Dat's - CJC-1295 & GHRP-6 (Basic Guides)

DatBtrue · Aug 28, 2008

fourthgen said:
However pre-bed I usually have plenty of fats in my system. I often (when not dieting) have peanut butter or some combo of fats/protein. I always wait at least 30 minutes after eating my last snack before administering the CJC/GHRP and going to bed.

I always thought carbs were the only food that interacted with these peptides. Its very interesting that fats do as well. My new method is cjc/ghrp pwo, then 30min cardio then shake and pre bed is 50g whey/olive oil, then 30min later cjc/ghrp. So the peptides can react with carbs and fats, how about protien? Would it be ok to have some amino acids with the cjc/ghrp pwo or should even protien not be present at time of injection? Thanks

Carbs aren't nearly as inhibitory as fatty acids.

Peino, R., Cordido, F., Peñalva, A., Alvarez, C.V., Dieguez, C. and Casanueva, F.F. (1996) Acipimox-mediated plasma free fatty acid depression per se stimulates growth hormone (GH) secretion in normal subjects and potentiates the response to other GH-releasing stimuli. J. Clin. Endocrinol. Metab. 81, 909–913

ABSTRACT:

Increases in plasma free fatty acids (FFA) inhibit the GH response to a variety of stimuli; however, the role of FFA depression in GH control is far from understood. In the present work, FFA reduction was obtained by the administration to normal subjects of acipimox, a lipid-lowering drug devoid of side-effects. Each subject tested underwent two paired tests. In one, acipimox was administered orally at a dose of 250 mg at -270 min and at a dose of 250 mg at -60 min; in the matched test, placebo was given at similar intervals.

To induce GH release, four stimuli acting through different mechanisms were used: pyridostigmine (120 mg, orally) at -60 min, GHRH (1 ug/kg, iv) at 0 min, GH-releasing peptide (GHRP-6; His-D-Trp-Ala-Trp-D-Phe- Lys-NH,; 1 ug/kg, iv) at 0 min, and finally, GHRH plus GHRP-6 at the same doses at 0 min. GH secretion was analyzed as the area under the secretory curve (AUC; mean +/- SE, micrograms per L/120 min).

Acipimox pretreatment alone (n = 6) induced a reduction in FFA levels compared with placebo treatment. The FFA reduction led to a sustained GH secretion that increased from 2.4 +/- 1.8 ug/L at -120 min to 14.2 +/- 4.0 at 120 min. The GH AUC for placebo was 266 +/- 100, and that for acipimox was 1781 +/- 408 (P < 0.05). In the pyridostigmine- treated group (n = 61, the acipimox-pyridostigmine AUC (2046 +/- 323) was higher (P < 0.05) than the placebo-pyridostigmine AUC (764 +/- lOl), but was not different from the AUC of acipimox alone. Previous FFA reduction nearly doubled the GHRH-mediated GH secretion (n = 6; placebo-GHRH AUC, 1817 +/- 365; acipimox-GHRH test, 3228 +/- 876; P < 0.05). A similar enhancement was observed when the stimulus employed was GHRP-6 (n = 6; placebo-GHRP-6 AUC, 2034 +/- 295; acipimox-GHRP-6, 4827 +/- 703; P < 0.05). Furthermore, even the most potent GH stimulus known to date, i.e. GHRH plus GHRP-6, was enhanced by the FFA suppression (placebo- GHRH-GHRP-6 AUC, 2034 +/- 277; acipimox-GHRH-GHRP-6,5809 +/- 758; P < 0.05). The enhancing effect of lowering FFA levels was additive regardless of the stimulus employed.

These results indicate that 1) FFA reduction per se stimulates GH secretion with a delayed time of action; 2) FFA reduction enhanced in an additive manner the GH secretion elicited by such different stimuli as pyridostigmine, GHRH, and GHRP-6; and 3) the observation that FFA reduction enhanced the response to the most potent GH stimulus, GHRH plus GHRP-6, suggests that FFA suppression acts by a separate mechanism. FFA reduction may have value in the clinical setting for assessing GH reserve.

GoneForever · Aug 28, 2008

Wow this is crazy. So what do you think about taking some amino acids or just a little whey with the shot, or will protien effect it as well?

DatBtrue · Aug 28, 2008

fourthgen said:
Wow this is crazy. So what do you think about taking some amino acids or just a little whey with the shot, or will protien effect it as well?

Protein is fine.

GoneForever · Aug 29, 2008

Very very cool. Now I will take my lba's with my shot pwo and hit my cardio for 30min and then have shake. I've been on it for 2days now. Cant tell much but we'll see. At night, I have been having my shake/olive oil and then taking my shot in a fatty area 30min later. Like straight into a love handle, so not quite subQ but more of directly into fat. I figure this may take absorption longer. Any thoughts?

kutch · Sep 2, 2008

So after re-reading this again, I'm back on to the question of intestinal growth. I think most people expect to see some fatloss and muscle gains out of the cjc/ghrp combo(granted, not as much as an aas cycle). To accomplish this, is it fair to say that igf levels have to be raised in the body? If cjc-1295 and ghrp-6 really raise the levels of hgh and eventually turn into free-flowing igf looking to bind to something...wouldn't the igf's first choice to bind to something be in the intestines?

Without hijacking this thread, wouldn't localized IM igf injections be a better alternative than the cjc/ghrp combo with respect to preventing intestinal growth and causing new muscle growth?

Maybe I need to read up more on having raised levels of hgh throughout the body(eventually turning into igf) vs. spot injected igf(IM injections PWO). Thanks.

DatBtrue · Sep 2, 2008

kutch said:
So after re-reading this again, I'm back on to the question of intestinal growth. I think most people expect to see some fatloss and muscle gains out of the cjc/ghrp combo(granted, not as much as an aas cycle). To accomplish this, is it fair to say that igf levels have to be raised in the body? If cjc-1295 and ghrp-6 really raise the levels of hgh and eventually turn into free-flowing igf looking to bind to something...wouldn't the igf's first choice to bind to something be in the intestines?

Probably the first choice would be to bind with an IGF-binding protein such as IGF-Binding protein-3 and form a complex. A complex which both enables IGF-1 to survive and a complex which regulates how and where it will be capable of acting.

Secondly the IGF-1 isoforms that are specific to muscle will be increased. These variants are not synthesized by the liver and don't represent circulating levels of IGF-1. They are locally produced & used within muscle tissue.

kutch said:
Without hijacking this thread, wouldn't localized IM igf injections be a better alternative than the cjc/ghrp combo with respect to preventing intestinal growth and causing new muscle growth?

No. Most IGF-1 that is sold is altered IGF-1 (named IGF-1 LR3). It is altered in such a way as to reduce its binding affinity for the IGF-Binding proteins. This removes the body's natural checks & "say" in determining how & where IGF-1 will be able/allowed to act. The body is pretty darn smart.

Second there is no such a thing as limiting an injection to a specific area (i.e. localized). especially when the solution is water based and not a gel/oil. There is the possibility for some localized benefit... in my estimation this is confined to a reduction in protein degradation or increase in protein synthesis locally...but this is of very limited benefit.

The injected IGF-1 LR3 will circulate throughout the body and bind to receptors where it finds them ...and as you pointed out there are a lot of receptors in the intestines.

kutch said:
Maybe I need to read up more on having raised levels of hgh throughout the body(eventually turning into igf) vs. spot injected igf(IM injections PWO). Thanks.

No don't put yourself down like that. Sure read up...but you raise valid points.

I'll let you in on something personal to me that relates to your question.

I suffered from gastro-intestinal problems all of my adult life (from the age of 20 till sometime in the past few years). These problems were debilitating. They took out my gall bladder when I was 20 years old and my intestines never could adjust. They were not able to absorb all the substances that the liver produced. In addition my Pancreas could not secrete sufficient digestive juice/enzymes...anyway I was on medications some for 20 years.

I decided I'd try to heal myself and I ran low doses of IGF-1 LR3. I began to heal. By the end of the third course course of IGF-1 LR3 I was totally healed. It took a year but it worked.

So what does my experience indicate. First IGF-1 LR3 even in low dose finds itself bound to receptors in the gastro-intestinal tract. Second those receptors make use of IGF-1 to heal and likely grow new tissue (probably more lining).

Third my gut does not protrude or stick out or look thick.

Gut growth is not something that happens over night. It didn't happen to Kevin Leverone while he was building a 2nd place Mr. Olympia body...but it did happen to him when he felt he needed to become much bigger...

...are you ever going to approach those levels of insulin/GH use? Don't you think you'd notice?

If you want to worry ...properly worry I might add...it would be better to think about cancer. IGF-1 & IGF-II as those growth factors relate to cancer and growth hormone releasing hormone and growth hormone as it relates to the ability of cancer to metastasize, break through bounderies and grow.

But at least as far as growth hormone releasing hormone/GH is concerned certain tumors are able to make their own locally and use it locally to grow. Cutting edge research in the field of antagonists for GHRH is showing outstanding promise at stopping all of these cancers from growing, which makes it easier to kill them. Now the GHRH-antagonists are not general antagonists...they don't shut off generalized production but rather need to be specifically constructed to target the exact tumor tissue...be it in prostate, breast, lung or brain.

Higher levels of IGF-1 circulating throughout the body is positively correlated with higher incidences of cancer. But note that the body produces checks & balances...and as you increase GH levels and subsequently IGF-1 levels you also increase the binding proteins and the body's ability to control IGF-1.

I understand my response has moved away from your original question...

...but if you are going to focus on GH you should also be aware that there are big differences between synthetic GH and the natural GH our body produces.

Our body produces a blend of isoforms, variants, fragments and binding proteins. The two largest forms are 22kDa (191 amino acids long) and 20kDa (identical with a deletion of 15 amino acid residues (32 to 46) ). Both forms are equally effective at stimulating growth. However the 20kDa appears to produce fewer side effects and be longer lasting. Perhaps as it relates to prolactin fed tumors 22kDa increases tumor growth while 20kDa does not.

The synthetic form is made up of ONLY 22kDa. Thats it.

So there is a difference between the synthetic GH and naturally produced. It may be that the body better utilizes this natural blend...a blend which includes a double 22kDa bonded stack known as 45kDa which circulates and is capable of interacting with receptors. *

What does any of this SPECIFICALLY mean? Research is ongoing and there are not a lot of definitive answers but I'd like to underscore something...the body knows best and works best when we don't create unnatural imbalances.

True we may create higher or lower levels but it is probably best not to create imbalances within the isoforms, variants, fragments and binding proteins the body has come to rely on for overall control.

* NOTE: Schooled by Bobaslaw on 45kDa

bobd400 · Sep 3, 2008

Wow!

I was directed over here for info on CJC 1295 and man, did I just learn a whole bunch. I'm sure I have quite a bit more to learn, but at least I have a good basic understanding now. Thank you for all the info.

One question (I think it was alluded to in a few posts, but never saw anything definitive).

All the studies/suggestions, were the dosings done SQ or IM? I can't imagine they would be IM (@ that frequency).

Again, Thanks!

DatBtrue · Sep 3, 2008

bobd400 said:
All the studies/suggestions, were the dosings done SQ or IM? I can't imagine they would be IM (@ that frequency).

Bottom line is you don't NEED to dose CJC-1295 that frequently.

But you MAY benefit by extra amplitude from a pulse if you dose it everyday with GHRPs.

Also GHRPs serve a dual purpose one of which is to reduce Somatostatin and make CJC-1295 even more effective.

Studies, especially animal studies, were done with an I.V. either a bolus or time released infusion. For a lot of human studies they were done via subcutaneous injection.

Never did I see specific reference to intra-muscular. The release curves for the subcutaneous administration looked very similiar to the release curves for I.V. There is not much delay ...a few minutes tops.

Aestheticlabs · Sep 4, 2008

re igflr3 and mgf

looking forward to your article on lr3 and mgf the two work great ,and they dont compete for the same receptors,but I'm waiting on your posts...you have done us all a huge service Thanks bro for posting here
Love & Respect

SCRAPSTER · Sep 4, 2008

awesome thread!!

Wow! I just learned more than my brain can cram in lol!!! Thanks again Dats!!!

DatBtrue · Sep 4, 2008

Aestheticlabs said:
looking forward to your article on lr3 and mgf the two work great ,and they dont compete for the same receptors,but I'm waiting on your posts...you have done us all a huge service Thanks bro for posting here
Love & Respect

Hey bro good to see you around.

As for IGF-1 & MGF I think they would work better w/ either GH or CJC-1295/GHRP-6 then they do by themselves.

From the studies, GHRP-6 is not sufficient to sustain IGF-1 levels and it also isn't really likely to increase the muscle forms of IGF-1. So IF for some you reason you wanted to use GHRP-6 w/o CJC-1295 to build muscle you'd benefit from MGF for sure.

On another board I was asked:

xxxx said:
Dat do you think there would be any synergy in adding in pegMGF or MGF into a cycle of ghrp6/cjc?

My response:

My general thoughts:

IGF Binding Proteins (particularly IGFBP-3) may be important in mediating the desired actions of IGF-1 in tissue & the inability of LR3 to bind w/ IGFBP-3 & form a complex may effect its ability to promote growth.

Growth Hormone (GH) is better at creating the "right kind" of IGF-1 isoform and targeting it to local tissue than IGF-1 administration alone.

GH is better at creating muscle isoforms of IGF-1 in older people than young.

Locally produced/locally used (i.e. autocrine/paracrine) IGF-1 is more important than overall circulating levels of IGF-1 in promoting muscle growth.

There is a relationship between overall levels of circulating IGF-1 and local IGF-1 expression. (I conjecture that it is often a positive one but that the relationship often changes.)

Since GH will raise levels but may not upregulate muscle IGF-1 locally in the young it may be of benefit to add those isoforms via local administration.

Snippets of science:

There are six IGF-binding proteins (IGFBPs). The IGFBPs were initially isolated from serum and are proteins of about 30 kDa able to bind IGF-I and IGF-II but not insulin. Most serum IGF-I is found in a tripartite complex with IGFBP3 and the acid labile subunit (ALS). IGF-IGFBP complexes can leave the circulation and access tissue unless they are bound to the ALS. In serum, they increase the circulating half-life and delivery of IGF-I to tissues. In tissues, they modulate IGF action as they have higher affinity for IGFs than the receptors. IGFs are released by proteolysis of IGFBPs or binding of the IGFBPs to the extracellular matrix. - Parker A, Rees C, Clarke J, Busby Jr WH, Clemmons DR (1998). Binding of insulin-like growth factor (IGF)-binding protein-5 to smooth-muscle cell extracellular matrix is a major determinant of the cellular response to IGF-I. Mol Biol Cell 9: 2383–2392.

There are effects that cannot be mimicked by infusion of IGF-I. It has been demonstrated that GH administration increases skeletal muscle IGF-I mRNA production in hypophysectomized rats 20-fold, whereas the increase observed after IGF-I treatment is only 2.5-fold. This may be relevant to skeletal muscle mass regulation as the autocrine/paracrine levels of IGF-I appear to be more important than the systemic/circulating levels of IGF-I. - Gostelli-Peter M, Winterhalter KH, Schmid C, Froesch ER, Zapf J (1994). Expression and regulation of insulin like growth factor I (IGF-I) and IGF binding protein messenger ribonucleic acid levels in tissues of hypophysectomized rats infused with IGF-I and growth hormone. Endocrinology 135: 2558–2567.

Critically, high levels of circulating IGF-I do not seem to be required for intrauterine growth as liver-specific IGF-I knockouts show similar body weight to controls at birth and up to 3 months of age. The liver-specific knockout has some postnatal growth reduction compared with wild types, but it is not as severe as in the total IGF knockout. This implies that locally produced, autocrine/paracrine IGF-I plays an important role in pre- and postnatal growth. - Sjogren K, Liu JL, Blad K, Skrtic S, Vidal O, Wallenius V et al. (1999). Liver-derived insulin-like growth factor I (IGF-I) is the principal source of IGF-I in blood but is not required for postnatal body growth in mice. Proc Natl Acad Sci USA 96: 7088–7092 & Baker J, Liu JP, Robertson EJ, Efstratiadis A (1993). Role of insulin-like growth factors in embryonic and postnatal growth. Cell 75: 73–82.

Direct infusion of either GH or IGF-I into rat muscle does result in increased mass providing evidence that it is the local autocrine/paracrine rather than systemic endocrine effects that are important for hypertrophy. - Adams GR, McCue SA (1998). Localized infusion of IGF-I results in skeletal muscle hypertrophy in rats. J Appl Physiol 84: 1716–1722.

GH administration alone has, however, been shown to affect the expression of a 3' splice variant of IGF-I (IGF-IEa) in the muscles of elderly men. - Hameed M, Lange KH, Andersen JL, Schjerling P, Kjaer M, Harridge SD et al. (2004). The effect of recombinant human growth hormone and resistance training on IGF-I mRNA expression in the muscles of elderly men. J Physiol 555: 231–240.

The interactions between circulating and local IGF-I expression may also play a role in regulating muscle mass. It is possible that increased circulating IGF-I affects GH and thus has consequences for the synthesis of autocrine/paracrine levels of IGF-I. Alternatively, increased circulating IGF-I may directly inhibit either muscle IGF-I synthesis or the effects of locally produced IGF-I. Indeed, it has been reported that IGF-I mRNA is downregulated in cultured muscle cells following IGF-I treatment. - Frost RA, Nystrom GJ, Lang CH (2002). Regulation of IGF-I mRNA and signal transducers and activators of transcription-3 and -5 (Stat-3 and -5) by GH in C2C12 myoblasts. Endocrinology 143: 492–503.

Recently, we observed that GH administration does not upregulate IGF-IEa in skeletal muscles of young men whereas in older men, GH resulted in increased skeletal muscle IGF-IEa. In the young men, GH administration led to serum IGF-I levels that were supraphysiological, whereas in older men serum IGF-I levels after treatment were equivalent to the pretreatment levels observed in young men. The effects of supraphysiological versus normal circulating IGF-I on muscle hypertrophy and local IGF-I production remain to be investigated in detail. - Aperghis M, Hameed M, Bouloux P, Goldspink G, Harridge S (2004). Two weeks of GH administration does not increase the expression of insulin-like growth factor-I mRNA splice variants in the skeletal muscle of young men. J Physiol 558P: C4. & Hameed et al.

cecray3 · Sep 5, 2008

All I can say is "holy shit!" I had never researched anything on peptides prior to reading this thread and needless to say I'm a bit overwhelmed however definitely intrigued by what I have "discovered". Thanks Dat for your contributions...once again making this one of, if not, the most SOLID forum/board, bar none!

This may come across as an uneducated series of questions and quite frankly it is!

But I'll ask anyways; any feedback is greatly appreciated!

-So, dosing at 100/200 pre-bed ED can be done either SC or IM, correct?

-And coupled with AAS, one can expect to acheive fat loss with simultaneous lean mass gain?

-Other than a lesser amount of side effects (as compared to AAS) and age-reversing/sparing effects, are there other benefits of usage?

Like I said above, I may sound like an idiot, but like many people on this board, up until now I knew absolutely nothing on this subject. Thanks again Dat!

GoneForever · Sep 6, 2008

Dat is it cool to use nolvadex while on cjc/ghrp6. I know its ok if on GH or IGF b/c nolvadex lowers naturally occuring IGF levels, not synthetic. So what about with cjc/ghrp6? I like to take a small dose like 10mg EOD to keep estro in check while on TRT since I keep my trt on the higher end. Thanks

DatBtrue · Sep 6, 2008

fourthgen said:
Dat is it cool to use nolvadex while on cjc/ghrp6. I know its ok if on GH or IGF b/c nolvadex lowers naturally occuring IGF levels, not synthetic. So what about with cjc/ghrp6? I like to take a small dose like 10mg EOD to keep estro in check while on TRT since I keep my trt on the higher end. Thanks

The Tamoxifen Citrate/Nolva won't noticably interfere with the IGF-1 that comes about from CJC...especially at that low dose.

DatBtrue · Sep 6, 2008

cecray3 said:
-So, dosing at 100/200 pre-bed ED can be done either SC or IM, correct?

Correct.

cecray3 said:
-And coupled with AAS, one can expect to acheive fat loss with simultaneous lean mass gain?

You can achieve fatloss w/o the AAS. It is all directly related to diet bro. The increased GH especially if you are older will help reduce visceral fat...i.e. the mid-section fat pad.

It takes calorie surpluses to gain muscle tissue. GH will help w/ nutrient partitioning and help keep fat off as you gain in a proper cycle.

Its not magic...just a component of a proper growth cycle or an aid to fatloss over s sufficient period of time with a proper diet.

cecray3 said:
-Other than a lesser amount of side effects (as compared to AAS) and age-reversing/sparing effects, are there other benefits of usage?

Very numerous benefits to Growth Hormone especially if you are older. The topic is too big & general for a single reply.

If you meant Growth Hormone Secretagogues such as GHRP-2, GHRP-6, Hexarelin & even Ghrelin itself the answer is YES. Keep in mind these GHRPs are the keys and their receptor is the lock they insert into. So where there are locks (i.e. receptors) there is opportunity for these GHRPs to bind and exert an effect.

GHS-R (the ghrelin receptor and the synthetic GHRP receptor) regulates the activity of GHRH neurons and GH release and maintains normal IGF levels during aging of young adults. GHS-R expression was found to be predominant in the anterior pituitary gland and specific regions of the brain.

More interesting and pertinent to your question is that the GHS-R is also expressed in regions besides those generally considered to be involved in GH release. For example, expression is seen in the anterior hypothalamus, suprachiasmatic nucleus, supraoptic nucleus, ventromedial hypothalamus, dentate gyrus, CA2 and CA3 regions of the hippocampal structures, tuberomamillary nucleus, pars compacta of substantia nigra, ventral tegmental area, dorsal raphe nuclei, and median raphe nuclei. Recently, GHS-R expression has also been measured in T cells and in the thymus.

The sites of expression of the GHS-R in the brain and thymus "could have profound significance to aging". It is reasonable to speculate that specific central nervous system functions might also be restored in elderly subjects. The hippocampus is enriched with neurotransmitter systems that affect memory and learning, and the substantia nigra and ventral tegmental areas are centers for the dopaminergic systems in the midbrain that affect motor control and reinforcement behavior. Furthermore, the dorsal and median raphe nuclei are enriched with serotonergic neurons that project to areas implicated in physiological pain (nociperception) and affective behaviors.

GHS-R expression in the thymus and on T cells suggests that in elderly subjects immune function might be restored by treatment with GHS. It has been demonstrated already that a GHRP derivative benefited thymic function in old mice by reversing its shrunken form brought on by aging and restoring it seems to optimal function.

There are studies all over the place that focus on different areas. GHRP-6 (and I assume all GHRPs) has been shown too protect the liver from inflamation & damage. Hexarelin (and I assume all GHRPs) is cardio-protective in some situations. These effects are mediated through the GHS-Rs found in those tissues.

The GHS-R is also found in skeletal muscle. Ghrelin (and again probably the GHRPs) has been found to promote differention & fusion of muscle cells. GHRP-2 (and I assume the GHRPs) has been shown to be anti-catabolic in muscle.

So the quick answer to your question is YES.

cecray3 said:
Like I said above, I may sound like an idiot, but like many people on this board, up until now I knew absolutely nothing on this subject. Thanks again Dat!

Don't put yourself down. You have a curious mind and that is what is important... and NO you don't sound like an idiot at all.

GoneForever · Sep 6, 2008

Im so glad this stuff can be done IM. My stomach is a pin coushin. Nice to have other options, esp since we use slin pins like traps,calves,lats,etc..

GoneForever · Sep 8, 2008

Dat, 2 quickies for yah whenever you get some time.

1.) There is no need for an anti-prolactin (ie, cabergoline) for cjc/ghrp, let along any peptide other than HGH correct?

2.) I presume there is no spot reduction and/or localized growth with cjc/ghrp?

Thanks brother.

DatBtrue · Sep 8, 2008

fourthgen said:
Dat, 2 quickies for yah whenever you get some time.

1.) There is no need for an anti-prolactin (ie, cabergoline) for cjc/ghrp, let along any peptide other than HGH correct?

Not likely. In fact natural growth hormone is made up of a blend of isoforms, the 2nd most predominant 20kDa lacks the amino-acids that enable it to interact with the prolactin receptor. True the most predominant member 22kDa (which is what synthetic GH is solely made up of) does interact with the prolactin receptor but the blend is liable to result in less such interaction than an equivalent amount of synthetic (i.e. 22kDa) growth hormone.

fourthgen said:
2.) I presume there is no spot reduction and/or localized growth with cjc/ghrp?

Not really. There are GHS-Rs in muscle and GHRP-6, GHRP-2 & Hexarelin could exert anabolic effects in skeletal muscle tissue but that effect to the extent it is noticable is likely to be systemic and not near the site of injection.

Spot reduction... science vs. what we witness.

The answer is no. Melantonin-II might though:

"peripherally administered MTII reduces the mass of specific WAT [white adipose tissue] depots without causing apoptosis." - MTII administered peripherally reduces fat without invoking apoptosis in rats, Yang-Ho Choi, et al., Physiology & Behavior 79 (2003) 331– 337

VictorZ06 · Sep 8, 2008

I can't believe the amount of information there is here! You ROCK Dat!!

I'm a total novice when it comes to peptides. I just ordered a couple bottles of CJC (and waiting for supplier to carry GHRP-6) and plan to run it for a couple of months in conjunction with HGH.

I have been body building for a good 12 years and am well versed with AS. But, I now want to try the HGH/peptide route. I'm want to order some slin pinz, but I don't know what size to use (I ran a search). 1cc, 1/2cc, or 3/10cc?

Thanks so much for the help.

lilned · Sep 8, 2008

VictorZ06 said:
I can't believe the amount of information there is here! You ROCK Dat!!

I'm a total novice when it comes to peptides. I just ordered a couple bottles of CJC (and waiting for supplier to carry GHRP-6) and plan to run it for a couple of months in conjunction with HGH.

I have been body building for a good 12 years and am well versed with AS. But, I now want to try the HGH/peptide route. I'm want to order some slin pinz, but I don't know what size to use (I ran a search). 1cc, 1/2cc, or 3/10cc?

Thanks so much for the help.

Dat does rock!!!
You will be fine with 1cc/100IU pins. Just make sure you double check your math when you reconstitute and dose : )