CJC-1295/GHRP-6 doses/duration?

[Swifto]

The study abstract you posted has NOTHING to do with gender differences, all it says is that the mass of Gh secreted (basically amount) is higher in females than males, and that its not as regular as male gh secretion. has nothing to do with what i stated previously.

Neuroendocrine control of pulsatile growth hormone release in the human: relationship with gender

Tell me you're joking.

Its states that the AMOUNT of a single GH burst is larger (in females).

It states the FREQUENCY is "less orderly" indicating, less constant.

You're telling me you dont understand that and that it doesn't contradict your previous statement of, "In males GH is released in spikes, in females its more of a constant release..."?

[Lemonada8]

Neuroendocrine control of pulsatile growth hormone release in the human: relationship with gender
Tell me you're joking.
Its states that the AMOUNT of a single GH burst is larger (in females).
It states the FREQUENCY is "less orderly" indicating, less constant.
You're telling me you dont understand that and that it doesn't contradict your previous statement of, "In males GH is released in spikes, in females its more of a constant release..."?

Orderly has nothing to do with 'constancy'. It is saying that there is no 'order' to the GH pulses in women when compared to men. Men have a large nocturnal GH pulse with much smaller pulses throughout the day. Women, on the other hand, have smaller amplitude pulses but a higher interpulse level throughout the day. they use 'orderly' because it doesnt follow the large nocturnal pulse (aka spike) like shown in males. Basically, it doesnt have a pattern like males show, so it has less order to pulses, so it is 'less orderly'. This is the general consensus on GH pulses. So no, it doesnt contradict my original statement. I really dont have time to try and argue this, im in the midst of finals. If you want a better expanation, go read dats board on the pulsation topic.

If you go back to the 2nd article i posted and look at figure 2, it is showing exactly what i am saying. Ill post an image of that figure. Here is what it says in the text about it. And since its a full free text from pubmed, it should be accessible to everyone. I forgot to add this: The subjects recieved saline infusion.


"The mean (6SE) GH concentrations for the
eight men and eight women are given in Fig. 2. The 24-h profiles
in men were characterized by the presence of a dominant
nocturnal pulse with much smaller pulses at other times of the
day. In contrast, GH secretion in women was more continuous,
with pulses of similar amplitude throughout the 24 h."

"We have compared pulsatile GH secretion profiles in young men and women in the baseline state and during a continuous intravenous infusion of recombinant human insulin-like growth factor I (rhIGF-I)."
Again, did you miss that bit?
I have outlined the differences in healthy males and females (women premenstral) and you've done what exactly...?
Take your blinkers off and try reading all of the study, specifically its "methods", not just what you want to read to "prove a point".

Well, since IGF1 is a negative feedback to GH release, and as shown below, exogenous IGF1 seems to block the negative feedbach for GH release. So without that feedback it still shows what i said.
Take your own advice and take the blinkers off. And women premenstral... seriously? thats pre-puberty, so not really applicable here, and same with the males used.. in pre-puberty. Infact they were Premature Infants...
At the end of that study, it acknowledges that aspect and provides a possible reason with not having the right response to negative feedback amount of somatostatin.

I saw what you are trying to say about estrogen and GH but the part you posted didnt really do much at all. I copied and pasted a section from the route of oestrogen delivery, which i think would be better understood by those here reading what is posted and w/o access to the full study.

Oral administration of oestrogen tends to decrease plasma IGF-I levels and increase GH secretion.47- 51 In
contrast, in some studies, transdertnal oestrogen delivery did not stimulate the GH axis. 52•53 A more recent
investigation, however, using higher doses of transdermal oestrogen, found that both oral and
percutaneous oestradiol stimulate pulsatile GH secretion and reduce circulating IGF-I concentrations. 51 Thus,
current evidence suggests that appropriate amounts of oral and transdermal oestrogen can diminish IGF-1
negative feedback by redudng plasma IGF-I concentrations, and perhaps thereby augment pulsatile GH
secretion. However, intravenous infusion of IGF-I has not been given to test this hypothesis directly. Thus,
additional actions of oestrogen are not excluded; for example, oestrogen may increase the central drive of the
GH axis via GHRH, GHRPs, etc. (with or without concomitantly decreased somatostatin tone). In addition, the preovulatory phase of the normal menstrual cycle and the maximal pubertal growth phase are both marked by hypersomatotrophism (increased mean serum GH
concentrations and daily GI-l secretion rates) and concomitantly higher plasma IGF-I concentrations.17•54
This pattern is seen not only in these two physiological states in women, and after testosterone injection in
men, 55-57 but also in acromegaly or in states in which the GH axis is driven pharmacologically (e.g. after pulsatile
or continuous GHRH infusions). (For review, see Giustina and Veldhuis.3) Thus, whereas a component of the
mechanism of action of orally replaced oestrogen is via presumptive partial withdrawal of the negative-feedback effect of IGF-I, the physiologically hyperoestrogenaemic states of the late follicular phase in young women and
during maximal growth in pubertal girls apparently Gender and GH release stimulate the hypothalamic-pituitary- IGF-1 axis centrally,
resulting in concerted increases in both GH and IGP-1.

Basically saying that estrogen can diminish some of the negative feedback of GH regulation, resulting in increased GH release.
This was also suggested in another study, because it compared the menstrual cycle and associated estrogen levels. And later in the menstrual cycle, when estrogen increases the GH pulses become more frequent rather than a larger amplitude.

[Swifto]

Orderly has nothing to do with 'constancy'. It is saying that there is no 'order' to the GH pulses in women when compared to men. Men have a large nocturnal GH pulse with much smaller pulses throughout the day. Women, on the other hand, have smaller amplitude pulses but a higher interpulse level throughout the day. they use 'orderly' because it doesnt follow the large nocturnal pulse (aka spike) like shown in males. Basically, it doesnt have a pattern like males show, so it has less order to pulses, so it is 'less orderly'. This is the general consensus on GH pulses. So no, it doesnt contradict my original statement. I really dont have time to try and argue this, im in the midst of finals. If you want a better expanation, go read dats board on the pulsation topic.

I also do not have time to argue the definition of "constant". Clearly, you dont understand.

Debating with you is like banging my f*cking head against a wall whilst you "try to prove a point".

Go knock yourself out.

Or better, go give women advice on Winstrol and "how they cant take it becuase dont have DHT receptors".

If you go back to the 2nd article i posted and look at figure 2, it is showing exactly what i am saying. Ill post an image of that figure. Here is what it says in the text about it. And since its a full free text from pubmed, it should be accessible to everyone. I forgot to add this: The subjects recieved saline infusion.


I've pointed out to flaws in your "studies", yet you seem to ignore them or think that being "GH deficient" and being given "IV GH" has no impact here.

You dont think studies in healthy adult males and females are relevant and wrong.

Are you GH dificient and do you inject IV GH?

I've just hit another brick wall.

"The mean (6SE) GH concentrations for the
eight men and eight women are given in Fig. 2. The 24-h profiles
in men were characterized by the presence of a dominant
nocturnal pulse with much smaller pulses at other times of the
day. In contrast, GH secretion in women was more continuous,
with pulses of similar amplitude throughout the 24 h."

See above.

Well, since IGF1 is a negative feedback to GH release, and as shown below, exogenous IGF1 seems to block the negative feedbach for GH release. So without that feedback it still shows what i said.
Take your own advice and take the blinkers off. And women premenstral... seriously? thats pre-puberty, so not really applicable here, and same with the males used.. in pre-puberty. Infact they were Premature Infants...
At the end of that study, it acknowledges that aspect and provides a possible reason with not having the right response to negative feedback amount of somatostatin.

I'll come back to this later as I'm on my phone.

Again, your study has its flaws.

"premenstral" was a typo, I meant "premenomausal", but you didnt even spot that did you. The study I posted was on "premenomausal".

Did you actually take the time to read the study?

I saw what you are trying to say about estrogen and GH but the part you posted didnt really do much at all. I copied and pasted a section from the route of oestrogen delivery, which i think would be better understood by those here reading what is posted and w/o access to the full study.

I have more info. on this, again, I'm on my phone...

Basically saying that estrogen can diminish some of the negative feedback of GH regulation, resulting in increased GH release.
This was also suggested in another study, because it compared the menstrual cycle and associated estrogen levels. And later in the menstrual cycle, when estrogen increases the GH pulses become more frequent rather than a larger amplitude.

bolds