hGH desensitization: Why you may not want to inject hGH everyday (heightmaxers GTFIH)

[axm]

Prevention of Growth Deceleration after Withdrawal of Growth Hormone Therapy in Idiopathic Short Stature​

Meir Lampit, Ze’ev Hochberg. The Journal of Clinical Endocrinology & Metabolism, Volume 87, Issue 8, 1 August 2002, Pages 3573–3577. Published 01 August 2002.

The treatment of children with idiopathic short stature by daily injections of human GH (hGH) is followed after its withdrawal by a growth deceleration with normal serum GH and IGF-I levels.

The present study was designed to understand and prevent growth deceleration. We hypothesized that this phenomenon is due to tolerance at the target organ level, that tolerance develops in response to the unphysiological pharmacokinetics of daily-injected hGH, and that alternate day hGH therapy will prevent it.

Thirty-eight prepubertal children with idiopathic short stature, aged 3.3–9.0 yr, were studied. Their heights were less than −2 SD score, growth rate was above the 10th percentile for age, bone age was less than 75% of chronological age, and the stimulated serum GH concentration was greater than 10 μg/liter.

The children were matched for sex, height, and growth velocity SD score to receive daily or alternate day hGH at the same weekly dose of 6 mg/m2 for a period of 2 yr. The 1st and 2nd year mean growth velocities were 3.4 and 2.3 SD score for the daily therapy group and 3.0 and 2.0 SD score for the alternate day group, respectively (P = NS).

Over the initial 6 months after withdrawal of therapy, and growth velocity decelerated to a nadir of −3.9 SD score in the daily therapy group, whereas it decelerated in the alternate day group to only −0.2 SD score (P < 0.01).

Over the entire 2 yr off therapy the latter group maintained mean growth rates of −0.2 to −1.2 SD score, similar to their pretreatment velocities. The daily group recovered slowly to resume their mean pretreatment rate only on the fourth semiannual evaluation off therapy.

The cumulative 4-yr growth velocity (2 yr on and 2 yr off therapy) of the alternate day group was greater than that of the daily therapy group (mean, 0.9 vs. 0.3 SD score; P < 0.002). At the end of the 4-yr therapy period, the adult height prediction of the alternate day group was greater than that of the daily group by a mean 6.5 cm (P = 0.06).

What does this mean?

Everyday injections of exogenous hGH seem to drastically lower your body's sensitivity to its own GH secretion.

In this study, 38 ISS children were given either everyday (ED) or every other day (EoD) injections of hGH for two years (doses equated). The treatment then ceased and their heights were tracked for an additional two years after the treatment.

During hGH therapy, both groups accelerated their growth substantially:

The ED group first and second year velocity was 3.4 and 2.3 SD.

The EoD group had 3.0 and 2.0 SD for first and second year, respectively.

Over the initial six months after withdrawal of therapy, growth velocity decelerated to a low nadir –3.9 SD score for the daily therapy group, whereas it decelerated in the alternate day group to only –0.2 SD score.

During the 2 years off therapy, the latter group taking EoD injections maintained growth rates of –0.2 to –1.2 SD score, which is similar to their SD score prior to the hGH treatment. The daily group also recovered but very slowly, on the fourth semiannual evaluation off therapy. The cumulative 4-year growth velocity—2 yrs on and 2 yrs off therapy—of the alternate day group was greater than that of the daily therapy group: mean, 0.9 vs. 0.3 SD score.

At the end of the 4-yr therapy period, the adult height prediction of the EoD group was greater than that of the daily group by a mean of 6.5 cm.

Why is this?

Typically, endogenous growth hormone comes in pulses or spikes, as opposed to a sustained release over many hours as seen in exogenous administration. It seems that the issue stems from desensitization of target tissues due to the unnatural release of growth hormone when exogenously administered subcutaneously. This is despite the fact that sustained GH release is known to boost IGF-1 higher than pulsatile secretion, further proving that GH itself contributes to growth as seen in some rodent models.

What Can We Do?

Alternate day dosing, as seen in the study, seems to ameliorate this. This is at the cost of short term height velocity though. We still do not understand how the desensitization may differ in other tissues, so it everyday dosing could maybe be considered if you believe your plates are soon to close and you want to max out height velocity during this time. Please keep in mind that the doses were equated, meaning double the dose once every other day. (as an example, from 3 IU's everyday, to 6 IU's every other day).

Another (theoretical) way this problem could be solved is through the use of peptidyl (not MK-677) growth hormone secretagogues and GHRH analogs. These peptides (especially in combination) seem to produce a spike much more similar to endogenous production. This (again, in theory) could mitigate desensitization and lead to better height gains. This is also combining with the multiple molecular weights your pituitary releases in response to the peptides as opposed to the 22 kDa exogenous hGH but that might be for a different thread.

I am not a medical professional, nothing written here should be considered medical advice. Do your own research. Thanks for reading!

 

[axm]

https://pubmed.ncbi.nlm.nih.gov/11133160/
This was the rodent model I was referring to by the way

 

[letsdoit]

@Osie

 

[Osie]

@Osie

I'll dm you about this

 

[Osie]

Why is this?

Typically, endogenous growth hormone comes in pulses or spikes, as opposed to a sustained release over many hours as seen in exogenous administration. It seems that the issue stems from desensitization of target tissues due to the unnatural release of growth hormone when exogenously administered subcutaneously. This is despite the fact that sustained GH release is known to boost IGF-1 higher than pulsatile secretion, further proving that GH itself contributes to growth as seen in some rodent models.

What Can We Do?

Alternate day dosing, as seen in the study, seems to ameliorate this. This is at the cost of short term height velocity though. We still do not understand how the desensitization may differ in other tissues, so it everyday dosing could maybe be considered if you believe your plates are soon to close and you want to max out height velocity during this time. Please keep in mind that the doses were equated, meaning double the dose once every other day. (as an example, from 3 IU's everyday, to 6 IU's every other day).

View attachment 3026171

Another (theoretical) way this problem could be solved is through the use of peptidyl (not MK-677) growth hormone secretagogues and GHRH analogs. These peptides (especially in combination) seem to produce a spike much more similar to endogenous production. This (again, in theory) could mitigate desensitization and lead to better height gains. This is also combining with the multiple molecular weights your pituitary releases in response to the peptides as opposed to the 22 kDa exogenous hGH but that might be for a different thread.

I am not a medical professional, nothing written here should be considered medical advice. Do your own research. Thanks for reading!

Great post, I always love seeing analysis of interesting studies on the forum. The best way to handle this is by injecting peptides once in the morning and once in the afternoon, so twice a day, and then injecting HGH at night. This essentially allows for constant spiking of both endogenous production and exogenous production. However, when you are taking both of them, they have different break times, so you'd have to take breaks from the peptides and then potentially decide to continue using the HGH or stop until your body is resensitized and ready to use the peptides.

You can never inject peptides and HGH at the same time, they need like at least a 5-8 hour distance in terms of use time of administration. This is because exogenous HGH creates a feedback loop that directly signals the pituitary gland to not produce as much endogenous HGH in it's presence. Now, this means that if you were to inject peptides in a similar time frame, it's effects would be completely halted, as it increases endogenous production.

Another way is to simply take a break after every 3-4 months when your body is just beginning to desensitize, then hop back on after 2 weeks. This seems like a simple way to circumvent it, but may feel odd to the traditional heightmaxxer as a majority of studies keep blasting the same dosage regardless of the decrease in growth velocity.

 

[axm]

You can never inject peptides and HGH at the same time, they need like at least a 5-8 hour distance in terms of use time of administration. This is because exogenous HGH creates a feedback loop that directly signals the pituitary gland to not produce as much endogenous HGH in it's presence. Now, this means that if you were to inject peptides in a similar time frame, it's effects would be completely halted, as it increases endogenous production.

I've heard on some forums (namely DatBTrue) that you could potentiate a huge spike in GH by pinning some peptides, letting them reach their peak in say 15 min or so, and then dosing exogenous hGH. Besides, isn't the negative feedback loop exerted by IGF-1? So the suppression would be chronic instead of acute

 

[Deleted member 70692]

then im fucked up

 

[letsdoit]

Great post, I always love seeing analysis of interesting studies on the forum. The best way to handle this is by injecting peptides once in the morning and once in the afternoon, so twice a day, and then injecting HGH at night. This essentially allows for constant spiking of both endogenous production and exogenous production. However, when you are taking both of them, they have different break times, so you'd have to take breaks from the peptides and then potentially decide to continue using the HGH or stop until your body is resensitized and ready to use the peptides.

You can never inject peptides and HGH at the same time, they need like at least a 5-8 hour distance in terms of use time of administration. This is because exogenous HGH creates a feedback loop that directly signals the pituitary gland to not produce as much endogenous HGH in it's presence. Now, this means that if you were to inject peptides in a similar time frame, it's effects would be completely halted, as it increases endogenous production.

Another way is to simply take a break after every 3-4 months when your body is just beginning to desensitize, then hop back on after 2 weeks. This seems like a simple way to circumvent it, but may feel odd to the traditional heightmaxxer as a majority of studies keep blasting the same dosage regardless of the decrease in growth velocity.

Can you check Whatsapp Osie

 

[Deleted member 33409]

Bunp

 

[heightmaxxer1133]

Prevention of Growth Deceleration after Withdrawal of Growth Hormone Therapy in Idiopathic Short Stature​

Meir Lampit, Ze’ev Hochberg. The Journal of Clinical Endocrinology & Metabolism, Volume 87, Issue 8, 1 August 2002, Pages 3573–3577. Published 01 August 2002.








What does this mean?

Everyday injections of exogenous hGH seem to drastically lower your body's sensitivity to its own GH secretion.

In this study, 38 ISS children were given either everyday (ED) or every other day (EoD) injections of hGH for two years (doses equated). The treatment then ceased and their heights were tracked for an additional two years after the treatment.

During hGH therapy, both groups accelerated their growth substantially:

The ED group first and second year velocity was 3.4 and 2.3 SD.

The EoD group had 3.0 and 2.0 SD for first and second year, respectively.

Over the initial six months after withdrawal of therapy, growth velocity decelerated to a low nadir –3.9 SD score for the daily therapy group, whereas it decelerated in the alternate day group to only –0.2 SD score.

During the 2 years off therapy, the latter group taking EoD injections maintained growth rates of –0.2 to –1.2 SD score, which is similar to their SD score prior to the hGH treatment. The daily group also recovered but very slowly, on the fourth semiannual evaluation off therapy. The cumulative 4-year growth velocity—2 yrs on and 2 yrs off therapy—of the alternate day group was greater than that of the daily therapy group: mean, 0.9 vs. 0.3 SD score.

At the end of the 4-yr therapy period, the adult height prediction of the EoD group was greater than that of the daily group by a mean of 6.5 cm.

Why is this?

Typically, endogenous growth hormone comes in pulses or spikes, as opposed to a sustained release over many hours as seen in exogenous administration. It seems that the issue stems from desensitization of target tissues due to the unnatural release of growth hormone when exogenously administered subcutaneously. This is despite the fact that sustained GH release is known to boost IGF-1 higher than pulsatile secretion, further proving that GH itself contributes to growth as seen in some rodent models.

What Can We Do?

Alternate day dosing, as seen in the study, seems to ameliorate this. This is at the cost of short term height velocity though. We still do not understand how the desensitization may differ in other tissues, so it everyday dosing could maybe be considered if you believe your plates are soon to close and you want to max out height velocity during this time. Please keep in mind that the doses were equated, meaning double the dose once every other day. (as an example, from 3 IU's everyday, to 6 IU's every other day).

View attachment 3026171

Another (theoretical) way this problem could be solved is through the use of peptidyl (not MK-677) growth hormone secretagogues and GHRH analogs. These peptides (especially in combination) seem to produce a spike much more similar to endogenous production. This (again, in theory) could mitigate desensitization and lead to better height gains. This is also combining with the multiple molecular weights your pituitary releases in response to the peptides as opposed to the 22 kDa exogenous hGH but that might be for a different thread.

I am not a medical professional, nothing written here should be considered medical advice. Do your own research. Thanks for reading!

i have some questions come in private please

 

[DR. NICKGA]

Hgh injections are usseles

 

[Deleted member 58492]

growth hormone secretagogues and GHRH analogs. These peptides

which ones would u reccomend
and also good thread

 

[Deleted member 58492]

and what do you think about this article as a solution to ed dosing's affects on desensitization?

https://journals.physiology.org/doi/full/10.1152/ajpendo.00414.2009

 

[axm]

which ones would u reccomend
and also good thread

the drugs that are well known to the forum, and have some human trials. GHRP-6,-2, Ipamorelin, Hexeralin, mod-GRF/CJC-1295 no DAC etc.

and what do you think about this article as a solution to ed dosing's affects on desensitization?

https://journals.physiology.org/doi/full/10.1152/ajpendo.00414.2009

This is about the growth hormone secretagogue receptor (ghrelin), not the growth hormone receptor itself.

Treatment of humans with lipid infusions suppresses the GH secretagogue effect of ghrelin (11). This modulation of the GH secretagogue response in vivo may well be complicated by additional effects of lipids in the pituitary, for example, on GH-releasing hormone receptor function (15). We have used an in vitro approach to directly examine the modulatory effects of OFAs (oleic and linoleic acids) and cholesterol on GHSR function.

This study referenced in your paper says that:

In humans, ghrelin exerts a strong stimulatory effect on GH secretion which is partially refractory to the inhibitory effect of both glucose and FFA load and is not enhanced by ARG. These factors almost abolish and potentiate, respectively, the GH response to GHRH

The fact that fatty acids and glucose in the bloodstream inhibits the release of GH from secretagouges is well known info.

Initial experiments showed that oleic and linoleic acid had no acute effects on the response of the GHSR to ghrelin, as assessed using the aequorin assay (120 μM OFA; Fig. 1A). In this case, GHSR/aequorin cells were exposed to OFAs only during the 20-s integration period required to measure aequorin's fluorescence response to ghrelin. A range of OFA concentrations ≤1 mM were tested, none of which had acute effects on the sensitivity of the receptor to ghrelin (data not shown). However, prolonged 96-h treatment of the GHSR/aequorin cells with OFA caused a significant increase in sensitivity of the cells to ghrelin relative to untreated controls. At 60 μM OFA the EC50 was significantly decreased, 2.4- (P < 0.001) and 2.9-fold (P < 0.001) for oleic and linoleic acid, respectively, relative to controls (Fig. 1B). At 120 μM OFA the EC50 was decreased 3.7-fold (P < 0.001) for both oleic and linoleic acid relative to controls (Fig. 1C). A possible mechanism for the improved response to ghrelin in OFA-treated cells is that receptor affinity for its ligand has been increased. Therefore, we next measured the ability of unlabeled ghrelin to displace radiolabeled ghrelin from GHSR/aequorin-expressing cells. We found that treatment for 96 h with either 60 or 120 μM oleic acid had a slight but nonsignificant effect on binding (P > 0.05, t-test; Fig. 2, A and B).

This is an in vitro cell culture experiment, where "Oleic and linoleic acids [oligounsaturated fatty acids (OFAs)] have no acute effect on responsiveness of GHSR to ghrelin, whereas long-term (96 h) treatment with OFAs increases the sensitivity of GHSR to ghrelin". I'm honestly not educated enough to draw many conclusions from this, but the fact that this was done in a Petri dish over 96 hours, and that this is with exogenous ghrelin (not its selective counterparts like the drugs I listed above) which is not commonly used for GH secreting properties, and that fatty acids are otherwise known to inhibit GH secreting properties from ghrelin/GHS' leads me to believe that this probably won't apply to humans. From what I've read, desensitization from GH releasing peptides only occurs with excessively high doses above saturation dose and can be easily ameliorated by switching drugs or taking a break for a few days.

Interesting read though.

 

[Deleted member 58492]

This is an in vitro cell culture experiment, where "Oleic and linoleic acids [oligounsaturated fatty acids (OFAs)] have no acute effect on responsiveness of GHSR to ghrelin, whereas long-term (96 h) treatment with OFAs increases the sensitivity of GHSR to ghrelin". I'm honestly not educated enough to draw many conclusions from this, but the fact that this was done in a Petri dish over 96 hours, and that this is with exogenous ghrelin (not its selective counterparts like the drugs I listed above) which is not commonly used for GH secreting properties, and that fatty acids are otherwise known to inhibit GH secreting properties from ghrelin/GHS' leads me to believe that this probably won't apply to humans. From what I've read, desensitization from GH releasing peptides only occurs with excessively high doses above saturation dose and can be easily ameliorated by switching drugs or taking a break for a few days.

Thanks for the response, high iq response and your def better at these things then me.
Yeah, after reading I agree with everything you said.

Great response

 

[Deleted member 90503]

Hgh injections are usseles

hgh increases igf1 if you take it with aromasin it will increase your height (correct me if im wrong)

 

[MyDreamIsToBe183CM]

Prevention of Growth Deceleration after Withdrawal of Growth Hormone Therapy in Idiopathic Short Stature​

Meir Lampit, Ze’ev Hochberg. The Journal of Clinical Endocrinology & Metabolism, Volume 87, Issue 8, 1 August 2002, Pages 3573–3577. Published 01 August 2002.








What does this mean?

Everyday injections of exogenous hGH seem to drastically lower your body's sensitivity to its own GH secretion.

In this study, 38 ISS children were given either everyday (ED) or every other day (EoD) injections of hGH for two years (doses equated). The treatment then ceased and their heights were tracked for an additional two years after the treatment.

During hGH therapy, both groups accelerated their growth substantially:

The ED group first and second year velocity was 3.4 and 2.3 SD.

The EoD group had 3.0 and 2.0 SD for first and second year, respectively.

Over the initial six months after withdrawal of therapy, growth velocity decelerated to a low nadir –3.9 SD score for the daily therapy group, whereas it decelerated in the alternate day group to only –0.2 SD score.

During the 2 years off therapy, the latter group taking EoD injections maintained growth rates of –0.2 to –1.2 SD score, which is similar to their SD score prior to the hGH treatment. The daily group also recovered but very slowly, on the fourth semiannual evaluation off therapy. The cumulative 4-year growth velocity—2 yrs on and 2 yrs off therapy—of the alternate day group was greater than that of the daily therapy group: mean, 0.9 vs. 0.3 SD score.

At the end of the 4-yr therapy period, the adult height prediction of the EoD group was greater than that of the daily group by a mean of 6.5 cm.

Why is this?

Typically, endogenous growth hormone comes in pulses or spikes, as opposed to a sustained release over many hours as seen in exogenous administration. It seems that the issue stems from desensitization of target tissues due to the unnatural release of growth hormone when exogenously administered subcutaneously. This is despite the fact that sustained GH release is known to boost IGF-1 higher than pulsatile secretion, further proving that GH itself contributes to growth as seen in some rodent models.

What Can We Do?

Alternate day dosing, as seen in the study, seems to ameliorate this. This is at the cost of short term height velocity though. We still do not understand how the desensitization may differ in other tissues, so it everyday dosing could maybe be considered if you believe your plates are soon to close and you want to max out height velocity during this time. Please keep in mind that the doses were equated, meaning double the dose once every other day. (as an example, from 3 IU's everyday, to 6 IU's every other day).

View attachment 3026171

Another (theoretical) way this problem could be solved is through the use of peptidyl (not MK-677) growth hormone secretagogues and GHRH analogs. These peptides (especially in combination) seem to produce a spike much more similar to endogenous production. This (again, in theory) could mitigate desensitization and lead to better height gains. This is also combining with the multiple molecular weights your pituitary releases in response to the peptides as opposed to the 22 kDa exogenous hGH but that might be for a different thread.

I am not a medical professional, nothing written here should be considered medical advice. Do your own research. Thanks for reading!

great thread

 

[ihatemySOST]

Thats why ghrp2 is the goat

 

[theübermenschboy]

I've heard on some forums (namely DatBTrue) that you could potentiate a huge spike in GH by pinning some peptides, letting them reach their peak in say 15 min or so, and then dosing exogenous hGH. Besides, isn't the negative feedback loop exerted by IGF-1? So the suppression would be chronic instead of acute

When did you read this on DatBtrue? It has been down a while

 

[axm]

When did you read this on DatBtrue? It has been down a while

I meant his threads on professionalmuscle.com

 

[theübermenschboy]

I meant his threads on professionalmuscle.com

Makes sense

 

[duduboy]

Prevention of Growth Deceleration after Withdrawal of Growth Hormone Therapy in Idiopathic Short Stature​

Meir Lampit, Ze’ev Hochberg. The Journal of Clinical Endocrinology & Metabolism, Volume 87, Issue 8, 1 August 2002, Pages 3573–3577. Published 01 August 2002.








What does this mean?

Everyday injections of exogenous hGH seem to drastically lower your body's sensitivity to its own GH secretion.

In this study, 38 ISS children were given either everyday (ED) or every other day (EoD) injections of hGH for two years (doses equated). The treatment then ceased and their heights were tracked for an additional two years after the treatment.

During hGH therapy, both groups accelerated their growth substantially:

The ED group first and second year velocity was 3.4 and 2.3 SD.

The EoD group had 3.0 and 2.0 SD for first and second year, respectively.

Over the initial six months after withdrawal of therapy, growth velocity decelerated to a low nadir –3.9 SD score for the daily therapy group, whereas it decelerated in the alternate day group to only –0.2 SD score.

During the 2 years off therapy, the latter group taking EoD injections maintained growth rates of –0.2 to –1.2 SD score, which is similar to their SD score prior to the hGH treatment. The daily group also recovered but very slowly, on the fourth semiannual evaluation off therapy. The cumulative 4-year growth velocity—2 yrs on and 2 yrs off therapy—of the alternate day group was greater than that of the daily therapy group: mean, 0.9 vs. 0.3 SD score.

At the end of the 4-yr therapy period, the adult height prediction of the EoD group was greater than that of the daily group by a mean of 6.5 cm.

Why is this?

Typically, endogenous growth hormone comes in pulses or spikes, as opposed to a sustained release over many hours as seen in exogenous administration. It seems that the issue stems from desensitization of target tissues due to the unnatural release of growth hormone when exogenously administered subcutaneously. This is despite the fact that sustained GH release is known to boost IGF-1 higher than pulsatile secretion, further proving that GH itself contributes to growth as seen in some rodent models.

What Can We Do?

Alternate day dosing, as seen in the study, seems to ameliorate this. This is at the cost of short term height velocity though. We still do not understand how the desensitization may differ in other tissues, so it everyday dosing could maybe be considered if you believe your plates are soon to close and you want to max out height velocity during this time. Please keep in mind that the doses were equated, meaning double the dose once every other day. (as an example, from 3 IU's everyday, to 6 IU's every other day).

View attachment 3026171

Another (theoretical) way this problem could be solved is through the use of peptidyl (not MK-677) growth hormone secretagogues and GHRH analogs. These peptides (especially in combination) seem to produce a spike much more similar to endogenous production. This (again, in theory) could mitigate desensitization and lead to better height gains. This is also combining with the multiple molecular weights your pituitary releases in response to the peptides as opposed to the 22 kDa exogenous hGH but that might be for a different thread.

I am not a medical professional, nothing written here should be considered medical advice. Do your own research. Thanks for reading!

isnt that pointless? because what really matters is igf1 levels, and Hgh can raise that more than any pep

 

[axm]

isnt that pointless? because what really matters is igf1 levels, and Hgh can raise that more than any pep

Roles of growth hormone and insulin-like growth factor 1 in mouse postnatal growth - PubMed

To examine the relationship between growth hormone (GH) and insulin-like growth factor 1 (IGF1) in controlling postnatal growth, we performed a comparative analysis of dwarfing phenotypes manifested in mouse mutants lacking GH receptor, IGF1, or both. This genetic study has provided conclusive...

pubmed.ncbi.nlm.nih.gov

This genetic study has provided conclusive evidence demonstrating that GH and IGF1 promote postnatal growth by both independent and common functions, as the growth retardation of double Ghr/Igf1 nullizygotes is more severe than that observed with either class of single mutant.

Both IGF-1 and GH independently increase growth. Height growth is FAR more complex than higher IGF-1 = taller.

 

[HardcoreLooksmaxxer]

Prevention of Growth Deceleration after Withdrawal of Growth Hormone Therapy in Idiopathic Short Stature​

Meir Lampit, Ze’ev Hochberg. The Journal of Clinical Endocrinology & Metabolism, Volume 87, Issue 8, 1 August 2002, Pages 3573–3577. Published 01 August 2002.








What does this mean?

Everyday injections of exogenous hGH seem to drastically lower your body's sensitivity to its own GH secretion.

In this study, 38 ISS children were given either everyday (ED) or every other day (EoD) injections of hGH for two years (doses equated). The treatment then ceased and their heights were tracked for an additional two years after the treatment.

During hGH therapy, both groups accelerated their growth substantially:

The ED group first and second year velocity was 3.4 and 2.3 SD.

The EoD group had 3.0 and 2.0 SD for first and second year, respectively.

Over the initial six months after withdrawal of therapy, growth velocity decelerated to a low nadir –3.9 SD score for the daily therapy group, whereas it decelerated in the alternate day group to only –0.2 SD score.

During the 2 years off therapy, the latter group taking EoD injections maintained growth rates of –0.2 to –1.2 SD score, which is similar to their SD score prior to the hGH treatment. The daily group also recovered but very slowly, on the fourth semiannual evaluation off therapy. The cumulative 4-year growth velocity—2 yrs on and 2 yrs off therapy—of the alternate day group was greater than that of the daily therapy group: mean, 0.9 vs. 0.3 SD score.

At the end of the 4-yr therapy period, the adult height prediction of the EoD group was greater than that of the daily group by a mean of 6.5 cm.

Why is this?

Typically, endogenous growth hormone comes in pulses or spikes, as opposed to a sustained release over many hours as seen in exogenous administration. It seems that the issue stems from desensitization of target tissues due to the unnatural release of growth hormone when exogenously administered subcutaneously. This is despite the fact that sustained GH release is known to boost IGF-1 higher than pulsatile secretion, further proving that GH itself contributes to growth as seen in some rodent models.

What Can We Do?

Alternate day dosing, as seen in the study, seems to ameliorate this. This is at the cost of short term height velocity though. We still do not understand how the desensitization may differ in other tissues, so it everyday dosing could maybe be considered if you believe your plates are soon to close and you want to max out height velocity during this time. Please keep in mind that the doses were equated, meaning double the dose once every other day. (as an example, from 3 IU's everyday, to 6 IU's every other day).

View attachment 3026171

Another (theoretical) way this problem could be solved is through the use of peptidyl (not MK-677) growth hormone secretagogues and GHRH analogs. These peptides (especially in combination) seem to produce a spike much more similar to endogenous production. This (again, in theory) could mitigate desensitization and lead to better height gains. This is also combining with the multiple molecular weights your pituitary releases in response to the peptides as opposed to the 22 kDa exogenous hGH but that might be for a different thread.

I am not a medical professional, nothing written here should be considered medical advice. Do your own research. Thanks for reading!

So then stay on HGH forever HGH is basically pointless in high doses after you’re done growing so you just need to inject 2-4IU a day and you’ll be fine

 

[introvertedextrover]

@Zagro i dnr ts is this legit or can i pin ed

 

[idnap]

Prevention of Growth Deceleration after Withdrawal of Growth Hormone Therapy in Idiopathic Short Stature​

Meir Lampit, Ze’ev Hochberg. The Journal of Clinical Endocrinology & Metabolism, Volume 87, Issue 8, 1 August 2002, Pages 3573–3577. Published 01 August 2002.








What does this mean?

Everyday injections of exogenous hGH seem to drastically lower your body's sensitivity to its own GH secretion.

In this study, 38 ISS children were given either everyday (ED) or every other day (EoD) injections of hGH for two years (doses equated). The treatment then ceased and their heights were tracked for an additional two years after the treatment.

During hGH therapy, both groups accelerated their growth substantially:

The ED group first and second year velocity was 3.4 and 2.3 SD.

The EoD group had 3.0 and 2.0 SD for first and second year, respectively.

Over the initial six months after withdrawal of therapy, growth velocity decelerated to a low nadir –3.9 SD score for the daily therapy group, whereas it decelerated in the alternate day group to only –0.2 SD score.

During the 2 years off therapy, the latter group taking EoD injections maintained growth rates of –0.2 to –1.2 SD score, which is similar to their SD score prior to the hGH treatment. The daily group also recovered but very slowly, on the fourth semiannual evaluation off therapy. The cumulative 4-year growth velocity—2 yrs on and 2 yrs off therapy—of the alternate day group was greater than that of the daily therapy group: mean, 0.9 vs. 0.3 SD score.

At the end of the 4-yr therapy period, the adult height prediction of the EoD group was greater than that of the daily group by a mean of 6.5 cm.

Why is this?

Typically, endogenous growth hormone comes in pulses or spikes, as opposed to a sustained release over many hours as seen in exogenous administration. It seems that the issue stems from desensitization of target tissues due to the unnatural release of growth hormone when exogenously administered subcutaneously. This is despite the fact that sustained GH release is known to boost IGF-1 higher than pulsatile secretion, further proving that GH itself contributes to growth as seen in some rodent models.

What Can We Do?

Alternate day dosing, as seen in the study, seems to ameliorate this. This is at the cost of short term height velocity though. We still do not understand how the desensitization may differ in other tissues, so it everyday dosing could maybe be considered if you believe your plates are soon to close and you want to max out height velocity during this time. Please keep in mind that the doses were equated, meaning double the dose once every other day. (as an example, from 3 IU's everyday, to 6 IU's every other day).

View attachment 3026171

Another (theoretical) way this problem could be solved is through the use of peptidyl (not MK-677) growth hormone secretagogues and GHRH analogs. These peptides (especially in combination) seem to produce a spike much more similar to endogenous production. This (again, in theory) could mitigate desensitization and lead to better height gains. This is also combining with the multiple molecular weights your pituitary releases in response to the peptides as opposed to the 22 kDa exogenous hGH but that might be for a different thread.

I am not a medical professional, nothing written here should be considered medical advice. Do your own research. Thanks for reading!

Are you stupid?
The already idiopathically short children due to their suboptimal GH efficiency went back to having suboptimal GH efficiency after they stopped pinning?

 

[axm]

Are you stupid?
The already idiopathically short children due to their suboptimal GH efficiency went back to having suboptimal GH efficiency after they stopped pinning?

What are you even trying to say?

Over the initial six months after withdrawal of therapy, growth velocity decelerated to a low nadir –3.9 SD score for the daily therapy group, whereas it decelerated in the alternate day group to only –0.2 SD score.

Only the ED group lost sensitivity (growth decelerated after therapy). Also, idiopathic literally means no known cause so it won't always be "suboptimal GH efficiency" whatever the fuck that means

So then stay on HGH forever HGH is basically pointless in high doses after you’re done growing so you just need to inject 2-4IU a day and you’ll be fine

I guess bro

 

[duduboy]

hgh increases igf1 if you take it with aromasin it will increase your height (correct me if im wrong)

Roles of growth hormone and insulin-like growth factor 1 in mouse postnatal growth - PubMed

To examine the relationship between growth hormone (GH) and insulin-like growth factor 1 (IGF1) in controlling postnatal growth, we performed a comparative analysis of dwarfing phenotypes manifested in mouse mutants lacking GH receptor, IGF1, or both. This genetic study has provided conclusive...

pubmed.ncbi.nlm.nih.gov

Both IGF-1 and GH independently increase growth. Height growth is FAR more complex than higher IGF-1 = taller.

should I take 300mcg of cjc no dac and 300mcg of ghrp2 so? I want to take hgh (15ui) after 4 months of that, what do you think?

 

[Zagro]

@Zagro i dnr ts is this legit or can i pin ed

It’s a retarded post you can pin everyday, this would only be a problem for those taking it for multiple years and even then it still works

 

[Zagro]

What are you even trying to say?

Only the ED group lost sensitivity (growth decelerated after therapy). Also, idiopathic literally means no known cause so it won't always be "suboptimal GH efficiency" whatever the fuck that means



I guess bro

There’s almost always a reason behind ISS

 

[axm]

There’s almost always a reason behind ISS

Controversies in the Definition and Treatment of Idiopathic Short Stature (ISS) - PMC

The term idiopathic short stature (ISS) refers to short children with no identifiable disorder of the growth hormone (GH)/insulin like growth factor (IGF) axis and no other endocrine, genetic or organ system disorder. This heterogeneous group of ...

pmc.ncbi.nlm.nih.gov

Shortness is defined as a condition in which the height of the individual is 2 SD below the corresponding mean height for a given age, sex and population group.1 Therefore, short stature is defined on the basis of a statistical cut−off point which does not automatically imply the presence of an underlying pathology. Height distributes in a definite population according to a Gaussian curve in which subjects with a height <−2 SD can either be considered as the necessary 2.3% shortest part of the normal distribution, or as individuals with a disorder that restricts growth.(5)

It's literally defined as 2 SD below mean. You can be perfectly healthy and qualify for ISS.

 

[pslgod15]

i read every molecule

 

[Zagro]

Controversies in the Definition and Treatment of Idiopathic Short Stature (ISS) - PMC

The term idiopathic short stature (ISS) refers to short children with no identifiable disorder of the growth hormone (GH)/insulin like growth factor (IGF) axis and no other endocrine, genetic or organ system disorder. This heterogeneous group of ...

pmc.ncbi.nlm.nih.gov

It's literally defined as 2 SD below mean. You can be perfectly healthy and qualify for ISS.

Doesn’t change the fact that arguably half of them actually have issues and the rest are just literal short kids cause majority of ISS do reach FAH or NFAH

There are multiple causes found in “ISS” mostly insensitivities to IGF-1/GH and mutations in genes so its issues at the molecular level which are hard to detect

Genetics of Short Stature - PMC

Short stature is a common and heterogeneous condition which is often genetic in etiology. For most children with genetic short stature, the specific molecular causes remain unknown, but with advances in exome/genome sequencing and bioinformatics ...

pmc.ncbi.nlm.nih.gov

Diagnostic yield of a multigene sequencing approach in children classified as idiopathic short stature - PMC

Most children with short stature remain without an etiologic diagnosis after extensive clinical and laboratory evaluation and are classified as idiopathic short stature (ISS). This study aimed to determine the diagnostic yield of a multigene ...

pmc.ncbi.nlm.nih.gov

 

[axm]

Doesn’t change the fact that arguably half of them actually have issues and the rest are just literal short kids cause majority of ISS do reach FAH or NFAH

There are multiple causes found in “ISS” mostly insensitivities to IGF-1/GH and mutations in genes so its issues at the molecular level which are hard to detect

Genetics of Short Stature - PMC

Short stature is a common and heterogeneous condition which is often genetic in etiology. For most children with genetic short stature, the specific molecular causes remain unknown, but with advances in exome/genome sequencing and bioinformatics ...

pmc.ncbi.nlm.nih.gov

Diagnostic yield of a multigene sequencing approach in children classified as idiopathic short stature - PMC

Most children with short stature remain without an etiologic diagnosis after extensive clinical and laboratory evaluation and are classified as idiopathic short stature (ISS). This study aimed to determine the diagnostic yield of a multigene ...

pmc.ncbi.nlm.nih.gov

It is true that seemingly ISS children would have growth pathologies due to the multi factorial nature of the normal distribution, but my overall point still stands in the study. It was an RCT and only the ED group lost sensitivity after treatment, while the EoD wasn’t effected. The likelihood that the ED group were ISS children ALL with GH specific pathologies related to their height is very unlikely. That’s the point of the trial.

During the 2 years off therapy, the latter group taking EoD injections maintained growth rates of –0.2 to –1.2 SD score, which is similar to their SD score prior to the hGH treatment. The daily group also recovered but very slowly, on the fourth semiannual evaluation off therapy. The cumulative 4-year growth velocity—2 yrs on and 2 yrs off therapy—of the alternate day group was greater than that of the daily therapy group: mean, 0.9 vs. 0.3 SD score

 

[Zagro]

It is true that seemingly ISS children would have growth pathologies due to the multi factorial nature of the normal distribution, but my overall point still stands in the study. It was an RCT and only the ED group lost sensitivity after treatment, while the EoD wasn’t effected. The likelihood that the ED group were ISS children ALL with GH specific pathologies related to their height is very unlikely. That’s the point of the trial.

And my point still also stands nigga, you’re acting as if it becomes instantly useless after a weeks of daily usage its a 30% decrease after one year of treatment

This is already known and water info

 

[axm]

you’re acting as if it becomes instantly useless after a weeks of daily usage

No I'm not. The treatment lasted 2 years in both groups. Not sure where you get "weeks" from.

its a 30% decrease

At the end of the 4-yr therapy period, the adult height prediction of the EoD group was greater than that of the daily group by a mean of 6.5 cm.

Not sure where you're getting 30% from either.

At the end of the day, most studies on ISS are on children (3-9 yrs old in this study) where doses are high and treatment last for years. Hardly applicable to teenagers running some stuff for a few months anyway. I thought this study would be interesting and perhaps help some people.

Why are you so offended anyway? Maybe get your e2 checked? It's not like I insulted you or anything.

 

[Zagro]

No I'm not. The treatment lasted 2 years in both groups. Not sure where you get "weeks" from.


Not sure where you're getting 30% from either.

At the end of the day, most studies on ISS are on children (3-9 yrs old in this study) where doses are high and treatment last for years. Hardly applicable to teenagers running some stuff for a few months anyway. I thought this study would be interesting and perhaps help some people.

Why are you so offended anyway? Maybe get your e2 checked? It's not like I insulted you or anything.

You literally have no idea what you’re talking about

I said weeks because no fucking teenager here even has more than 2 years of longitudinal growth left so they wont even reach a point where “desentisation” will matter

You also don’t even know how it happens i assume, its because of SOCS2/3 and it has been seen that when its over expressed there’s 30% less growth. It takes one year to reach this 30% mark thats why i said 30% fucking faggot grey

You need to dose higher as a healthy individual to see effects and no one should run it for a few months as they will see almost zero difference in FAH, this thread helped no one kill yourself

Because i have to argue with fucking morons like you every other week and funny fact my e2 is nuked but I’m on a gram of 19-nors you fucking natural twink

“Yes bro dose EOD for less efficiency almost as if we all use rhGH for 4 years+ like the kids with ISS/GHD!”

There’s like 4 threads just like this one