Long acting rHGH

Scientists have recently created long-acting rHGH by modifying the C-terminus of rHGH to use the C-terminal peptide sequence of hCG.

It only requires injection once per week.

Will UGL be catching up on this anytime soon?

Doesn't sound super difficult to make.
 
Pegylated rhgh is nothing new. Russian OneQ team made it.

Somalong is one of best UG growths ive ever used. OneQ is second best, but i like long better because i dont hold so much water on it compared to others.

Actually today i acquired it again, after 3 years of not using.

It keeps me a lot leaner than regular somatropin. I guess its because it is active in system 24/7 for 5 days.

I would love to have more discussions around forums about it, but it still is very exotic product rare heard about. In Russia its quite popular, because it isnt regulated under classic 191aa law
 
would long acting HGH not be a nightmare for insulin sensitivity?
Theoretically. Ive not checked mine, while on long, but will do after couple months.

As much ive seen on Russian forums, its not an issue more than a regular GH.

There are some scientific research available, and they dont seem to point out any extra negatives compared to regular during years of usage
 
Ohhh. Also. Forgot to mention. There is another "side effect" of pegylated hgh. Ive always shot mine IM. But this time i will do my shots around belly button (my problem site) to try get this side.
 

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would long acting HGH not be a nightmare for insulin sensitivity?
Only if you actually use your rhGH thrice weekly (3X/w, or less). Otherwise, they become practically equivalent.

Daily administration of rhGH actually increases IGF-I > thrice weekly, but benefits insulin sensitivity mostly by keeping fasting insulin, glucose & FFAs lower.

I'd expect the long-acting GH to cause a worse decrement in GH response, such that the decrease to IGF-I that occurs by 6 mo and probably between months 4 - 5 with daily rhGH at a constant dose, might occur after only half that time.
 
Only if you actually use your rhGH thrice weekly (3X/w, or less). Otherwise, they become practically equivalent.

Daily administration of rhGH actually increases IGF-I > thrice weekly, but benefits insulin sensitivity mostly by keeping fasting insulin, glucose & FFAs lower.

I'd expect the long-acting GH to cause a worse decrement in GH response, such that the decrease to IGF-I that occurs by 6 mo and probably between months 4 - 5 with daily rhGH at a constant dose, might occur after only half that time.
 

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A couple distinctions between this study's population vs. ours & between IGF-I vs. SDS should be made.

First, going from sub-normal IGF-I standard deviation score (-1.24 SDS) to normal (1.09 - 1.26 SDS) in the case of Growth Hormone Deficiency children (childhood GHD) is qualitatively different than going from normal to acromegalic IGF-I (as SDS, or raw) in the case of rhGH-using bodybuilders are not actually closely comparable.

Any decrement that does (in fact) occur at 4 - 5 mo, but with sampling at 6, 12, and 24 mo, will still result in an improved health outcome in GHD children & ΔIGF-I (raw), despite there in fact being this significant decrement in GH response (Δ IGF-I)... by 6 months, to the tune of -11%, and by 9 months to the tune of -42% in a more valid comparison population to bodybuilders, of healthy but abdominally obese men given 2.85 IU * 100 kg⁻¹ body weight daily.
Decrement-in-serum-IGF-I-rhGH-treatment-Table.MesoRx.png
[1].

SDS (Standard Deviation Scores) require explanation because these cannot be viewed the same as a raw IGF-I value for the purpose of comparison. SDS are intended to describe dispersion about the mean for a population's IGF-I in terms of the Z-score. Since distribution of IGF-I values in a healthy population is non-Gaussian, mathematical transformation is necessary to obtain reference intervals for each age group. Here, that population must include healthy Chinese children; whose IGF-I levels differ significantly from other populations, e.g., even between Caucasian population-wide data there is considerable variation in IGF-I concentrations.

This ties in to the impact of known heritable factors (i.e., genes and genotypes) on GH response (Δ IGF-I). Take the GHR gene that controls the expression of GH receptor in our bodies. Its d3 homozygous genotype (those that are d3d3) see substantially increased IGF-I, far greater than in those d3fl and especially flfl. These differences likely underlie why some individuals see rapid increases in IGF-I at initiation versus others seeing little change (hypo- or even non- responders). Besides GHR genotype, rhGH dose & age at diagnosis (e.g., Growth Hormone Deficiency) affect the Δ IGF-I at 6, 12, & 24 mo. In some populations, the d3 homozygous (d3-GHR) genotype has a prevalence of > 50%!

Important general considerations that arise out of the use of SDS to describe IGF-I distribution are that:

1. Data is not applicable to BMI > 28 kg/m² (i.e., bodybuilders), or those on exogenous estrogens (especially oral estrogens); e.g., excluding exogenous estrogen use yielded IGF-I in women > than in men, until age 50 (menopause).
2. Use of different populations is the greatest source of variation.
3. Lack of specificity (i.e., IGFBP interference removal; specificity and/or affinity to the IGF-I antibody used) arises as a source of variation, with significant implications for patients with disorders that affect IGFBP profile, such as acromegaly (analogous to high dose rhGH use) or chronic kidney disease.

The very fact of this study's failing to describe a significant decrement in its proxy for IGF-I (raw) – (I have not sought out its supplementary materials for more for more particularized data on SDS vs. months followup) – vis-a-vis rhGH use belies its insufficient sensitivity & power for this task.

References
[1] Johannsson G, Mårin P, Lönn L, Ottosson M, Stenlöf K, Björntorp P, Sjöström L, Bengtsson BA. Growth hormone treatment of abdominally obese men reduces abdominal fat mass, improves glucose and lipoprotein metabolism, and reduces diastolic blood pressure. J Clin Endocrinol Metab. 1997 Mar;82(3):727-34. doi: 10.1210/jcem.82.3.3809.
 
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