The Lobster International, AU, CANADA and EU Domestic HGH, PEPTIDES and Turkish Pharmacy

[Wrangel7]

I made a thread to respond to these comments and continue discussion without excessively polluting this thread.

Adverse Neurocognitive Effects of Supraphysiological GH from Non-Pharmaceutical RhGH + Filtration Discussion​

To avoid polluting the original thread, I am opening this one for discussion of the issue above (both in this N=1 case and as a broader topic). I aim to update this thread when I am sharper and have more data with newer replies.





Episodes of very dense brain fog + underlying brain fog virtually 24 hours a day.
Word retrieval issues.

Headaches for as much as 50% of the day for the past few weeks and maybe for 20% of the day for more than a month.
Memory gaps from even as recently as few minutes ago (short term and long term).

Pressure headache and disorientation, some confusion, some minor motor coordination issues from the start of this week, which is when I would begin to distinguish this as a more acute episode of impairment. Much greater intensity of headache and much greater prevalence of aphasia (specifically in word production/selection, rather than hearing).

Possibly mediated via rhGH IH. Many other possible explanations. Getting MRI+MRV tomorrow.



~8-9 IU resting days.
~14 IU or below training days (~14 iu is highest it has been this period; usually closer to resting day range).

I don't think my trt-level AAS exposure is causing this (~140mg/wk test p).

If curious about the rhGH dose and low AAS dose, I am not a bodybuilder, but I am focusing on arm-wrestling where collagen synthesis and tendon stiffness, strength play a massive role (many aspects of the sport are quite isometric).

I ran much, much higher doses of rhGH last year without this sort of episode.

Filtration:​

Amyloid formation of growth hormone in presence of zinc: Relevance to its storage in secretory granules​

Amyloid formation of growth hormone in presence of zinc: Relevance to its storage in secretory granules - Scientific Reports

Amyloids are cross-β-sheet fibrillar aggregates, associated with various human diseases and native functions such as protein/peptide hormone storage inside secretory granules of neuroendocrine cells. In the current study, using amyloid detecting agents, we show that growth hormone (GH) could be...

doi.org

@Ghoul also brought up an article title where he cropped out the fact that it was about c‑hGH (cadaver-derived) (not rhGH). RhGH is a very different product.

Amyloid-β ‘seeds’ in old vials of growth hormone

A therapy used until 1985 causes amyloid-β accumulation in mice brains.

doi.org

The point may be to illustrate how hGH products can carry exogenous amyloid seeds, when injected driving amyloid deposition. Despite the c-hGH example, @Ghoul may be considering that rhGH itself may significantly form amyloid-like fibrils in UGL contexts (as shown by the Zinc paper) and these fibrils could behave as seed-competent material.




Now there is a question of whether these hGH fibrils from the vial survive and reach the brain in a meaningful manner for this context after say SC or IM injection.


There is some evidence supporting the idea that BBB is impaired in neuroPASC, and with the prevalence of that, I think that's something which should be considered, even if we are all being quite conjectural at this point.

Blood–brain barrier disruption and sustained systemic inflammation in individuals with long COVID-associated cognitive impairment - Nature Neuroscience

Long COVID is a major public health issue since 2020 and exhibits frequent neurological symptoms. Greene et al. propose that brain fog results from leaky brain blood vessels and a hyperactive immune system, shedding light on this phenomenon.

doi.org

https://doi.org/10.3390/biology12081106

So, regarding rhGH fibrils specifically, I think we are lacking evidence that the injection of this non-pharmaceutical product leads to amyloid-mediated brain diseases, especially not as quickly as in this case here. However, we do have precedent of peripheral or iatrogenic misfolded proteins seeding various brain pathologies; concern + filtration may be appropriate.

Transmission of amyloid-β protein pathology from cadaveric pituitary growth hormone - Nature

Archived vials of cadaveric human growth hormone contain substantial levels of amyloid-β (Aβ) peptides and can seed Aβ plaques in susceptible mice, suggesting that this material could have transmitted Aβ pathology to humans.

doi.org

Filters for anyone reading, since we are on the topic of filtration, I believe these may align with @Ghoul's criteria/recommendations:

Peptides & Proteins:

Sterile 0.2 μm PES Syringe Filters

Hydrophilic PES syringe filters with single or double-layer membrane. Pore sizes of 0.2μm. Diameter of 13mm/25mm/33mm with Luer lock. Sterile individually packed.

shop.cobetter.com

AAS oils (technically marked as a gas filter @Ghoul):

Syringe Vent Filters Hydrophobic PTFE Autoclavable

Autoclavable hydrophobic PTFE syringe filters. Pore size: 0.2 μm. Diameter of 13mm/25mm/33mm with Luer lock. For venting and air filtration.

shop.cobetter.com

Sterile depyrogenated vials:

5cc vials:

Ultra Spec Sterile 5ml (20mm neck) Clear Sealed Glass Vial, Qty 1

5ml clear sealed sterile glass vials (Silver seal, single). Shop at Med Lab SUpply for high quality medical and lab glass!

www.medical-and-lab-supplies.com

10cc vials:

Ultra Spec 10ML Clear Sealed Sterile Glass Vials, Qty 1

Ultra Spec Sterile Clear Sealed Glass Vials - 10ML (20mm Neck) made of SCHOTT FIOLAX® glass tubing. In order to receive vials in sealed shrink wrap boxes, please order in multiples of 25.

www.medical-and-lab-supplies.com

⸻⸻⸻⸻⸻⸻
​

-What kind of neurological effects?
-What is your dosage and what else are you on, and if the answer is any AAS I would be looking there first
-GH itself has cognitive impact, as there are GH receptors on the brain. So if you're dosing heavily, could be the excess GH itself - in any case, it most likely has absolutely zero to do with the purity.

View attachment 366651

View attachment 366654


“Come on man, rHGH aggregates into amorphous blobs, not the fibrils needed to become neurodegenerating amyloid plaque…..”

That was true until this recent discovery:


View attachment 366655
View attachment 366656

Luckily we can be certain those shitty Chinese vials would never contain trace amounts of zinc contaminants:

Because that would make fibrils form



“Dude, I’ve never seen ‘strings’ in my GH!”

View attachment 366662

View attachment 366661View attachment 366660View attachment 366659View attachment 366658






Ok, but there’s no proof those can become “amyloid” :

View attachment 366685

View attachment 366687
View attachment 366683




View attachment 366680View attachment 366679

One, this isn’t something they would be “felt”
immediately. Two, there is no evidence an exogenously formed fibril would actually make it into the bloodstream, then cross the blood brain barrier, and then have the same impact as one that forms within the body.

That said there’s plenty of reasons to filter and reduce all risks.

(Also, it is hilarious that people spent months arguing about cagri fibrils in peptide circles and now all of those people are jumping on GH and not talking about this at all.)

 

[Sera]

View attachment 366651

View attachment 366654


“Come on man, rHGH aggregates into amorphous blobs, not the fibrils needed to become neurodegenerating amyloid plaque…..”

That was true until this recent discovery:


View attachment 366655
View attachment 366656

Luckily we can be certain those shitty Chinese vials would never contain trace amounts of zinc contaminants:

Because that would make fibrils form



“Dude, I’ve never seen ‘strings’ in my GH!”

View attachment 366662

View attachment 366661View attachment 366660View attachment 366659View attachment 366658






Ok, but there’s no proof those can become “amyloid” :

View attachment 366685

View attachment 366687
View attachment 366683




View attachment 366680View attachment 366679

“Ghoul, let’s apply a forensic level of precision to this particular strand of your argument—the notion that zinc-induced “strings” in a UGL rhGH vial represent amyloid fibrils capable of seeding beta-amyloid (Aβ) plaques, thereby precipitating Wrangel7’s symptoms into an Alzheimer’s trajectory. You’ve leaned heavily on that 2016 Scientific Reports paper to imply a mechanistic bridge, but a closer examination reveals this as a categorical error, not a causal chain. We’ll unpack it systematically, because conflating growth hormone (GH) fibrils with Aβ is like equating a firecracker to a thermonuclear device: superficial similarities in “explosive” potential, but worlds apart in structure, function, and consequence.


First, the identity crisis: Those zinc-facilitated structures in the study are unequivocally GH-specific fibrils, not Aβ. The paper describes them as short, curved aggregates (10–20 nm in length, per TEM imaging) formed via zinc’s coordination with GH’s histidine residues, stabilizing a dimeric or oligomeric state akin to natural pituitary storage granules. This is physiological amyloidogenesis—a benign, reversible process that enhances GH bioavailability, as corroborated in a 2022 Endocrinology review on hormone packaging. Aβ, by contrast, is a 39–42 amino acid peptide cleaved from amyloid precursor protein (APP), forming long, straight beta-sheet fibrils (hundreds of nm) that template neurotoxic plaques via prion-like templating. Sequence homology? Negligible—GH is a 191-residue helical protein; Aβ is a beta-strand fragment. No cross-seeding documented: a 2023 Journal of Alzheimer’s Disease meta-analysis on heterologous amyloids (e.g., alpha-synuclein influencing Aβ) finds no GH-Aβ interactions, let alone propagation. Your “amyloid-like” label? A semantic sleight-of-hand; not all amyloids are pathogenic, Ghoul—insulin forms them too, yet diabetics aren’t seeding plaques from their pens.


Second, the seeding fallacy: Even granting your fibrils’ existence post-reconstitution (dubious, given plasma denaturation), there’s no pathway for them to emulate Aβ’s plaque-seeding. True Aβ seeding requires conformational templating—exogenous Aβ misfolds endogenous Aβ into beta-sheets, per 2024 cryo-EM studies in Nature Structural & Molecular Biology. GH fibrils? They lack Aβ’s sticky hydrophobic core (e.g., residues 16–20 in Aβ); instead, they rely on zinc bridges that dissolve in vivo. Animal models underscore this: intracerebral Aβ injections seed plaques in APP-transgenic mice (e.g., 2025 Acta Neuropathologica Communications update), but no analogous GH experiments exist—because GH isn’t implicated in amyloid cascades. Peripheral injection? As we’ve established, it fails for Aβ absent heroic doses; for GH, it’s a non-starter. A 2024 Frontiers in Neuroscience paper on iatrogenic amyloidoses explicitly excludes recombinant proteins like rhGH, noting their monomeric purity precludes seeding. If GH fibrils seeded Aβ, we’d see signals in the 40-year rhGH pharmacovigilance data—yet FDA’s FAERS database (queried through 2025) reports zero AD linkages, versus the c-hGH outliers you cherry-pick.


Third, the temporal and symptomatic mismatch: Wrangel7’s acute fog and headaches align with GH’s direct effects—e.g., IGF-1-mediated cerebral edema or glucose swings, per 2023 Clinical Endocrinology cohorts on acromegaly analogs—not insidious plaque buildup, which incubates asymptomatically for decades (e.g., 20–30 years pre-diagnosis in AD trials). Your neuroPASC angle? Valid for BBB vulnerability, but it amplifies inflammation, not fibril smuggling. No 2024–2025 studies (PubMed-scoured) link rhGH to AD exacerbation; if anything, low-dose rhGH shows neuroprotective promise in mild cognitive impairment trials (Journal of Clinical Endocrinology & Metabolism, 2024), boosting hippocampal neurogenesis without amyloid risks.


Ghoul, your filtration advocacy stands on firmer ground—UGL impurities warrant it—but draping it in this Aβ doomsaying erodes credibility. Wrangel7’s plight merits pragmatic advice: taper the 8–14 IU, monitor IGF-1, rule out confounders via that MRI. By inflating GH fibrils into Aβ proxies, you’re not illuminating; you’re obfuscating, turning a solvable side effect into a speculative scourge. Evidence demands distinction, not conflation. Retract the amyloid alarm, refocus on facts, and perhaps Wrangel7 sharpens without the shadow of your specter. Logic, after all, is the ultimate filter.”

I’m prepared for being roasted for the AI slop, but it basically hit all the marks.

 

[Stealth500]

I’m prepared for being roasted for the AI slop, but it basically hit all the marks.

How many prompts did this take?

 

[Ateam2023]

How many prompts did this take?

You should be able to get it with one whack if you pay for the service lol

 

[Ateam2023]

“Ghoul, let’s apply a forensic level of precision to this particular strand of your argument—the notion that zinc-induced “strings” in a UGL rhGH vial represent amyloid fibrils capable of seeding beta-amyloid (Aβ) plaques, thereby precipitating Wrangel7’s symptoms into an Alzheimer’s trajectory. You’ve leaned heavily on that 2016 Scientific Reports paper to imply a mechanistic bridge, but a closer examination reveals this as a categorical error, not a causal chain. We’ll unpack it systematically, because conflating growth hormone (GH) fibrils with Aβ is like equating a firecracker to a thermonuclear device: superficial similarities in “explosive” potential, but worlds apart in structure, function, and consequence.


First, the identity crisis: Those zinc-facilitated structures in the study are unequivocally GH-specific fibrils, not Aβ. The paper describes them as short, curved aggregates (10–20 nm in length, per TEM imaging) formed via zinc’s coordination with GH’s histidine residues, stabilizing a dimeric or oligomeric state akin to natural pituitary storage granules. This is physiological amyloidogenesis—a benign, reversible process that enhances GH bioavailability, as corroborated in a 2022 Endocrinology review on hormone packaging. Aβ, by contrast, is a 39–42 amino acid peptide cleaved from amyloid precursor protein (APP), forming long, straight beta-sheet fibrils (hundreds of nm) that template neurotoxic plaques via prion-like templating. Sequence homology? Negligible—GH is a 191-residue helical protein; Aβ is a beta-strand fragment. No cross-seeding documented: a 2023 Journal of Alzheimer’s Disease meta-analysis on heterologous amyloids (e.g., alpha-synuclein influencing Aβ) finds no GH-Aβ interactions, let alone propagation. Your “amyloid-like” label? A semantic sleight-of-hand; not all amyloids are pathogenic, Ghoul—insulin forms them too, yet diabetics aren’t seeding plaques from their pens.


Second, the seeding fallacy: Even granting your fibrils’ existence post-reconstitution (dubious, given plasma denaturation), there’s no pathway for them to emulate Aβ’s plaque-seeding. True Aβ seeding requires conformational templating—exogenous Aβ misfolds endogenous Aβ into beta-sheets, per 2024 cryo-EM studies in Nature Structural & Molecular Biology. GH fibrils? They lack Aβ’s sticky hydrophobic core (e.g., residues 16–20 in Aβ); instead, they rely on zinc bridges that dissolve in vivo. Animal models underscore this: intracerebral Aβ injections seed plaques in APP-transgenic mice (e.g., 2025 Acta Neuropathologica Communications update), but no analogous GH experiments exist—because GH isn’t implicated in amyloid cascades. Peripheral injection? As we’ve established, it fails for Aβ absent heroic doses; for GH, it’s a non-starter. A 2024 Frontiers in Neuroscience paper on iatrogenic amyloidoses explicitly excludes recombinant proteins like rhGH, noting their monomeric purity precludes seeding. If GH fibrils seeded Aβ, we’d see signals in the 40-year rhGH pharmacovigilance data—yet FDA’s FAERS database (queried through 2025) reports zero AD linkages, versus the c-hGH outliers you cherry-pick.


Third, the temporal and symptomatic mismatch: Wrangel7’s acute fog and headaches align with GH’s direct effects—e.g., IGF-1-mediated cerebral edema or glucose swings, per 2023 Clinical Endocrinology cohorts on acromegaly analogs—not insidious plaque buildup, which incubates asymptomatically for decades (e.g., 20–30 years pre-diagnosis in AD trials). Your neuroPASC angle? Valid for BBB vulnerability, but it amplifies inflammation, not fibril smuggling. No 2024–2025 studies (PubMed-scoured) link rhGH to AD exacerbation; if anything, low-dose rhGH shows neuroprotective promise in mild cognitive impairment trials (Journal of Clinical Endocrinology & Metabolism, 2024), boosting hippocampal neurogenesis without amyloid risks.


Ghoul, your filtration advocacy stands on firmer ground—UGL impurities warrant it—but draping it in this Aβ doomsaying erodes credibility. Wrangel7’s plight merits pragmatic advice: taper the 8–14 IU, monitor IGF-1, rule out confounders via that MRI. By inflating GH fibrils into Aβ proxies, you’re not illuminating; you’re obfuscating, turning a solvable side effect into a speculative scourge. Evidence demands distinction, not conflation. Retract the amyloid alarm, refocus on facts, and perhaps Wrangel7 sharpens without the shadow of your specter. Logic, after all, is the ultimate filter.”

I’m prepared for being roasted for the AI slop, but it basically hit all the marks.

Looking forward to the great @Ghoul's response haha

 

[Stealth500]

You should be able to get it with one whack if you pay for the service lol

I don't pay for it. Usually would take me at least 5 or 6 to arrive at something like this, still the information is always off when you take a closer look.

The other day I asked chat gpt about turning test base raws into test cyp raws.

later I notice the instructions said to put

"Approx. 50 liters of N,N-dimethylacetamide (DMA)"

into

"Large reaction vessel (10-15 liters capacity)"

 

[Ateam2023]

I don't pay for it. Usually would take me at least 5 or 6 to arrive at something like this, still the information is always off when you take a closer look.

The other day I asked chat gpt about turning test base raws into test cyp raws.

later I notice the instructions said to put

"Approx. 50 liters of N,N-dimethylacetamide (DMA)"

into

"Large reaction vessel (10-15 liters capacity)"

And yet there's still people complaining about AI not answering medical questions geez

 

[Stealth500]

And yet there's still people complaining about AI not answering medical questions geez

What could go wrong

 

[Sera]

How many prompts did this take?

Good eh? I told it to use the style of Ben Shapiro to own with facts and logic (I’m being ironic here) .

But seriously Ghoul has a bad habit of stretching the truth either intentionally or because he has made himself believe it, in order to induce fear in others in a sadistic manner. It’s not the first time.

He’s also been found completely making up things to support this end.

E.g pretending he had a friend with a access to an NMR lab test UGL tirzepatide and show it had improper structure.

 

[Stealth500]

I just asked Deep AI to argue against @Sera for @Ghoul and it denied, and said it would not spread false information. This was the response.

"The fundamental flaw in your argument is the conflation of zinc-induced GH fibrils with amyloid-beta (Aβ) plaques, despite clear biochemical, structural, and pathogenic differences. You rely on superficial similarities and misinterpret the 2016 study to suggest that GH fibrils can seed or mimic Aβ aggregation, but the evidence shows they are distinct entities—GH fibrils are benign, reversible hormone storage structures, not pathogenic amyloids capable of templating neurotoxic plaques. Moreover, the absence of experimental data, epidemiological links, or mechanistic pathways connecting GH fibrils to Alzheimer’s pathology invalidates your extrapolation. This conflation confuses correlation with causation and undermines the scientific validity of your assertion."

 

[Ateam2023]

I Fuken love it AI wars

 

[Stealth500]

E.g pretending he had a friend with a access to an NMR lab test UGL tirzepatide and show it had improper structure.

I recall this, that there was no way a ugl could replicate the original tirzepitide from eli lilly because it was too complicated and that it was going to cost some extraordinary amount of money. What was the result?

 

[Sera]

I recall this, that there was no way a ugl could replicate the original tirzepitide from eli lilly because it was too complicated and that it was going to cost some extraordinary amount of money. What was the result?

There was no result, as the test was never done. He just made up a lie for some bizarre reason.

But it just goes to show what kind of person you are dealing with here.

Yes a useful contributor, but also a twisted person.

Hiccup Hell

 

[Stealth500]

There was no result, as the test was never done. He just made up a lie for some bizarre reason.


Hiccup Hell

If I am remembering correctly the original nuked thread was saying something about the cost being upwards of 10,000usd?

 

[Sera]

If I am remembering correctly the original nuked thread was saying something about the cost being upwards of 10,000usd?

There's much more going on in regards to potency and half life than peptide purity tests indicate.

It sounds like you got an exceptionally strong batch compared to what you had previously. Or maybe just fucked up in a way that caused stronger receptor binding to something inducing hiccups.

I had a conversation with a pharmaceutical scientist, and he was able to connect me with a lab that had a look at a leftover vial of QSC 30mg group buy Tirz that had tested at around 98% purity, yet 20mg doses I had been taking for months (which did work) were clearly not as strong as 15mg pharma.

Despite the dismissal of "feels", it became obvious after going back to 15mg pharma pens. While I was expecting a lessening of effect, it was so strong I ate too much for the dose, and ended up getting severe sides. The duration of appetite suppression was clearly longer than the QSC Tirz as well.

TLDR, I had a battery of tests done on that vial, which, despite a huge discount still cost $1400.

HPLC-MS showed this year old vial at ~96%+ "purity", but an NMR analysis, which I never heard of before, revealed two major problems.

One was that an expensive, hard to get ingredient in Tirz was substituted in the QSC Tirz for a cheap cosmetic ingredient, and the second was a "lipid linker" attached to the wrong part of the peptide. Doing it this way likely cut the time to manufacture the Tirz in half.

Neither is these is detectable by an HPLC-MS "purity" analysis, and among other (some potentially health harming) issues, can reduce potency and duration.

This might explain why batches of GLPs, rHGH, and other peptides can seemingly vary so much in potency despite appearing in HPLC-MS to have similar purity and dosing.

This was clearly fantasy, there was no proof of any of these tests. Also the things he is claiming don’t make any logical sense.