. Aging, 7(7), 500-512.
(11) Sotiropoulos, A., Ohanna, M., Kedzia, C., Menon, R. K., Kopchick, J. J., Kelly, P. A., & Pende, M. (2006). Growth hormone promotes skeletal muscle cell fusion independent of insulin-like growth factor 1 up-regulation. Proceedings of the National Academy of Sciences, 103(19), 7315-7320.
(12) Hameed, M., Lange, K. H. W., Andersen, J. L., Schjerling, P., Kjaer, M., Harridge, S. D. R., & Goldspink, G. (2004). The effect of recombinant human growth hormone and resistance training on IGF‐I mRNA expression in the muscles of elderly men. The Journal of physiology, 555(1), 231-240.
(13) Iida, K., Itoh, E., Kim, D. S., Del Rincon, J. P., Coschigano, K. T., Kopchick, J. J., & Thorner, M. O. (2004). Muscle mechano growth factor is preferentially induced by growth hormone in growth hormone‐deficient lit/lit mice. The Journal of physiology, 560(2), 341-349.
(14) Matheny Jr, R. W., Nindl, B. C., & Adamo, M. L. (2010). Minireview: Mechano-growth factor: a putative product of IGF-I gene expression involved in tissue repair and regeneration. Endocrinology, 151(3), 865-875.
(15) Okazaki, R., Durham, S. K., Riggs, B. L., & Conover, C. A. (1995). Transforming growth factor-β and forskolin increase all classes of insulin-like growth factor-I transcripts in normal human osteoblast-like cells. Biochemical and biophysical research communications, 207(3), 963-970.
(16) Chew, S. L., Lavender, P. A. U. L., Clark, A. J., & Ross, R. J. (1995). An alternatively spliced human insulin-like growth factor-I transcript with hepatic tissue expression that diverts away from the mitogenic IBE1 peptide. Endocrinology, 136(5), 1939-1944.
(17) Dai, Z., Wu, F., Yeung, E. W., & Li, Y. (2010). IGF-IEc expression, regulation and biological function in different tissues. Growth Hormone & IGF Research, 20(4), 275-281.
(18) Yi, Q., Feng, J., He, L., Wan, R., Zeng, H., Yang, L., ... & Tang, L. (2017). The structure-function relationships of insulin-like growth factor 1 Ec in C2C12 cells. Cell Adhesion & Migration, (just-accepted), 00-00.
(19) Mavalli, M. D., DiGirolamo, D. J., Fan, Y., Riddle, R. C., Campbell, K. S., van Groen, T., ... & Clemens, T. L. (2010). Distinct growth hormone receptor signaling modes regulate skeletal muscle development and insulin sensitivity in mice. The Journal of clinical investigation, 120(11), 4007-4020.
(20) Imanaka, M., Iida, K., Murawaki, A., Nishizawa, H., Fukuoka, H., Takeno, R., ... & Chihara, K. (2008). Growth hormone stimulates mechano growth factor expression and activates myoblast transformation in C2C12 cells. Kobe J Med Sci, 54(1), E46-54.
(21) Goldspink, G. (2012). Age-related loss of muscle mass and strength. Journal of aging research, 2012.
(22) Hill, M., & Goldspink, G. (2003). Expression and splicing of the insulin‐like growth factor gene in rodent muscle is associated with muscle satellite (stem) cell activation following local tissue damage. The Journal of Physiology, 549(2), 409-418.
(23) Nederveen, J. P., Joanisse, S., Snijders, T., Ivankovic, V., Baker, S. K., Phillips, S. M., & Parise, G. (2016). Skeletal muscle satellite cells are located at a closer proximity to capillaries in healthy young compared with older men. Journal of cachexia, sarcopenia and muscle, 7(5), 547-554.
(24) Snijders, T., Smeets, J. S. J., Kranenburg, J., Kies, A. K., Loon, L. J. C., & Verdijk, L. B. (2016). Changes in myonuclear domain size do not precede muscle hypertrophy during prolonged resistance‐type exercise training. Acta Physiologica, 216(2), 231-239.
(25) Roth, S. M., Martel, G. F., Ivey, F. M., Lemmer, J. T., Tracy, B. L., Metter, E. J., ... & Rogers, M. A. (2001). Skeletal muscle satellite cell characteristics in young and older men and women after heavy resistance strength training. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 56(6), B240-B247.
(26) Kadi, F., Schjerling, P., Andersen, L. L., Charifi, N., Madsen, J. L., Christensen, L. R., & Andersen, J. L. (2004). The effects of heavy resistance training and detraining on satellite cells in human skeletal muscles. The Journal of physiology, 558(3), 1005-1012.

Last one, Brad clarifies some points after some questions he got.

Brad's response to some of the feedback he received from everybody regarding his report on HGH and Bodybuilding
Brads initial report is a few posts below, just under Furions breakdown of HGH

Bradley Clarke
Master of Human Factors Engineering and Health Science
DipAppSci;AdvDipEnv;AdvDipBus;GradCertForensInv;MESH;MA; MSIA;MHFESA
Scientific Investigator and Performance Chemist

It would be fair to say that I am old school and would prefer to go Chat Board over FB because it lasts longer. But here we are so I will respond in part as we go to keep the answers congruent with the questions and interesting for people who do not have an opinion or so you can come back with better material.

By the look of some comments I may have been mistaken to have said one does not need growth hormone and or that growth hormone has no value as a pharmacological intervention for disease. This is not what I meant to convey. An above average growth hormone level may confer some advantages to a low level for day to day operation and healing although for the emerging evidence, even this might not be the case. In a 2003 report Evolutionary medicine: from dwarf model systems to healthy centenarians? from the American

Association for the Advancement of Science I quote:
GH treatment can increase body mass and decrease adipose tissue in 61- to 81-year-old men with low plasma IGF-I concentration, and long-term GH replacement therapy causes some improvements in patients with GH deficiencies. However, the "antiaging" effects of GH therapy are typically observed after short-term treatment of patients with low plasma GH. By contrast, chronically high GH levels increase the incidence of diseases, including cancer and kidney diseases in rodents, and increase cardiovascular diseases and cancer in human acromegaly patients. GH administration also increases the development of diabetes and glucose intolerance in healthy, older women and men and increases morbidity and mortality in patients that are clinically ill, even after short-term treatment). It is clear that a major and chronic increase in plasma GH/IGF-I levels increases morbidity and mortality.[1]

My intention was not really to argue about life extension however one of my bug bears is the sale of goods which do not work to people who do not need them; a consumer advocate if you will. 90% of bodybuilders will never walk on stage with Luke, do not have the genetics, time to train, funds to supplement. Where is your dollar best put? I can only speak to the published trials.

Consider a 6 month program (which I haven’t found any studies in athletes going that long to answer one question) at 10iu per day. Let’s assume growth hormone is $10 at iu. That’s $100 per day for 185 days; $18,500. That is a serious investment. Short term administration at 16iu had no real BB effect (unless you sprint) over 28 days. This should be our starting point. Not Broscience, actual controlled studies with a placebo group. At 16iu for six months the bill is $29,600. For reference that is a bottle of red wine and 4kg of steak a day for six months. The critical point here is the WADA study found that over 28 days the lean mass accretion was attributable to extracellular water weight. I am happy to entertain that over a longer period some genes may be expressed at a greater level (Furion has suggested some) but in the long term trials soon to be discussed, there was no evidence of this, at least at 2.4iu/day.

It has been suggested that there are thousands of studies saying I am wrong. This is not the case but I concede that there are studies which do support the alternative. When one cites a study you should look at various key attributes beyond the title and abstract. I always do a quick search of the authors and whether the institute is funded and by who. Especially when forming legal arguments. This is why-

A number of links were attached by one reader who disagrees with my assertions. I like being disagreed with and hope to even change my mind. But these studies are not the ones to convince me of a number of key points to my argument:
1. Growth hormone is not worth the investment even if it does work.
2. It does not work.
3. The side effects are not worth the gain in lean muscle mass.
Effect of growth hormone (GH) on the immune system. [2]
This study is not relevant. The full study is not available and may have been retracted. If not it supports my contention. To quote: However, in humans GH deficiency is not usually associated with immunodeficiency and only minor abnormalities of immune function have been reported, as compared to those observed in GHD animals. It is possible that in humans the GH produced locally in the immune system compensates for the lack of endocrine GH. Thus compensatory growth hormone is not required for immune function.

Two years of treatment with recombinant human growth hormone increases bone mineral density in men with idiopathic osteoporosis. [3]

This study was in idiopathic osteoporosis patients who were administered calcium and vitamin D at the same time as growth hormone replacement. There was no control group and no calcium and vitamin D group only. We know one of the treatments for osteoporosis is calcium and vitamin D. In the two treatment groups, 1.2iu and 2.4iu per day were administered for three years.

The results did not impress the researchers and they conclude:
• A barrier to GH as a plausible therapy for osteoporosis is that the improvements in BMD in this present and other studies are not as impressive as those usually seen with antiresorptive agents.
• A second barrier to GH treatment is side effects. However, the side effects of GH treatment are well known from numerous studies in GHD and GH-sufficient subjects and are usually well tolerated and seldom cause interruption of treatment
• The GH treatment did not have any effect on bone size, according to the method used in this study.
• However, the absence of a placebo-treated control group strongly limits the conclusions that can be drawn about the efficacy of the treatment in this study; and double blind, placebo-controlled studies are needed to further elucidate the effects of GH on BMD and fracture risk in male idiopathic osteoporosis.
Moreover, this study was funded by a growth hormone producer (Upjohn and Pharmica Swdn). That must have been disappointing for them given other treatments were recommended over GH for increasing bone mass density over long term.

Growth hormone modulates migration of developing T cells. [4]
This study is about thymus atrophy and AIDS patients who are growth hormone deficient. The study concludes: Interestingly, enhancement of thymopoieisis in aging animals was also achieved with the use of IGF-1 as well as ghrelin, a potent GH secretagogue.
Grelin receptor activation can be achieved through ipamorelin (or GHPR-6/2, hexarhelin etc) or MK677. I come back to cost if thymus atrophy is an issue. The study is speculative but say 2iu GH per day $20 vs 10mg MK677 for $2. The study does not call for supraphysiological growth hormone administration in anycase.
The final link was an ad for MK-677. I have not commented on growth hormone secretagogues which may have a place due to the cost effective nature. They may increase growth hormone to supraphysiological levels transiently.

If we are to study whether growth hormone is a cost effective mass gainer, beyond 4kg of steak and a bottle of Pepperjack Shiraz per day then the argument needs to be better than those studies.
In regards to why growth hormone makes you feel better, simply it is a gene switch which manipulates genes. That is not is not to say you are not taking quality of life from your latter years and enjoying the experience now.

I’ll do a list of the genes which may include mu-opiod gene expression (reducing pain) and nerve tissue regeneration genes. Sleep is great for recovery and I am a big fan (at $1 per day not $20). Sleep is not reliant on growth hormone. Aspiring to a long nose, long ears and longer fingers and toes are a personal choice. I assume growth hormone is the only way to achieve those and may be worth the investment. It is for short statured children.

Why are body builders bigger? Check out Coleman’s published cycle, 1100mg per day. Dan Duchaine is dead and not even he used that much (1100mg per week). Training techniques have changed (thanks to the science) food is better. Gene therapy, myostatin, IGF-1, growth hormone (sure) and are they really any different? Dorian Yates and Phil Health have similar stats, size and look. https://forum.bodybuilding.com/showthread.php?t=162829521

1 Longo, V. D., & Finch, C. E. (2003). Evolutionary medicine: from dwarf model systems to healthy centenarians?. Science, 299(5611), 1342-1346.
2 Meazza, C., Pagani, S., Travaglino, P., & Bozzola, M. (2004). Effect of growth hormone (GH) on the immune system. Pediatric endocrinology reviews: PER, 1, 490-495.
3 Gillberg, P., Mallmin, H., Petrén-Mallmin, M., Ljunghall, S., & Nilsson, A. G. (2002). Two years of treatment with recombinant human growth hormone increases bone mineral density in men with idiopathic osteoporosis. The Journal of Clinical Endocrinology & Metabolism, 87(11), 4900-4906.
4 Dardenne, M., Smaniotto, S., Mello‐Coelho, D., Villa‐Verde, D. M. S., & Savino, W. (2009). Growth hormone modulates migration of developing T cells. Annals of the New York Academy of Sciences, 1153(1), 1-5.

A lot of great info in this thread.

muj that's a lot to read over. Thanks for posting it.

No probs, yeah it's a lot to read lol but it's honestly very interesting and will challenge a lot of people's previous thoughts of hgh which is great for this thread

I have never used HGH, so I can't give an informed opinion on its usage. One thing I did notice in the first few studies he listed is that they were done for 12-16 weeks. I have read some peoples board posts that have said you have to use HGH for 6 months to get real benefits from it. For any experienced HGH users here...does the 6 month time frame sound correct?

Racepicks said:

I'm not going to really dispute any of the points made in Bradley Clarke's article or Podcast. Especially muj's first post. Frankly, Brad is saying what we all knew, that low dosed HGH will not result in strength or muscle mass, and may result in an increase in insulin resistance. I have no studies to back up my claim but, I do believe in the benefits of anti-aging. I believe that more than I believe that HGH caused a reduced life-span in mice and rats of 30-70%. Also anyone who would make this claim, "There is no evidence that black market hGH has not come from cadavers.", automatically makes me question the remainder of his arguments.

By the way, I too would like to hear Scott Stevenson's view on muj's posts. He did say he would check out the thread, which he did, but also said he was busy and would try to respond when he had a chance. I believe he would agree with most of what Brad has stated, minus a few things I have noted.

Click to expand...

Yeah that cadaver point was a bit weird. He did address it later but I won't post it just basically said he was referring to the past.

I disagree with a lot of what Brad posted (and agree with parts too), I think the second one which is Furion has a bit more of a positive spin on hgh so I tend to agree more with him. But I think regardless of agreeing or disagreeing I found them to be interesting reads anyway as it challenges the conventional thinking of hgh by bodybuilders since it probably is the most misunderstood PED out there so it makes for good discussion.

gungalunga said:

I have never used HGH, so I can't give an informed opinion on its usage. One thing I did notice in the first few studies he listed is that they were done for 12-16 weeks. I have read some peoples board posts that have said you have to use HGH for 6 months to get real benefits from it. For any experienced HGH users here...does the 6 month time frame sound correct?

Click to expand...

It starts working as soon an you inject it. If you have a tight diet and are in a leaning out phase you will notice it immediately.

Racepicks said:

Please expand, Techno. Notice what exactly? Fat loss?

Click to expand...

:yeahthat:I have run more gh over the years then most people I know (mainly to help with my eating distorter (eat until I'm sick lol)...But there were plenty of times in the beginning where I kept shit on point and never noticed any effects immediately?! I mean, after some days or a week I would start getting the carpel-tunnel syndrome, arms and hands falling asleep all the time and pain (and that may have been a little longer then a week for that to show but don't really remember)...But never any energy, fat loss or hardening or any type of positive effect out of the norm?!

But like everything there are so many variables...I also always ran mine right before bed (unless I was doing 10+ui/ed) and have always heard the argument back and forth about timing so I know about as much as anyone that hasn't researched, experimented or followed any of the published facts about hGH...So I really know jack-shit:sFun_zipit:

Racepicks said:

Hey Sandpig! We talked on ProMuscle about World Gym in Providence. I remember Hank, but what was his Partners name (I can see his face)? I remember his Son Chris, they also started a fitness equipment company, Big Fitness. What was his name?

Click to expand...

Hey sorry it took so long here.

His partners name was Al. Same as mine BTW.

Sent from my SM-G900V using Tapatalk

gungalunga said:

I have never used HGH, so I can't give an informed opinion on its usage. One thing I did notice in the first few studies he listed is that they were done for 12-16 weeks. I have read some peoples board posts that have said you have to use HGH for 6 months to get real benefits from it. For any experienced HGH users here...does the 6 month time frame sound correct?

Click to expand...

TeknoViking said:

It starts working as soon an you inject it. If you have a tight diet and are in a leaning out phase you will notice it immediately.

Click to expand...

Racepicks said:

Please expand, Techno. Notice what exactly? Fat loss?

Click to expand...

This whole you need to run growth for 6+ months to see its effects is false. Maybe some people who are loose with their diet it will take that long to see some fatloss but not for those of us that are leaner or in a dieting phase. The fat loss will start immediately if you are in a calorie deficit. Run a 2-3 week cycle with dnp and run another 2-3 week cycle with dnp along with hgh the 2nd cycle you will see much better results in terms of fat loss.

Have I noticed an increase in muscle that I attribute to growth? I can't say I have. It gives me a really full look (intramuscular water weight others describe it as 3d). I have used doses of 10ius ed, 4ius ed and everything in between for years at a time (all in one shot, split doses, 2ius am 2ius pre workout 2ius pre bed etc) even when I was just rock climbing, playing video games and not training with weights at all but I never felt that it added muscle. It helps me push the food and stay lean while making gains though. When I am blasting and throw in some slin it helps me stay lean. Does staying more lean create a better environment for gaining muscle we know it does. Now the slin/anabolics/hgh combo is amazing for gains but I don't think the hgh is carrying this combo in terms of LBM gains.

For me personally I can be off growth for an extended period of time shoot 2ius 1-3 hours before the gym and be more pumped and more vascular while I am training. For those of you that have never taken growth take 2ius pre bed and you will sleep like a baby. I consider all these things benefits and feeling the effects of growth hormone.

For people who have more flab I don't think the cosmetic effects are going to be as pronounced compared to someone who has lower body fat...but that can be said with all these drugs.