Complete step by step for peptides

theartofwar

theartofwar

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Complete step-by-step guide for peptide beginners
1 - You are on this site because you have heard of and want to become more familiar with Growth Hormone Releasing Peptide (GHRP) and/or Growth Hormone Releasing Hormone (GHRH). These 2 materials administered can give you an increased quality of life in ways of anti-aging, muscular hypertrophy, fat loss, injury repair, higher bone density, and better sleep.

2 - GHRP can be used on its own to increase our natural Growth Hormone (GH) pulse release from the Pituitary Gland in the brain. GHRP dosed in conjunction with GHRH will amplify our growth hormone release significantly to gain maximal benefit.

3 - There are various types of GHRH's. The only GHRH to consider is tetra-substituted CJC-1295 / CJC-1295(without DAC) / modGRF(1-29). They are all the same thing but with a different name. They come in vials ranging in material weights measured in milligrams (mg) consisting of a solid freeze-dried (lyophilized) substance.

4 - There are various types of GHRP's. GHRP-6, GHRP-2, Hexarelin, and Imaporelin. The differences between them are potency and side effects. GHRP-6 is very potent and makes you quite hungry. GHRP-2 is potent and can slightly affect your sleep somewhat. Hexarelin is very potent but you can desensitize from higher dosages. Imaporelin is potent with the minimalist side effects of all 4 GHRP's.

5 - Peptides are dosed via a regular 1mL needle syringe typical to what a diabetic would use. It is administered Subcutaneously (SubQ) (just under the skin into the fat tissue), most usually around the abdomen region.

6 - The required amount (saturation dose) is 1mcg (microgram) per Kg (Kilogram) of bodyweight. The typical usage and for ease of measuring is 100mcg of modGRF(1-29) and/or 100mcg of your choice of GHRP. Lower dosages will simply result in less GH release due to a slightly weaker GH pulse and reduce any side effects you may have. A higher dose will have minimal benefit and is more a waste of money than anything else. But, in saying that, the more frequently dosed in any given day would result in more frequent pulses.

7 - Mixing (reconstitution) the lyophilized product in their vials with Bacteriostatic Water (BW) can take some getting used to. The idea is not to add too much dilution. Typical rule of thumb is to add 0.5mL of BW to 1mg of Peptide. So a 2mg vial should reconstitute with 1mL BW. 5mg with 2.5mL, 10mg with 5mL, etc. Squirt the BW along the inside wall of the vial in a smooth controlled manner being cautious not to agitate the mixture too much. It will dissolve itself and become clear. You can roll the vial gently between your fingers or hands but don't shake it to dissolve. The reconstitute is ok to be drawn once fully dissolved.

8 - On a 1mL needle, there are either 50 tick marks from 0-100, skipping every odd number OR 100 international units (IU). A 100mcg dose is half way between the 2nd and 3rd tick mark, OR 5 IU's (if you followed the above reconstitution). There are no half tick marks. It is OK to draw modGRF and GHRP into the one needle for a single shot. It is NOT OK to mix peptides in the same vial or syringe for storage.

9 - Reconstituted peptide should be stored in the refrigerator to prevent degradation. Left at room temperature, peptide will degrade within days but kept in the fridge will last months. You can pre-load syringes and store in freezer if you want but it is more of a hassle than being worth the effort.

10 - Doses can be taken throughout the day but at no less than 3 hour intervals between doses. 1 dose a day is typical for light injury repair, anti-aging effects, deeper sleep, and better quality of life. The most beneficial would be to dose immediately prior to going to bed for your daily sleep period. Sleep is the time when our pituitary is most active. 2 or 3 doses per day will give the added benefit of lean tissue build, and fat loss, considering your diet consists of good quality foods.

11 - Doses should be taken on empty stomach to benefit the most. This is usually 3 hours or more.

12 - Do not consume food for between 15-30 minutes after your dosage. Best time is around 20-25 minute mark. GH pulses should peak within about 10 minutes after dosage. Fats and Carbohydrates affect the pulse dramatically. Protein has no effect on pulse and you can have a pure protein source in your stomach at anytime if you so choose to.

13 - Dosage timing can be beneficial to your goals. For muscle growth, the 2nd most beneficial time to dose is post workout (PWO). Best time is pre-bed because sleep is when we recover and our cells repair and grow. Within 30 minutes should be fine but sooner the better. Remember to have your meal 20-25 minutes after dose.

14 - For fat loss, your supplemental dose is 1 hour pre-cardio exercise after a long fasting without food. Best time is after waking up and before breakfast. During cardio exercise, maintain a moderate intensity for between 30-60 minutes. 45 minutes is a good session. You do not want to go too hard or too long. A moderate pace will utilize Free Fatty Acids (FFA) at the highest rate for energy. Refrain from eating for approximately 2 hours after your exercise because this is the time the body is still burning fat as fuel. You must eat throughout the day to reduce the chance of muscle catabolism (breakdown).

15 - These Peptides can be used on a daily basis for the rest of your life without any harm. Enjoy!!!
Written and Thanks goes to Aussie
 
I will say I personally use acetic acid for igf1lr3 - not BW - BW for GHRP 2 , 6 - but I wouldn't buy 6 personally , 2 is much better imo.
 
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Nice post, the CJC GHRH analog is a very quality substance. I find it really helpful for getting good recovery sleep following a night of strong psychedelic use (i.e., an MDMA binge) and not putting my strength training at as much of a loss in the following days.

It also gives really good muscle pumps if taken before a workout but sometimes this can result in pain during heavy lifting and can actually hurt the workout from a power perspective.

Probably the worst thing is that it gives me added muscle soreness and especially bone sensitivity. The first few times I used it, I had full body soreness after simply injecting at night and waking up the next morning. The soreness effect faded away and is not a problem anymore, but I still feel like my bones are more sensitive than before I started using it on a semi-regular basis (once or twice a week usually). It seems when I accidentally hit my hands and arms on things it hurts more than in previous years.

Of course I also recently hit a 230 lb clean & snatch at 178 lb bodyweight and am increasingly lean so it's all good.

You can also keep CJC in the freezer and thaw it each time you want to use it. A solution like this could last longer than in the fridge, just keep in mind to not make too huge of a solution so you do not freeze and thaw the same sample every day or few days for 8-12 months. Peptides are not entirely stable for extended storage times (many months to years) in solution unless kept at -20 or below.
 
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im hungry as FUCK on 6 , feel more hypo.

I'm already hungry as shit 24/7 2 makes me hungry as is !!!!
 
i remember the 6 hypo feeling

i just got a slin test kit since i been usisng GH (which makes me go hyper).

I'll test the GHRP6 I reckon it will make me go hyper though. The hypo feeling you are having is actually ghrelin release.
 
^^ There you have it boys n girls. My meathead PHD is not up to par with it all - I simply know what I do and try to pass along to the rest of us out there.

But yes brother , I absolutely feel MUCH more hypo and slin like on 6 , 2 - zilch nada , but christ help me bro I literally cannot tell you guys the food bill. Any of you who know the cycle I'm running atm - it's NOTHING compared to m yfood bill - THIS IS HOW IT SHOULD BE. I've been to my gym twice for cardio, and for the iron, in between then I've eaten clean and heavy specifically along the guidelines I live by. Mind you I have 3 fucking funerals today, 2 for overdoses. I am never more happy to be out of that game and back where i belong. Peace to you all and let's get this right and get swole.
 
^ If you are very strict with it is not a problem , you simply have to do be doing plenty of shit man. I do am / pm cardio , so my shots / diet is regulated around that.

I think it's worth it , but legit kits have been fewer and farther as we all know for awhile. Thankfully their are few good kinds available now. Also i think GHRPs depend entirely what your cycle / stats are . I run a cycle around 2 grams total now , and will be while vary compounds for nearly 10 months brother. It's only worth a shit if you put in the diet dedication as you know. So for me GHRPs are nothing new , you want it you gotta work for it , self control with hunger is a fucking bitch tho man, i feel ya guys.

I could fuck a 90 year old goat , eat its offspring. And walk away shameless some days on tren lmao.
 
^ I wish for me brother !!!! I am one starving fucker esp the am shot before cardio. Brutal brother, i want to eat everything i just stay zoned and drive hahaha.
 
only third week brother - EQ just is starting to feel it brother. I've run EQ plenty - I know the GHRP2 when I feel it bro !! :) It's just gonna get worse tho you are right hahaha. I don't mind though - it's the important part where the dedication comes into play is the kitchen as we all know.
 
Matsuo Munefusa. said:
i remember the 6 hypo feeling

i just got a slin test kit since i been usisng GH (which makes me go hyper).

I'll test the GHRP6 I reckon it will make me go hyper though. The hypo feeling you are having is actually ghrelin release.
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Heh, that's not what you originally said.

Anyways growth hormone stimulates a variety of systems and can cause both hypo- and hyperglycemia.

Hypoglycemia can come from stimulation of excess IGF-1 secretion from the liver where IGF-1 (at high enough concentrations) begins to agonize the insulin receptor, resulting in blood glucose lowering. IGF-1 also has insulin-like action, but cross-reactivity appears to be the main reason as IGF-1 is only 100X selective for the IGF-1 receptor over insulin receptor which means there is not much "wiggle room."

Hyperglycemia can come from desensitization to the effects of insulin. Read the abstracts below, specifically the second where they say GHD can cause some people to go hypo and others hyper so in each of us (who presumably do not have GHD) it is probably a case by case issue largely dependent upon diet, body composition and exercise schedule.

This is further complicated by the fact that GH has lipolytic effects which can increase insulin sensitivity, thus making people more prone to hypoglycemia virtually all the time so long as they are experiencing the effect of the drug when they induce insulin secretion (eating) or administer it exogenously (injections).

I can tell you that in myself, as a type 1 diabetic, I notice the hypo effects a lot more than hyper from using GHRH (never tried GH or a GHRP, don't plan to). I do generally notice hyperglycemia shortly (<1 hour) after using it, and will usually dose some insulin along with it to prevent it.

Outside the insulin desensitization thing, there may be an unknown link between the stimulated growth hormone secretion and glucagon secretion from the liver that people are not fully aware of. The GH receptor has links to fatty acid metabolism, but I question if this effect in myself could be solely due to short-term decreases in insulin sensitivity. Glucagon is a potent stimulator of lipolysis (and glucose release from the liver!) and with GH causing strong lipolysis along with so much IGF-1 secretion (which promotes nutrient storage - not breakdown) I wonder if there is a missing link in the physiology. Maybe not, I am not too familiar with GH physiology beyond what I have stated/posted here.

Glucagon itself stimulates GH in the short-term (as well as FGF21), and a lot of times biology works best (or the way it is supposed to ;P) with what we have traditionally thought of as "opposing" hormonal activities functioning simultaneously (see the last abstract I posted). So it makes sense to me that it could be part of the equation as well, assuming it needs to be accounted for in the first place.

Anyways, generally I have to watch out a lot more for overnight hypoglycemia or hypoglycemia from accidentally overdosing insulin in the next 24-48 hours because I am generally a bit more sensitive to it (presumably because my fat cells are more depleted) in the long-run after having used the GHRH.

Nat Clin Pract Endocrinol Metab. 2007 Mar;3(3):302-10.
Mechanisms of disease: metabolic effects of growth hormone and insulin-like growth factor 1.

LeRoith D, Yakar S.

Division of Endocrinology, Diabetes and Bone Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029-6574, USA.

Abstract

Insulin-like growth factor (IGF) 1 is a member of a family that is involved in growth, development, cell differentiation, and metabolism. IGF1, IGF2 and insulin act primarily through tyrosine-kinase-linked receptors--the IGF1 receptor (IGF1R) and insulin receptor (IR). The IGF1R binds IGF1 and IGF2 with high affinity and the IR binds insulin with high affinity; however, since both receptors share a high degree of structural and functional homology, the IGF1R can bind insulin and the IR can bind the IGFs with reduced affinity. These two receptors can, moreover, form heterodimers, which bind both ligands. Upon binding to the receptors, cascades of tyrosine and serine kinases are stimulated to facilitate growth or metabolism. The IGF2 receptor is a scavenger receptor, and is, therefore, not involved in mediation of growth or metabolic effects of the IGF family and will not be discussed in the current article. IGF1 is a major gene target of growth hormone and its product mediates many of the actions of growth hormone on growth and development; however, IGF1 has actions distinct from those of growth hormone in carbohydrate, lipid, and protein metabolism. For example, excess growth hormone causes insulin resistance and hyperglycemia, whereas IGF1 has insulin-like effects that reduce blood glucose levels and has been used experimentally to treat both type 1 and type 2 diabetes.
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Horm Res. 2004;62 Suppl 3:51-5.
Growth hormone and glucose homeostasis.

Jørgensen JO, Krag M, Jessen N, Nørrelund H, Vestergaard ET, Møller N, Christiansen JS.

Medical Department M (Endocrinology and Diabetes) and Institute of Experimental Clinical Research, Arhus University Hospital, Arhus, Denmark.

Abstract

Patients with active acromegaly are insulin-resistant and glucose-intolerant, whereas children with growth hormone (GH) deficiency (GHD) are insulin-sensitive and may develop fasting hypoglycaemia. Surprisingly, however, hypopituitary adults with unsubstituted GHD tend to be insulin-resistant, which may worsen during GH substitution. During fasting, which may be considered the natural domain for the metabolic effects of GH, the induction of insulin resistance by GH is associated with enhanced lipid oxidation and protein conservation. In this particular context, insulin resistance appears to constitute a favourable metabolic adaptation. The problem is that GH substitution results in elevated circadian GH levels in non-fasting patients. The best way to address this challenge is to employ evening administration of GH and to tailor the dose. Insulin therapy may cause hypoglycaemia and GH substitution may cause hyperglycaemia. Such untoward effects should be minimized by carefully monitoring the individual patient.
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Growth Horm IGF Res. 2010 Feb;20(1):1-7. Epub 2009 Oct 1.
Biological effects of growth hormone on carbohydrate and lipid metabolism.

Vijayakumar A, Novosyadlyy R, Wu Y, Yakar S, LeRoith D.

Division of Endocrinology, Diabetes and Bone Diseases, The Samuel Bronfman Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA.
Abstract

This review will summarize the metabolic effects of growth hormone (GH) on the adipose tissue, liver, and skeletal muscle with focus on lipid and carbohydrate metabolism. The metabolic effects of GH predominantly involve the stimulation of lipolysis in the adipose tissue resulting in an increased flux of free fatty acids (FFAs) into the circulation. In the muscle and liver, GH stimulates triglyceride (TG) uptake, by enhancing lipoprotein lipase (LPL) expression, and its subsequent storage. The effects of GH on carbohydrate metabolism are more complicated and may be mediated indirectly via the antagonism of insulin action. Furthermore, GH has a net anabolic effect on protein metabolism although the molecular mechanisms of its actions are not completely understood. The major questions that still remain to be answered are (i) What are the molecular mechanisms by which GH regulates substrate metabolism? (ii) Does GH affect substrate metabolism directly or indirectly via IGF-1 or antagonism of insulin action?
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Horm Res. 2005;64 Suppl 3:45-50. Epub 2006 Jan 20.
Insulin sensitivity in adults with growth hormone deficiency and effect of growth hormone treatment.

Groop L, Segerlantz M, Bramnert M.

Department of Endocrinology, Malmö University Hospital, Lund University, Malmö, Sweden.
Abstract

Adult growth hormone deficiency (GHD) is a multifactorial disorder in which pituitary dysfunction associated with pituitary adenomas or their treatment plays a major role. The introduction of recombinant growth hormone (GH) for the treatment of GHD has opened up new treatment avenues but has also raised concerns about possible untoward long-term metabolic effects of GH, such as the potential effect of GH on insulin sensitivity and a deterioration in glucose tolerance. Research has shown that GH induces insulin resistance by the stimulation of lipolysis and a concomitant switch from oxidation of glucose to oxidation of lipids, during both acute and chronic treatment. However, although this is a consistent effect of GH therapy, it does not mean per se that it leads to abnormal glucose tolerance and diabetes mellitus. This article discusses this and other potential long-term metabolic effects of GH, and raises a number of questions to be addressed by future research.
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Diabetes. 2010 Nov;59(11):2941-4. Epub 2010 Aug 10.
Glucagon supports postabsorptive plasma glucose concentrations in humans with biologically optimal insulin levels.

Cooperberg BA, Cryer PE.

Division of Endocrinology, Metabolism and Lipid Research, Washington University School of Medicine, St. Louis, Missouri, USA.
Abstract

OBJECTIVE: Based on the premise that postabsorptive patients with type 1 diabetes receiving intravenous insulin in a dose that maintains stable euglycemia are receiving biologically optimal insulin replacement, we tested the hypothesis that glucagon supports postabsorptive plasma glucose concentrations in humans.

RESEARCH DESIGN AND METHODS: Fourteen patients with type 1 diabetes were studied after an overnight fast on up to five occasions. Insulin was infused intravenously to hold plasma glucose concentrations at ∼100 mg/dl (5.6 mmol/l) overnight and fixed from -60 to 240 min the following morning. From 0 through 180 min the patients also received 1) saline, 2) octreotide 30 ng · kg(-1) · min(-1) with growth hormone replacement or octreotide with growth hormone, plus 3) glucagon in doses of 0.5 ng · kg(-1) · min(-1), 4) 1.0 ng · kg(-1) · min(-1), and 5) 2.0 ng · kg(-1) · min(-1).

RESULTS: Compared with a mean ± SE of 98 ± 5 mg/dl (5.4 ± 0.3 mmol/l) at 180 min during saline, mean plasma glucose concentrations declined to 58 ± 1 mg/dl (3.2 ± 0.1 mmol/l) (P < 0.001) at 180 min during octreotide plus saline and were 104 ± 16 mg/dl (5.8 ± 0.9 mmol/l) (NS), 143 ± 13 mg/dl (7.9 ± 0.7 mmol/l) (P = 0.004), and 160 ± 15 mg/dl (8.9 ± 0.8 mmol/l) (P < 0.001) at 180 min during octreotide plus glucagon in doses of 0.5, 1.0, and 2.0 ng · kg(-1) · min(-1), respectively.

CONCLUSIONS: In the setting of biologically optimal insulin replacement, suppression of glucagon secretion with octreotide caused a progressive fall in plasma glucose concentrations that was prevented by glucagon replacement. These data document that glucagon supports postabsorptive glucose concentrations in humans.
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interesting points however GH has always reliably caused a BG spike in me. It goes from like 70ish (resting stable levels) to about 110-120 and then slowly drops as the sugars are absorbed.

this is why insulin is best used in conjunction with GH.
 
Gotta say I love GHRP2 , but holy fuck man , try TRY not eating and doing cardio 5 days a week like suggested in the read - it's brutal. I'm eating around the clock as is but this shit makes you dial it in or waste serious gains. Do love the stuff.
 
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