GHRP’s have been used whilst steroid cycling, but due to their nature and comparative weakness to steroids and the like, I find the best use of these compounds is during and after post cycle therapy in an attempt to keep as much of the steroid-induced gains as possible as well as helping the users mind-set as they still feel like they are ‘on’ something…sad but true. GHRP’s are also cycled in an alternate fashion with GH (and IGF), so as to keep the body’s natural GH production systems from de-sensitizing and shutting down completely…much in the same way that steroid users alternate HCG with steroids; to keep the natural testosterone system functioning optimally.
"In circumstances where a medicine is widely known to be used in connection with modifying a physiological process in persons (as appears to be the case with some SARMs and other peptide products), that medicine is likely to satisfy the definition of a therapeutic good despite any disclaimer to the effect that it is for research purposes only and/or not for human use."
Molly Hunsinger is a communications professional and certified group exercise instructor and fitness trainer. Her medical, health and fitness industry background spans nearly three decades with experience working as an instructor trainer, staff trainer, facility manager, group exercise program manager, physician relations manager and marketing director. As a media professional, she has developed and launched award-winning allied marketing and advertising campaigns for luxury retailers, leading nonprofit organizations and foundations and written numerous articles and blogs for both digital and print publications. Molly holds a bachelor’s degree in mass communications from the University of South Florida with a concentration in journalism and digital media studies.
In August 2010, the delegate confirmed the decisions of the June 2010 meeting of the NDPSC to transfer leflunomide to Appendix L. Appendix L was a new appendix created to list all of the requirements for dispensing labels previously included in the body of the Poisons Standard (i.e. paragraph 45, Dispensed Medicines, of Part 3, Miscellaneous Regulations) as part of the transitional amendments required to change the Standard for the Uniform Scheduling of Drugs and Poisons No. 24 into the Standard for the Uniform Scheduling of Medicines and Poisons No. 1, under the revised scheduling arrangements commencing 1 July 2010.
The evidence derived from these experiments supports the notion that CD36 is an active and approachable receptor to modulate the healing process. Here we have observed that CD36 occupation by GHRP-6 attenuates wound inflammation, accelerates wound closure, and above all improved wound’s esthetic outcome by impacting ECM proteins accumulation. To our knowledge these findings are unprecedented for GHRP-6 within the context of cutaneous healing.
The response to GHSs is not gender related, except during puberty, when girls exhibit a greater response than do boys. The GH responses to both GHSs and ghrelin are similar during the early-follicular, late-follicular, and luteal phases of the menstrual cycle, suggesting that they are not affected by changes in estrogen levels. However, estrogen as well as estrogen-progestin supplementation enhances the GH response to ghrelin after menopause.
But for maintenance of adequate and natural IGF-1 and growth hormone, and to achieve that sweet spot of not becoming to pro-growth while also not becoming a weak, muscle-less noodle, that sweet spot of producing adequate insulin without producing too much, and that sweet spot of increasing cellular repair without letting cellular division get “out of control”, I have indeed been implementing three specific strategies: my IGF-1 “trilogy”.
Author Contributions: Conceived and designed the experiments: JBA, AAC, DGBH, YMM, ARU, AGO, VFC, FHB, GGN. Analyzed the data: JBA, AAC, DGBH, YMM, ARU, AGO, VFC, FHB. Wrote the first draft of the manuscript: JBA. Contributed to the writing of the manuscript: JBA, AGO, YMM. Agree with manuscript results and conclusions: JBA, AAC, DGBH, YMM, ARU, AGO, VFC, FHB, QB, GGN. Jointly developed the structure and arguments for the paper: JBA, AGO, GGN. Made critical revisions and approved final version: QB, GGN. All authors reviewed and approved of the final manuscript.
Prolactin, or estrogen gynecomastia issues: Those that are sensitive to prolactin based gynecomastia are open to problems with GHRP-6. Luckily, this is a rare occurrence, and it can be easily combated with dostinex. However, those who stack this compound with anabolic androgenic steroids may have a greater chance of getting gynecomastia. Thats why an AI (aromatase inhibitor) should be used during this kind of cycles.
Cerebrolysin—also known as FPE 1070—is a synthetic nootropic drug. Nootropic drugs are substances that enhance cognitive functions such as memory, creativity, and motivation in otherwise healthy individuals. This peptide is extremely small, allowing it to penetrate the blood-brain barrier and act directly on the neurons of the central nervous system. Cerebrolysin has been found to improve the metabolic activity of brain tissue, shield neurons from harmful substances, and stimulate the peripheral and central nervous systems. In addition to its utility as a nootropic substance, the drug has potential as part of a treatment plan addressing Alzheimer’s disease, stroke, and moderate to severe head injury.
Essentially a synthetic version of ghrelin analogue, GHRP-6 (like GHRP-2) stimulates the release of an endogenous growth hormone (GH) within the somatotropes of the anterior pituitary in the animal and human body. Specifically, GHRP-6 will increase the number of somatotropes in a GH pulse by limiting the amount of somatostatin present, while standard GHRH increases the amplitude at which the pituitary cells pulse. Unlike ghrelin, GHRP-6 is not specifically used to increase appetite, but it may have secondary actions that impact hypothalamic neurons. These effects last for approximately an hour after the initial application, which mimics the natural application of GH, and consists of an eight hour circulation period.
Then there’s colostrum. Colostrum is packed with growth factors, including IGF-1, that amplify lean muscle gains and increase the body’s ability to burn fat. In many studies, colostrum has been shown to restore IGF-1 and stimulate IGF-1 production. Colostrum is also a natural immunity drug, containing antibodies and antigens that knock out disease-causing agents such as bacteria, viruses, and fungi.
There is no “one right way”, to use Ipamorelin. For example, if you are using 500 to 1000 mcg doses daily, twice a day, your cycle might run for an 8 week period. If on the other hand, you are an athlete training for a competition, you might be on 3 injections per day, at 300-500 mcg, and will stay on for a 12 week period. For new users, you might find a 300 mcg injection is too high, and you will cut back to 200 mcg until your body gets used to it, for an 8-week cycle.
In this one you have a peptide with potential to stimulate GH release without resulting in issues associated with others. Just like GHRP-6, it both stimulates the pituitary and suppresses somatostatin. This is not the most powerful growth hormone releasing peptide. But neither causes your appetite to surge drastically nor your prolactin or cortisol levels to rise. These reasons make them a favorite for some users.
Athletes will greatly benefit from using Ipamorelin. For example, if you use CJC 1295 along with Ipamorelin, the results are going to be even greater. HGH increase will result in greater muscle mass levels, less time for muscle mass to develop, and increased levels of lean muscle tissue. The more peptides your body produces, the greater your lean muscle mass is going to be. And, over time, with gradual increases in HGH, you are going to realize a leaner, more muscular definition to your body.
You’ve already learned that sufficient protein intake (above 0.5g/lb of body weight) can assist with adequate IGF-1 and growth hormone production. Whey protein provides your body with a complete profile of necessary amino acids, including leucine. Leucine is an amino acid that promotes greater muscle protein synthesis and assists the body while gaining lean muscle mass and losing fat tissue simultaneously.
Figure 2: GHRP-6-mediated response to inflammation. Images are representative of (a) wounds topically treated with vehicle (1% CMC); (b) wounds topically treated with GHRP-6. GHRP-6 treatment reduced the inflammatory infiltration of mononuclear basophilic round cells. In contrast, CMC-treated wounds exhibit a physiologically normal infiltration, which matches the biological stage of the wound. 5 μm section, H/E, 20x magnification.
A remarkable specific (125)I-Tyr-Ala-hexarelin binding was observed in the human cardiovascular system where the highest binding levels were detected in ventricles, followed by atria, aorta, coronaries, carotid, endocardium, and vena cava. In other experiments on H9c2, cardiomyocyte-specific GHRP binding was found along with a potent antiapoptotic activity.3 The primarily investigated receptor was the growth hormone secretagogue receptor type 1a (GHS-R1a), which was detected in isolated human cardiomyocytes, myocardium, and aorta samples.17 It has been recently shown that GHS-R1a is a sort of “promiscuous receptor” involved in many systems and behavioral patterns such as reward, feeding, and memory, which makes it an attractive pharmacological target.18 Years later, the synthetic GHRP hexarelin was acknowledged as a ligand of another protein identified as CD36, a scavenger receptor that is expressed in various tissues, including monocytes/macrophages and the endothelial microvasculature. Activation of CD36 in perfused hearts by hexarelin was shown to increase coronary perfusion pressure in a dose-dependent manner. Contrariwise, this effect was lacking in hearts from CD36-null mice and hearts from spontaneous hypertensive rats genetically deficient in CD36.19,20 Thus, it is currently accepted that two cardiac receptor subtypes mediate the pharmacological actions of GHRP-6, GHRP-2, and hexarelin.21,22
These studies on human subjects were paralleled by contemporary experimental progresses in basic science, which demonstrated that hexarelin enhanced H9c2 cardiomyocyte proliferation in a dose-dependent manner. Since these were in vitro experiments, they completely excluded a potential intervention of the GH axis and clearly indicated a direct GHRP binding to cardiac cells membranes.32 Weekers et al33 demonstrated that 14 days of pretreatment with GHRP-2, but not GH, selectively protected against the postischemic diastolic dysfunction and myocardial stunning of excised hearts submitted to ischemia/reperfusion in isolated, perfused rabbit hearts.
MuscleSport PCT Revolution ADVANCED POST-CYCLE THERAPY PCT Revolution should be used after the use of any SARM. This ensures natural testosterone production increases and excess estrogen production is reduced. When your body produces abnormally high levels of testosterone for an extensive period of time you need to get your system back firing on all cylinders. Post-Cycle Therapy does just that.…
Ryan also brings up a good point to bring up the fact that GHRH receptors are typically not desensitized with higher dosing but again not much accomplished with CJC-1295, ,MOD GRF 1-29 where we know the 100mcg is a saturation dose. on the other hand we can desensitize the GHRP receptor if we start increasing the dosing significantly above the saturation dosing of 100mcg. I think you are fine at a 150 mcg dosing but again how much more benefit are you really getting.
Injections of other compounds along with IGF-1 (which is a popular practice) can also cause serious health issues. The idea is that after an user administers a GHRP (like Ipamorelin) along with IGF-1, a selective pulse is then sent that stimulates the hypothalamus and pituitary to release even more growth hormone. But this may result in an eventual negative feedback loop that leaves you unable to produce your own growth hormone and stuck on injections forever. GHRP and synthetic HGH use has also been shown to cause joint pain, huge spikes in cortisol, excessive hunger, and splitting headaches.
 Blocked growth hormone-releasing peptide (GHRP-6)-induced GH secretion and absence of the synergic action of GHRP-6 plus GH-releasing hormone in patients with hypothalamopituitary disconnection: evidence that GHRP-6 main action is exerted at the hypothalamic level. V Popovic, S Damjanovic, D Micic, M Djurovic, C Dieguez, and F F Casanueva. JCEM 1995 80: 942-7; doi:10.1210/jc.80.3.942.
One submission was received, which did not support the delegate's interim decision, as available data support that the fixed dose paracetamol/caffeine combination product provides clinically meaningful efficacy over paracetamol alone; has an excellent safety profile; a very low risk of nephrotoxicity, toxicity in overdose, misuse, abuse or illicit use; and a highly favourable risk/benefit profile.
The experiment in rats, based on clean full-thickness controlled wounds, indicated that GHRP-6 pharmacodynamics has likely involved attenuation of immunoinflammatory mediators, their effector cells, and the reduction of fibrosis-inducing cytokines. The concerted action of these two elemental mechanisms may have theoretically translated into a particular modulation of fibroblasts response to injury, leading to precocious closure with a reduced scarring. Outstandingly, the mechanisms underlying this pattern of healing do not appear to interfere with the angiogenic repopulation nor with the reepithelialization process.
But IGF-1 injections may soon be a thing of the past. Future use of IGF-1 will no doubt involve gene therapy, which directly targets genes that produce IGF-1 in muscle, usually by attaching specific gene activators to an inactive virus or vector that then enters into muscle cells. Studies in mice show that a procedure like this can cause a 15% increase in muscle mass, along with a 14% increase in strength. Gene therapy in old mice has been shown to cause to a 27% increase in strength, along with regeneration of aging muscle. In one mouse study, the IGF-1 gene was placed in the animals’ glutes and calves, which resulted in up to a 115% increase in muscle-cross-sectional area.
Your level of physical activity also affects IGF-1, and heavy weight training for your legs is a particularly potent way to increase it. Some studies suggest that the effects of the popular anti-aging supplement DHEA actually arise due to this same type of increase in IGF-1 in the body that occurs with with weight training (so you choose: heavy barbell squats or a bottle of DHEA from the drugstore).