purplehaze

I remember DFG and Scorpious Orge...They brought me in over here and gave me my first mod position...Nice guys to me.{Don't know the details of their bust}

 

Crank was a good fella as well and helped me build UBB back in the day and then dropped off and I never heard from him again.

 

A lot of us old guys are from vipbb...Most of the staff we have now has been around for 10 plus years.

Exactly,,,I wish that Crank was still active and around the boards....Too many of the really good dudes from back in the day have left the scene...I was on this site a very long time ago, and then the board changed and changed hands...I really like this site and hope it remains here for another 10 yrs....

MU there are still a few of us dinosaurs still around...I really enjoy seeing so many members here and on other boards for that matter that were on vipbb,AU, and some of the other vet sites that are no longer with us....

Welcome.....Glad to have you with us..PH

Nice to see you here and Welcome...PH

Welcome to AB....Glad to have you with us..PH

Knowing that loser B2J he WAS trying to get money/gear or both from this guy and get one of his get rich quick schemes rolling like he did on VIP and IWF a year or so ago...drama queen is right and also a status whoring look good who doesnt really know shit.

I like the part where he gives 'options' to stay quiet- if this guy was such a shit bag then he should have gave him up and posted him as such- but I guess extorting him seemed a better option.

Good to see you here buddy....You Board Whore You!!!!!!!!!

Bloodhound Im a little confused. You say that you make good lean gains at 100-125mcgs. From what I have read and from experience as well T3 is extremely catabolic. Are you combating the T3 with high amounts of AAS or are you stating that it helps with gains? Also I noticed great results when taking great quality t3 at 100mcg a day for getting lean. For some reason I am extremely sensitive to carbs and dieting is extremely hard and would love to run it longer than just a few weeks. So my second question is, are you saying that you dont have a longer shut down of your thyroid (rebound effect) if your on for longer?

 

Much respect,

-Chief-

Another Study,Posted and used By Nandi

In (1) subjects were put on a month long T3 cycle: 50 mcg/day week 1; 75/day week 2; then 100/day weeks 3 & 4, then stopped abruptly. Six days after withdrawal TSH was back in the normal range; 8 days after withdrawal it had returned to baseline and then spiked above baseline until dropping back to baseline by day 42. The point being TSH recovery is very fast.

As for thyroid hormone levels, after going cold turkey T3 dropped to only 22% below baseline and had returned to normal within 2 weeks. The 22% drop in T3 compared to a 60% drop in T4 represents the "thermostat" upregulating conversion of T4 to T3 in a state of thyroid suppression.

Your thyroid will come back quickly after only a minor suppression of T3 (22%) during a relatively heavy cycle (100 mcg/day). I would not even worry about trying to speed recovery.

(1) J Clin Invest. 1984 Feb;73(2):570-5.

Peripheral tissue mechanism for maintenance of serum triiodothyronine values in a thyroxine-deficient state in man.

Lum SM, Nicoloff JT, Spencer CA, Kaptein EM.

Also,

In 1951, Greer reported the pattern of recovery of thyroid function after stopping suppressive treatment with thyroid hormone in euthyroid [normal] subjects based on sequential measurements of their thyroidal uptake of radioiodine. He observed that after withdrawal of exogenous thyroid therapy, thyroid function, in terms of radioiodine uptake, returned to normal in most subjects within two weeks. He further observed that thyroid function returned as rapidly in those subjects whose glands had been depressed by several years of thyroid medication as it did in those whose gland had been depressed for only a few days" (3)

These results have been subsequently verified in several studies.(3)(4) So contrary to what has been stated in the bodybuilding literature, there is no evidence that long term thyroid supplementation will somehow damage your thyroid gland."

Antony Roberts a dirt bag? I mean come on really,... why pick on dirt, more like a pile of money crap.

LMAO....How are you my old friend?...Good to see you over here..PH

I have used up to 100mcg but I dont know if i would go over that, Ive actually never even heard of someone going to 200mcg, im not sure how safe that is...but maybe i havent met the right people yet lol.

I have seen studies conducted and the dosing was around 250mcgs for several months...I don't go over 100mcgs for health reasons,,but more for the way it makes me feel..I will try and find the studies..

Great read Titan. But I can't imagine doing more than 100mcg of T3. At 100mcg i'm sweating like crazy and even my voice is shaky. Let alone go up to 200mcg (And adding clen).

Same with me....Not a big fan of going over 100mcgs...

Here is another great read on t-3

It is by Nandi....It is one of the better threads posted you will find around the net..Nandi was very knowledgeable and always backed his posts and threads up with Medical Studies.

Thyroid Hormone for Weight Loss:

Physiologic and Metabolic Effects

by Nandi

Introduction

It has been over 100 years since the discovery by Magnus-Levy that thyroid hormones play a central role in energy homeostasis, and 75 years since the hormones were first used for weight loss. Despite this great length of time, the precise mechanisms by which thyroid hormones exert their calorigenic effect are not completely characterized, and still actively debated. Despite numerous clinical studies having shown that the administration of thyroid hormone induces weight loss, it is not currently indicated as a weight loss agent. This is probably due to the number of side effects observed during thyroid hormone use at the relatively high doses used in the majority of obesity treatment studies. These deleterious effects include cardiac problems such as tachycardia and atrial arrhythmias, loss of muscle mass as well as fat, increased bone resorption and muscle weakness. Nevertheless, thyroid hormones, particularly triiodothyronine (T3) are a mainstay in the arsenal of drugs used by bodybuilders for fat loss. The widespread underground use of T3 warrants an understanding of its mechanism of action, as well as a knowledge of how it is most effectively and safely used, with an eye to minimizing side effects.

Thyroid Function and Physiology

Before jumping right into a discussion of the use of thyroid hormone for fat loss, a little review of thyroid function and physiology might be in order. The thyroid gland secretes two hormones of interest to us, thyroxine (T4) and triiodothyronine (T3). T3 is considered the physiologically active hormone, and T4 is converted peripherally into T3 by the action of the enzyme deiodinase. The bulk of the body's T3 (about 80%) comes from this conversion. The secretion of T4 is under the control of Thyroid Stimulating Hormone (TSH) which is produced by the pituitary gland. TSH secretion is in turn controlled through release of Thyrotropin Releasing Hormone which is produced in the hypothalamus. This is analogous to testosterone production, where GnRH from the hypothalamus causes the pituitary to release LH, which in turn stimulates the testes to produce testosterone.

In addition to T3, it has recently been recognized that there exist two additional active metabolites of T3: 3,5 and 3,3' diiodothyronines, which we will collectively call T2. Studies have shown that 3,3'-T2 may be more effective in raising resting metabolic rate when hypothyroid subjects are treated with T3, than when normal (euthyroid) subjects are given T3. Therefore in normal subjects 3,5-T2 may be the principal active metabolite of T3 (1)

Like the hypothalamic-pituitary-gonadal axis, the thyroid gland is under negative feedback control. When T3 levels go up, TSH secretion is suppressed. This is the mechanism whereby exogenous thyroid hormone suppresses natural thyroid hormone production. There is a difference though between the way anabolic steroids suppress natural testosterone production and the way T3 suppresses the thyroid. With steroids, the longer and heavier the cycle is, the longer your natural testosterone is suppressed. This is not the case with exogenous thyroid hormone.

An early study that looked at thyroid function and recovery under the influence of exogenous thyroid hormone was undertaken by Greer (2). He looked at patients who were misdiagnosed as being hypothyroid and put on thyroid hormone replacement for as long as 30 years. When the medication was withdrawn, their thyroids quickly returned to normal.

Here is a remark about Greer's classic paper from a later author:

"In 1951, Greer reported the pattern of recovery of thyroid function after stopping suppressive treatment with thyroid hormone in euthyroid [normal] subjects based on sequential measurements of their thyroidal uptake of radioiodine. He observed that after withdrawal of exogenous thyroid therapy, thyroid function, in terms of radioiodine uptake, returned to normal in most subjects within two weeks. He further observed that thyroid function returned as rapidly in those subjects whose glands had been depressed by several years of thyroid medication as it did in those whose gland had been depressed for only a few days" (3)

These results have been subsequently verified in several studies.(3)(4) So contrary to what has been stated in the bodybuilding literature, there is no evidence that long term thyroid supplementation will somehow damage your thyroid gland. Nevertheless, most bodybuilders will choose to cycle their T3 (or T4 which in most cases works just as well) as part of a cutting strategy, since T3 is catabolic with respect to muscle just as it is with fat. As previously mentioned, long term T3 induced hyperthyroidism is also catabolic to bone as well as muscle.

The proviso about T4 vs T3 for weight loss alluded to above needs some elaboration. There have been a number of studies that have shown that during starvation, or when carbohydrate intake is reduced to approximately 25 to 50 grams per day, levels of deiodinase decline, hindering the conversion of T4 to the physiologically active T3.(5) From an evolutionary standpoint this makes sense: during periods of starvation the body, teleologically speaking, would like to reduce its basal metabolic rate to preserve fat and especially muscle stores. However, a recent study demonstrating the effectiveness and safety of the ketogenic diet for weight loss recorded no change in circulating T3 levels.(6) So this issue not completely settled. Nevertheless, persons contemplating thyroid supplementation during ketogenic dieting might prefer T3 over T4 since the bulk of the research does suggest a decline in the peripheral conversion of T4 to T3 during low carb dieting.

Now that we have reviewed a little about thyroid function, let's consider just how it is that thyroid hormone exerts its fat burning effects.

Increased Oxidative Energy Metabolism

Thyroid hormone has long been recognized as a major regulator of the oxidative metabolism of energy producing substrates (food or stored substrates like fat, muscle, and glycogen) by the mitochondria. The mitochondria are often called the "cell's powerhouses" because this is where foodstuffs are turned into useful energy in the form of ATP. T3 and T2 increase the flux of nutrients into the mitochondria as well as the rate at which they are oxidized, by increasing the activities of the enzymes involved in the oxidative metabolic pathway. The increased rate of oxidation is reflected by an increase in oxygen consumption by the body.

T3 and T2 appear to act by different mechanisms to produce different results. T2 is believed to act on the mitochondria directly, increasing the rate of mitochondrial respiration, with a consequent increase in ATP production. T3 on the other hand acts at the nuclear level, inducing the transcription of genes controlling energy metabolism, primarily the genes for so-called uncoupling proteins, or UCP (see below). The time course of these two actions is quite different. T2 begins to increase mitochondrial respiration and metabolic rate immediately. T3 on the other hand requires a day or longer to increase RMR since the synthesis of new proteins, the UCP, is required (1).

There are a number of putative mechanisms whereby T2 is believed to increase mitochondrial energy production rates, resulting in increased ATP levels. These include an increased influx of Ca++ into the mitochondria, with a resulting increase in mitochondrial dehydrogenases. This in turn would lead to an increase in reduced substrates available for oxidation. An increase in cytochrome oxidase activity has also been observed. This would hasten the reduction of O2, speeding up respiration. These and a number of other proposed mechanisms for the action of T2 are reviewed by Lannie et al.(7)

What is the fate of the extra ATP produced during hyperthyroidism? There are a number of ways by which the increased ATP promotes an increase in metabolic activity, including the following:

Increased Na+/K+ATPase. This is the enzyme responsible for controlling the Na/K pump, which regulates the relative intracellular and extracellular concentrations of these ions, maintaining the normal transmembrane ion gradient. Sestoft(7) has estimated this effect may account for up to to 10% of the increased ATP usage.

Increased Ca++-dependent ATPase. The intracellular concentration of calcium must be kept lower than the extracellular concentration to maintain normal cellular function. ATP is required to pump out excess calcium. It has been estimated that 10% of a cell's energy expenditure is used just to maintain Ca++ homeostasis. (1)

Substrate cycling. Hyperthyroidism induces a futile cycle of lipogenesis/lipolysis in fat cells. The stored triglycerides are broken down into free fatty acids and glycerol, then reformed back into triglycerides again. This is an energy dependent process that utilizes some of the excess ATP produced in the hyperthyroid state (8). Futile cycling has been estimated to use approximately 15% of the excess ATP created during hyperthyroidism (8)

Increased Heart Work. This puts perhaps the greatest single demand on ATP usage, with increased heart rate and force of contraction accounting for up to 30% to 40% of ATP usage in hyperthyroidism (9)

Mitochondrial Uncoupling

As mentioned, the mitochondria are often characterized as the cell's powerhouse. They convert foodstuffs into ATP, which is used to fuel all the body's metabolic processes. Much research suggests that T3, like another much more potent agent DNP, has the ability to uncouple oxidation of substrates from ATP production. T3 is believed to increase the production of so called uncoupling proteins. Uncoupling protein (UCP) is a transporter family that is present in the mitochondrial inner membrane, and as its name suggests, it uncouples respiration from ATP synthesis by dissipating the transmembrane proton gradient as heat. Instead of useful ATP being produced from energy substrates, heat is generated instead. There are conflicting studies about the importance of T3 induced uncoupling. Animal studies have demonstrated an actual increase in ATP production commensurate with increased oxygen consumption as we discussed above. Other studies in humans have shown that in fact uncoupling in skeletal muscle does occur. This would contribute to T3 induced thermogenesis, with a resulting increase in basal metabolic rate.(10)

To make up for the deficit in ATP production (as well as provide fuel for the extra ATP production discussed above) more substrates must be burned for fuel, resulting in fat loss. Unfortunately, along with the fat that is burned, some protein from muscle is also catabolized for energy. This is the downside of T3 use, and the reason many people choose to use an anabolic steroid or prohormone during a T3 cycle to help preserve muscle mass. Studies have shown this to be an effective strategy (11). (Muscle glycogen is also more rapidly depleted, and less efficiently stored during hyperthyroidism. This may account for some of the muscle weakness generally associated with T3 use.)

Countering T3 induced muscle loss with AAS or prohormones makes sense from a physiological viewpoint as well. Thyroid hormone muscle protein breakdown is mainly mediated via the so-called ubiquitin-proteasome pathway. (12). (There are several independent metabolic pathways of protein breakdown in the body. For instance, another pathway, the lysosomal pathway, is responsible for the accelerated rate of muscle protein breakdown during and after exercise.) Testosterone administration has been shown to decrease ubiquitin-proteasome activity. (13) So AAS specifically target the muscle protein breakdown process stimulated by T3.

What may not be an effective strategy to maintain muscle mass during a T3 cycle is the use of exogenous growth hormone (GH). Studies have shown that when GH and T3 are administered concurrently, the increased nitrogen retention normally associated with GH use is abolished. This has been attributed to the observation that T3 increases levels of insulin like growth factor binding protein, reducing the bioavailability of igf-1 (14). Nevertheless, GH has fat burning properties independent of igf-1, so using GH with T3 would act additively to speed fat burning, but with little if any preservation of lean body mass. So again, if GH is used in conjunction with T3, anabolic steroid/prohormone use would be indicated.

Andregenic Receptor Modulation

Administration of T3 has been shown to upregulate the so-called beta 2 adrenergic receptor in fat tissue. What is the significance of this effect for fat loss? Before fat can be used as fuel, it must be mobilized from the fat cells where it is stored. An enzyme called Hormone Sensitive Lipase (HSL) is the rate-controlling enzyme in lipolysis, or fat mobilization. The body produces two catecholamines, epinephrine and norepinephrine, which bind to the beta 2 receptor and activate HSL. The upregulation of the beta 2 receptor due to T3 results in an increased ability of catecholamines to activate HSL, leading to increased lipolysis.

Bodybuilders often use drugs like clenbuterol, which bind to the beta 2 receptors and activate them in the same way as the body's endogenous catecholamines. The use of clenbuterol along with T3 can produce an additive lipolytic effect: T3 increases the number of receptors, while clenbuterol binds to the receptors activating HSL and increasing lipolysis. Since clenbuterol itself downregulates the beta 2 receptor, most bodybuilders use clenbuterol in a two week on/ two week off cycle, the rationale being that this minimizes downregulation and allows receptor recovery. Another option is to use the antihistamine Ketotifen concurrently with the clenbuterol. Studies have shown that Ketotifen attenuates the beta 2 receptor downregulation caused by clenbuterol (15). Moreover, research in AIDS patients has shown that Ketotifen blocks the production of the proinflammatory and catabolic cytokine TNF-alpha (16). This may be of relevance to bodybuilders since there is evidence showing TNF lowers both testosterone and IGF-1 levels quite significantly (17) (18), while strenuous exercise elevates TNF levels. (19)

Besides increasing beta 2 receptor density in adipose tissue, T3 upregulates this receptor in human skeletal muscle (12). This has some very intriguing if somewhat speculative implications for the combined use of clenbuterol and T3. Animal studies have shown that catecholamines, particularly clenbuterol, inhibit Ca++ dependent skeletal muscle proteolysis (20). Like the lysosomal and ubiquitin-proteasome pathways discussed above, Ca++ regulated proteolysis is yet another way for the body to degrade muscle protein. Again the implications are enticing: Increased beta 2 receptor density from T3 use, coupled with the beta 2 agonist clenbuterol, could slow this pathway of muscle catabolism.

Another adrenergic receptor important to lipolysis is the alpha 2 receptor, which impedes fat mobilization by counteracting the effects of the beta 2 receptor. There are some conflicting studies about the effects of T3 on the alpha 2 receptor, with studies showing either a downregulation (21) or no effect (22). If T3 does in fact downregulate alpha 2 receptors, this would further aid lipolysis.

Studies in rats have shown that inducing hyperthyroidism increases the lipolytic beta 3 receptor density in white adipose tissue by 70% (23). Beta 3 receptors are abundant in human white adipose tissue as well, and if T3 administration has the same effect in humans, this could could contribute significantly to T3 induced fat loss. This might also argue for taking a currently available beta 3 agonist such as octopamine along with T3 and perhaps clenbuterol.

Decreased Phosphodiesterase Expression

In hyperthyroid patients as well as in normal subjects given T3, levels of the enzyme phosphodiesterase are lowered in fat cells (20). When lipolytic hormones like epinephrine (adrenaline) bind to the beta 2 receptor described above, they initiate a signaling cascade mediated by the so called “second messenger” cyclic AMP (cAMP). cAMP in turn acts on other cellular enzymes to initiate and maintain lipolysis. The original signal is terminated when cAMP is degraded by the enzyme phosphodiesterase. Clearly, maintaining elevated cAMP levels, by lowering phosphodiesterase concentrations with T3, will prolong lipolysis.

As an aside, caffeine is thought to exert at least a portion of its lipolytic action by lowering phosphodiesterase in fat cells. Interestingly, Viagra and cialis are also phosphodiesterase inhibitors but their action seems to be limited to relaxing vascular smooth muscles.

Increased Growth Hormone Secretion

In vitro, animal, and human studies have all demonstrated that T3 administration increases growth hormone production. (24)(25) Since GH is calorigenic aside from any increase in igf-1, elevated GH may contribute to some of the fat burning associated with T3 administration. This effect may obviate the need for the use of expensive recombinant HGH, as mentioned above.

Decreased Insulin Secretion

Insulin is well known as a lipogenic hormone. It promotes fat storage by facilitating the uptake of fatty acids by adipocytes, and reducing lipid oxidation in muscle tissue. Several studies have shown that thyroid hormone is associated with glucose intolerance resulting from decreased glucose stimulated insulin secretion (26).

This defect in insulin secretion is believed to result from an increase in the rate of apoptosis (programmed cell death) of pancreatic beta cells as a direct effect of thyroid hormone excess.(27) This process is reversible, since when thyroid hormone is withdrawn the rate of beta cell replication increases until homeostasis returns. However, there are conflicting studies regarding the effects of T3 on insulin. For example, Dimitriadis et al (28) showed a decrease in glucose stimulated insulin secretion, consistent with (25), but an increase in basal insulin. They also observed increased insulin clearance, with a compensatory increase in basal insulin secretion.

So if in fact the hyperthyroid state is associated with lower insulin levels, this could explain a portion of hyperthyroid stimulated lipolysis. The obvious downside here is that insulin is also an anabolic hormone. Basal insulin concentration is thought to limit the action of the ubiquitin-proteasome degradative pathway of muscle protein breakdown (29). Of course supplementing with insulin during T3 use would be counterproductive. However, as mentioned above, anabolic steroids inhibit ubiquitin-proteasome activity, so their use could counter any loss in muscle anabolism resulting from a drop insulin levels.

The Future

As mentioned at the beginning of this article, a major roadblock in the adoption of T3 by the medical community as an antiobesity agent is its deleterious effect on the heart. Recent research has identified two isoforms of the thyroid hormone receptor, TRalpha and TRbeta. The TRalpha-form may preferentially regulate the heart rate, and an experimental agent, GC-1, has been developed that selectively binds the TRbeta receptor, with minimal effects on the heart (30). The distribution and actions of TRalpha and TRbeta throughout the body are not yet well characterized. However should it turn out that TRalpha is specific to the heart, then drugs like GC-1 may turn out to be effective fat burning agents with a much safer profile that T3 or T4.

One alleged “futuristic” agent that is here now is T2, or 3,5-Di-iodo-L-thyronine, the T3 metabolite discussed above. Unfortunately, this product does not live up to its hype. It has been claimed to be as or more effective that T3 for fat burning with minimal suppression of endogenous thyroid production. Regarding the relative effectiveness of T2 as a lipolytic agent, and its effect on TSH, this topic was thoroughly covered in a recent article by Bryan Haycock in Muscle Monthly:

All of my research into this subject has led me to the same conclusion reached by Mr. Haycock. That is, T2 is only slightly less suppressive of TSH than is T3, and only packs a portion of the lipolytic punch of T3, with no ability to increase the expression of the UCPs, which is a major determinant of the action of thyroid hormone.

Summary

We have discussed a number of ways by which T3, and its active metabolite T2 act to increase resting energy expenditure. Also discussed were some drawbacks of T3 use, such as cardiac stress, as well as the potential loss of muscle mass. It is ironic that the latter may be of more concern to many bodybuilders that the other more serious potential impacts on health. Nevertheless, used moderately and for short periods (a couple of months or less) in people with no preexisting cardiovascular disease T3 has a relatively safe medical profile, compared to other lipolytic agents like DNP. Perhaps most importantly we have presented substantial evidence that even the long-term use of supra-physiological levels of T3 does not damage the thyroid gland.

__________________

Welcome...PH

just to throw my 2 cents in...

 

I think the mods do a good job keeping on top of things here at AB.

 

. .

db

. .

#1 Thanks DB

#2 This thread is getting a little off topic and out of hand..Lets please remain civil and constructive while dealing with this problem...

#3 Mods are here to help and dedicate time to problems and share knowledge and info with the members of this site...However, we all have lives outside the boards..Jobs, Family, Hobbies etc...We try to be here for you,,but it helps us to be contacted by members when these problems arise so we can address them and help...Believe me the last thing we want is for anyone to get scammed here in our community....

#4 None of us here have heard from BB and would like to think his longtime rep would be worth more than 500$...I would like to get all of the facts before making any assumptions...500$ is 500$,,but not enough for a well respected mod to reverse scam. I do understand the frustration incurred by Hal.....

Not sure I want to see it in 3d.....

Welcome to AB...PH

Welcome to AB..PH

Glad to have you with us...Welcome PH

The same as Titan posted..BTW, thanks for sharing that link Titan.

At this time, we do not have any info on Stormy...From the looks of it, he owes a few people and is not returning emails etc...PH

Some might know me from bodybuilding.com where i mod, and i've been ALL over... triedia, osbb (the original) ssb, etc. like the new set up I'm not a real fan of black boards like it used to be...

good to see you BOZZ...Longtime, how you been?

See Some Famailiar Faces Here...i'm Here To Help Gk And Woody With Any Issues

Nice to have you with us 69...How are you?

Looking to buy a new laptop....So far I have had a few dells, and a gateway, and both crapped out a little early....Any ideas/

For the most part, he has had trouble in the past with customs etc...Also, in the past he was labeled as somewhat of a selective scammer around the net...He has been around the sites for as long as I can remember and that is about 10yrs or so...I used him in the past, long ago, and sometimes the packs would never make it or get seized...However, he did always resend and it may take awhile but for the most part, I always got what I ordered....Again, look around and do some homework, read reviews, ratings and make your own call...Nothing is ever a sure thing...No matter how a ****** is rated...PH

I to thought he was good to go and he was till he fucked up. Made couple order registered with dc# all good. Made another order registered with DC# got first pack record time, tracked second pack returned to sender illegible address. Wrote O an email no reply for a week and half. Finally he replied go to PO and pick it up. Wrote him back tried that it was returned to sender. Asked about 100% reship guarantee after another week got reply pack shipped gave me dc# well tracked it It was delivered about 30states over from mine. Wrong DC# sent O mail again been 3 more weeks and have not heard shit nothing nadda. Not the only one over there going through this he may be turning scammer. All it wouold take is a fucking email explaining whats up but guess thats to much to ask for him. Alot of paople say he selling fakes as well

In the past he has been slow to answer emails...So, dont loose all hope yet..P

Thanks guys!! wasn't sure because I know some area codes are HOT! Thanks again ...cLeRks

Well, I live here and no big worries...Alot of times, some sources would prefer sending to 0-3 zips..P

by Jbig on SSB....

This is a very common question, and instead of retyping this in every PM, I'll just make a sticky. This will be applicable to any brand of GH and any vial size.

OK, you have your vial of lyophilized GH (powder). No matter the brand, you know how many IUs are in each vial, as that will be noted on the vial. If it's in terms of mgs, just assume (estimate) that 1mg = ~3IU.

It does NOT matter how much water (BW or sterile water) you use. I tend to use more than what most kits include, because this makes it more dilute and means that you're less likely to leave some behind in the vial and syringe.

Pick a volume of water to add to your vial....I don't care what it is. For a 10IU vial, I use 2mL, but between 1 and 2mLs is good IMO.

use a syringe with a 1" or better yet a 1.5" needle attached to reconstitute. Load the syringe with water (BW ideally, but sterile water is fine, despite popular belief). Hold the plunger so that when inserting the needle into the GH vial the vacuum doesn't suck the water out. Once the needle is inserted, angle it so that the needle tip is pointed at the side of the vial....not directly at the powder. Now, simply release the plunger and allow the vacuum force to suck the water out into the vial. Remove the needle and gently swirl the GH vial until fully reconstituted.

Now measuring....this is much easier than people make it out to be. Just use this generic formula:

You know how many IUs are in your vial. You also know how much water was used to reconstitute it (since you just added it). how many IUs do you want to inject? 2IU? Fine, so be it. say your vial was a 10IU vial, 2IU is 20% of 10IU, so you simply draw up 20% of the total volume used to reconstitute your GH. If you used 1mL for a 10IU vial, and you want to draw 2IU, then you simply draw 0.2cc. if you used 2mL for a 10IU vial, you'd draw 0.4cc (since 20% of 2mL is 0.4cc). Most everyone is using a U-100 insulin syringe for GH injections. Each 10IU mark is 0.1cc, so the 20IU mark is 0.2cc, you can figure out the rest.