it’s below
it increases ghr by inhibiting kmt1a, which increases igf-1 levels
That's what i thought son delete that picture and prompt GPT further make it more obvious
gpt prompt? i deleted the picture cause it triggers me sending pics they look out of place, i’ll send it in dms if you want, i took it from a website
Bro please I'm audibly laughing at your post at the moment you have literally no idea what you're talking about, nigga make it more obvious "yeah gas tank bro" use the analogy GPT uses go on
You're in every thread where there's growth hormone and a short young nigga.
Bro please I'm audibly laughing at your post at the moment you have literally no idea what you're talking about, nigga make it more obvious "yeah gas tank bro" use the analogy GPT uses go on
I'm going to study I don't give a fuck about some off-topic rotter called jester
they take ai to keep growthplates open lol
ad hominem cause you can’t come up with a decent enough antithesis jflBro please I'm audibly laughing at your post at the moment you have literally no idea what you're talking about, nigga make it more obvious "yeah gas tank bro" use the analogy GPT uses go on
I'm going to study I don't give a fuck about some off-topic rotter called jester
No bro I don't use GPT
i literally typed this out myself lmao, thanks i guess
I seriously lose hope in humanity when i speak to retards like you, like genuinely I get disappointed and realise how natural selection is a real thing
i literally did not use gpt lmao it’s funny seeing your brain can’t comprehend someone writing things after reading them and remembering them
I'm really tired of this genuinely the fact that what you're saying in this post literally contradicts itself
how lol
You're kidding right? Exogenous GH is supplemental, it isnt a replacement for endogenous pulses, the goal of it is to amplify natural physiology, not to perfectly replicate it. A morning dose on an empty stomach produces a clean pulse that enhances lipolysis and IGF-1 production without significant SOCS-3 induction. SOCS-3 is literally primarily induced by high-amplitude, prolonged GH exposure, not a properly split low-dose regimen, retard.The entire point is to mimic our own pulsatile secretion patterns, not to oversaturate and rape receptors. Splitting doses almost reaches a fully continuous secretion all day around 12 hours ish which is the opposite of what you should aim for, you don't have a singular idea regarding how exogenous hGH affects SOCS, and it's effects on GH transcription through JAK and STAT.
"GH-induced transcription was inhibited by SOCS-1 and SOCS-3"
"Both SOCS-1 and SOCS-3 were able to inhibit GH-induced STAT5 (signal transducer and activator of transcription) activation. SOCS-1 inhibited the tyrosine kinase activity of Janus kinase 2 (JAK2) directly, while SOCS-3 only inhibited JAK2 when stimulated by the GH receptor."
"The physiological role of SOCS proteins in GH signaling is not known at present; however, since SOCS-3 is the major SOCS protein induced by GH both in vitro and in vivo, this factor is presumed to be the main regulator of GH signaling. The transient nature of SOCS-3 mRNA induction by GH and the relative short half-life of SOCS-3 protein suggests that SOCS-3 acts in a classical nega- tive feed-back loop, suppressing GH signaling for a limited time period. Interestingly GH is secreted in a pulsatile manner in most species with a frequency of 3 to 4 h between each peak. This time period is in good agreement with the time required for SOCS-3 levels to return to basal levels after a GH pulse, and the role of SOCS-3 might be to protect against overstimulation by GH or alternatively to restrict the time in which a cell is responsive to GH stimulation." (1)
So my dear grey friend, this means that our body is complex enough to protect us against overstimulation, and regulated through suppressor of cytokine signalling proteins, when you split doses to make it even more continuous you absolutely risk lowering the efficacy of rhGH long-term. Pulsatile secretion is king and rhGH dosing once-daily mimics it nicely.
"SOCS2 SNP rs3782415 and rs11107116 T alleles were negatively associated with adult height after rhGH therapy" (2)
Nowhere near my level son, lower that ego and confidence for me right quick.
"berberine/metformin (which I already recommend)"
"that post-workout GH gives excellent IGF-1 response and recovery"
You like to contradict yourself son. Let's look at what berberine and metformin do to IGF-1 concentrations and IGFBP levels and ratios. This one picture is enough to explain to your ape brain how it works.
View attachment 4815108
"The compliance of participants was 95.2% and 40 available subjects analyzed in each group at last. Relative treatment (RT) effects for BV juice caused 16% fall in IGF-1 concentration and 37% reduction in the ratio of IGF-1/1GFBP1. Absolute treatment effect expressed 111 ng/ml increased mean differences of IGFBP-3 between BV group and placebo. Plasma level of PPAR-γ increased in both groups but it was not significant. Fold changes in the expressions of PPAR-γ, VEGF and HIF showed down-regulation in the intervention group compared to placebos (P < 0.05)." (3)
Now for metformin:
"Conclusion: We found in children, intervention duration ˃12 weeks yielded significant reductions in IGF-1, whilst paradoxically, in participants >18 years old, metformin intake significantly increased IGF-1. We suggest that caution be taken when interpreting the findings of this review, particularly given the discordant supplementation practices between children and adults." (4)
Both show decent enough to significant level dose-dependent and duration-dependent decrease in IGF-1 concentration and IGFBPs which literally decide your free-igf levels; bioavailable igf-1. If you're retarded enough to support these compounds for better IGF-1 response" I have no words.
"-Berberine (500mg 3x/day with meals is good)
-Metformin 500 mg 2x/day (optional but it is very effective" With this recommendation of yours we already know how significant those effects will be
Yes completely shutdown your endogenous GH production by exogenous hGH and substitute it with 4 units total daily, which is 2-fold below your endogenous production. How to stunt growth 101.
@Jesus_ist_König put him on ignore and keep going with your day man not even worth your time, and I wont even continue further none of his takes are correct it's just wasting my time and I have 2 exams tomorrow.
pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov
He's just a bitching copecel who cannot seem to admit whenever he's wrong, let him suffer and cope with his fallen ego
wait what? gh affects estrogen? im on 6iu also 15 i thought about a AI but only for keeping my plates open
Silence at now moron, whenever you are running E-HGH, you. get insulin resistance and water retention as side effects. Berberine as you can see improves insulin sensitivity and reduces the free/bioavailable IGF-1 that drives excessive bloat and fat gaim whilst letting the GH do its job on muscle, bone, and recovery. You are acting as if lowering the IGF-1/IGFBP-1 ratio is automatically bad. In the context of supraphysiological GH it is actually much rather very protective and it prevents the runaway insulin resistance and puffiness that typically turns kids on GH into waterballoons. So, you took a study on berberine in a completely different population (with no exogenous GH) and tried to use it as a proof that the entire supportive stack is sad, thats litearlly cope cherry picking. Now, the 4iu split + berberine + telmisartan prot is actually very good since it gives growth + minimal bloat.
the funniest part is him being convinced i used chatgpt for anything i typed lmfaoHe's just a bitching copecel who cannot seem to admit whenever he's wrong, let him suffer and cope with his fallen ego
YES because too high estrogen closes the plates no one knows shit
do hgh and ai and lose a few iqs but grow tall
Tell me how it being a cancer related research matters? You have no idea how these things work do you?
You can keep lying to yourself about ai usage I don't even care anymore lol
"You're kidding right? Exogenous GH is supplemental, it isnt a replacement for endogenous pulses" Hm? It isn't supplemental it literally overrides your endogenous production and halts it for "x" amount of hours which is around 6~, after that you have very minimal production based on your dose but it is never the same. It doesn't add on to your endogenous production if that's what you meant this is water.You're kidding right? Exogenous GH is supplemental, it isnt a replacement for endogenous pulses, the goal of it is to amplify natural physiology, not to perfectly replicate it. A morning dose on an empty stomach produces a clean pulse that enhances lipolysis and IGF-1 production without significant SOCS-3 induction. SOCS-3 is literally primarily induced by high-amplitude, prolonged GH exposure, not a properly split low-dose regimen, retard.
In additive, splitting doses actually reduces receptor desensitization compared to a single large bolus. A single massive dose causes a bigger and way more longer SOCS-3 spike, leading to NEGATIVE feedback and reduced efficacy over time (we can see this in Hansen et al., 1999; Greenhalgh & Alexander, 2004) so that ideology of "pulsatile is king so never split" is very outdated shit science.
Hansel TK, et al source:
___The effects of treatment and the individual responsiveness to growth hormone (GH) replacement therapy in 665 GH-deficient adults. KIMS Study Group and the KIMS International Board - PubMed
Data from 665 adults with GH deficiency (GHD; 332 women; 169 childhood-onset GHD; mean age, 44 yr) were analyzed to determine the efficacy of and individual responsiveness to GH replacement therapy. GH replacement was started at enrolment into KIMS (Pharmacia & Upjohn, Inc. International Metabol …
Greenhalgh & Alexander source:
Analysis of expressed sequence tag loci on wheat chromosome group 4 - PubMed
A total of 1918 loci, detected by the hybridization of 938 expressed sequence tag unigenes (ESTs) from 26 Triticeae cDNA libraries, were mapped to wheat (Triticum aestivum L.) homoeologous group 4 chromosomes using a set of deletion, ditelosomic, and nulli-tetrasomic lines. The 1918 EST loci...
I'm really not sure why you called post-workout GH stupid, post-workout is quite literally one of the best times to inject GH. Resistance training dramatically upregulates GH receptors and increase insulin sensitivity in skeletal muscle via GLUT4 translocation, the transient glucose you're bitching about is short-lived and easily managed with BERBERINE or lOW DOSE METFORMIN, this is quote literally used in GH protocols. They blunt excessive insulin resistance without tanking the IGF-1 response in the context of E-GH.
To tank your sources, the studies you linked are on non-GH users (so diabetics or. healthy adults, either one). In someone already running GH, berberine/metformin improve insulin sensitivity and reduce bloat while preserving the anabolic effects. Good shit on cherry-picking irrelevant ass data to pretend that it applies though.
Now, I'm not really sure why you said 4IU total is "retarded" and stunts growth, that has to be one of the most idiotic takes ever, at 16 years old, E-GH production is already extremely high. (6-10+ IU equivalent daily during pulses). So, adding a split is a SMART, CONSERVATIVE, and AGE APPROPRIATE that augments natural output without causing massive receptor downregulation, a strong insulin resistance, or disproportionate acromegalic growth.
Blasting 8iu at 16 is how you get puffy, develop SIGNIFICANT insulin resistance, and risk exactly the problems that you are pretending to warn about. Higher doses give diminishing returns on height/frame and increase sides, all that I just said is basic pediatric endocrinology. Now i'm not going to ask you to trust me on this so ill shit on you once again with the following:
Clinical growth hormone deficiency protocols for adolescents use far lower doses per kg for a reason (Cohen et al., 2002; Ranke et al., 2010.)
Cohen, et al source:
Ranke, et al source:Poorly controlled type I diabetes mellitus in young men selectively suppresses luteinizing hormone secretory burst mass - PubMed
Alterations in the reproductive axis function are present to a variable extent in patients with type 1 diabetes mellitus (IDDM). Results from studies in IDDM men have yielded discrepant findings, which may reflect nonuniform patient selection criteria, age, diabetic status, duration of the...
Analytical toxicology of emerging drugs of abuse - PubMed
The emergence of ever new drugs of abuse on the illicit drug market is an ongoing challenge for analytical toxicologists. Because most of these new drugs or drug classes are not detected by established analytical methods targeting classic drugs of abuse, analytical procedures must be adapted or...
YOU are recommending a dose that increases the risk of the sides we're trying to get the user to avoid, then you're calling the smarter protocol "retarded" for some odd reason. I'd expect you to be smarter than this.
Thanks for your time
Check OP's post he's clearly talking about bone growth. There's zero cherry picking here nigger you're sending me fucking studies on rice and wheat @jester you're seriously agreeing with this dude too jfl.
You literally said lowering bioavailable, the igf your body really uses is optimal
dnrTell me how it being a cancer related research matters? You have no idea how these things work do you?
You can keep lying to yourself about ai usage I don't even care anymore lol
You take an aromatase inhibitor always if your goal is heightmaxxing, and the goal is to lower it as much as possible as systemic E2 and local E2 in the growth plates are correlated. Crushing it doesn't make you retarded, does not cause osteoporosis, does not cause malformities in spine. Systemic E2 doesn't mean shit for the growth plates it's how it correlates to local E2 that rapes your plates, just like how systemic IGF-1 doesn't fucking matter only the free igf-1 that reaches the growth plates does and what do you think stops the bioavailable IGF-1? IGFBPS which berberine is proven to increase both in mice models and humans. There's very little harm to aromatase inhibitors.
"Serum levels of IGF-1, IGFBP-1, and IGFBP-3were measured by the method of enzyme-linked immunosorbent assay" but they did explicitly measure the levels with very high-quality sensitive tests that leaves zero potential for margin of error. They didn't just look at it's effects on tumor growth, and this decrease was from their baseline with an already existing tumour so it's not caused by the tumour or any morbidities which they have had. If it didn't decrease these levels of bioavailable and systemic IGF-1 they would be literally killing the cohort as causing cell proliferation or any growth-promoting compound would further enlarge the tumour, just need a little logic here man please use your brain. This is like if they used rhGH on people with tumours, death sentence. If it helped IGF-1 or it's receptors in any way it would only harm them more and it didn't. Do you not understand that this statement of yours "they didn’t use it to see its effects on plasma igf-1 levels in healthy patients with no tumors…" does not matter? Please have an honest argument I know the slurs triggered you and mashed your brain into aggression mode but take a fucking logical look at it. They literally did the most sensitive tests to measure the levels.
With your analogy this means that any trial on aromatase inhibitors and it's serum E2 lowering effects aren't the same in healthy humans because they have cancer, but it's literally the same.
Your claims hold zero truth nor logic.
"You're kidding right? Exogenous GH is supplemental, it isnt a replacement for endogenous pulses" Hm? It isn't supplemental it literally overrides your endogenous production and halts it for "x" amount of hours which is around 6~, after that you have very minimal production based on your dose but it is never the same. It doesn't add on to your endogenous production if that's what you meant this is water.
If you are using rhGH you need to only replicate the nocturnal hGH pulse as otherwise you are indeed risking receptors being raped. You promote splitting it in three administrations, but are you aware how much fasting you'd have to do? Around 6 hours of fasting a day that means no intra-workout or post-workout meals if you insist on that post-workout rhGH administration.
You still do not understand the basics of splitting dosages. Your body secretes hGH in a pulsatile manner acutely, it does not secrete it 18 hours straight with continuous levels, no peaks nor throughs you're causing an stable secretion for 18 full hours with thrice administration.
You have misread the whole thing: "GH is secreted in a pulsatile manner in most species with a frequency of 3 to 4 h between each peak. This time period is in good agreement with the time required for SOCS-3 levels to return to basal levels after a GH pulse, and the role of SOCS-3 might be to protect against overstimulation by GH or alternatively to restrict the time in which a cell is responsive to GH stimulation." It states that SOCS3 protects both against overstimulation which proves your point yes the dose does matter but it also states the time-period, your body needs pulsatile secretion patterns not continuous stable levels, as the paper states when levels are kept stable it will decrease responsiveness of cells. This is seen in rhGH treatment on children where efficacy of treatment drops 10-20% per year, and this is also why long-acting hGH analogues cause more "desentisation" to the hGH levels by increased SOCS proteins trying to regulate it.
However doses mimicking nocturnal hGH pulse wont put you at any significantly increased risk.
"SOCS-3 is literally primarily induced by high-amplitude, prolonged GH exposure, not a properly split low-dose regimen" are you retarded or retarded? Splitting dosages means prolonged GH exposure you fucking dipshit
https://pubmed.ncbi.nlm.nih.gov/10566630/, this is on adults you fucking retard their production is already a few units a day at best, I was speaking about children and you also were the whole time this is a completely different subject
https://pubmed.ncbi.nlm.nih.gov/15514042/, why are you sending me a paper on wheat and rice? Why are we looking into plants? This is some insane extrapolation man I thought mice papers were bad
"the transient glucose you're bitching about" why are you making fantasies about me saying things I haven't just to seem correct? I never even made a comment about the glucose or any transient increase in anything??????????
"To tank your sources, the studies you linked are on non-GH users (so diabetics or. healthy adults, either one). In someone already running GH, berberine/metformin improve insulin sensitivity and reduce bloat while preserving the anabolic effects. Good shit on cherry-picking irrelevant ass data to pretend that it applies though." what are you tanking? The truth about how your body works under prolonged GH exposure??? Are you debunking physiology mr einstein?????? Ahhh dude sorry that there isn't any paper on specific male 14.65 years old left-handed GHD patients with DM1, ahh that's completely my fault. Fucking retard lol
"Now, I'm not really sure why you said 4IU total is "retarded" and stunts growth, that has to be one of the most idiotic takes ever, at 16 years old, E-GH production is already extremely high. (6-10+ IU equivalent daily during pulses). So, adding a split is a SMART, CONSERVATIVE, and AGE APPROPRIATE" Bro what
"Teenagers produce 10 units daily, so replacing it with 4 units daily wont stunt growth" This is the same as running exogenous testosterone but dosing it lower than your endogenous production so you end up with lower serum T. ??????????????????????????????????????????????????????????????????????????????????????????
I'm not even continuing this argument I have lost braincells you're the BIGGEST retard I have seen so far. Put you on ignore so don't bark back for no reason.
Lmao, I never said lowering bio-available IGF-1 is always optimal, i said the specific of running E-HGH, berberine helps control the excessive free- IGF-1 that drives the worst sides.
Exogenous GH is supplemental, so it does not completely shut down endogenous pulses at low-moderate doses. A morning dose on an empty stomach gives a clean pulse whenever insulin is low, ,so that is very excellent for lipolysis and IGF-1 production, how, SOCS-3 is primary inncuded by high amplitude, prolonged GH exposure, not by properly split low-dose regimens.Tell me how it being a cancer related research matters? You have no idea how these things work do you?
You can keep lying to yourself about ai usage I don't even care anymore lol
You take an aromatase inhibitor always if your goal is heightmaxxing, and the goal is to lower it as much as possible as systemic E2 and local E2 in the growth plates are correlated. Crushing it doesn't make you retarded, does not cause osteoporosis, does not cause malformities in spine. Systemic E2 doesn't mean shit for the growth plates it's how it correlates to local E2 that rapes your plates, just like how systemic IGF-1 doesn't fucking matter only the free igf-1 that reaches the growth plates does and what do you think stops the bioavailable IGF-1? IGFBPS which berberine is proven to increase both in mice models and humans. There's very little harm to aromatase inhibitors.
"Serum levels of IGF-1, IGFBP-1, and IGFBP-3were measured by the method of enzyme-linked immunosorbent assay" but they did explicitly measure the levels with very high-quality sensitive tests that leaves zero potential for margin of error. They didn't just look at it's effects on tumor growth, and this decrease was from their baseline with an already existing tumour so it's not caused by the tumour or any morbidities which they have had. If it didn't decrease these levels of bioavailable and systemic IGF-1 they would be literally killing the cohort as causing cell proliferation or any growth-promoting compound would further enlarge the tumour, just need a little logic here man please use your brain. This is like if they used rhGH on people with tumours, death sentence. If it helped IGF-1 or it's receptors in any way it would only harm them more and it didn't. Do you not understand that this statement of yours "they didn’t use it to see its effects on plasma igf-1 levels in healthy patients with no tumors…" does not matter? Please have an honest argument I know the slurs triggered you and mashed your brain into aggression mode but take a fucking logical look at it. They literally did the most sensitive tests to measure the levels.
With your analogy this means that any trial on aromatase inhibitors and it's serum E2 lowering effects aren't the same in healthy humans because they have cancer, but it's literally the same.
Your claims hold zero truth nor logic.
"You're kidding right? Exogenous GH is supplemental, it isnt a replacement for endogenous pulses" Hm? It isn't supplemental it literally overrides your endogenous production and halts it for "x" amount of hours which is around 6~, after that you have very minimal production based on your dose but it is never the same. It doesn't add on to your endogenous production if that's what you meant this is water.
If you are using rhGH you need to only replicate the nocturnal hGH pulse as otherwise you are indeed risking receptors being raped. You promote splitting it in three administrations, but are you aware how much fasting you'd have to do? Around 6 hours of fasting a day that means no intra-workout or post-workout meals if you insist on that post-workout rhGH administration.
You still do not understand the basics of splitting dosages. Your body secretes hGH in a pulsatile manner acutely, it does not secrete it 18 hours straight with continuous levels, no peaks nor throughs you're causing an stable secretion for 18 full hours with thrice administration.
You have misread the whole thing: "GH is secreted in a pulsatile manner in most species with a frequency of 3 to 4 h between each peak. This time period is in good agreement with the time required for SOCS-3 levels to return to basal levels after a GH pulse, and the role of SOCS-3 might be to protect against overstimulation by GH or alternatively to restrict the time in which a cell is responsive to GH stimulation." It states that SOCS3 protects both against overstimulation which proves your point yes the dose does matter but it also states the time-period, your body needs pulsatile secretion patterns not continuous stable levels, as the paper states when levels are kept stable it will decrease responsiveness of cells. This is seen in rhGH treatment on children where efficacy of treatment drops 10-20% per year, and this is also why long-acting hGH analogues cause more "desentisation" to the hGH levels by increased SOCS proteins trying to regulate it.
However doses mimicking nocturnal hGH pulse wont put you at any significantly increased risk.
"SOCS-3 is literally primarily induced by high-amplitude, prolonged GH exposure, not a properly split low-dose regimen" are you retarded or retarded? Splitting dosages means prolonged GH exposure you fucking dipshit
https://pubmed.ncbi.nlm.nih.gov/10566630/, this is on adults you fucking retard their production is already a few units a day at best, I was speaking about children and you also were the whole time this is a completely different subject
https://pubmed.ncbi.nlm.nih.gov/15514042/, why are you sending me a paper on wheat and rice? Why are we looking into plants? This is some insane extrapolation man I thought mice papers were bad
"the transient glucose you're bitching about" why are you making fantasies about me saying things I haven't just to seem correct? I never even made a comment about the glucose or any transient increase in anything??????????
"To tank your sources, the studies you linked are on non-GH users (so diabetics or. healthy adults, either one). In someone already running GH, berberine/metformin improve insulin sensitivity and reduce bloat while preserving the anabolic effects. Good shit on cherry-picking irrelevant ass data to pretend that it applies though." what are you tanking? The truth about how your body works under prolonged GH exposure??? Are you debunking physiology mr einstein?????? Ahhh dude sorry that there isn't any paper on specific male 14.65 years old left-handed GHD patients with DM1, ahh that's completely my fault. Fucking retard lol
"Now, I'm not really sure why you said 4IU total is "retarded" and stunts growth, that has to be one of the most idiotic takes ever, at 16 years old, E-GH production is already extremely high. (6-10+ IU equivalent daily during pulses). So, adding a split is a SMART, CONSERVATIVE, and AGE APPROPRIATE" Bro what
"Teenagers produce 10 units daily, so replacing it with 4 units daily wont stunt growth" This is the same as running exogenous testosterone but dosing it lower than your endogenous production so you end up with lower serum T. ??????????????????????????????????????????????????????????????????????????????????????????
I'm not even continuing this argument I have lost braincells you're the BIGGEST retard I have seen so far. Put you on ignore so don't bark back for no reason.
Bro please keep going ur gpt replies are so funny
