Phenylephrine is a direct alpha-1 adrenergic agonist, with weak alpha-2 adrenergic agonist activity. It also has very weak beta-adrenergic effects, but at therapeutic doses there are no significant stimulating beta-1 adrenergic effects on the heart, or on the bronchial airways, or on peripheral blood vessels. This contrasts with pseudoephedrine, which has greater beta-adrenergic activity. The effect on the alpha-adrenergic receptors leads to local vasoconstriction and shrinking of mucous membranes. There is no anti-histamine effect. The drug is readily and completely absorbed following oral administration, undergoing extensive first pass metabolism in the intestinal wall and in the liver leading to some variability in individual pharmacokinetics. Nasal decongestion is apparent within 15 to 20 minutes and persists for up to 4 hours (AHFS 2007).
There were concerns regarding the number of contraindications and precautions and whether consumers would be able to interpret these appropriately without a requirement for pharmacist advice. There were concerns regarding gastro-intestinal, renal and other adverse effects related to the potential interactions of ibuprofen and paracetamol. Also raised were concerns regarding the potential for paracetamol overdose.
In 1982, the natural hormone "Growth Hormone Releasing Hormone" (GHRH) was identified after a prolonged search. Soon, researchers discovered that those GH-Releasing Peptides (specifically GHRP-6 & GHRP-2) followed a mode of action which bound them to and was mediated through receptors different from those for GHRH. Furthermore, researches discovered that these GH-Releasing Peptides acted synergistically with the natural hormone Growth Hormone Releasing Hormone (GHRH), which is related to Sermorelin, in both laboratory animals and humans to produce large releases of Growth Hormone. In the 1980s, the first highly potent GH-Releasing peptide, GHRP-6, was developed. Due to a strong GH release response from the the peptide, it became the first member of a class called Growth Hormone secretagogues. GHRP-6 is a hexapeptide composed of 6 amino acids: L-Histidine, D-Tryptophan, L-Alanine, L-Tryptophan, D-Phenylalanine and L-Lysine. The "L" form of an amino acid is the naturally occurring form and often in the nomenclature the "L" is dropped. The "D" form does not occur in nature and is the isomeric form (i.e. mirror image) of the naturally occurring "L" form. GHRP-6 (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) is composed of both natural and isomeric forms of those 6 amino acids.This sequence provides a signal to the body to begin secreting Growth Hormone release while also blocking Somatostatin, a hormone that inhibits the release of Growth Hormone.
The effect of GHSs on GH release is dose dependent and more reproducible than that of GHRH. The peptide GHSs (e.g., GHRP-6, GHRP-1, GHRP-2, and hexarelin) and the nonpeptide GHSs differ in terms of their pharmacokinetics. The nonpeptides MK-0677 and macimorelin have been developed specifically as orally active agents. The peptidyl GHSs are also active PO, but only at doses several hundred times higher than that required when administered IV.
Ipamorelin is a man-made peptide that is part of the growth hormone family. Rated as one of the safest in the peptide industry, it has strong growth hormone releasing properties. From this, it is a huge winner with athletes and bodybuilders. This is because it builds muscle and keeps weight down quickly. It works by sending signals to the pituitary gland at the base of the brain and adjusts and controls various body functions through the endocrine system. It binds certain receptors inside cells. This allows cells to respond and change, encouraging growth and regulation of hormones. Ipamorelin can help with:
Used for muscle building, weight loss and anti-aging purposes, this is a very powerful peptide for promoting growth hormone release. GHRP-6 also helps in fighting inflammation and boosting recovery. Some professional bodybuilders are believed to use it together with steroids for greater potency. The peptide not only stimulates the pituitary to produce growth hormone, but also suppresses somatostatin which could impede release.
Dosing will ordinarily be at least twice per day and preferably 3x/day for best effect, taken at least 30-60 minutes before a meal and at a time of non-elevated blood sugar (in other words, after blood sugar has had time to fall since the most recent meal.) The amount taken generally will be from 50-300 mcg at a time. When using a GHRH along with GHRP-6, dosing should be reduced to 50-100 mcg at a time.
Peptide therapy, or the use of specific peptides in treatment, has gained great popularity in recent years. This is due largely to the fact that these peptides are highly specific (i.e., only do what you want them to do) while also being well-tolerated and safe. As of January 2015, there were over 60 US FDA-approved peptide medications, 140 peptide drugs being evaluated in clinical trials, and 500 in pre-clinical development.
Exercise and sports have, in recent times gained the credit it is due. Not only are these sports a testament to the fortitude of the athletes, but they are also a science in themselves. Each sport has different exercise regimes and different dietary requirements. While some athletes face the same environment in each competition, there are those who have to face a different environment every time they compete. What remains constant however is the importance of growth hormone and the effect it has on the athlete’s body.
Very tough to say. I am not a doctor and this is not to be taken, interpreted or construed as medical advice. Please talk with a licensed medical professional about this. These are just my own personal thoughts and not a prescription or a diagnosis or any form of health care whatsoever. I could possibly help but would need to see your health history, blood, biomarkers, etc. I'd be happy to help you via a personal one-on-one consult. Just go to https://bengreenfieldfitness.com/coaching. and then choose a 20 or 60 minute consult, whichever you'd prefer. I can schedule ASAP after you get that.
In June 2011 the Advisory Committee on Medicines Scheduling was referred a proposal by the delegate to consider up-scheduling of five (5) then unscheduled substances contained in cold and cough preparations into Schedule 2. One of these substances was phenylephrine and many public submissions received rejected this proposal on the grounds of the paracetamol/phenylephrine exemptions in the Schedule 2 entry. The committee made similar comments and the delegate agreed that the current exempt from scheduling status of phenylephrine was appropriate.
Technically, it is a “protein-peptide hormone” which means that it consists of 70 amino acids bonded together. Just like the peptides I’ve written about in the past, this means that it must be injected, because otherwise IGF-1 simply degrades in the gut, rendering it useless. Your own human growth hormone release promotes the synthesis of IGF-1 in your liver (and to smaller amounts, synthesis of IGF-1 by your muscles), your liver and muscles then synthesize IGF-1 and then, in the case of your liver, subsequently package the IGF-1 with binding proteins for transport into the blood. In a type of anabolic positive-feedback loop, IGF-1 then further increases growth hormone’s anabolic effects.
Finally, patients deficient in growth hormone who get IGF-1 injections have shown increased rates of fat loss and fat oxidation. One theory for this is that, as you’ve just learned, IGF-1 can suppress circulating insulin, which would allow more burning of fatty acids from fat cells. This makes sense, since we do know that fat cells contain IGF-1 receptors, and this means that IGF-1 can interact with fat cells.
TGA evaluator concluded that the consistent absence of any clinically meaningful effects on blood pressure (BP) or heart rate (HR) in the applicant's bioavailability studies, and the absence of any ADR reports of BP, HR or other cardiovascular problems, indicate that "there is no valid reason for concern and no need to take any regulatory against the combination products currently in the ARTG and available in the Australian market", i.e. no demonstrated safety risk, and no evidence provided of efficacy of paracetamol 1000 mg / phenylephrine HCl 5 mg adult dose.
In November 1999, the National Drugs and Poisons Schedule Committee (NDPSC) decided to reschedule mometasone from Schedule 4 to Schedule 3 for use in aqueous nasal sprays for the treatment of seasonal allergic rhinitis, with certain dose and age conditions. The NDPSC considered that this rescheduling was appropriate given mometasone's safety in use based on pharmacokinetic parameters, and that the treatment of seasonal allergic rhinitis has a place in Schedule 3.
These compounds may be considered an improvement on GHRH in terms of ability to induce growth hormone secretion. GHRP, it is thought, causes secretion of greater amounts of GH in the body. Unlike in the case of GHRH, you do not need to aim at specific times to take advantage of pulse produced by your body. Growth hormone releasing peptides produce growth hormone burst practically any time you take them. They are also available in different types, including the following:
For those who are just getting started, make sure you go gradually. Start off with an eight-week cycle, and start off with 200 mcg (rather than 300) per day. Doing a test run will allow you to see how your body is going to react. If all goes well, you can then increase your dosage cycle to an 8 to 12 week period, and possibly add an additional injection dose daily, or increase to 300 mcg with each use.
Peptides is from the latin word pepsis which means digestion. So in reality they cover anything in the body that aids digestion and since we get all our nutrients from this process the use of peptides is seemingly limitless. Recently biologically active peptides have been discovered in the heart, brain and skin so the potential uses and benefits of peptides in the future is really exciting.
ADV Research ADV-17 Post Cycle Therapy PRODUCT STRENGTH (CONCENTRATION): 30MG/ML KEY BENEFITS Raises testosterone levels Lowers estrogen levels Raises luteinizing hormone (LH) levels Lowers cortisol levels Enhances recovery speed Promotes vascularity (hardening and drying out) Increases libido Inhibits gynecomastia (male breast enlargement) Promotes fat loss Not liver toxic GENDER SUITABILITY ADV-17 is suitable for use by males. Females should not…
In June 2007, the NDPSC decided to extend the exemption from the limit on paracetamol combinations being allowed as general sale products to include phenylephrine (as long as it also qualified as exempt from scheduling through the phenylephrine entries). At that time, the NDPSC considered that the safety profile of these substances was such that allowing a fixed combination to be unscheduled was reasonable.
The scheduling of paracetamol and caffeine when combined in a compound analgesic as the only active ingredients was again reviewed by the NDPSC at its 57th Meeting in October 2009 after the Committee had received a request to reconsider the scheduling on the grounds of potential toxicity if used in excess. This issue had been extensively reviewed at the June 2007 meeting and it was decided that Schedule 2 remained appropriate.
Thymosin alpha-1 (T α 1) is a peptide, or small protein, consisting of 28 amino acids. T α 1 is produced naturally by the thymus gland. The thymus is located behind the sternum and between the lungs, and is where immune cells known as T cells mature and are released, prompted to do so by the T α 1 peptide. T cell production and action within the body is vital to adaptive immunity—the mode by which immune cells are able to recognize and eradicate foreign invaders.
Excerpt: I started taking Ipamorelin and CJC 1295 without DAC yesterday. I dont see many logs and i see a lot of people wondering what kind of results you can get wiith these peptides. I have enough to go a couple of months right now and see what this stuff is really about. Im taking each 3x a day. Morning, pwo, and before bed. Im taking 100mcgs of each in the morning and before bed. After my workout, I'll take 100mcgs of cjc and 100-200mcgs of Ipa. I weigh 215 and i have no idea what my bodyfat
GHRH/GHRP-6 was the first of a family of synthetic peptides that enhance the release of the GH by the pituitary gland in a dose-dependent manner. Since its discovery, it has been used as a benchmark and starting point for many of the research aims to obtain new drugs, but none of its implications are more engaging than the treating of the obesity epidemic.
CJC 1295 can be compounded in two forms (DAC and non-DAC). Drug affinity complex (DAC) prevents enzymatic degradation thus increasing the half-life. Consequently CJC 1295-DAC can be dosed as a single weekly injection. Administration of CJC 1295-DAC provides a GHRH-like stimulation around the clock. A potential drawback when using a weekly protocol can be attributed to ineffective GHRH stimulation when the body is due for a GH spike (usually 1:00am). This is referred to as a GH-bleed and the overall result is inferior to using CJC 1295-NON-DAC daily for 5 days out of 7. Therefore using CJC 1295-NON-DAC daily (between 6-8pm) provides a more effective GH spike at 1:00am.
Studies have shown that individuals fighting infection have a lower amount of circulating T α 1 and suppressed helper T cell numbers compared to healthy individuals. This is problematic, as optimal immune function is vital to recovery from infection. Supplementation with T α 1 has the potential for great therapeutic benefit for patients suffering from infection or autoimmune disease.
Similar to other enhancers, it is observed that administrating GHRP-6 along with insulin gets an increased GH response. However, in presence of elevated glucose levels, GHRP-6 does not work well. As a result, consuming carbohydrates or dietary fats before administrating GHRP-6 is a bad idea. Thus the dose should be taken two hours after your last meal and at least thirty minutes before your next meal. Also, GHRP-6 has saturation points. As a result, you want to put a healthy interval between two doses so that your receptors are clear. The best schedule is one dose upon waking up, one post workout, and one before sleeping.
Administration of peptides is normally subcutaneous or intramuscular. Peptides come as a fine white and delicate powder that must be reconstituted with bacteriostatic water or medical grade saline. An insulin syringe should always be used to administer the dose. When targeting muscles, look for a place where the layer of skin and fat are lean. Mixing two peptides in the same syringe is totally fine but I personally would advise not drawing/mixing doses and storing pins for future use.
GH-releasing peptides (GHRPs) are synthetic peptides that like GHRH act directly on pituitary somatotrophs to stimulate GH release. Growth hormone (GH) release is stimulated by a variety of synthetic secretagogues, of which growth hormone-releasing hexapeptide (GHRP-6) has been most thoroughly studied; it is thought to have actions at both pituitary and hypothalamic site.
Hypertrophic scarring is a form of abnormal, exuberant healing, locally aggressive, and recurrent cutaneous fibroproliferative condition, characterized by excessive extracellular matrix (ECM) accumulation during the cutaneous healing process. Including keloids and hypertrophic scars (HTS), these aberrant processes lead to esthetically disfiguring scars, patients’ psychological stress, and functional impairment . The cellular and molecular mechanisms underlying the formation of these raised dermal scars are poorly understood. Recent whole genome profiling and proteomic studies have led to the identification of regulatory elements with different expression profiles in HTS and keloid tissues . The limited understanding of the pathophysiology of these processes has led to investigating a broad spectrum of potential antihypertrophic scarring candidates .
Conclusions: Subcutaneous administration of CJC 1295 resulted in sustained, dose-dependent increases in GH and IGF-I levels in healthy adults and was safe and relatively well tolerated, particularly at doses of 30 or 60 ug/ kg. There was evidence of a cumulative effect after multiple doses. These data support the potential utility of CJC 1295 as a therapeutic agent.
It is also important to note that whether you are a long-time user or a first-time user of Ipamorelin, your body is going to react differently to that of the next user. Like the benefits you will experience, the side effects you are going to experience will occur differently, and at different dosage levels. So, it truly is a trial and error period you are going to go through with a test run of Ipamorelin for new users. You have to find what works for you, how your body will react, and what potential side effects are lingering ahead, in order for you to achieve the greatest results, and eventually find the proper dosage and cycle level, which is going to work the best for your body and system.
Years ago, our group examined the cytoprotective effects exerted by the GHRP-6 preventive administration in the hepatic tissue subjected to I/R, as in other distal organs from the ischemic site (ie, lungs, kidneys, and small intestine). Histological and biochemical results allowed us to conclude that the pharmacological preconditioning induced by the GHRP-6 treatment attenuated I/R liver damage. Besides respiratory distress syndrome like pulmonary changes, intestinal transmural infarct and acute tubular necrosis in kidneys were significantly reduced. These results indicated for the first time a systemic cytoprotective effect for the GHRP-6, suggesting its potential efficacy to control the inflammatory response associated with acute I/R and shock, which eventually originated multiple organs damage (MOD). Cytoprotection induced by GHRP-6 treatment was also related to the attenuation in the generation of ROS and preservation of the antioxidant defense reserves. Histological analysis as the assessment of myeloperoxidase activity evidenced a clear anti-inflammatory GHRP-6-induced effect in the liver and remote organs. Moreover, the molecular mechanism mediating the action of GHRP-6 peptide was shown to involve the phosphatidylinositol 3-kinase/RAC-alpha serine/threonine-protein kinase (PI-3K/AKT1) pathway, as the induction of the hypoxia-inducible factor-1 alpha (HIF-1α) all committed in cellular survival.51 Subsequently, Granado et al52 examined the potential anti-inflammatory impact of GHRP-2 in lipopolysaccharide (LPS)-challenged rats. GHRP-2 administration attenuated the effects of LPS on the elevation of circulating levels of transaminases, nitrites/nitrates, and tumor necrosis factor-alpha (TNF-α), via direct interaction with liver nonparenchymal cells. Globally, the exogenous administration of these two synthetic GHRPs appeared to exert a potent hepatoprotective role by attenuating the inflammatory response orchestrated by liver-resident macrophages. Another line of evidences document the benefits of 15-daily injections of GHRP-2 (100 μg/kg) in arthritic rats, so that the treatment ameliorated the external symptoms of arthritis and decreased the circulating levels of interleukin 6 (IL-6) as the nitrite/nitrate release from peritoneal macrophages in vitro. This experiment extrapolated the counter-inflammatory properties of GHRP-2 to a nonepithelial organ and suggested again a direct interaction with ghrelin receptor of immune cells.53 Similarly, effects have been attributed to ghrelin by inhibiting the inflammatory response via AKT1-activated pathway with a concomitant reduction of myeloperoxidase activity, the rate of apoptosis, and oxidative stress.54 All these data suggest that GHRPs exert a mutually inclusive beneficial effect by directly protecting parenchymal organs epithelial cells, and simultaneously by modulating the magnitude of the inflammatory response by direct interaction with the effector immune cells. Supporting the protective effect of GHRP-6 on epithelial organs, a recent study has excellently described and dissected the mechanistic bases on how GHRP-6 prevented gastric mucosal damage induced by water immersion restraint (WRS) and other forms of stress. The data indicated that the protective effect of GHRP-6 on WRS-induced gastric mucosal injury is somehow mediated by peripherally suppressing the vagal efferent effect on the stomach, including gastric acid secretion. Although more studies are clearly demanded, the present findings open the possibility to use GHRP-6 in preventing Curling ulcers.55
GHRP mechanism of action. GHRPs are endowed with the ability to bind two different receptors that seem to mediate its cytoprotective and other pharmacological properties (GHS-R1a and CD36). The main biological properties/pharmacological actions of GHRP-6 as cyto- and cardioprotective candidates are summarized as follows: Inotropic: mediated by an elevation of Ca2+ influx via PLC/DAG/PKC, through the voltage-gated calcium channel, triggering Ca2+ release from thapsigargin-sensitive intracellular stores, which translated in a positive inotropic response without a chronotropic effect. Anti-fibrotic: via upregulation of PPARγ, which is followed by a transforming growth factor-beta (TGF-β), CTGF, and platelet-derived growth factor (PDGF) downregulation. Anti-inflammatory: blunts NFκB expression and activation. Cell survival: it involves the phosphatidylinositol 3-kinase/RAC-alpha serine/threonine-protein kinase (PI-3K/AKT1) pathway, as the induction of the hypoxia-inducible factor-1 alpha (HIF-1α). Cardioprotective: as shown, it involves different biological actions that converge to enhance cardiomyocytes survival. Vasodilatory: it seems to involve e-NOS upregulation and endothelin activity reduction. Anabolic: it is mediated by the IGF-1/AKT1 and mTOR pathway activity.
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