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Minimalus tarpai tarp suviu 3h.
Kiekis ir leidimo laikas priklauso nuo konkreciu tikslu,geriau leistis po maziau bet daugiau kartu.
Maksimalus efektas isgaunamas vartojant GHRH+GHRP.(Pvz: MOD-GRF+GHRP-2), po viena juos vartoti neefektyvu.
Pradzioje galima pavartoti viena kart per diena,pries miega. Jei viskas gerai dadedam karta ryte, ar po treniruotes.Pvz: GHRH 100mcg+GHRP 100mcg einant miegot,galima pradeti ir nuo 50/50mcg.
Dozuoji tiek kiek tavo kisene leidzia, o ne kazkokiam forume kazkas kabliuoja+ dar pajunges 1g testo, daugiau nereiskia geriau, realiai jauciasi ir 50/50mcgx2 dienoj.
Nevalgykit angliu  30min. pries saunant ir po bent 30min.
Pagereja miegas, atsistatymas po treniruotes, pamazinus kcl po truputi tirpsta riebalas, nebeskauda sanariu.
Gali truputi pritraukt vandens
Geriau nevartoti CJC1295-DAC.
Vien peptidu raumenu auginimui nelabai kas vartoja prie ju jungia AAS.

Paskutinį kartą taisė MBQuart (2012-09-10 16:14)

MBQuart rašė:

Minimalus tarpai tarp suviu 3h.
Kiekis ir leidimo laikas priklauso nuo konkreciu tikslu,geriau leistis po maziau bet daugiau kartu.
Maksimalus efektas isgaunamas vartojant GHRH+GHRP.(Pvz: MOD-GRF+GHRP-2), po viena juos vartoti neefektyvu.
Pradzioje galima pavartoti viena kart per diena,pries miega. Jei viskas gerai dadedam karta ryte, ar po treniruotes.Pvz: GHRH 100mcg+GHRP 100mcg einant miegot,galima pradeti ir nuo 50/50mcg.
Dozuoji tiek kiek tavo kisene leidzia, o ne kazkokiam forume kazkas kabliuoja+ dar pajunges 1g testo, daugiau nereiskia geriau, realiai jauciasi ir 50/50mcgx2 dienoj.
Nevalgykit angliu  30min. pries saunant ir po bent 30min.
Pagereja miegas, atsistatymas po treniruotes, pamazinus kcl po truputi tirpsta riebalas, nebeskauda sanariu.
Gali truputi pritraukt vandens
Geriau nevartoti CJC1295-DAC.
Vien peptidu raumenu auginimui nelabai kas vartoja prie ju jungaia AAS.

Nori pasakyt kad tik su aas jie efektyvus raumenu augime?Jai vienus varai tai tik savijauta,atsistatymas geresnis ir po truputi tirpsta riebalas?
Palei tave tai tik tos 2 kombinacijos veza? O tarkim tradicine cjc 1295 ir ghrp-2,tai jau nekokia konbinacija?

mod grf ir yra cjc tik kitas pavadinimas: kaip kad buna anavaras-oxandrolonas ir pan..

vakar kai sushoviau doze snd tik po 11.15 prabudau

su tais valgiais, tai as pavalgau ir tada shaunu, pakyla apetitas, ir jauciu kaip virskinasi geriau, tada vel valgau, shaunu tiesiai i raumeny..  siaip yra tyrimai padaryti, bei experimentai DATbe true forume, bet lab daug knistis ir ieskot reikia..

MBQuart rašė:

rolka78 rašė:

MBQuart rašė:

Minimalus tarpai tarp suviu 3h.
Kiekis ir leidimo laikas priklauso nuo konkreciu tikslu,geriau leistis po maziau bet daugiau kartu.
Maksimalus efektas isgaunamas vartojant GHRH+GHRP.(Pvz: MOD-GRF+GHRP-2), po viena juos vartoti neefektyvu.
Pradzioje galima pavartoti viena kart per diena,pries miega. Jei viskas gerai dadedam karta ryte, ar po treniruotes.Pvz: GHRH 100mcg+GHRP 100mcg einant miegot,galima pradeti ir nuo 50/50mcg.
Dozuoji tiek kiek tavo kisene leidzia, o ne kazkokiam forume kazkas kabliuoja+ dar pajunges 1g testo, daugiau nereiskia geriau, realiai jauciasi ir 50/50mcgx2 dienoj.
Nevalgykit angliu  30min. pries saunant ir po bent 30min.
Pagereja miegas, atsistatymas po treniruotes, pamazinus kcl po truputi tirpsta riebalas, nebeskauda sanariu.
Gali truputi pritraukt vandens
Geriau nevartoti CJC1295-DAC.
Vien peptidu raumenu auginimui nelabai kas vartoja prie ju jungaia AAS.

Nori pasakyt kad tik su aas jie efektyvus raumenu augime?Jai vienus varai tai tik savijauta,atsistatymas geresnis ir po truputi tirpsta riebalas?
Palei tave tai tik tos 2 kombinacijos veza? O tarkim tradicine cjc 1295 ir ghrp-2,tai jau nekokia konbinacija?

O HGH labai efektyvus vienas raumens auginime?,
Tos kombinacijos buvo tik pvz, nori kazko daugiau domekis pats, CJC daznaiusiai tas pats kas ir MOD-GRF,tik kitu pavadinimu.

Viskas cia aisku su tais cjc ir grf.Siaip tik uzklausiau.Domiuosi as nemazai,tikrai neklausiu taves patarimo gali but ramus

beje kam idomus palyginimas hgh ir peptidu(derinio ghrp+cjc) imetu biski info:

In comparison to synthetic GH administration we find that:

22iu of synthetic GH results in 495 - 585 ng/ml
Saturation doses of GHRH & GHRP results in 130 - 170 ng/ml

These results indicate that 22iu is between 3.8 and 3.4 more efficacious then a single administration of GHRH & GHRP which means that a single dose of GHRH & GHRP has the potential to produce better then the equivalent of 5iu of GH in plasma.

A dosing protocol of GHRH + GHRP at saturation dose, administered 3 times per day has the potential to exceed the equivalent of 15iu.

Note though that using this methodology GHRP-6 at a saturation dose by itself may add the equivalent of 1.4 to 1.8 iu per administration... or 4.2 to 5.4 iu per day if administered three times.

gal yra savanoriu pavertejaut?



    What's known about GH and IGF-1 Feedback Regulation?


    The release of Growth Hormone (GH) is a regulated event. There are positive (+) signals and negative (-) signals. Signals are transmitted through neurons... if we need a simple mental image we can think of wires and attached to one end of a wire is some sort of sensor that can detect a change and at the other end of the wire is something that can do something based on receiving the information that a change has taken place. We can picture a thermometer attached to a wire. If the temperature gets too high it may trigger the sending of that information or signal down the wire. That's how the body works thanks to that wonderful area we refer to as the spinal column. In fact the entire brain and spinal column circuitry is called the Central Nervous System (CNS). Now when that information travels through that wire it ends up somewhere. In humans that somewhere is the brain and in regard to many of the hormones and actions that we are interested in, the region of the brain that receive the signals is the hypothalamus. In our example of the wire sending the temperature signal, it could be attached to a device that electronically dumps a bucket of water based on that signal. If the temperature never gets hot enough for the programmed thermometer setting, no signal is sent and no bucket is dumped. In our brains the end points of those wires are often co-localized next to hormonal secretion points.


    This is how the body can tell the brain what's going on. The brain can make a stop or go decision and communicate that by releasing hormones, stopping the release of hormones or even sending further signal elsewhere such as into the pituitary. One reason why GHRP-6 can trigger hunger as well as the release of Growth Hormone Releasing Hormone (GHRH) from the hypothalamus is that the wires trigger serveral responses one of which is triggering the Neuro Peptide Y hunger cascade.


    Obviously no one should try to become a doctor or scientist based on the above... but as an armchair scientist it suffices.


    Let's take a look at some of what is known about this topic in specific regard to GH and IGF-1 Feedback.


    There are several feedback loops (i.e. that thermometer, wire and bucket dumper). Some of the mechanisms operate on a short-term basis; others continue to exert negative feedback on GH release over the long-term.


    Short-term (physiological)


    The ultrashort feedback loops are those in which the presence of a hormone inhibits its own secretion. It's as if a nightclub room has a maximum occupancy of 100 people. When more than 100 people try to enter a signal is sent that tells some bouncer not to let any more people in. Fairly quickly people do leave the room and more are allowed to enter. GHRH, or the presence of GHRH in the very short-term can inhibit its own further secretion.1,2 GHRH is the the "go" hormone or positive growth hormone releaser. Now Somatostatin the "stop" hormone or the negative growth hormone inhibitor also will suppress its own release from neurons.3 In other words with this mechanism, these hormones actually stop their own further release. This is self inhibition and doesn't last very long at all.


    The short feedback loops involve the interplay between the "stop" and "go" hormones. There is more complexity here because this interplay occurs across both the hypothalamus in the brain and into the sack-like pituitary right below it. Remember that the brain/hypothalamus releases precursor hormones to the pituitary which then releases the actual end hormone that will circulate throughout the body often making its way to some specific organ. The brain/hypothalamus releases precursors for the hormones which will eventually interact with the thyroid, adrenal glands, ovaries/testis and the liver. In regard to the GH circuit the brain releases GHRH which goes to the pituitary and binds to the cells their which in turn release GH which makes its way to the liver where it binds to receptors and initiates certain events one of which results in the eventual release of the horomone IGF-1.


    In this short feedback loop we do not leave the brain/hypothalamus + pituitary area. The secretion of the "stop" hormone somatostatin is encouraged or stimulated directly by the presense of GHRH. If this were a nightclub room, again we have the limitation on the number of people (ultrashort feedback loop) but now we are adding the rule that there must be a female for every male in the club. So if there are a lot of males in the room (called GHRHs), the bouncer will be instructed to let in more females (called somatostatins). The presence of GHRHs directly stimulates the release of its own inhibitor somatostatin. 4 What happens when females begin to crowd the room. More males are crowded out. That rise in somatostatin directly stimulated by GHRH leads to inhibiting any further release of GHRH.5


    Now there is another factor that is able to bring about that balance. That factor is the presence of GH in the pituitary. Of all places GH could end up, when it is in the pituitary at a certain level it sends a signal to the brain/hypothalamus which inhibits hypothalamic GHRH secretion 6,7 and stimulates somatostatin release from hypothalamic neurons 8.


    As of 2011 the scientific thought on this short term feedback loop is that a hypothalamic stimulus (from GHRH, somatostatin or GH) which alters GH secretion automatically extinguishes its own effect. It is this mechanism that plays a primary role in the creation of pulsatile GHRH secretion, somatostatin secretion patterns and ultimately results in the maintenance of pulsatile GH release from the pituitary.


    It is this dynamic interaction between the pituitary and the hypothalamus and not just some sort of biological clock function in the hypothalamus itself that is important in creating the pulsatile GH release pattern.


    Now these feedback mechanisms operate on a short term basis (3 hours which result in the physiological 3 hour pulse to trough period).9,10


    There are longer-term feedback mechanisms which involve IGF-1 and are disruptive to the normal physiological response. (I use the term physiological response as meaning something like "in conformance with nature... [I seem to often imply this to be better no matter what the goal...]".


    Long-term (excessively inhibitory)


    The long-term negative feedback on GH secretion occurs through a loop involving the end product of GH action (i.e. GH binding to a receptor), the hormone IGF-1. An important point to underscore is that although both liver-derived circulating IGF-1 (endocrine) and local bone-derived IGF-1 (autocrine/paracrine/juxtacrine) can redundantly replace each other in the maintenance of normal longitudinal bone growth, locally derived IGF-1 cannot replace liver-derived IGF-1 as a regulator of GH secretion. 11 In other words it is systemic liver-made endocrine IGF-1 that creates long-term negative feedback on GH secretion and not local IGF-1. I used the term bone-derived because this understanding was derived from studies in bone. However it applies to all locally derived IGF-1. Muscle derived IGF-1 will not create a negative feedback loop hindering GH secretion and neither will local IGF-1 in any tissue, because it is made and it acts in that tissue. It will not circulate. [For other liver IGF-1 differences see the end NOTE]


    Before moving on I want to get a graph up for you. I want you to understand that natural levels of somatostatin and indeed IGF-1 play a role in keeping GH pulsatile and natural. There is often talk of suppressing somatostatin. If you do this and also if you were to suppress natural IGF-1 you raise the GH troughs. In other words you create GH bleed. In the instance of somatostatin suppression, you won't even increase the amplitude of pulses. Thus the effects of natural levels of both somatostatin and IGF-I seem be the maintenance of low GH trough levels and thereby the masculinizing effect of pulsatile GH secretion.


    The highlighted sections below represent abnormality. If we suppress somatostatin we get elevated GH troughs with a shorter pulse amplitude. If we suppress IGF-1 we get elevated troughs without an effect on pulse amplitude.


    Name: F5.medium.jpg Views: 257 Size: 82.9 KB

    The specific mechanism for precisely how IGF-1 exerts feedback is presently unknown. Note: State of knowledge 2011 It is known that regulation of IGF-1 production by GH is mediated via "signaling through the
    Janus kinase (JAK)-2 pathways, via the phosphorylation of the transcriptional factor, signal transducer, and activator of transcription (STAT)-5b" 12. But that understanding does not point to an exact site for IGF-1 negative feedback on GH secretory mechanisms. However we can look at the effect. We can see what happens when there is a rise in systemic IGF-1.


    Let's look at a continuous infusion of IGF-1 which will be similar to a long lasting analog of IGF-1. A continuous infusion of IGF-1 in young men and women increased plasma IGF-1 concentrations three to four times above the upper limit of the normal range. This reliably suppressed plasma GH concentrations by approximately 50–80% in both sexes, at the expense of grossly diminished GH pulse amplitude. 13


    Name: IGFSupression.jpg Views: 259 Size: 50.8 KB


    What happens if you administer GHRH in that IGF-1 induced GH suppressive environment? Well in the same study, administration of exogenous GHRH to the same individuals, showed a sexually dimorphic effect. In men, IGF-1 infusion grossly suppressed plasma GH response to GHRH, suggesting that the negative feedback of IGF-1 was expressed either directly at the pituitary level or at the hypothalamic level by stimulating somatostatin secretion. On the other hand, administration of exogenous IGF-1 to women was completely ineffective in suppressing their GH responses to GHRH. This suggests that, in women, elevated IGF-1 suppresses GH secretion by selective suppression of the hypothalamic GHRH output.13


    What is the lesson?

    In men somatostatin rises up when levels of IGF-1 rise. In a rising systemic (but not local) IGF-1 environment this underscores a need to suppress somatostatin and do it correctly. A GHRP (Growth Hormone Reasing Peptides) (Ipamorelin, GHRP-6, GHRP-2) is capable of doing just that and must be used. In women there is no urgency to supress somatostatin, rather GHRH is supressed and thus the need to provide Mod GRF (1-29) (the best analog of GHRH (Growth Hormone Releasing Hormone for humans). As we know both work synergistically and together have the potential to overcome some of the suppression engendered by a rise in systemic IGF-1.

    NOTE Liver derived IGF-1 plays a role in the following where as local IGF-1 does not - the regulation of a large number of other parameters including cortical bone mass, kidney size, prostate size, peripheral vascular resistance, spatial memory, sodium retention, insulin sensitivity, liver size, sexually dimorphic liver functions, and progression of some tumors.
    References:

    1 - Lumpkin MD, McDonald JK. Blockade of growth hormone-releasing factor (GRF) activity in the pituitary and hypothalamus of the conscious rat with a peptidic GRF antagonist. Endocrinology. 1989;124:1522–31.
    2 - Lumpkin MD, Mulroney SE, Haramati A. Inhibition of pulsatile growth hormone (GH) secretion and somatic growth in immature rats with a synthetic GH-releasing factor antagonist. Endocrinology. 1989;124:1154–9.
    3 - Peterfreund RA, Vale WW. Somatostatin analogs inhibit somatostatin secretion from cultured hypothalamus cells. Neuroendocrinology. 1984;39:397–402.
    4 - Mitsugi N, Arita J, Kimura F. Effects of intracerebroventricular administration of growth hormone-releasing factor and corticotropin-releasing factor on somatostatin secretion into rat hypophysial portal blood. Neuroendocrinology. 1990;51:93–6.
    5 - Yamauchi N, Shibasaki T, Ling N, Demura H. In vitro release of growth hormone-releasing factor (GRF) from the hypothalamus: somatostatin inhibits GRF release. Regul Pept. 1991;33:71–8.
    6 - Frohman MA, Downs TR, Chomczynski P, Frohman LA. Cloning and characterization of mouse growth hormone-releasing hormone (GRH) complementary DNA: increased GRH messenger RNA levels in the growth hormone-deficient lit/lit mouse. Mol Endocrinol. 1989;3:1529–36.
    7 - Chomczynski P, Downs TR, Frohman LA. Feedback regulation of growth hormone (GH)-releasing hormone gene expression by GH in rat hypothalamus. Mol Endocrinol. 1988;2:236–41.
    8 - Chihara K, Minamitani N, Kaji H, Arimura A, Fujita T. Intraventricularly injected growth hormone stimulates somatostatin release into rat hypophysial portal blood. Endocrinology. 1981;109:2279–81.
    9 - Sato M, Chihara K, Kita T, Kashio Y, Okimura Y, Kitajima N, Fujita T 1989 Physiological role of somatostatin-mediated autofeedback regulation for growth hormone: importance of growth hormone in triggering somatostatin release during a trough period of pulsatile growth hormone release in conscious male rats. Neuroendocrinology 50:139–151 Medline
    10 - Carlsson L, Jansson JO 1990 Endogenous growth hormone (GH) secretion in male rats is synchronized to pulsatile GH infusions given at 3-hour intervals. Endocrinology 126:6–10
    11 - Ohlsson C, Mohan S, Sjögren K, Tivesten A, Isgaard J, Isaksson O, et al. The role of liverderived insulin-like growth factor-I. Endocr Rev. 2009;30:494–535.
    12 - Rosenfeld RG, Hwa V. The growth hormone cascade and its role in mammalian growth. Horm Res. 2009;71 Suppl 2:36–40.
    13 - Bermann M, Jaffe CA, Tsai W, DeMott-Friberg R, Barkan AL. Negative feedback regulation of pulsatile growth hormone secretion by insulin-like growth factor I. Involvement of hypothalamic somatostatin. J Clin Invest. 1994;94:138–45.

azuolyno bicas rašė:

IGF1 Studies:

This IGF-1 Study on males subjects injected daily for 6 weeks (with either HGH alone, IGF-1 alone or IGF-1 + HGH together) indicated increased lean body mass, increased strength and decreased fat mass in all groups. An interesting point to note though was that the increases only persisted for the whole 3 months in those injecting IGF-1 + HGH, giving validity to the point that IGF-1 loses its effectiveness after a certain period of time and therefore should be used 1 month on and 1 month off to re-sensitize the muscle receptors.

http://www.annals.org/content/125/11/865.short



PEG MGF (Mechano growth factor) studies:

This 2005 MGF Scientific Report discusses the potential of the peptide to enhance physical training and also potentially be misused as a doping agent in sports due to its difficult detection. The article mentions the finding in a previous study that a single intramuscular injection of MGF into the muscle of a mouse caused a 25% increase in muscle size within just 3 weeks.

http://www.ncbi.nlm.nih.gov/pmc/arti...v039p00787.pdf



HGH Fragment 176-191 Studies:


This 2004 HGH Fragment 176-191 Study (also known as AOD9604) indicates that the peptide was highly successful at stimulating the metabolism of body fat in humans and is the first drug to ever do so - all other weight loss drugs (such as Sibutramine) contribute to loss of body weight indirectly by reducing appetite and not actually burning fat itself.
The study was conducted over 3 months at 6 different doses with one of the most interesting conclusions being that the lowest daily dose of 1mg (1000mcg) was found to be the most effective. Since the 1mg dose was taken orally, it would be the equivalent of approximately 250mcg (0.25mg) by injection. The average overall weight loss in 3 months was 3kg of fat, 300% more than for those test subjects not taking the peptide.
Additionally, unlike normal HGH injections which have negative effects on blood glucose, HGH Fragment 176-191 did not negatively effect glucose tolerance, but rather improved it and also improved cholesterol levels.

http://www.news-medical.net/news/2004/12/16/6878.aspx



CJC1295 (Mod. GRF-1-29) or GHRH Studies:

This 2005 Modified GRF 1-29 Study (referred to as GHRH 1-44) on women who injected the peptide for 90 days (3 months) indicated several key benefits of the peptide such as: an increase in Growth Hormone (GH) and IGF-1 levels; reduction in fat mass (stomach fat) and an increase in athletic physical performance (such as walking and stair climbing) - all of which occurred 100% as a result of simply taking the peptide (they did not do any special physical training or dieting in conjunction with the injections).
A 2004 Study, in men, indicated similar findings after 3 months of Modified GRF 1-29 injections: a 200% increase (doubling) of both GH and IGF-1 levels; an increase in fat free mass (muscle) as well as a reduction in abdominal fat; and an improvement of physical performance, measured by the time it took to walk 30 minutes and to ascend four flights of stairs. Once again these excellent results were achieved by the injections alone, no special diet and weight or cardio training were followed. So you can well imagine the sort of results which could be achieved with the addition of careful dieting and training.

Both studies serve to indicate 5 things:

1. CJC-1295 (Modified GRF 1-29) is anti-aging as it's a potent increaser of GH and IGF-1 levels which decline with age
2. Results don't happen overnight and you should take the product for 3 months minimum
3. The peptides are effective on their own (however results would be far superior with diet and exercise)
4. CJC-1295 Peptides are safe and have been used for many years in scientific circles
5. The peptides improve athletic performance, fat loss (particularly stomach fat) and increase muscle mass

The two studies:

2005: http://www.ncbi.nlm.nih.gov/pubmed/16260425
2004: http://j***.endojournals.org/content/89/12/6325.full


CJC1295 DAC Studies:

The following 2006 CJC-1295 DAC Study shows that the peptide is a potent and long-lasting stimulator of GH and IGF-1 levels. After just one injection of the product, GH levels increased by 200-1000% for 6 days and remained higher than normal for up to 1 month in healthy subjects aged 21-61 years.
While no studies have been undertaken to test for the fat-loss, muscle building and performance enhancing effects of CJC-1295 DAC it would be safe to assume that since it is a potent and long-lasting increaser of Growth Hormone and IGF-1 levels, all of the associated benefits indicated in the CJC-1295 (Modified GRF 1-29) studies would be realised with long term use with the added benefit of fewer injections. Additionally, with the long half-life, there is no concern regarding any potential food interactions which might cause the peptide to be less effective.
CJC-1295 DAC, with its long half-life (i.e. 1-2 weekly injections) is therefore a much more convenient alternative to GRF 1-29 and/or GHRP peptides. Furthermore, feedback from experienced users indicates it is much more effective at achieving the desired results on body composition. Since however no long-term studies have been conducted using CJC-1295 DAC, we recommend never using it for more than 6 months at a time to give your pituitary gland a break from the continual pulses of GH.

http://j***.endojournals.org/content/91/3/799.full



GHRP-6/GHRP-2 Studies:

This GHRP-6 Study makes a number of interesting conclusions about the efficiency of GHRP-6 at releasing Growth Hormone including that it is much more effective than Modified GRF 1-29 at releasing GH (although a combination of both GHRP and Modified GRF 1-29 is much more effective than either product alone). It indicates that a dosage of as little as 10mcg can induce a significant GH pulse, however a dosage of 100mcg is much more effective than 10mcg.
The following GHRP Study (the second) shows that Ipamorelin has similar effectiveness to GHRP-6 at promoting GH release at dosages of 100mcg, however unlike GHRP-6 and GHRP-2 it does so without increasing the detrimental hormones cortisol, aldosterone or prolactin which can be responsible for such negative side effects as stress, water retention and decreased sex drive.
The study also indicates that at a comparable dosage, GHRP-2 is approximately 30% more efficient at creating a GH pulse than GHRP-6 making it the strongest and most cost effective GHRP peptide.

First studie: http://www.professionalmuscle.com/fo...es-figure5.jpg
Second studie: http://www.ncbi.nlm.nih.gov/pubmed/9849822

na kad niekas man nepadeda, isskyrus google translator

rolka78 rašė:

Angliskai irgi gerai.Manau siais laikais daug kas supranta anglu kalba

as sovietu vaikis,nieks manes angliskai neismoke:D

mgf, mgf peg, igf1 lr3, hgh

kuo jie skiriasi? cjc1295  - cjc1295 dac

Laisviss rašė:

HRS rašė:

kuo jie skiriasi? cjc1295  - cjc1295 dac

Dac ilgesnis veikimas. Jo užtenka kartą, du per savaitę.
cjc be dac reiktų kasdien vartot.

Cjc 1295-DAC isvis nereikia vartoti.

Todel kad zmogaus organizme GH isskiriamas pulsacijos budu, isskyre kazkiek tam kartui  ir viskas, o susileidus DAC, GH isskyrimas pasidaro pastovus, kas nera labai gerai organizmui ir receptoriamas. Angliskai yra daug apie tai parasyta. Galima pabandyt ta DAC jei norisi, vartojant su GHRP galima ji vartot dazniau ir mazesnem dozem,  DAC dideles dozes vartojamos tada kai jis vartojamas vienas, nes ji labai greit organizmas neutralizuoja.
Nuo DAC vaikstai pastovei nutirpusiom galunem, nuo paprasto CJC nutirpsti  tik trumpam.

Paskutinį kartą taisė MBQuart (2012-10-06 16:22)