TweetI know we all have heard that HGH is good for tendons and other connective tissues, but how many of us have actually looked at studies to prove it? Lets find out!

I will break down the studies with tidbits and such as I go along.

The tendon study is: Growth hormone stimulates the collagen synthesis in human tendon and skeletal muscle without affecting myofibrillar protein synthesis and can be found here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821728/

To test the hypothesis that GH promotes matrix collagen synthesis in musculotendinous tissue, we investigated the effects of 14 day administration of 33-50 microg kg(-1) day(-1) recombinant human GH (rhGH) in healthy young individuals.

1mg is 2.7IUs of HGH. A 200 pound person is about 90kg (yeah, 91, but 90 makes the math easier). Lets use the top end of the range in the study to see the max amount they used in it, which is 50 micrograms/kg per day. This means they used 50 X 90 = 4000 micrograms per day, which is also 4mg. Continuing the math, we find that 4 X 2.7 = 10IUs. If we use the bottom end, 33 micrograms, we find 33 X 90 = 2970 (lets round to 3000). 3000 micrograms is 3 milligrams, so 3 X 2.7 = 8.1IUs. Both are VERY VERY high, so keep that in mind. Anecdotally, lower doses should do the same thing, just to lesser effect.

A significant correlation between local IGF-I mRNA and collagen mRNA in both muscle and tendon was demonstrated, whereas no significant correlations between sGH or sIGF-I and collagen expression were observed in the rhGH-supplemented participants. This suggests a role for local IGF-I signalling, a notion that is supported by animal studies, showing that circulating IGF-I has little effect on overall growth in mice (Sjogren et al. 1999), while locally produced IGF-I is a prerequisite for GH stimulatory effects in muscle and cartilage (Schlechter et al. 1986; Kim et al. 2005).

These findings are in accordance with our results and support the view that IGF-I rather that GH directly is responsible for the elevated collagen expression and protein synthesis seen in the present study (Figs 3 and ​and44).

This basically says that the overall IGF-1 in the body is not important, what is important is the LOCAL IGF-1 level. This supports the view of those who say doing many small injections in the area you want to improve your tendon strength is superior to doing one large injection. It also says that IGF-1 is the source of the improvement, not HGH itself. I think we all already knew that, but it is nice to see it proven.

In contrast to the effect on connective tissue, elevated GH did not increase myofibrillar protein synthesis. With rhGH supplementation, both circulating and local IGF-I was increased by 3-fold but this did not enhance myofibrillar protein FSR (Fig. 4). This finding is in contrast to the well-established positive effect of GH and IGF-I on muscle protein and strength found in animals with a large growth potential (Musaro et al. 2001; Quinn et al. 2007), but it is in concert with previous human experiments where no effect on muscle strength and protein FSR was observed (Yarasheski et al. 1993; Blackman et al. 2002; Lange et al. 2002; Berggren et al. 2005; Ehrnborg et al. 2005). So rather than causing muscle fibre growth, GH/IGF-I appear to stimulate the supporting connective tissue that would help force transmission from the contracting muscle fibres to the bone.

This one shocked me as it goes directly against Bro-Science. It basically says that, even at 10IUs a day, NO increase in the size and strength of muscle fibers was seen at all. It DOES increase it in animals, but has been proven more than once that it DOES NOT increase it in humans. But since it makes the tendons stronger, you can work harder without feeling pain and therefor the extra work you are doing will increase your muscles.

In this study, just 14 days of rhGH supplementation in healthy individuals increased collagen synthesis by up to 6-fold without causing any side effects.

WOW! Only 14 days of 10IUs caused a 6 times increase, or 600% increase, in collagen synthesis! Anecdotally, if you take 2IUs a day, you can see a doubling of your collagen synthesis. Just wow.

Very few studies have investigated the effects of GH or IGF-I treatment in relation to human musculoskeletal tissue injuries. Tentatively indicative of a beneficial effect of GH treatment is a case control study with six patients, in whom application of a mixture of growth factors, including IGF-I, increased foot range of motion and decreased recovery time after Achilles tendon rupture (Sanchez et al. 2007). However, more convincing evidence is given in a placebo-controlled trial with 406 patients, in whom a significantly shorter time to healing of closed fractures was observed after high-dose GH treatment (Raschke et al. 2007). This is consonant with the increased collagen synthesis in muscle and tendon we observed after GH treatment given in similar high doses.

This says if you have injured yourself (which almost always will include tendon damage - just the way we humans tend to break), using a dose HGH regimen WILL reduce your recovery time.

GH/IGF-I apparently reinforces the supporting collagen framework around muscle fibres rather than the muscle contractile apparatus per se in adult skeletal muscle. GH/IGF-I may be more biologically important for strengthening the supportive matrix in tissues than for muscle cell hypertrophy in adult human musculotendinous tissue.

In conclusion, HGH will not cause the growth of your muscles. It WILL strengthen your muscles' supportive matrix (tendons, etc). This will then allow you to push more weight and therefor get stronger.



The first fat reduction study is: Growth hormone treatment of abdominally obese men reduces abdominal fat mass, improves glucose and lipoprotein metabolism, and reduces diastolic blood pressure. It can be found here: https://www.ncbi.nlm.nih.gov/pubmed/9062473

Thirty men, 48-66 yr old, with abdominal/visceral obesity were treated with recombinant human GH (rhGH) in a 9-month randomized, double-blind, placebo-controlled trial. The daily dose of rhGH was 9.5 micrograms/kg.

1mg is 2.7IUs of HGH. A 200 pound person is about 90kg (yeah, 91, but 90 makes the math easier). 9.5 is basically 10, which makes for very easy math. 90 X 10 = 900. 900 micrograms is 0.9 milligrams. 0.9 X 2.7 = 2.43 IUs. That is in the range that most people use, since most people will use from 2IUs to 4IUs per day.

In response to the rhGH treatment, total body fat and abdominal sc and visceral adipose tissue decreased by 9.2 +/- 2.4%, 6.1 +/- 3.2%, and 18.1 +/- 7.6%, respectively. After an initial decrease in the glucose disposal rate (GDR) at 6 weeks, the GDR increased in the rhGH-treated group as compared with the placebo-treated one (P < 0.05). The mean serum concentrations of total cholesterol (P < 0.01) and triglyceride (P < 0.05) decreased, whereas blood glucose and serum insulin concentrations were unaffected by the rhGH treatment. Furthermore, diastolic blood pressure decreased and systolic blood pressure was unchanged in response to rhGH treatment. This trial has demonstrated that GH can favorably affect some of the multiple perturbations associated with abdominal/visceral obesity. This includes a reduction in abdominal/visceral obesity, an improved insulin sensitivity, and favorable effects on lipoprotein metabolism and diastolic blood pressure.

The average fat loss after 9 months of about 2.5IUs of HGH was 9.2%, with some losing as much at 18%!! Overall health was improved as well. The only negative effect was the 2 hour glucose level (GDR). It was harder for the body to remove glucose immediately after its induction, so keep that in mind. After that 2 hour period, the glucose levels were better for those using HGH than those not using it.


And not to leave out the post-menopausal women and fat reduction, here is another study: Growth Hormone Treatment Reduces Abdominal Visceral Fat in Postmenopausal Women with Abdominal Obesity: A 12-Month Placebo-Controlled Trial Found here: https://press.endocrine.org/doi/full/....WtSPw6w1.dpuf

Abdominal obesity is associated with blunted GH secretion and a cluster of cardiovascular risk factors that characterize the metabolic syndrome. GH treatment in abdominally obese men reduces visceral adipose tissue and has beneficial effects on the metabolic profile. There are no long-term data on the effects of GH treatment on postmenopausal women with abdominal obesity. Forty postmenopausal women with abdominal obesity participated in a randomized, double-blind, placebo-controlled, 12-month trial with GH (0.67 mg/d). The primary aim was to study the effect of GH treatment on insulin sensitivity.


Forty women with a mean age of 57.3 yr (range, 51–63 yr) were studied. The initial dose of GH was 0.13 mg/d (0.4 IU/d), which was then increased to 0.27 mg/d (0.8 IU/d) after 2 wk, 0.4 mg/d (1.2 IU/d) after 4 wk, 0.53 mg/d (1.6 IU/d) after 5 wk and, after 6 wk, to the target dose of 0.67 mg/d (2.0 IU/d).

The target dose was 2IU a day. A nice low number that most users will be at or above.

A reduction in serum total cholesterol and LDL cholesterol was observed in the GH-treated women, although the reduction in LDL cholesterol was more marked after the first 6 months (10%) compared with 12 months (5%). In some studies dealing with GH-deficient patients receiving GH replacement therapy, a transient reduction in total cholesterol, LDL cholesterol, and the total cholesterol/HDL ratio and an increase in Lp (a) have been reported (36, 37). In contrast to these data, no significant changes in Lp (a) or total apoB were observed in our study. One plausible explanation is that the target dose of GH in our study was considerably lower than that used in these previous trials and that men may respond more markedly/differently than women in terms of the lipoprotein metabolism (38). Assessments of body composition by CT scan showed a clear reduction in VAT and an increased amount of thigh muscle mass in the GH-treated women. In contrast to a similar study involving middle-aged men with abdominal obesity who received GH treatment for 9 months (17), we did not find any changes in abdominal or thigh sc AT, suggesting that postmenopausal women are less responsive to the lipolytic effect of GH in the sc fat depots.

HGH is great for reducing cholesteral in women. VAT is visceral adipose tissue, which is the inner belly fat (as opposed to the belly fat found just under the skin). It seems that women will lose the fat on the upper thigh, but not the inner belly fat. Men lose the inner belly fat (and tend to not store fat on the upper thighs anyway, so hard to lose fat that is not there). Sorry ladies, no or very little spot reduction in the belly for you at 2IUs, though you WILL lose fat on the upper thighs. The study does say the results might be different at 4IUs, but they did not test at that level.

The lack of belly fat loss in women was also proven in another study: Effect of Recombinant Human Growth Hormone (rhGH) on Abdominal Fat and Cardiovascular Risk in Obese Girls found here: https://www.ncbi.nlm.nih.gov/pmc/arti...rticle_359.pdf

It mirrors the first female study, just on a younger group of women (under 18 years but past puberty). So again, sorry ladies, no belly fat reduction for you. Still, it does improve many other things (cholesteral, the look and feel of skin and nails, and a better overall feeling of well being) so do not discount using HGH.

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