Steroids confiscated in the investigation were marketed to be used with animals via public web sites.
DEC 15–WASHINGTON, DC – DEA Administrator Karen P. Tandy today announced the arrest of Albert Saltiel-Cohen, owner of three of the world’s largest anabolic steroid manufacturers, as part of the largest steroid enforcement operation in U.S. history. Operation Gear Grinder is a 21-month Organized Crime Drug Enforcement Task Force (OCDETF) investigation that targeted eight major steroid manufacturing companies, their owners, and their trafficking associates. By reviewing the sources of all seized and analyzed steroids submitted to the DEA’s forensic laboratories, DEA intelligence analysts and diversion investigators found that 82 percent of the steroids seized and analyzed are of Mexican origin. A large majority of those 82 percent seized and analyzed steroids originate from the eight companies identified in Operation Gear Grinder. These businesses conducted their sales via the Internet, and DEA estimates their combined total U.S. steroid sales are $56 million per year.

“Steroid traffickers market their product by luring young people with promises of enhanced performance and appearance,” DEA Administrator Karen P. Tandy said, “but what they don’t say is the illicit use of these harmful drugs can destroy the very bodies that they are supposed to improve. Drug traffickers prey on the belief that steroids enhance ability, but steroids only rob that ability, as we have seen so often from the affected lives of too many youth and professional athletes.”

Operation Gear Grinder is part of the Virtual Enforcement Initiative, a coordinated DEA effort to target illegal Internet drug trafficking, which was launched in April with Operation Cyber Chase and continued in September with Operation CYBERx. DEA’s cyber initiative acknowledges drug traffickers are embracing the use of 21 st century technology to further spread their virus into U.S. communities.

The steroid manufacturers involved in this investigation tried to mask the true consumers of these products by marketing them as being developed and sold for use in animals. The veterinary manufacturers (“laboratorios”) took notice of the demand for anabolic steroids and created a marketing strategy tailored to the needs of the U.S. consumer – to include high-quality products and internet websites. Communications via the Internet and parcel distributions were the core of these companies’ operations. The websites showcase the products and offer an email address to exchange prices and tracking numbers, and give ordering and payment instructions.

These eight companies used U.S.-based email addresses and listed each manufacturer utilizing a business website to place their products in the hands of American consumers. Some manufacturers provided direct referrals to distributors through the Contact Us section of the websites. The steroids were smuggled into the United States, and shipped to customers. In addition, steroids from the eight companies were also shipped to U.S. traffickers, who re-sold the products to their customers. Financial transactions were primarily done via Western Union wire transfers, as well as bank transfers and credit card payments.

These groups also supplied numerous pharmacies along the U.S./Mexico border, where U.S. customers could purchase steroids and smuggle them back across the border into the United States.

In addition to the Saltiel-Cohen arrest and indictments, DEA today arrested 4 steroid trafficking suspects in San Diego and Laredo, TX. As part of Operation Gear Grinder, DEA also identified over 2,000 U.S. customers that have received steroids from the businesses indicted today. These customers consist of individual users, street-level dealers, and organized trafficking groups in dozens of cities across the country.

The Southern District of California has issued indictments charging the companies and individual defendants with the following:Title 21, U.S.C., Secs. 952, 960 and 963 – Conspiracy to Import Anabolic Steroids; Title 21, U.S.C., Secs. 846 and 841(a)(1) – Conspiracy to Distribute Anabolic Steroids; Title 18, U.S.C., Sec. 2; Title 18, U.S.C., Secs. 1956(h) and 1956(a)(1)(A)(I) – Conspiracy to Launder Money; Title 21, U.S.C.,Sec. 853(a), Title 18, U.S.C.,Sec. 982 and Title 21, U.S.C.,Sec. 853(p) – Criminal Forfeiture.

Manufacturing Targets

1. Companies: Quality Vet, Denkall, and Animal Power
Owners: Alberto Saltiel Cohen, Joaquin Garcia Rivas, and Javier Garcia de la Pena.
These manufacturers are significant U.S. suppliers of Nandrolone

2. Company: Laboratorios Tornel
Owner: Luis Bravo-Tornel
Manager: Mauricio Bravo-Berentsen
This manufacturer is a top U.S. supplier of Testosterone Decanoate

3. Company: Laboratorios Brovel

Owner: Arturo Bravo-Valdes
This manufacturer is a top U.S. supplier of Nandrolone Decanoate

4. Company: Pet’s Pharma
Owner: Ramon Vargas
Co-Owner-Eduardo Hernandez
This manufacturer is a top U.S. source of Testosterone Enanthate

5. Company: Syd Group
Owner: Armando Guzman-Armenta
Associate: Amalia Lara
This manufacturer is a top U.S. source of Stanozolol

6. Company: Loeffler

Officer: Jose Angel Garcia-Hinojosa
This manufacturer is a top U.S. source of Methandrostenolone

Operation Gear Grinder was coordinated by the DEA Special Operations Division. DEA offices in San Diego, Mexico City, Tijuana, New York, Houston, San Antonio, and Laredo, Texas participated in the investigation.

This investigation was a collaborative effort involving DEA, numerous U.S state and local law enforcement agencies, and the Mexican Federal Agency of Investigation (AFI).

Study: bodybuilders grow on 10mg dianabol per day

Way back in 1975, sports scientists at Manchester University in England made a discovery that mainstream science would only come to accept twenty years later. The researchers gave bodybuilders who worked out in fitness centres pills containing the anabolic steroid Dianabol, produced by the CIBA Laboratories. They discovered that these accelerated muscle growth. “Their improvements were significantly greater on methandienone than on placebo”, the Brits wrote.

The researchers got thirteen athletes to participate in their experiment, and gave them either a placebo or Dianabol. They had known since 1969 that bodybuilders used steroids and that there was lively clandestine trade in the substances. They also knew that women sometimes took steroids and that stories were doing the rounds of users who took over 300 mg of Dianabol per day. The scientists did their experiment to find out whether steroids really had any effect on athletes.

They gave their test subjects either 10 or 25 mg of Dianabol per day. Some of the athletes started with the steroids and ended with a placebo, and the others did it the other way round. All athletes could tell whether they were using a steroid or the fake. When they were using the blue CIBA pills they felt “prima-donna-ish”, or made, in their own words, “fantastic improvements”. The athletes’ progression is shown below. It is not clear from the article how the researchers measured progress. They did mention though that the group on 10 mg of Dianabol per day made as much progress as the group on the higher dose.

Anabolic steroids in athelics: crossover double-blind trial on weightlifters.

Any more than 500IU of HCG per day causes too much aromatase activity. Some feel aromatase is actually toxic to the Leydig cells of the testes. You are then inducing primary hypogonadism (which is permanent) while treating steroid-induced secondary (hypogonadotrophic) hypogonadism (which is temporary–hopefully).

If 250IU or 500IU on two days each week isn’t enough to stave off testicular atrophy, then I recommend using it more days each week (as opposed to taking larger doses). In fact, I wouldn’t mind having a guy use 250IU per day ALL THROUGH the cycle. Those that have tell me they thus avoid that edgy, burned-out feeling they usually get. They also say they simply feel better each day. Subjective reports, to be sure, but they are hard not to appreciate. Especially when HCG is so inexpensive.

The testes are then ready, willing and able to again produce testosterone at the end of the cycle. LH levels rise fairly rapidly, but endogenous testosterone production is limited by lack of use. I also want to make sure a SERM, such as Clomid or Nolvadex, is at effective serum dosage (around 100mg QD for Clomid, 20-40mg QD for Nolvadex) when serum androgen levels drop to a concentration roughly equal to 200mg of testosterone per week. That is when androgenic inhibition at the HP no longer dominates over estrogenic antagonism with respect to inducing LH production. Of course, if the fellow has been doing Clomid or Nolvadex all along the way (and I now prefer Nolvadex over Clomid, due to the possibility of negative sides from the Clomid), he is all set to simply continue it at the end (no need to switch from one to the other). BTW, I see no evidence of any benefit in using BOTH SERM’s at the same time. I used to think a couple of weeks of the SERM was enough; now I like to see an entire month after the last shot of AAS (and migration of long to short esters as the cycle matures). Tapering the SERM is probably a good idea during the last week, as well.

I want my patients to stop taking HCG within a week after the end of the cycle. The testosterone production it induces will further inhibit recovery, as will using Androgel, or any other testosterone preparation, while in recovery. There is no escaping this, as there is no such thing as a “bridge”. Just because you are not inhibiting the HPTA for the entire 24 hours does not mean you are not suppressing it at all. IOW, you can’t “fool” the body—it is smarter than you are.

I like arimidex during the cycle (in fact, consider use of an AI while taking aromatisables a necessity) but it ABSOLUTELY should not be used post cycle (even though it has been shown to increase LH production) because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile, is too great (this also drives libido back into the ground—and we don’t want that, do we?).

All this is meant to get my guys through recovery as fast as possible (the real goal, yes?). So far, all of them who have tried it have reported they are recovering faster than when they have tried other protocols.

One of the most significant side effects of anabolic/androgenic steroid (AAS) use is inhibition of natural testosterone production. There is no way to entirely avoid the problem, but there are ways to minimize the problem and recover natural testosterone levels reasonably quickly after a cycle. In this article, we will look at the problem of inhibition, its causes, and the best solutions currently known.
The Causes of Inhibition

Elevated hormone levels, in general, will cause inhibition of natural testosterone production. Many bodybuilders have come to believe that elevated estrogen levels alone are the sole cause of inhibition, and believe that by blocking estrogen, they can block inhibition.

This is not true. For example, consider the results seen in the second 2-on / 4-off cycle case study reported on Meso-Rx where Jim used 50 mg/day of trenbolone acetate, which does not aromatize, 50 mg/day of Dianabol, which does aromatize, with 250 mg/day of Cytadren as an aromatase inhibitor and 50 mg/day Clomid as an estrogen receptor blocker. His estrogen levels remained in the normal range, though elevated from baseline, since apparently the Cytadren was not sufficient to block aromatization completely. The Clomid should easily have been able to overcome normal estrogen levels, and so if the estrogen-only theory of inhibition were correct, Jim should have been suffering no inhibition. But the fact is, his testosterone levels dropped to only 1/10 his baseline value. Estrogen alone was not the cause of his inhibition. It could not have been the cause of any of it, given the normal levels and the Clomid use.

So much for the estrogen-only theory of inhibition that has been claimed by other writers. That isn’t to say, though, that estrogen is not also inhibitory: it is.

What then besides estrogen can cause inhibition? DHT, which does not aromatize, has been extensively shown to cause inhibition of testosterone production. Androgen alone, then, is sufficient to cause inhibition. In Jim’s case, androgen use was moderately heavy, and androgen alone would seem the cause of the inhibition.

Progesterone is another hormone that can cause inhibition, when used long-term. Paradoxically, in the short term it can be stimulatory. Other relevant factors include beta agonists, opiates, melatonin, prolactin, and probably other compounds. With the exception of beta agonists (e.g. ephedrine and Clenbuterol) and opiates (natural endorphins on the one hand being inhibitory, and Nubain blocking such inhibition) manipulation of these would not seem useful in bodybuilding.
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The Hypothalamic/Pituitary/Testicular Axis (HPTA)

To understand inhibition of testosterone production, we need to know first how it is produced and how production is controlled. The broad general picture is that the hypothalamus receives a variety of inputs, for example, levels of various hormones, and decides whether or not more sex hormones should be produced. If the inputs are high, for example, high estrogen or high androgen or both, then it decides that little or no sex hormones should now be produced, but if all inputs are low, then it may decide that more sex hormones should be produced. It seems that the hypothalamus doesn’t respond only to current hormone levels, but also to the past history of hormone levels.

The hypothalamus itself cannot produce any sex hormones – instead it produces LHRH, or luteinizing hormone (LH) releasing hormone, also called GnRH (gonadotropin releasing hormone.) This then stimulates the pituitary gland.

The pituitary uses the amount of LHRH as one of its signals in deciding how much LH it should produce. Proper response depends on having sufficient receptors for LHRH. These receptors must be activated for LH to be produced. The pituitary also uses sex hormone levels, both current and the past history, in deciding how much LH to produce. Some aspects of the pituitary’s behavior are peculiar. For example, too much LHRH results in the pituitary downregulating LHRH receptors, with the result that very high LHRH production, which one would think should result in high testosterone production, actually lowers testosterone production. Another oddity is that while high estrogen levels inhibit the pituitary, still some estrogen is required to maintain a high number of LHRH receptors. So both very low and high levels of estrogen can inhibit LH production.

LH produced by the pituitary then stimulates the testicles to produce testosterone. Here, the amount of LH is the main factor, and high levels of sex hormones do not seem to cause inhibition at this level.
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Inhibition From AAS Cycles

Because high androgen levels sustained around the clock will cause inhibition, traditional cycles simply cannot avoid inhibition of LH production while on cycle. There are three ways to avoid it:

Avoid having high androgen levels around the clock. This can be done, for example, by using oral AAS only in the morning, with the last dose being approximately at noontime. Even 100 mg/day Dianabol can be used in this fashion with little inhibition. The problem with this approach is that gains are not very good compared to what is seen when high androgen levels are sustained around the clock.
Use an amount and kind of AAS that is low enough to avoid much inhibition. Primobolan at 200-400 mg/week may achieve this effect. Again, gains will be compromised compared to a more substantial cycle. Testosterone esters and Deca are substantially inhibitory even at 100 mg/week so using a low dose of these drugs will simply result in both inhibition and poor gains.
In principle, one could use an antiandrogen, but this would totally defeat the purpose of the cycle.
Where AAS doses are sufficient for good gains, an interesting pattern is seen. For the first two weeks of the cycle, only the hypothalamus is inhibited, and it produces much less LHRH as a result of the high levels of sex hormones it senses. The pituitary is not inhibited at all: in fact, it is actually sensitized, and will respond to LHRH (if any is provided) even moreso than normally. After two weeks however, the pituitary also becomes inhibited, and even if LHRH is provided, the pituitary will produce little or no LH. This then is a deeper type of inhibition. After this point, there seems to be no definite further “switching point” where inhibition again becomes deeper and harder to reverse. As a general rule, I would say that there seems to be little difference between using AAS for 3 weeks vs. 8 weeks: recovery is about the same either way. Between 8 and 12 weeks, it becomes more and more likely that recovery will be difficult and slow, though even at 12 weeks it is common for recovery to not be too problematic, taking only a few weeks. Cycles past 12 weeks seem much more likely to cause substantial problems with recovery. In the hundreds of consultations I have done for people with recovery problems, very few (I can recall two) were for very short cycles such as 6 weeks, while most were for usages of 12 weeks straight or more.

I do not know what changes take place in the hypothalamus and pituitary over a long period of time that result in this problem, but it certainly is true that long-term inhibition makes recovery more difficult on average. I suspect the problem may have to do with change in the “clock” that regulates the pulse rate of LHRH secretion, but I am not sure that that is so.
Drugs of Use With Regard to Inhibition

Cytadren: This drug can be used to reduce conversion of testosterone, Dianabol, and Equipoise (not an exclusive list of aromatizable AAS, but the main ones) to estrogen. Some feel that when estrogen levels are kept under control during the cycle, recovery is faster after the cycle is over, though that is not proven. It is a good idea though. And if testosterone esters were used prior to ending the cycle, some levels of these will remain for weeks, and continued use of Cytadren will help prevent conversion to estrogen, and thereby reduce inhibition. The best dosing pattern, in my opinion, is to take ½ tab (125 mg) on arising, and then ¼ tab at six and 12 hours later. Use of more Cytadren than this, or a different pattern, may lead to an adverse effect on cortisol production, with subsequent cortisol rebound after discontinuing the drug. Some individuals suffer some lethargy (feeling of tiredness and laziness, or sleepiness) from Cytadren, but that is uncommon at this dose.

Arimidex: This accomplishes the same purposes as Cytadren but without the possible side effects mentioned above. It is however far more expensive. A typical dose is 1 mg./day. The timing of the dosage does not matter, since the drug has a long half-life.

Clomid: After a cycle is over, Clomid at 50 mg/day is usually very effective in restoring natural testosterone production. It acts by blocking estrogen receptors at the hypothalamus and pituitary. If androgen levels are not elevated, this is enough to cause production of at least normal amounts of LH, or often more LH than normal. During the cycle Clomid cannot prevent inhibition, though some think using it during the cycle will allow a faster recovery afterwards. That is not proven though. If nothing else, though, it is useful as an antigyno/antibloating agent during the cycle.

Nolvadex: This works in the same manner as Clomid, but not nearly so well with regard to reversing inhibition. It is better to use this only as an anti-gyno/antibloating agent, if at all. If Clomid is used, there is no need for Nolvadex.

HCG: This does nothing with regard to inhibition of the hypothalamus and pituitary. Rather it acts like LH, and causes the testicles to produce testosterone just as if LH were present. It is useful then for avoiding testicular atrophy during the cycle. The best dosing method is to use small amounts frequently: 500 IU per day is sufficient, and 1000 IU may optionally be used. The amount may be given as a single daily dose or divided into two doses. Administration may be intramuscular or subcutaneous. More is not better: too much HCG can result in downregulation of the LH receptors in the testes, and is therefore counterproductive. Overdosing of HCG can also result in gynecomastia.

Ephedrine/clenbuterol: It is possible that the beta agonist activities of these drugs may assist in recovery. Personally, I do recommend the use of ephedrine post-cycle to those who can use it. Clenbuterol has the same effect but acts around the clock, having a longer half life, and allowing a higher effective dose (amount times potency) due to having less relative effect on beta receptors in the heart. I am not sure that Clenbuterol has any better effect with regard to recovery though.

Oral AAS: These do not assist recovery of natural testosterone production, but if used only in the morning, can help sustain muscle mass while in the recovery phase, with little or no adverse effect on recovery.

Tribulus: If this is of benefit, I have not been able to observe it myself. I have only tried the Tribestan brand, but this is the brand that earned tribulus its reputation.

Melatonin: While disrupted sleep patterns definitely inhibit recovery, I have seen no evidence that taking melatonin at night speeds recovery. It is useful though for those who have allowed their sleep patterns to be disrupted and who wish to reset their natural clocks.
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General Recommendations

Pharmaceutical drugs should of course not be self-prescribed: the following are simply recommendations of what works well, not of what to do without physician’s advice. Enough said.

The best cycle plans are either brief two week cycles with short acting drugs, which allow a very fast recovery (less than one week) or cycle of approximately 6-10 weeks, which usually allow reasonable recovery and allow quite a bit of time to make gains. Cycles in the 3-5 week range are less efficient because they combine the disadvantage of relatively little time gaining with the disadvantage of slower recovery.

If a cycle lasts 8 weeks or longer, I think it is best to use HCG during the cycle if possible, as described above. HCG should not be used during the recovery itself since it will increase androgen and estrogen levels, which will be inhibitory to the hypothalamus and pituitary. Clomid use should begin, if it was not used during the cycle, as soon as androgen levels drop enough that recovery becomes possible. This would be about two weeks after the last injection of long acting steroid esters, assuming reasonable doses such as 500 mg/week. Clomid use should start with 300 mg on the first day (50 mg six times) to quickly get blood levels as high as needed, and then maintained with 50 mg/day. This is needed because of the half-life of the drug. It should be continued until one is sure that natural testosterone production is back and testicle size is returned to normal, with the exception that if use has been more than about 6 weeks, one might try dropping it for a few weeks to see what happens. If no further improvement occurs, then Clomid would be resumed. It has been studied medically for long-term use and found safe for periods of at least a year. However, a small percentage of users develop vision problems from Clomid, which are generally reversible upon discontinuing the drug. So if you have this problem, certainly the drug should be discontinued.

If aromatizable injectables were used, an antiaromatase would be useful for 3 weeks or so after the last injection, or 4 weeks if dosage was high (a gram per week or more.)

Lastly, ephedrine seems to be of some help. The same dose as used for dieting (e.g. 25 mg three times per day) seems quite sufficient.

Long term inhibition can potentially be a serious side-effect of AAS use, and this risk should be minimized by avoiding excessively long cycles. This really does not compromise gains greatly, since the body cannot grow rapidly week in, week out, 52 weeks per year anyway. And even moderate post-cycle inhibition is something we wish to minimize, since it is frustrating to lose much of one’s gains in the first few weeks after a cycle as a result of low natural testosterone and no AAS being used. The advice given above is generally successful in minimizing such losses, and I hope you will find it useful

If you use a long ester such as deca at xmg/week, it will take you 4-5 weeks to build up to max blood concentrations possible for xmg/week. So half of your cycle is not wasted, but you are not maximizing efficiency.

When coming off a cycle, the waiting period before Clomid therapy begins will vary depending on the type and dose of the AAS. If you ran 500mg/week of deca for 10 weeks, a month after your last shot, you will still have around 200mg of esterified deca in your system. This is more than enough to prevent recovery. This is the reason why recovery is more difficult with a deca (or another long acting ester).

Let’s calculate the amount accumulated in the body after 6 weeks of 500mg/deca. Let’s say you inject it once a week and we’ll give it a 1.5 week half life. Note that injection frequency makes a huge difference in blood concentration stability but no difference in amount of esterified in the system

E (greek letter “sigma”) 500*e^(ln(1/2)n/1.5) from n=0 to n=6. So after 6 weeks, about 1300mg of esterified nandrolone remain in the body.

Now lets see how long, after the initial injection, it takes to reduce to a small enough amount that permits recovery.

1300*e^(ln(1/2)n/1.5) After 3 weeks, 325 mg of esterified remain

after 6 weeks, 81 mg of esterified remain.

After 8 weeks, 32mg of esterified remain.
Most guys go with “time on=time off.” This will not work with long esters as I have demonstrated above. For at least a month after your last shot you are in what I call a “time in-effiency” period where you are no longer reaping the benefits of you AAS but you are not recovering either. The goal of the modern cycle is to minimize this wasted time.

The key components are:
1) Front end loading this cuts down on wasted time in the beginning of your cycle waiting for the doses to reach full theraputic levels. This concept has been used before but (as far as I know) I was the first one to quantify it mathmatically. Zyg has taken the math one step further with a graph showing, visually, the importance. Graph of eq loading

The use of orals in the beginning of a cycle is a popular component of a cycle. While I don’t feel it is a nessecity, it too is a (different) type of front end load. For the advnaced BBer, dbol should be taken in the beginning of a cycle as well as loading the injectables since the anabolic response from dbol is alleged to be by a different mechanism than most injectables. If one had to chose between a dbol load and and injectable load, in most cases, the injectable load should be prefered over the dbol load.

2) Injection frequency This is crucial to obtaining even blood concentrations of androgens. Ideally, the more often injected, the better. An acceptable rule of thumb is “inject at half of the half life.” For instance, if the half life of a steroid is 7 days, this should be injected at least twice weekly. For cycles that involve multiple injectables, the injections should be fractioned out and divided up based on the injectable with the shortest half life. For instance, if you were doing a test propionate and deca cycle, the old school way to do it would be to inject the prop EOD and the deca once a week. Both compounds should not be viewed as separate, but together with total androgen concentration taken into consideration. If you injected the deca only once a week, probably along with one of the propionate injections, that day will have a much larger spike on total blood androgen concentrations. Instead, the deca should be split up and taken with the propionate injections, EOD. This way there is no one day of the week that has a “spike” and even blood concentrations are maintained throughout the week.

3) Ending the cycle Switching to shorter esters toward the end of a cycle makes perfect sence however not too many guys incorporate this practice- perhaps because of the lack of variety of drugs. The modern cycle should include replacing long ester injectables with shorter ones so that recovery time is made more efficient. The necesity of switching to shorter esters toward the end of a cycle depends on the type of drugs used. Longer esters such as deca and eq should be replaced with shorter acting versions of these compounds no later than four weeks before the end of a cycle. Medium length esters such as t-enanthate and cypionate should be replaced no later than three weeks before the end of a cycle. A couple examples of appropriate replacements are: trenbolone acetate and testosterone propionate. There is no need to “load” these compounds in the middle of a cycle since 1) they are already “fast acting” and 2) blood androgen concentrations are already high.

4) Recovery With the replacement of the faster acting injectables toward the end of a cycle, the “wasted” time between the end of a cycle and beginning of Clomid therapy is reduced. For instance, if 100mg TA is used ED, Clomid therapy may begin in as little as 5 days after the last shot. This tremendously impoves time efficiency. Clomid therapy usually last for four weeks. An excellent thread posted by The Iron Game describes this in further detail Clomid FAQ’s .

When the above recomendations are made, your cycle itself is made much more efficient and if recovery time is made more efficient as well, time “off” AAS may very well be reduced so that the overall efficiency of AAS use over time is tremendously improved.
Andy

Androgen use is very prevalent in society. Much of this is due to androgen abuse among athletes and bodybuilders, where black market androgen abuse has reached epidemic proportions. Indeed, in various studies of high school boys, it has been found that 4-12% had used androgens at least once (JAMA 27O:12l7, 1993). Androgens have also been prescribed for many conditions by physicians throughout the last several decades.

Despite the prevalence of legal and illegal androgen use, the science of androgen effects has greatly lagged behind the understanding of biological effects of estrogen and indications for estrogen replacement therapy. Female oral contraceptives have been in use for many years, but only recently have we seen studies regarding hormone contraceptive agents in men. Although there are a few very well-defined clinical syndromes of male hypogonadism which require androgen therapy, the use in other clinical situations, such as mild hypogonadism and hypogonadism associated with aging is less well established.

During this lecture, I would hope that some of the mystery of androgen therapy in older men is overcome.

II. Normal Androgen Physiology

Testosterone is present in very low levels in boys prior to puberty. At puberty, pulsatile secretion of GnRH causes the anterior pituitary to produce LH and FSH. Circulating LH induces the Leydig cells of the testis to produce testosterone, with the resultant development of secondary sex characteristics. As the level of testosterone rise in the circulation, there is a negative feedback on the production of GnRH at the hypothalamic level, and LH and FSH at the pituitary level.

A high intratesticular level of testosterone is an absolute prerequisite for sperm production. The levels in the seminiferous tubules remains high due to the proxitimity of production in the Leydig cells, and well as by binding in the tubules by androgen binding-protein (ABP). This binding to ABP probably also prevents fluctuation of the levels, by maintaining a reservoir of hormone immediately available to buffer changes in production. Although testosterone is the only absolute requirement for sperm production, FSH has a promotional effect, and quantitatively normal spermatogenesis requires the action of FSH on the Sertoli cell. When sperm production is proceeding in a quantitatively normal manner, a peptide hormone called inhibin is released into the circulation (also by the Sertoli cell) and is responsible for negative feedback of FSH (but not LH) production by the pituitary.

Circulating testosterone is present in several forms. Testosterone may be present as a free hormone (not bound to any protein) or bound relatively weakly to albumin. The majority of testosterone in circulation, however, is bound to sex hormone binding globulin (SHBC). The testosterone bound to SHBC is not available for biological activity. The free testosterone and that weakly bound to alburnin comprise the so called “bioavailable” testosterone fraction which is responsible for peripheral androgenic effects. Which is the most important measurement in diagnosing hypogonadism, the total T, or free T remains controversial.

Testosterone is converted to other clinically important compounds in the peripheral circulation and/or peripheral tissues. Dihydrotestosterone (DHT) is produced by reduction through the action of 5 reductase, which is present in genital tissue, skin and the prostate. DHT is responsible for prostatic growth and has other trophic effects on the prostatic tissue. Estradiol (E2) is produced by esterification of testosterone. The rate of conversion of T to E2 can be increased in obese men and in men with liver failure. Elevated levels of E2 can down regulate the hypothalamic-pituitary-gonadal axis, resulting in decreased gonadotropin secretion and decreased circulating T levels.

III. Changes in Testosterone Levels With Aging

There is no corollary of the menopause seen in females as men age. The menopause in women is caused by ovarian failure. Although no such similar event of complete testicular failure occurs in men, it has been well established that mean T levels drop progressively with age and the percentage of men with T levels in the abnormal range increases (J Clin Endocrinol Metab 56:1278, 1983;J Clin Endocrinol Metab 73:1016, 1991). When one looks at the levels of bioavailable testosterone, probably more accurate measure of the decreasing androgenic effects, more marked changes may be evident. Other evidence of a relatively hypogonadal state in older men includes elevated LH, as well as an exaggerated response of LH to the administration of GnRH (GnRH stimulation test).

Although T levels drop with aging, it is less clear whether any of the generalized manifestations of aging, such as impotence, osteoporosis, CNS changes, are due to the decrease in circulating androgen. Since it is not established that these age-related changes are due to hormonal deficiencies, the simple presence of a decline in circulating hormones cannot be taken as de facto evidence that hormone replacement therapy will be beneficial in reversing or preventing these changes. An example of this would be in the case of erectile dysfunction. There are certain cases of impotence where the only abnormality seen in testing is a low T level, and in such cases, T replacement therapy may very well be beneficial. However, in the vast majority of older men, one can also identify a very high prevalence of penile arterial insufficiency, tissue dysfunction dysfunction resulting in venous leak, and neuropathic problems, and all of these cases would not be cured simply with hormonal therapy.

IV. Types of Androgen Replacement Therapy.

A. Oral agents -

Testosterone itself cannot be given orally because in the first pass through the liver after oral administration, the breakdown is substantial and very little androgenic effects would be seen. Alkylated forms of testosterone (see table below) are much more resistant to hepatic metabolism and can exert a clinical effect when ingested. Alkylated forms of testosterone are weaker than T itself. The clinical efficacy is further complicated by irregular absorption and varying degrees of hepatic breakdown on the first pass through the liver. Therefore, varying results can be seen when giving these agents. Liver toxicity may be substantial with oral androgens, and such toxicity may range from an elevation of liver enzymes to development of hemorrhagic liver cysts. Liver neoplasms have also been reported in men undergoing oral androgen therapy.
Because of these problems, oral androgen therapy has very little place in the treatment of hypogonadism.

B. Injectable agents-

Testosterone esters (see table) have certain advantages as injectable agents. They are relatively resistant to hepatic breakdown, are released slowly from oil-based carriers, and are hydrolyzed to yield testosterone itself. Therefore, delivery in a long-acting injection is possible, and the biological effects of the injected form of T is indistinguishable from the native hormone. The usual dosage is approximately 100mg. of drug per week is given and the interval can be varied to smooth out these wide swings, i.e. 100mg. every week, 200mg every two weeks, 300mg. every three weeks, etc. acting injection is possible, and the biological effects of the injected form of T is indistinguishable from the native hormone.

Following a testosterone injection, the serum T level rises to high normal or supranormal range for the first few days, followed by a progressive drop until the next injection is administered. The T level may drop below the normal range during this time. These wide swings may cause varying efficacy from the treatment.

V. Testosterone patch therapy

There are currently two available testosterone patch therapies, Testoderm and Androderm. (Please note that Dr. Ohl is a consultant for Alza Pharmaceuticals, and Smith-Kline Beecham for these two products).

Testoderm is a patch that must be worn on the scrotum. In this location skin absorption is increased due to the thin nature of the skin and because of this property of the scrotal skin, permeation enhancers do not need to be placed into the formulation to achieve adequate drug absorption. The potential advantages less potential for skin irritation. Disadvantages include the necessity to shave the scrotal hair and difficulty with adherence of the patch (which has been partially circumvented with the addition of adhesive strips). Another potential disadvantage of Testosderm is the high level of 5-reductase activity in the scrotal skin with the potential of elevation of DHT levels. At this point, however, there is no evidence that an elevation of peripheral DHT levels will have any adverse effects on the prostatic tissue. Testosderm is applied to the scrotum each morning, and comes in 4 and 6 mg dosages.

Androderm is a patch that may be worn anywhere on the body. Because of the increased thickness of the skin and a relative resistance to absorption of the testosterone, it is necessary to place permeation enhancers within the drug vehicle. Because permeation enhancers are present, this patch should never be worn on the scrotal skin where extreme absorption might be seen. Two patches (only one dose available) are worn on flat areas of the skin, not overlying any joints or high movement areas. The pharmacokinetics dictate that Androderm patches are placed in the evening (see below). Patch sites are rotated on a weekly basis so a patch is not placed in the same site anytime during the same week. Advantages of Androderm include non-scrotal application and good adhesion. Disadvantages include a non-discrete location and potential for skin reactions.

Both Androderm and Testoderm, when placed properly at the correct time of day, cause a rise to the mid to upper normal range of serum testosterone in the morning and a decrease to the low normal range in the evening. Therefore, patch therapy mimics the diurnal variation of normal testosterone secretion and appears to be more physiological. Wide swings seen with injection therapy are not seen. Whether or not this more physiological pattern of delivery is more beneficial has not been proven.

TABLE 1. Types of testosterone replacement therapy

Oral (Alkylated forms)

Methyl testosterone
Fluoxymes terone
Injectable (Esterified) Testosterone:

Propionate
Cypionate
Enanthate
Undecanoate

Patch therapy (both testosterone)

Testoderm
Androderm

VI. Potential Benefits of Androgen Replacement Therapy

A.Sexual function

It has been thought for years that testosterone effect on sexual function is mainly through libido. Although libido is certainly increased by the administration of testosterone in hypogonadal men, there is also some recent experimental evidence in rats to suggest that there may be peripheral effects in penile tissue from testosterone also. Nitric oxide is the primary mediator of penile erection and investigators have shown that nitric oxide synthase in penile tissue is androgen-dependent (Fertil Steril, 63:1101, 1995). Therefore, in the hypogonadal state, it is possible that nitric oxide production in penile tissue may be deficient, with substandard penile smooth muscle relaxation and a poor quality erection. Thus, we may have both central and peripheral effects from testosterone on sexual function.

In men who are identified as having a low testosterone (total and or bioavailable) and have difficulties with erectile function, testosterone therapy may be tried prior to moving on to more invasive tests or therapies. In the event that normal sexual function returns with replacement, then further evaluation is of Testoderm include the hidden site of application and the lack of the permeation enhancers, leading to unnecessary. However, as mentioned above, many elderly men with impotence will have multiple factors leading to their impotence problem and simple hormonal replacement will not result in return of normal sexual activity in most When a trial of testosterone is unable to return a man to normal sexual function, but there are beneficial effects on libido, the wisdom of proceeding on with ongoing androgen therapy is less well established. The physician in this circumstance will have to balance the subjective improvement with potential for adverse effects.

B. Body composition/muscle strength

Androgenic steroids have general effects of making favorable changes in body composition. Several studies in older men have identified decreased fat mass, increased lean body mass, and increased strength ( J Clin Endocrinol Metab 75:1092, 1992; Obesity Res 1:245, 1993; J Am Geratric Soc 41:149, 1993). Supraphysiologic dosages of androgens in normal have been proven to increase muscle strength,”and act synergistically with exercise in this regard (NEJM 335:1, 1996). Larger, as well as long-term outcomes studies regarding the effect of androgens on body composition and strength in older men with hypogonadism are necessary.

C. Osteoporosis

Bone mass does decrease as men age. Very little data exists regarding the efficacy of testosterone in reversing or arresting these changes. Some small studies show beneficial effects on bone with androgen therapy (J Clin Endocrinol Metab 75:1092, 1992; J Am Geratric Soc 41:149, 1993), but more research in this area is also necessary. There is no long-term data to assure that androgen therapy will reduce fractures/disability, etc.

D. Cognitive behavior

There is evidence that spatial cognition in older men improves with androgen therapy (Behav Neurosci 108:325, 1994). Another area that is not studied terribly well.

VII. Potential Adverse Effects of Androgen Therapy

A. Hepatotoxidty

As mentioned above, the oral, alkylated forms of testosterone can create a situation of liver toxicity (Semin Liver Dis 7:230, 1987; Liver 42:73, 1992). Since I believe that these oral agents should never be given, this problem can in general be circumvented. There is little evidence that other methods of administration cause liver dysfunction, but I think it is prudent that in men on testosterone therapy, liver function tests be performed at approximately six month intervals.

B. Water retention

Androgen therapy can cause water retention, with the fear of exacerbation of hypertension or inducing or worsening congestive heart failure in older men undergoing such therapy. Weight gain thought to be due to water retention has been demonstrated ( J Clin Endocrinol Metab 75:1092, 1992; JAm Geratr Soc 41:149, 1993), but no study has shown clinically significant pathology due to this retention.

C. Erythropoiesis

Androgens cause an increase in hematocrit. Two~studies showed a rise in hematocrit between 3.6 and 7.0% in older men receiving T supplementation (J Clin Endocrinol Metab 75:1092, 1992; J Am Ceratr Soc 41:149, 1993). Typically this rise in hematocrit, although measurable, is not clinically significant. Since many older men are also anemic prior to testosterone therapy due to their hypogonadism and/or aging/nutritional changes, the rise in hematocrit may be beneficial.

D. Sleep apnea

Sleep apnea may be worsened in men on testosterone therapy (Clin Endocrinol (Oxf) 22:713, 1985). This may be due to changes in tissue surrounding the posterior pharynx. Therefore, if there is a clinical history of sleep apnea in a man considered for T therapy, this should be investigated and treated prior to institution of therapy.

E. Changes in plasma lipoproteins

This area is perhaps one of the more controversial areas in testosterone replacement therapy. The differences in incidence of atherosclerotic vessel disease between men and women has been ascribed to hormonal differences. Since HDL levels begin to drop in males coincident with the rise of testosterone seen at puberty, the evidence has been compelling. However, a large review of studies that attempted to compare HDL levels with circulating T levels failed to reach. the conclusion that T level is correlated with lower HDL (Diabetes Metab 21:156, 1995). In fact, most of the evidence shows that higher endogenous T levels are associated with a higher HDL, and presumably a lower cardiovascular risk.

This data has been interpreted by some clinicians to indicate that testosterone replacement therapy will cause beneficial changes in HDL. However, when one looks at multiple studies regarding replacing testosterone- in- men who are hypogonadal, a mix of results are seen. Administration of alkylated testosterone derivatives causes a substantial reduction in HDL-C (JAMA 261:1165, 1989). This further adds to the recommendation that these drugs should not be given. When parenteral T esters are administered in weekly 100 mg injections, no change is generally seen, but there is a significant decline in HDL when 200 mg injections are given every 2 weeks (Metabolism 42:446, 1993; Ann Intern Med 116:967, 1992; JAMA 261:1165, 1989). Data on patch therapy is still being generated.

I think it is safe to say that one should view this issue with caution. It would be prudent to get a fasting cholesterol/HDL profile on all hypogonadal men in whom androgen replacement therapy is being suggested and then another profile at three months to look for these potentially unfavorable changes.

F. Prostatic changes

It is clear that without androgens present, prostatic pathology does not develop. Prostatic cancer and benign prostatic hyperplasia never develops in eunuchs. Prostatic diseases represent very clinically significant problems in the elderly and the effect of androgen replacement therapy on the prostate needs to be very carefully considered.

The prostate increases in size during androgen replacement therapy in older men (J Clin Endocrinol Metab 75:1092, 1992). Therefore, symptomatic prostatism may potentially become worse with androgen therapy. Because of this one needs to take a careful voiding history prior to initiation of therapy to uncover such problems.

Prostate cancer has never been proven to be associated with androgen replacement therapy. While there are scattered case reports of development of prostate cancer while on such therapy it is commonly accepted that prostatic cancer which is present (and may be occult when considering androgen replacement therapy) will probably be accelerated by elevation of the serum androgens. In this way an occult prostatic cancer may become apparent during therapy. Surveillance for prostate cancer development and growth is essential during therapy.

G. Infertility

Via suppression of the hypothalamic-pituitary-gonadal axis, administration of exogenous androgens results in suppression of spermatogenesis. In many cases, this will lead to complete azoospermia. Indeed, administration of testosterone as a contraceptive agent has been proven to be effective in recent multi-center studies (Lancet 336:955, 1993). Therefore, in all men who are considering treatment of hypogonadism, and in whom fertility is a concern, exogenous androgens must not be given.

SOURCE: ESPN

There should not be a controversy over anabolic steroid use in athletics — non-medical use of anabolic steroids is illegal and banned by most, if not all, major sports organizations. Still, some athletes persist in taking them, believing that these substances provide a competitive advantage. But beyond the issues of popularity or legality is the fact that anabolic steroids can cause serious physical and psychological side effects.

In light of these hazards, measures to curtail the use of anabolic steroids are escalating. One of the nation’s foremost authorities on steroid use, Dr. Gary Wadler, is part of a concerted effort to educate the public about the dangers of anabolic steroids. Dr. Wadler, a New York University School of Medicine professor and lead author of the book Drugs and the Athlete, serves as a consultant to the U.S. Department of Justice on anabolic-androgenic steroid use. He has also won the International Olympic Committee President’s Prize for his work in the area of performance-enhancing drugs in competitive sports. He joined us to address the issue of steroids and sports.

What are anabolic steroids?

Anabolic steroids — or more precisely, anabolic-androgenic steroids — are the synthetic derivatives of the naturally occurring male anabolic hormone testosterone. Both anabolic and androgenic have origins from the Greek: anabolic, meaning “to build,” and androgenic, meaning “masculinizing.” Testosterone’s natural androgenic effects trigger the maturing of the male reproductive system in puberty, including the growth of body hair and the deepening of the voice. The hormone’s anabolic effect helps the body retain dietary protein, which aids in the development of muscles. “Although there are many types of steroids with varying degrees of anabolic and androgenic properties, it’s the anabolic property of steroids that lures athletes,” says Dr. Wadler. “They take them to primarily increase muscle mass and strength.”

How are steroids taken?

Steroids can be taken orally or they can be injected. Those that are injected are broken down into additional categories, those that are very long-lasting and those that last a shorter time. In recent years, use has shifted to the latter category — shorter-lasting, water-soluble injections. “The reason for that is that the side effects associated for the oral form were discovered to be especially worrisome for the liver,”says Dr. Wadler. “But the injectable steroids aren’t free of side-effects either. There is no free ride and there is a price to be paid with either form.”

Who takes anabolic steroids and why?

It is not only the football player or weightlifter or sprinter who may be using anabolic steroids. Nor is it only men. White- and blue-collar workers, females and, most alarmingly, adolescents take steroids — all linked by the desire to hopefully look, perform and feel better, regardless of the dangers.

Anabolic steroids are designed to mimic the bodybuilding traits of testosterone. Most healthy males produce less than 10 milligrams of testosterone a day. Females also produce testosterone but in minute amounts. Some athletes however, may use up to hundreds of milligrams a day, far exceeding the normally prescribed daily dose for legitimate medical purposes. Anabolic steroids do not improve agility, skill or cardiovascular capacity.

What are the health hazards of anabolic steroids?

“There can be a whole panoply of side effects, even with prescribed doses,” says Dr. Wadler. “Some are visible to the naked eye and some are internal. Some are physical, others are psychological. With unsupervised steroid use, wanton ‘megadosing’ or stacking (using a combination of different steroids), the effects can be irreversible or undetected until it’s too late.” Also, if anabolic steroids are injected, transmitting or contracting HIV and Hepatitis B through shared needle use is a very real concern.

Additionally, Dr. Wadler stresses that “unlike almost all other drugs, all steroid based hormones have one unique characteristic — their dangers may not be manifest for months, years and even decades. Therefore, long after you gave them up you may develop side effects.”

Physical side effects

Men – Although anabolic steroids are derived from a male sex hormone, men who take them may actually experience a “feminization” effect along with a decrease in normal male sexual function. Some possible effects include:

• Reduced sperm count
• Impotence
• Development of breasts
• Shrinking of the testicles
• Difficulty or pain while urinating

Women – On the other hand, women often experience a “masculinization” effect from anabolic steroids, including the following:

• Facial hair growth
• Deepened voice
• Breast reduction
• Menstrual cycle changes

With continued use of anabolic steroids, both sexes can experience the following effects, which range from the merely unsightly to the life endangering. They include:

• Acne
• Bloated appearance
• Rapid weight gain
• Clotting disorders
• Liver damage
• Premature heart attacks and strokes
• Elevated cholesterol levels
• Weakened tendons

Special dangers to adolescents

Anabolic steroids can halt growth prematurely in adolescents. “What happens is that steroids close the growth centers in a kid’s bones”, says Dr. Wadler. “Once these growth plates are closed, they cannot reopen so adolescents that take too many steroids may end up shorter than they should have been.”

Behavioral side effects

According to Dr. Wadler, anabolic steroids can cause severe mood swings. “People’s psychological states can run the gamut.” says Wadler. “They can go from bouts of depression or extreme irritability to feelings of invincibility and outright aggression, commonly called “‘roid rage. This is a dangerous state beyond mere assertiveness.”

Are anabolic steroids addictive?

Recent evidence suggests that long-time steroid users and steroid abusers may experience the classic characteristics of addiction including cravings, difficulty in stopping steroid use and withdrawal symptoms. “Addiction is an extreme of dependency, which may be a psychological, if not physical, phenomena,” says Dr. Wadler. “Regardless, there is no question that when regular steroid users stop taking the drug they get withdrawal pains and if they start up again the pain goes away. They have difficulties stopping use even though they know it’s bad for them.”

SOURCE: ESPN

Clenbuterol FAQ: Everything you need to know about Clen I wrote this because of all the confusion that surrounds this drug. Enjoy.

What is Clenbuterol? Clenbuterol is a beta-2 agonist and is used in many countries as a broncodilator for the treatment of asthma. Because of it’s long half life, Clenbuterol is not FDA approved for medical use. It is a central nervous system stimulant and acts like adrenaline. It shares many of the same side effects as other CNS stimulants like ephedrine. Contrary to popular belief, Clenbuterol has a half life of 35 hours and not 48 hours.

Dosing and Cycling Clenbuterol comes in 20mcg tablets, although it is also available in syrup, pump and injectable form. Doses are very dependent on how well the user responds to the side effects, but somewhere in the range of 5-8 tablets per day for men and 1-4 tablets a day for women is most common. Clenbuterol loses its thermogenic effects after 6-8 weeks when body temperature drops back to normal. It’s anabolic/anti-catabolic properties fade away at around the 18 day mark. Taking the long half life into consideration, the most effective way of cycling Clen is 2 weeks on/ 2 weeks off for no more than 12 weeks. Ephedrine can be used in the off weeks. Clenbuterol vs Ephedrine vs DNP

Ephedrine will raise metabolic levels by about 2-3 percent and 200mg of DNP raises metabolic levels by about 30 percent. Clenbuterol raises metabolic levels about 10 percent and it can raise body temperature several degrees.

DNP is by far the most effective fat burner but many people will never use it because of the risks associated with it. It also offers no anti-catabolic benefit. Although it does have anti-catabolic effect, ephedrine short half life prevents it from being all that effective.

As far as side effects, Clenbuterol’s are certainly milder than DNP’s, and some would even say milder than an ECA stack. There is no ECA-style crash on Clenbuterol and many users find it easier on the prostate and sex drive. This may in part be due to the fact that Clen is generally used for only 2 weeks at a time.

Side effects

NAUSEA
NERVOUSNESS
DIZZINESS
DROWSINESS
DRY MOUTH
FACIAL FLUSHING
HEADACHE
HEARTBURN
INCREASED BLOOD PRESSURE
INCREASED SWEATING
INSOMNIA
LIGHTHEADEDNESS
MUSCLE CRAMPS
TREMORS
VOMITING
CHEST PAIN

The most significant side effects are muscle cramps, nervousness, headaches, and increased blood pressure.

Muscle cramps can be avoided by drinking 1.5-2 gallons of water and consuming bananas and oranges or supplementing with GNC potassium tablets at 200-400mg a day taken before bed on an empty stomach.

Headaches can easily be avoided with Tylenol Extra Strength taken at the first signs of a headache. You may need to take double the recommended dose.

Common Uses

Post-Cycle Therapy: Clen is used post cycle to aid in recovery. It allows the user to continue eating large amounts of food, without worrying about adding body fat. It also helps the user maintain more of his strength as well as his intensity in the gym. Diet: Roughly the same as on cycle.

Fat loss: The most popular use for Clen, it also increases muscle hardness, vascularity, strength and size on a caloric deficit. For the most significant fat loss, Clen can be stacked with t3. Diet: A high protein(1.5g per lb of bodyweight), moderate carb(0.5g to 1g per lb of bodyweight), low fat diet(0.25g per lb of bodyweight) seems to work best with Clen.

Alternative to Steroids: Clenbuterol has mild steroid-like properties and can be used by non AS using bodybuilder to increase LBM as well as strength and muscle hardness. Diet: A moderate carb, high protein, moderate fat diet work well.

Stimulant/Performance Enhancement: It can be used as a stimulant, but an ECA stack may be a better choice because of it’s much shorter half-life. Diet: To take full advantage of the stimulatory effects of Clen, Carbs must be included in the diet. Keto diet do not work well in this case.

Precautions: Is Clen for you?

The same precautions that apply to Ephedrine must be applied to Clen, although some people find ECA stacks harsher than Clen. It should not be stacked with other CNS stimulants such as Ephedrine and Yohimbine. These combinations are unnecessary and potentially dangerous. Caffeine can be used in moderation before a workout for an extra kick, although its diuretic effects may shift electrolyte balance. Drink more water if you use Caffeine.

What else do I need to know?

Most users that report bad side effects and discontinue use are those who use high doses right at the start of the cycle. The worst side effects occur within the first 3-4 days of use.

A first time user should not exceed 40mcg the first day.

Example of a first cycle:

Day1: 20mcg
Day2: 40mcg
Day3: 60mcg
Day4: 80mcg
Day5: 80mcg(Note: Increase the dose only when the side effects are tolerable)
Day6-Day12: 100mcg
Day13: 80mcg (Tapering is not necessary, but it helps some users get back to normal gradually)
Day14: 60mcg
Day15: off
Day16: off
Day 17: ECA/ NYC stack

Example of a second cycle:

Day1: 60mcg
Day2: 80mcg
Day3: 80mcg
Day4: 100mcg
Day5: 100mcg
Day6-Day12: 120mcg
Day13: 100mcg
Day14: 80mcg
Day15: off
Day16: off
Day 17: ECA/ NYC stack

Do not take Clen Past 4pm and drink plenty of water: 1.5-2 gallons a day.

All brands are not equal when it comes to Clen, different brands will yield different results.

That about covers everything.

Type- IGF-1 Long R3 (Anything else is not as effective, and if the person providing it for you doesn’t know anything about it, you are asking for trouble.)
2. Storage- the most popular (and most effective) way to store, transport, preserve IGF is by suspending it in sterile BA in a sterile vial.
This will keep your IGF 99% potent for many months at a time in just about ANY indoor storage, I.E.-closet, drawer, etc. (Take it from me, I stored mine because I wasn’t ready to use it for about 6 months in my closet… I had fears about its potency, then I started my first week, and BAM I practically cleaned out the fridge.
3. Use- Usage should not exceed 4-5 weeks, and an OFF period should be about the same. Daily dosages work best (split up into 2 seems to make little difference in the Long R3 version) Most people see results at about 40mcg/day, some use as low as 30mcg/day, and some folks even use 80-100mcg. I SUGGEST to ALL first time users no matter what level, to start at about 40-50mcg/day.
4. Administration- I believe in IM injections over sub q, but either seems to be effective. I like IM better because IM using a slin pin is probably the least painful thing one could imagine, even at two times per day. Also, sub Q shots that contain BA, even diluted BA, can leave little nodules that you may not want to feel on your stomach.
5. Mixing- Most IGF comes suspended in BA. Hopefully it is @ 500mcg/ml or even 333mcg/ml (that would be at 2ml/mg and 3ml/mg respectively) Draw out your desired amount and back load a slin pin. Add enough bacteriostatic Water to fill the U100 syringe completely.
Some inject immediately before training, while others choose to do 2 shots spread throughout the day… THEY BOTH WORK WELL. Try both; see which method makes your muscles pop out of your skin.
6. Add plenty of protein, and don’t shy away from carbs immediately after training. I used up to 100g of carbs after training, and my body fat went down, all without cardio.

I hope that helps a little, and I’m glad to be lurking around this board again.
More to come.

MORE

The most effective form of IGF is Long R3 IGF-1, it has been chemically altered and has had amino acid changes, which cause it to avoid binding to proteins in the human body and allow it to have a much longer half-life, around 20-30 hours. “Long R3 IGF-1 is an 83 amino acid analog of IGF-1 comprising the complete human IGF-1 sequence with the substation of an Arg(R) for the Glu (E) at position three, hence R3, and a 13 amino acid extension peptide at the N terminus. This analog of IGF-1 has been produced with the purpose of increasing the biological activity of the IGF peptide.”

“Long R3 IGF-1 is significantly more potent than IGF-1. The enhanced potency is due to the decreased binding of Long R3 IGF-1 to all known IGF binding proteins. These binding proteins normally inhibit the biological actions of IGF’s.”

It is also not as expensive since a media grade version is available which is sufficient for bodybuilding use. There is also a receptor grade available but it is VERY expensive and the only noticeable difference between the two would only be able to be noticed in a laboratory setting. The price on the black market for Long R3 IGF-1 can be seen anywhere from $300-$500 per milligram depending on the source, be wary of black market dealers of any IGF since it is a VERY difficult item to obtain. As mentioned IGF is a research product and is only available from a few laboratories in the world and is only available to research companies and biotechnology institutions. For the rest of this article when I say IGF I am now referring to Long R3 IGF-1 for simplicity sake.

Any form of IGF is ONLY supplied in a lyophilized form, which means a dry powder state. NEVER PUCHASE PRE-DILUTED LIQUID IGF!!!! There is no such product made anywhere in the world and even if there were real IGF ever present in the vial it would all be dead by the time you receive it. IGF is a very delicate peptide and must be diluted by yourself, where you have access to a refrigerator and freezer. There has also been a lot of talk by certain sources claiming to have IGF made by the Eli Lilly company, to clear things up Lilly is a pharmaceutical company and as stated IGF is a research drug and has not yet been approved, Lilly does not and never has manufactured research drugs for retail sale.

The diluents you will need for the IGF are a weak concentration of hydrochloric acid and a sterile buffer (sterile water or bacteriostatic water) the procedure for diluting the IGF is not very difficult, the diluents can be obtained from most local chemical suppliers and a good source of IGF would also be able to supply the necessary diluents.

The most effective length for a cycle of IGF is 50 days on and 20-40 days off. The most controversy surrounding Long R3 IGF-1 is the effective dosage. The most used dosages range between 20mcg/day to 120+mcg/day. IGF is only available by the milligram, one mg will give you a 50 day cycle at 20mcg/day, 2mg will give you a 50 day cycle at 40mcg/day, 3mg will give you a 50 day cycle at 60mcg/day, 4mg will give you a 50 day cycle at 80mcg/day and so on. The dosage issue mainly revolves around how much money you have to spend, plenty of people use the minimum dosage of 20mcg/day and are happy with the results, and in fact several top bodybuilders use the 20mcg/day dosage and are pleased with the results. IGF is most effective when administered subcutaneous and injected once or twice daily at your current dosage. The best time for injections is either in the morning and/or immediately after weight training.

Another frequently asked question of IGF refers to the real world results; in terms of pure weight gain don’t expect to gain 5 lbs. a week like you may off of anadrol or a similar steroid. The only weight you will gain from IGF use is pure lean muscle tissue, with steroids most of the weight gained is water weight. With an effective dosage you can expect to gain 1-2 lbs of new lean muscle tissue every 2-3 weeks and these effects can be increased with the use of testosterone, anabolic steroids, and insulin use. Increased vascularity is also very common, people report seeing veins appear where they never have before. And yet another effect reported is the ability to stay lean while bulking with heavy dosages of steroids and TONS of food while on an IGF cycle, this is perhaps the most pleasing effect. Increased pumps are also noticeable almost immediately, the pumps can almost become painful, and pumps are even noticeable when doing cardio.

Overall, IGF is a very exciting drug due to its ability to alter ones genetic capabilities. If you can find a trustworthy source and you use it correctly it can be a VERY useful tool in your bodybuilding drug arsenal.

Insulin-Like Growth Factor Recombinant 3
IGF-1 R3
IGF1 stands for insulin like growth factor. It mimics insulin in the human body and also at the same time makes the muscles more sensitive to insulin’s effects. It is a growth factor and is the most potent one in the human body at that. IGF causes muscle cell hyperplasia, which is an actual splitting and forming of new muscle cells. This was thought to only be possible during puberty. IGF is much more potent at this effect than growth hormone is, in fact almost all of the effects you see from growth hormone come from the increased amount of IGF that your liver produces when the GH is destroyed. So it would be very easy to say that IGF is a much more potent and cheaper alternative to GH use, although GH is more effective for fat loss than IGF due to some other effects that it causes such as metabolism increase and the ability to effectively use more insulin, t3, and anabolic steroids.
Another advantage that IGF has over GH is that it has much more of an affinity to attach to muscle cells instead of bone and organ cells. Growth hormone has been know to cause a lot of organ enlargement and bone elongation since it attaches to all types of receptor cells. IGF is much more likely to go where we want it, our muscle cells. IGF-1 attaches to myogenic stem cells, which are only located in muscle and connective tissues. These myogenic stem cells are responsible for the production of myoblast cells, which in turn are responsible for the buildup and repair of connective tissues (ligaments, tendons, cartilage, and joints to a certain extent).
So from this you can see that IGF-1 is great for increasing the strength of tendons and also for helping to heal existing injuries while at the same time helping to prevent them. IGF-1 is also responsible for increased protein synthesis and amino acid synthesis.
IGF does not have to be used along with anabolic steroids, GH, insulin, or thyroid hormones to be effective. It causes muscle growth on its own. In fact some people prefer to use it during their breaks from steroid cycles since IGF has no effect on natural test production. It could effectively be used along with HCG, Clomid, and PGF2a for a hell of an off cycle stack which would allow your body to return to normal and still allow you to grow!! On its own IGF will give an increase of around 2 lbs. of new solid lean muscle tissue every two weeks, and is also is know for its ability to strip off body fat and GREATLY increase vascularity, body fat decreases of 5-8% over a 50 day cycle are not uncommon. But, of course you will be much happier with the results if you use the IGF along with anabolic steroids, testosterone, and insulin.
The use of steroids along with the IGF allow you to quickly mature and strengthen the new muscle tissue that the IGF has formed, and may also speed the process of hyperplasia. If you need any help setting up a great stack to
use along with the IGF just let me know and I can help you out. I speak with lots of top bodybuilders and guru’s so I am very knowledgeable.
The dosage issue for IGF is where the most controversy lies. Dosages used by competitive athletes most commonly range anywhere between 60mcg/day to 100+mcg/day. The trick is finding the dosage that works best for YOU. For most the best results appear when you reach a dosage of 80mcg/day, while some do
receive good results from only 40mcg/day. I personally feel the best results begin to be noticed at a dosage of 100mcg/day. I personally am using 150mcg/day during my current cycle.
Also I should let you know that the form of IGF is the Long R3 analog. It has been chemically altered and has a longer half-life than regular IGF, which only lasts about 10 minutes in the human body once injected. The Long R3 IGF-1 has a half-life of 6-10 hours, so you will only need to inject once or twice per day. The best time to inject is after lifting and in the morning, so it would be best to use half the dosage in the morning and the other half after lifting. This will take maximal advantage of IGF’s insulin
mimicking effects.

Something I put together that may help some of the new comers out there as well
as some of the more experienced.

Question: What is Clomid?

Answer: Clomid is a synthetic estrogen and is generally prescribed by doctors
to trigger ovulation in females.

Question: Why Should Bodybuilders use Clomid?

Answer: Almost all anabolic androgenic steroids will cause an inhibition of
the bodies own testosterone production. When he comes off the steroids he has
no natural test production and no more steroids. The body is left in a state
of catabolism (catabolic hormones are high and anabolic hormones are low) and
as a result much of the muscle tissue that was gained on the cycle is now going
to be lost. Clomid stimulates the hypophysis to release more gonadotropin so
that a faster and higher release of follicle stimulating hormone aud luteinizing
hormone occurs. This results in an increase of the body’s own testosterone production.

Question: Does Clomid also work as an anti estrogen?

Answer: Clomid is a synthetic estrogen, however it does also work as an anti-estrogen.
How does it work? Because it is a weak synthetic estrogen, it will bind to the
estrogen receptor (ER) and not cause any problems. At the same time the increase
in estrogen from steroids are blocked from attaching to the ER.

Question: How effective is Clomid as an anti-estrogen?

Answer: It is very weak and should not be relied upon if you are going to be
using steroids that aromatise at any rapid rate, or if you are pre disposed
to gyno. arimidex, Proviron and Nolvadex will all make better choices for this
purpose.

Question: Some say Clomid during a cycle is a waste, is this true?

Answer: Lets first examine what happens when someone is using anabaolic androgenic
steroids. When the level of androgens in the body get too high, the androgen
receptor becomes more highly activated, and the hypothalamus stops sending a
signal to the pituitary. In short the signal tells our body to stop producing
testosterone. During a cycle the body has higher levels than normal of androgens
and as long as this level is high enough Clomid will not help to keep natural
test production up. It will be almost all but completely shut off. The only
purpose of Clomid during a cycle is as an anti-estrogen.

Question: When do I start Clomid? Some say 2 weeks others 3.

Answer: When you start using your Clomid all depends on what steroids you were
using during your cycle. Different steroids have different half lifes and you
should adjust your Clomid intake accordingly. As we have seen above, if we take
Clomid when the androgen levels in our body is still high it will be a waste.
We need to wait for androgen levels to fall before implementing our Clomid therapy.
However if we take it too late we could possibly lose gains. Look at the list
below to determine when you should start Clomid therapy. By selecting from the
list all the steroids you used in your cycle and which ever one has the latest
starting point then go with that. For example if I cycled dbol, sustanon and
winstrol I would use sustanon as it remains active in the body for the longest
period of time.

Anadrol/Anapolan: 8 – 12 hours after last administration

Deca: 3 weeks after last injection and Clomid for 4 weeks

Dianabol: 4 – 8 hours after last administration

Equipoise: 3 weeks after last injection

Fina: 3 days after last injection

Primobolan depot: 10 – 14 days after last injection

Sustanon: 3 weeks after last injection

Testosterone Cypionate: 2 weeks after last injection

Testosterone Enanthate: 2 weeks after last injection

Testosterone Propionate: 3 days after last injection

Testosterone Suspension: 4 – 8 hours after last administration

Winstrol: 8 – 12 hours after last administration

Question: What is the most effective way for Clomid therapy.

Answer: Clomid has a long half life and as such there is no need to split up
doses throughout the day. I read some where that it was 5 days (any feedback
on this). Now if we used sustanon and we start using Clomid 3 weeks after our
last injection we anticipate that androgen levels are low enough to start sending
the correct signals. If androgen levels are still a little high then the normal
50mgs/day of Clomid for 1 week is not going to be effective. We need to start
at a high enough amount that will work or help even if androgen levels are still
a little high. 300mgs on day 1. I know I said don’t split it up due to
its long half life but try and split this up 2 tabs 3 times a day. After we
have finished this first day we seek to use 100mgs for 10 days and then followed
by 50mgs for 10 days.

Question: Do I need to use Clomid for 3 weeks?

Answer: Why don’t you want too? It is very cheap, very effective and can
mean the difference between maintaining gains and losing them.

Question: How cheap is Clomid?

Answer: Clomid normally comes in 50mg tablets but also comes in capsule form
of 25mgs. A 50mg tablet can be anywhere between 25 cents and $2.50. (15 pence
and 75 pence in England).

Question: Do all steroids cause shut down of the hpta.

Answer: Not all steroids do. Everyone is different and you must also take into
account how long you have been using a certain steroid and at what dose in order
to determine if you need Clomid or not. However as the price is so cheap, why
risk not using it.