MESO-Rx
Anabolic Steroids
Natural GH level suppression during exogenous supplementation
- Thread starter bigtex69
- Start date
johnnyBALLZ
New Member
I did a lot of research on this awhile back, the only reason not to take it everyday would be money..
hotdog23
New Member
A very thorough well controlled 4 year study published on
The Journal of Clinical Endocrinology & Metabolism Vol. 87, No.8
clearly shows every other day (EOD) hGH injections to be much more beneficial in
the long run to everyday injections. Everyday injections seems to drastically lower
your body's sensitivity to it's own GH secretion. The study included children with idiopathic
short stature, but can be ever casting on us, normal non-deficient hGH individuals who
may use hGH periodically for bodybuilding, sports and health purposes.
The 38 children were divided into 2 groups:
Group I received daily hGH injections.
Group II received alternate day hGH injections.
It is important to note that the total weekly dosage of hGH
was the same for both groups.
Both groups received the hGH therapy contiguously for 2 years.
Their natural growth was followed for an additional 2 years after hGH therapy ended.
They were all measured at 3-month intervals during the 4 years period (2 years
with hGH therapy and 2 years after). Their Serum GH was measured by double antibody RIA kit.
During hGH therapy, both groups accelerated their growth substantially.
Group I receiving the daily hGH injections first & second year velocity was 3.4 and 2.3 SD
Group II receiving the alternate hGH inj. had 3.0 and 2.0 SD for first and second year respectively.
Over the initial 6 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 later 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 (2yrs 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 alternate day group was greater
than that of the daily group by a mea of 6.5cm (that's over 2.5" in height, quite a lot of difference)
In even simpler English, to translate what it may mean to us is that using hGH everyday will only
negligibly give better short-term results. Yet using alternate day hGH will give radically better long-term
results and much better recovery. As the body may get back to homeostasis much faster.
Remember the two groups got the same weekly total hGH dosage,
so your every other day hGH injections would be twice as if you used
it every day.
The researchers said, the dose was of less impotency than the schedule of the injections.
Daily hGH therapy for 3 years caused subnormal growth persisting for 1.5 years (very bad)
It may be that the problem is not enough hGH or IGF-1 secretion but rather
the body's decreased sensitivity to it. The interesting part is that the serum GH levels
and serum IGF-I and IGF-binding protein remained unaffected or relatively mutely affected.
Even your body's endogenous pulsatile secretion of GH resumes within just days
even after long-term hGH therapy.
The researchers hypothesis is that the tolerance may be in the "GH signal transduction in
selective target organs in response to the disappearance of the unique pulsatile
pattern of serum GH during GH therapy". You see, hGH taken via sc injections
do not imitate the your body's own GH secretion.
"Indeed, daily sc administration of GH results in an unphysiological serum GH profile, with peak
levels at 4 h and a slow decline over the course of the following 12–24 h. This pattern can be
regarded as continuous administration, rather than the physiological GH pulses,
with a frequency of about eight per day."
"Assuming that the withdrawal syndrome is related to tolerance that might have developed toward
hGH or IGF-I, we tried to prevent it by alternate day treatment. Moreover, hGH doses used in
therapy often stimulate IGF-I to supraphysiological serum levels, suggesting that target
tissues IGF-I may also be higher than normal. The mechanism seems, therefore, to rest
with hGH and IGF-I action at their target tissues. We now show that alternate day therapy
with hGH in children with an intact GH-IGF-I axis prevents the withdrawal syndrome"
Researchers mark the analogy to another endocrine tolerance and withdrawal syndrome:
"alternate day therapy with glucocoricoids prevents tolerance to that hormone to a substantial degree,
"Interestingly, glucocoricoids withdrawal syndrome can also occur while the ..... Blah blah blah you get the point. Found this on another forum, it's what got me into EOD but I use peptides on my non-GH days
The Journal of Clinical Endocrinology & Metabolism Vol. 87, No.8
clearly shows every other day (EOD) hGH injections to be much more beneficial in
the long run to everyday injections. Everyday injections seems to drastically lower
your body's sensitivity to it's own GH secretion. The study included children with idiopathic
short stature, but can be ever casting on us, normal non-deficient hGH individuals who
may use hGH periodically for bodybuilding, sports and health purposes.
The 38 children were divided into 2 groups:
Group I received daily hGH injections.
Group II received alternate day hGH injections.
It is important to note that the total weekly dosage of hGH
was the same for both groups.
Both groups received the hGH therapy contiguously for 2 years.
Their natural growth was followed for an additional 2 years after hGH therapy ended.
They were all measured at 3-month intervals during the 4 years period (2 years
with hGH therapy and 2 years after). Their Serum GH was measured by double antibody RIA kit.
During hGH therapy, both groups accelerated their growth substantially.
Group I receiving the daily hGH injections first & second year velocity was 3.4 and 2.3 SD
Group II receiving the alternate hGH inj. had 3.0 and 2.0 SD for first and second year respectively.
Over the initial 6 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 later 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 (2yrs 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 alternate day group was greater
than that of the daily group by a mea of 6.5cm (that's over 2.5" in height, quite a lot of difference)
In even simpler English, to translate what it may mean to us is that using hGH everyday will only
negligibly give better short-term results. Yet using alternate day hGH will give radically better long-term
results and much better recovery. As the body may get back to homeostasis much faster.
Remember the two groups got the same weekly total hGH dosage,
so your every other day hGH injections would be twice as if you used
it every day.
The researchers said, the dose was of less impotency than the schedule of the injections.
Daily hGH therapy for 3 years caused subnormal growth persisting for 1.5 years (very bad)
It may be that the problem is not enough hGH or IGF-1 secretion but rather
the body's decreased sensitivity to it. The interesting part is that the serum GH levels
and serum IGF-I and IGF-binding protein remained unaffected or relatively mutely affected.
Even your body's endogenous pulsatile secretion of GH resumes within just days
even after long-term hGH therapy.
The researchers hypothesis is that the tolerance may be in the "GH signal transduction in
selective target organs in response to the disappearance of the unique pulsatile
pattern of serum GH during GH therapy". You see, hGH taken via sc injections
do not imitate the your body's own GH secretion.
"Indeed, daily sc administration of GH results in an unphysiological serum GH profile, with peak
levels at 4 h and a slow decline over the course of the following 12–24 h. This pattern can be
regarded as continuous administration, rather than the physiological GH pulses,
with a frequency of about eight per day."
"Assuming that the withdrawal syndrome is related to tolerance that might have developed toward
hGH or IGF-I, we tried to prevent it by alternate day treatment. Moreover, hGH doses used in
therapy often stimulate IGF-I to supraphysiological serum levels, suggesting that target
tissues IGF-I may also be higher than normal. The mechanism seems, therefore, to rest
with hGH and IGF-I action at their target tissues. We now show that alternate day therapy
with hGH in children with an intact GH-IGF-I axis prevents the withdrawal syndrome"
Researchers mark the analogy to another endocrine tolerance and withdrawal syndrome:
"alternate day therapy with glucocoricoids prevents tolerance to that hormone to a substantial degree,
"Interestingly, glucocoricoids withdrawal syndrome can also occur while the ..... Blah blah blah you get the point. Found this on another forum, it's what got me into EOD but I use peptides on my non-GH days
HuckingFuge
New Member
the study is talking about bone growth for adolescents with deficient HGH production in the first place and not muscle growth for fully grown men and women with properly functioning HGH. nice read, but I'm sure doesn't effect a fully grown man or woman the same way.
hotdog23
New Member
Agreed not perfectly translatable but if you ever plan on coming off growth it's something to think about. I've seen more than a couple IGF tests that had levels UNDER 100 for youngish guys after coming off a long GH run. I don't know how long those numbers stayed low tho
HuckingFuge
New Member
your HGH drops with age, just like Test. HGH drops sooner than Test drops. the bad thing is HGH costs out the ass and Test is cheap, so easier to do TRT over HRT.
90-8-08-080-8=08=0809759807867hjbhcturdy87r9rp9ghig75difyugiug86fiuuubouiugoutd
Hmm what's missing? Why didn't the authors evaluate GNRH levels rather than IGF and or GH.
What may also have been overlooked (I say MAY bc I've not yet reviewed the study) is the RIA assay ONLY provides data on the the 22KD GH yet to determine whether HTPA responsiveness to GNRH has occurred BOTH the 22KD and 20KD GH subunits MUST be measured!
The point is the authors did not perform an assay which adequately evaluates HTPA recovery from GH supplementation, the latter requiring only a few days.
jim
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That's NOT my opinion mate, (I underlined the answer) but rather evidence based. Perhaps another just as important question, what is the interval for IGF levels to return to baseline post GH supplementation!
Oh sorry we miscommunicated BUT since the half life of GH is SOOOO short (minutes) I would tend to believe more frequent injections would be more apt to maintain SS levels and for this reason I use A QD dosing schedule.
hotdog23
New Member
Wat? They only brought up hpta as an analogy. Did u read the study?
And what is 20KD? Molecular weight? Cuz 20kd isn't even hgh
Excuse me if I'm being dense but you are making zero sense
That's the whole subtext of what I posted. Do you have any related info on this topic? I think this is what we are all after
Thanks
GH is secreted by the pituitary under the influence of GNRH thus there IS a HTPA relationship between the two which is quite similar to AAS absent the gonads.
Moreover endogenous GH is secreted by the pituitary in "TWO primary FORMS" the active 22kd MW hormone AND a 20kd inactive polypeptide.
This difference can be used to identify when endogenous GH production resumes or one could measure GNRH levels BUT using changes in supplemented rHGH levels or IGF to determine the resumption of endogenous GH secretion or effectiveness of therapy can skew the data significantly AND I DONT KNOW IF THE AUTHORS "OVERLOOKED" THAT POSSIBILITY.
Thats bc I have not YET read the study which I already mention in my post, thus my comments were limited to what appears to be the abstract that you posted.
Nonetheless pose your question in more specific terms and I'll try to elaborate further.
Moreover endogenous GH is secreted by the pituitary in "TWO primary FORMS" the active 22kd MW hormone AND a 20kd inactive polypeptide.
This difference can be used to identify when endogenous GH production resumes or one could measure GNRH levels BUT using changes in supplemented rHGH levels or IGF to determine the resumption of endogenous GH secretion or effectiveness of therapy can skew the data significantly AND I DONT KNOW IF THE AUTHORS "OVERLOOKED" THAT POSSIBILITY.
Thats bc I have not YET read the study which I already mention in my post, thus my comments were limited to what appears to be the abstract that you posted.
Nonetheless pose your question in more specific terms and I'll try to elaborate further.
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hotdog23
New Member
Hmm never heard of gonadotropin releasing hormone having anything to do with this... Ghrh coupled with somastatin inhibition was the primary mechanism for growth hormone from my limited understanding.
Ok my question aligns with the OP and your post about IGF returning to baseline. Does exogenous synthetic suppress ghrh/ghrelin and natural pituitary output during use? How long does this suppression linger upon cessation? When can we expect full recovery and baseline levels of IGF-1?
Ok my question aligns with the OP and your post about IGF returning to baseline. Does exogenous synthetic suppress ghrh/ghrelin and natural pituitary output during use? How long does this suppression linger upon cessation? When can we expect full recovery and baseline levels of IGF-1?
No I've not forgotten ya HD but since you posed several questions that I oversimplified, (such as using the misnomer "gonadotropin" rather than the more appropriate term which is an "hepatotropin) in an attempt to relay a CONCEPT about how the physiologic control mechanisms of AAS and GH are actually quite similar in many respects.
I believe approaching a topic of this nature in such a manner (while I agree, IF one reads between the lines, it may also create a certain degree of confusion) can be very helpful since MOST AAS users have a relatively solid understanding of GONADAL/HPTA functioning.
Consequently comparing the former to the (GHRF-GH-IGF) HEPATIC/HTPA feedback loop, simplifies that which is most important and better enables the reader to comprehend why alterations in any part of EITHER feedback loop may effect another component.
Actually the control somatostatin exerts on GHRF is prototypical of an ULTRA SHORT FEEDBACK LOOP. This particular control mechanism results in the predominantly pulsitile nature of GH secretion bc the interaction is a local phenomena between the neurohypophysis and the anterior pituitary.
Of course there are significant differences between the above and the control of GH secretion as regulated by IGF and it's influence on GHRF levels, the latter being an example of a long feedback loop.
I hope that clarifies some of the confusion I created earlier by using the comparative term "gonadotropin" and HTPA.
I'll be back to elaborate further on the questions you posed with evidence based citations where applicable and if possible.
Regs
JIM
I believe approaching a topic of this nature in such a manner (while I agree, IF one reads between the lines, it may also create a certain degree of confusion) can be very helpful since MOST AAS users have a relatively solid understanding of GONADAL/HPTA functioning.
Consequently comparing the former to the (GHRF-GH-IGF) HEPATIC/HTPA feedback loop, simplifies that which is most important and better enables the reader to comprehend why alterations in any part of EITHER feedback loop may effect another component.
Actually the control somatostatin exerts on GHRF is prototypical of an ULTRA SHORT FEEDBACK LOOP. This particular control mechanism results in the predominantly pulsitile nature of GH secretion bc the interaction is a local phenomena between the neurohypophysis and the anterior pituitary.
Of course there are significant differences between the above and the control of GH secretion as regulated by IGF and it's influence on GHRF levels, the latter being an example of a long feedback loop.
I hope that clarifies some of the confusion I created earlier by using the comparative term "gonadotropin" and HTPA.
I'll be back to elaborate further on the questions you posed with evidence based citations where applicable and if possible.
Regs
JIM
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That's all fine and dandy Dr. Jim, but can you please type "hpta" and "ghrf" and "igf" and "aas" in lower-case instead? I feel rather offended by all these insulting upper case words.
Thanks
j/k
Thanks
j/k
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