A GH and fat loss protocol (rhGH lipolysis) that is science-based

Does it make a difference where the sub q injection is done?


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You're a fuckin beauty, bud.
Thanks
 

Front paper in previous post:

On injection to the SQ region low molecular weight drugs and proteins (<16kD) can be absorbed through capillaries and then enter systemic circulation (2). Since their size precludes entry however, higher molecular weight proteins and antibodies must traffic through the lymphatic system where they enter general circulation at the interface of the thoracic lymph duct with the subclavian vein (3). As lymphatic flow rates can vary between 0.2% and 2% to that of blood, understanding lymphatic uptake is of key importance (2).


See section titled

Injection site considerations​

 
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You're a fuckin beauty, bud.
Thanks
Hey sure. It's an interesting paper. They make the argument that bioavailability may be altered by injection site location for high molecular weight proteins. Pretty interesting. Probably pays to get the right site and massage well after injection.
 
Mechanical stimulation of the lymphatic system
Interstitial fluid dynamics and lymphatic flow are known to be both temperature and exercise dependent which has been attributed to filtration forces acting across capillary walls (38). Tissue compression [e.g. when walking] increases interstitial flow whereas stretching impedes this in a process that may be governed by fibroblasts (39). The impact of these mechanical phenomena on SQ drug dispersion and uptake has not been extensively studied though models have been developed (40). In an effort to promote lymphatic flow [and thus drug uptake] it is also possible to employ other mechanical methods. Clinical studies have been conducted on the impact of manual lymph drainage (MLD) in fibromyalgia patients (41). The methods, which include use of soft tissue massage regimens, targeted physical exercise [e.g. yoga], use of graduated compression bandages and pneumatic devices (e.g. the Lympha Press system) have shown a dramatic increase in lymph flow, reducing edema and other clinical markers (Figure 3) (42). Studies have also shown synergistic impact of ultrasound with manual drainage to increase lymph flow (43), which may afford additional benefits. The connective tissues are not fully hydrated at physiological state, and compression/stretching cycles results in substantial flux as GAG’s attract water based on their net negative charges.
 
Hello guys and @Type-IIx big information here, i have a small question, I'm person with low bodyfat, the problem is when injecting the hgh into the abdomen subq i feel like only inject into the skin, is that a problem and should I do it somewhere else?
Thanks
Screen-Shot-2018-09-20-at-2.14.36-PM.png

You should not inject into either the skin nor the adipose tissue. Rather, you inject into the subcutaneous space (subcutis).

Basically, the lower your abdominal & iliac crest ("love handles") fat levels, the more you need to rotate from 90° to 45° instead, and pinch, to get into this space.
 
I do have a question I want to ask you involving the biomechanics of rhgh and metformin in a fasted state, but I'll type it up tommorow with study references so I only sound mildly ignorant
 
rhGH does promote recovery from exercise including resistance training by procollagenous activity (primarily affecting the extracellular matrix), anticatabolic effects (reduced catabolism of amino acids, improved nitrogen balance), improved sleep (increased slow wave sleep), and improved mitochondrial oxidative capacity.

Dose-response is individualized, but do consider that 2IU 5 days weekly is less than the average (mean) weekly production of a healthy 22 - 28 year old male. So a lot of the dosages I see are very low and often are mere replacement.
I know you posted this three years ago but I'm lurking now. Wouldn't this dose ADD do our natural production, rather than replace it? Assuming we already produce a decent amount of IGF1 and HGH, I see value in adding a small amount like 1-2iu if it's for the purpose of "longevity."

Am I wrong by saying that?
 
I know you posted this three years ago but I'm lurking now. Wouldn't this dose ADD do our natural production, rather than replace it? Assuming we already produce a decent amount of IGF1 and HGH, I see value in adding a small amount like 1-2iu if it's for the purpose of "longevity."

Am I wrong by saying that?
It's not additive, unfortunately a bolus of rhGH (subcutaneously applied) suppresses endogenous GH secretion for ~ 22 h +/- with some inter-individual variation in escape from suppression.
 
It's not additive, unfortunately a bolus of rhGH (subcutaneously applied) suppresses endogenous GH secretion for ~ 22 h +/- with some inter-individual variation in escape from suppression.
I see.

So with this in mind, I am 38 and my IGF1 was testing at about 300 even without taking any HGH (I guess my Testosterone dose of 20mg per day pushed my IGF1 up pretty high). I know IGF1 and HGH levels are not the same but we can't reliably measure HGH in the body as far as I know.

Is my 1.5iu HGH dose that I am on actually counter productive in your opinion? I do notice slightly fuller muscles and some intramuscular fluid even from this dose.
 
I see.

So with this in mind, I am 38 and my IGF1 was testing at about 300 even without taking any HGH (I guess my Testosterone dose of 20mg per day pushed my IGF1 up pretty high). I know IGF1 and HGH levels are not the same but we can't reliably measure HGH in the body as far as I know.

Is my 1.5iu HGH dose that I am on actually counter productive in your opinion? I do notice slightly fuller muscles and some intramuscular fluid even from this dose.
I cannot stand in your shoes and make that judgment for you, only say that 1.5 IU GH daily is the mean (average) secretion for a normal BMI, height, 75 kg (165 lb) adult male in his twenties (22 - 28 years).
 
I cannot stand in your shoes and make that judgment for you, only say that 1.5 IU GH daily is the mean (average) secretion for a normal BMI, height, 75 kg (165 lb) adult male in his twenties (22 - 28 years).
How about I ask you the following instead:

If someone has a pretty strong IGF1 level without HGH from just testosterone replacement, does that also mean that their GH level is also likely to be equally as good or are these things totally separate and it's possible to have a low GH level (on par with the person's age) with a high IGF1 level?

This is one thing I have been trying to figure out but have had trouble finding the answer.
 
How about I ask you the following instead:

If someone has a pretty strong IGF1 level without HGH from just testosterone replacement, does that also mean that their GH level is also likely to be equally as good or are these things totally separate and it's possible to have a low GH level (on par with the person's age) with a high IGF1 level?

This is one thing I have been trying to figure out but have had trouble finding the answer.
Keep your exogenous GH in.
exogenous hgh has many more advantages than just increasing IGF levels.
 
How about I ask you the following instead:

If someone has a pretty strong IGF1 level without HGH from just testosterone replacement, does that also mean that their GH level is also likely to be equally as good or are these things totally separate and it's possible to have a low GH level (on par with the person's age) with a high IGF1 level?

This is one thing I have been trying to figure out but have had trouble finding the answer.
Aromatizing androgen (e.g., T, Nand, EQ, Dbol) augment GH secretion via in situ aromatization (the process), but estrogens negatively feedback on IGF-I bioavailability by increasing IGFBP-1 levels that unleash GH secretion by feedback withdrawal.
 
Aromatizing androgen (e.g., T, Nand, EQ, Dbol) augment GH secretion via in situ aromatization (the process), but estrogens negatively feedback on IGF-I bioavailability by increasing IGFBP-1 levels that unleash GH secretion by feedback withdrawal.

If price and sides aren't limiting, the protocol of Chase Irons the Younger doesn't seem too crazy (tapering up to >10 IU/d).

Allegedly Chase the Elder is up to 36 IU/d and I don't know man that's a really fucking lot of GH.
 
If price and sides aren't limiting, the protocol of Chase Irons the Younger doesn't seem too crazy (tapering up to >10 IU/d).

Allegedly Chase the Elder is up to 36 IU/d and I don't know man that's a really fucking lot of GH.
I'm not familiar with the protocol; don't need to see it here, off-topic. But 36 IU q.d. if you can handle it (!) confers (i.e., body composition) benefits that are > 10 IU q.d.

I couldn't handle it myself, though. And I doubt many can.

Believe it or not there's a sizeable number of studies with dosages in this approximate range. It seems to me that, since these researchers typically acquire reference grade rhGH that is donated by the manufacturer and/or paid for using institutional funding, they're perfectly happy using high dosages. They tend to think: (a) these dosages reflect common bodybuilding use patterns; (b) rhGH is mostly harmless; and (c) there is scientific value in testing the effects at these high doses & concentrations.
 
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Aromatizing androgen (e.g., T, Nand, EQ, Dbol) augment GH secretion via in situ aromatization (the process), but estrogens negatively feedback on IGF-I bioavailability by increasing IGFBP-1 levels that unleash GH secretion by feedback withdrawal.
This is good info but I'm not sure that this answers my question unless there is something about IGFBP-1 I didn't understand. I'm going to re-phrase it:

Is it possible to simultaneously have a good natural IGF1 level but also a low natural GH level? Let's assume the person is on TRT but isn't taking any exogenous HGH.

Thanks
 
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This is good info but I'm not sure that this answers my question unless there is something about IGFBP-1 I didn't understand. I'm going to re-phrase it:

Is it possible to simultaneously have a good natural IGF1 level but also a low natural GH level? Let's assume the person is on TRT but isn't taking any exogenous HGH.

Thanks
Your question definitely confused me, so I just described the processes involved in increasing IGF-I by aromatizing androgen including T.

TRT increases GH that in turn increases IGF-I. But while T does so, it also negatively feeds back on IGF-I and increases GH disproportionately (because high estrogens cause a resistance to IGF-I stimulation by GH).

RhGH just (mostly) directly stimulates IGF-I dose-dependently.

It's possible (e.g., d3-GHR homozygosiity, a genetic factor) to have high-normal IGF-I and unremarkable GH secretion.

But if a peron is on TRT and has high IGF-I, it's because their GH secretion is elevated.
 
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