+ 6 AASDirect HgH IGF1 Results
6'2 - 220lbs 9%bf
Started cycle : Test + Deca (2weeks ago)
2.5 mg Reta x2 a week
No orals
results-only update:
Switched to HGH Celtrope: IGF-1 moved 116→179→ 220 (Z ≈ +1).
179 was from another source at using 5.1iu
Ran Celtrope hgh at 6iu a day - 3iu am + 3iu pre-workout
AM glucose steady at 81–85.
The math from my baseline to last source to now and difference:
IGF-1 per IU (vs baseline 116):
Old: (179−116)/5.1 = 12.4
New: (220−116)/6.0 = 17.3 → ~+40%
Now let’s say with these numbers if I wanted to figure out what my score would be on this new Hgh we got on the dose of 5.1iu, which is what my first result of 179 came from:
Baseline = 116
New-source lift per IU = (220−116)/6.0=17.3
At 5.1 IU → 116 + (17.3 × 5.1)
= 116 + (86.5 + 1.73)
= 116 + 88.23 = ~204 Would be the #
Now if we wanted to find out how much percentage was it better:
Equal-dose outcome (old 179 → new ~204):
(204−179)/179≈14% higher IGF-1 on the same dosage
These calculations are using IGF-1 per IU vs baseline and not Raw IGF-1 per IU
Sharing for transparency and data.
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I feel like factoring actual results you get from hgh has a higher place than igf numbers, unfortunately. I know people that just don’t get crazy igf numbers but still reap the benefits
itszoot89I’m agreeing with this, at the end of the day it’s just very interesting to see the vast differences in our physiology
Right, I think IGF-1 is an indicator but unfortunately it’s not the end all be all to determine if the growth is effective. I really wish it was. Would make this all easier. Everyone’s different and I believe having lower IGF numbers (baseline and reaction to growth) isn’t even a solely negative thing at all. It’s relative.
People may disagree with this and that’s fine
https://stackingplates.com/2018/01/the-most-effective-growth-hormone-pro...
There’s some very good info in that article about IGF1 and exogenous GH. Interestingly enough, Kurt Havens’ GH book is almost a copy of that article, I wonder if he wrote the original one from 2018. Also super useful is the YouTube vid from Scott Stevenson from like 3 months ago;
https://youtu.be/PikSSK_2rpU?si=xcJf4q1IiSjsjqat
There’s so many genetic and environmental factors that can influence systemic IGF1 response, plus the fact that we can’t get info into how local/autocrine/paracrine IGF1 plays with exogenous GH administration. All we know about the local stuff comes from exercise, and this involves different IGF1 versions (cut up versions) that are released via weightlifting (MGF, etc.). I’ve been doing a lot of research into this stuff and there’s honestly A TON of info we don’t truly know. More than likely the people that get huge liver IGF1 response have either one copy or two copies of the growth hormone receptor version D3. But we don’t know if that translates to higher effect from the receptors at the muscle.
Kurt havens is confusing me lately. He was on Todd’s podcast not too long ago and they were talking about local IGF-1 and even giving exact dosages for max local IGF-1 production. And saying it should be injected IM. It was like 8ius every 6hrs during the day and 4ius before bed. But then I saw him on another podcast the other day saying the exact opposite. no point in IM, you won’t get any local IGF-1/MGF production, it all should be taken in 1 bolus at night, and the bioavailability is higher sub q. So I’m not really sure what to believe. They also mentioned that systemic IGF-1 which were measuring in these blood tests can be inhibitory to local IGF-1.
That article has same number of sources as his book so It seems pretty likely that this was the first rendition of it.
Yeah some of the stuff he says is completely contradictory, depending on when he said it or who he was talking to he’ll change his views. The video with Scott Stevenson shows that IM injection actually creates a larger spike effect, but then decreases very quickly. With subQ it’s a smaller spike but area under curve is longer. I believe in that same video there’s a comment stating that they’re pretty much the same since the overall net effect is the same, if you calculate area under curve overall it’s the same. As far as systemic IGF1 being inhibitory it seems that data comes from animal cell models and there’s no actual proof of that happening for human IGF1 receptors. Also, if it were inhibitory then that means that systemic/liver IGF1 would affect muscle hypertrophy, which is not the case, since a very tiny amount makes it to muscle tissue. If you compare the amount generated locally from muscle during exercise vs the minuscule amount that comes from liver IGF1 the difference is enormous. It just seems to me that no one truly knows the answers to these questions.
I have to watch the rest of that video, it was very informative. There’s no doubt serum GH levels spikes nearly double with IM injection vs subq. But I haven’t seen that translate into higher IGF-1 levels for me personally. I’ve tested on the same doses using both ways and I’m always around the same place. So thats kind of odd. You’d think with double the GH serum levels we’d see significantly more IGF-1 production.
So IGF-1Ec (MGF) is released most when hitting sets of 80% of 1rm. You’re saying those levels exceed the amount of systemic IGF that makes it to muscle tissue?
EMD says most of the anabolic effects of serostim is from igf-1, but not all. They don’t explain the other pathways as far I could find.
But it sounds like you’re saying high systemic igf-1 is largely useless? If not much of that makes it to them muscle hopefully the same can be said for all the things we don’t want to go, like organs and such.
There’s a comment left by Dean St Mark on that same video that’s really insightful; “measuring IGF1 levels between IM and SubQ results in very similar levels”, also, “the research consensus is that the overall area under the curve between IM and subQ is almost the same”. So to me this means that yes, you have a larger spike with IM, but that spike is very short lived since the increase from 0 dies down very quickly. With subQ, the spike is smaller but it takes a long while for it to completely die out. If you take the sum of the area under the curve for IM and compare it to subQ, then the total sum for both should be about equal. Maybe with IM you create a huge flux of IGF1 quickly but then it stops, but with subQ you reach that same amount of IGF1 but it takes longer since it doesn’t spike as high but maintains for longer.
As far as the other part, less than 5% of systemic/liver IGF1 is free/unbound from large complexes. The great majority are bound to IGFBP with ALS, forming this clunky as hell macromolecule. Because of this only the small amount that’s free can get into the capillaries that feed blood to muscle tissue (a). There’s also evidence that IGF1 surrounding muscle tissue AKA interstitial fluid contains 6-8ng/mL of IGF1, whereas plasma free IGF1 is around 0.4-0.6ng/mL, much, much lesser amount than the locally secreted (b). This was tested using microdialysis. Also, mice that are genetically engineered to lack liver specific IGF1, so they have 75-80% less systemic/liver IGF1, they still have normal growth, implying that autocrine/paracrine IGF1 sustains tissue growth (c). I attached the sources I used to state the arguments.
a) https://www.jci.org/articles/view/15463?
b) https://www.sciencedirect.com/science/article/pii/S0022316622080361?
https://jme.bioscientifica.com/configurable/content/journals$002fjme$002f54$002f1$002fR1.xml?t:ac=journals%24002fjme%24002f54%24002f1%24002fR1.xml&
c) https://pubmed.ncbi.nlm.nih.gov/10377413/
Keep Trying to tell you my guy the more the better......
itszoot89After I run the pharma and goldtrope new batch and get tests I’m going nuts on it lmao
Did this source go under or something? They were number 2 for the US and now they are no where on the charts.
itszoot89Nah I doubt that.. It could just be me, not saying the source has bad stuff- too many variables to consider. I just wanted to share my personal results as data. I am going to be using pharma hgh these next coming days and following that with a igf-1 test.
This will be the key to seeing if I am just a low responder or something is going on with QC
Well I think Eroids put them on timeout if you click on them it says this source is on a Hiatus excluded from ranking. They done something bad.
They haven't done anything bad just inactive since Sep 11th. I put them on hiatus just in case. They're back since.
He just posted a new promo 2 days ago and just commented on it about an hour ago.
yes but they are out of rankings but he said something to the effect that it was their email sever went down and he had no idea about it. I used them several times and they always got me gear quick.
Oh, I didn't see that
I'm pretty sure I read BFG say somewhere that they haven't logged in for some time now. Wonder if there is more to it?
Weak. You should be at 400ish. You will be happy with the K4L
No he shouldn’t. Where he’s at is exactly where he should be and Is no indicator of the quality of the GH. And there’s no standard level of elevation on a given dose. Some people get 15ng/ml per 1iu, and I get 120ng/ml per 1iu.. You must have missed my post yesterday. zoot was 176 on 5.1ius of another sources GH. And I said the same thing as you, it’s underdosed. So I did a run on that same sources GH and I was 535 on 4-5ius ED Which is around where I always am on that dose, even a little above actually. Zoot was 176 on that source at 5ius ed and 220 on 6ius of this new source. His liver just doesn’t produce that much systemic IGF-1, which is the case for a significant % of users. Chase irons igf-1 was around 200 on 18ius ed of serostim from CVS.
Nor does it mean him or Chase irons are low responders. They just don’t produce much systemic IgF-1, which may actually be a good thing. It’s quite possible that low systemic IGF-1 means high local IGF-1, and local IGF-1 is what we’re really after. It’s been said that systemic IGF-1 is inhibitory to local IGF-1. After all these years I don’t think we really understand GH and its anabolic pathways all that well.
I was about to bring up chase irons lol
Got it. Good to know. Thanks !
itszoot89Appreciate the breakdown brother. I don’t want people to think km saying this Hgh is underdosed —my liver just runs low on systemic IGF-1 (per what Iron said). Bottom line is high labs don’t automatically mean better GH. I’ll keep pulling data with Iron so we can get to a better understanding of dosages and scores.
itszoot89I was expecting more... but it was an increase from previous source.
Not sure if I had a one off batch or what.
It’s not an increase, you’re running 1iu more per day. You were getting 35ng/ml per 1iu on the other source and 36ng/ml per 1iu on this stuff. It’s an irrelevant difference.
itszoot89the issue is if you do the scores vs my baseline you get
IGF-1 per IU (vs baseline 116):
Old: (179−116)/5.1 = 12.4
New: (220−116)/6.0 = 17.3 → ~+40%
Now let’s say with these numbers if I wanted to figure out what my score would be on this new Hgh we got on the dose of 5.1iu, which is what my first result of 179 came from
Baseline = 116
New-source lift per IU = (220−116)/6.0=17.3
At 5.1 IU → 116 + (17.3 × 5.1)
= 116 + (86.5 + 1.73)
= 116 + 88.23 = ~204 Would be the #
Now if we wanted to find out how much percentage was it better:
Equal-dose outcome (old 179 → new ~204):
(204−179)/179≈14% higher IGF-1 on the same dosage
Your baseline is irrelevant. The GH you’re on is not adding to what you were producing naturally. Your natural production has been shutdown since your first dose and has been completely replaced by exogenous GH. So the GT brought you from 0-176 on 5ius and this stuff brought you from 0-220 on 6ius.
If you took 5ius of this stuff you would have been 183 vs 176. Not really a big difference. Or in Theory on 6ius of GT you would have been 207 vs 220. Also an insignificant difference in the context of IGF-1 levels. There’s so many factors that could swing it 7-13 points. You could have done a 2nd blood test an hour later, or before and been 20 points higher or lower. You could test the same batch of GT again and i wouldn’t be the least bit surprised if you were 10-20 points higher. It’s just not a significant difference. I got bloods on the same brand of pharm grade GH where I was getting 103ng/ml per IU and 112ng/ml per 1iu. The product doesn’t get any more consistent than that. And the difference is meaningless to me.
itszoot89That is very interesting brother. I am very glad we have someone as knowledgeable as you on the forum , really!
I think you’ll find this interesting as well. I think Baseline is useful to ensure the exogenous GH you’re paying a lot of money for is elevating your levels beyond where you are naturally. It Doesn’t make any sense to pay to just get you right where you were naturally. When I was 25 before getting on GH for the first time I had my baseline done and I was 124. Seemed pretty low for a 25 year old, but regardless I still got 100-120mg/ml per iu IGF-1 elevation. 124 isn’t far from where yours is. When I recently got back on GH after a few years off I was plannng on just doing a low anti aging dose, like 2ius per day. I figured if I was 124 at 25, 10+ years later I must be even lower, so 2ius will get me into the 200s which must be above where I am naturally. But I decided to recheck my baseline and much to my surprise I was nearly 2.5x higher, 304ng/ml. So that was weird, but, I’m still getting the same 100-120ng/ml per iu. So baseline IGF-1 doesn’t even have any predictive value in how well you’ll respond to exogenous GH. I had a low a baseline very similar to yours and still was at the hyper responder level atleast in terms of serum IGF-1. And now my natural IGF-1 is high for whatever reason and Im still a hyper responder.
I’m sure you’re getting better results with 200 IGF levels than I was naturally at 300. Because IGF doesn’t tell the whole story.
Johnny2biigIsn’t using his own baseline a good KPI when comparing different HGH against himself vs previous results and how he reacts to HGH.
Not sure I understand the question? Exogenous GH will fully shut down endogenous production. So you’re not adding to what you’re producing naturally. You’re completely replacing it. So your baseline doesn’t have any impact on your IGF-1 levels while on exogenous GH. Nor does your baseline seem offer any predictive value in how you’ll respond to GH. Low natural levels does not mean you’ll have low levels when taking GH. And high natural levels doesn’t mean you’ll respond really well and have high IGF-1 levels on GH. There doesn’t seem to be any correlation there.
Where a baseline is helpful Is determining your dose. The goal of taking GH is to elevate your igf-1 levels. So if you’re 200 naturally you need to be taking enough to surpass that, ideally by a decent amount. It doesn’t make any sense to be paying money for GH at a dose that just gets you to 200, since you were already producing that for free.
itszoot89That’s exactly how I understood it, yup
I hear u champ. Let me know how the K4L one goes. Keep crushing it!
itszoot89I got that standard L, snowcaps and dragon.
To my knowledge the standard L is their premium right?
Not sure I only use the Titan and dragon