While working out recently in a local Gold’s Gym in Latham, New York, a man named Chad Brothers, 32, described as a “gentle giant” by his family, reportedly went berserk, toppling weight machines, throwing dumbbells, and assaulting a patron. After being Tasered numerous times by law enforcement officers and even allegedly taking a Taser from an officer and using it on himself, he suffered a heart attack an hour later and died. Brothers was a large man at 6’1″ and 235 to 240 pounds, he was working out in a gym, and toxicology reports apparently found anabolic steroids in his blood.

The local District Attorney’s office announced that Brothers’ spontaneous and unprovoked rampage was a case of excited or agitated delirium (AD). AD is usually characterized by extremely high body temperature, loss of contact with reality, out of control aggressive and agitated behavior, superhuman strength and an unwillingness to back down from confrontation in the face of overwhelming numbers (e.g., Grant, Southall, Mealey, Scott, & Fowler, 2009; Vilke, Payne-James, & Karch 2012). Not surprisingly, those suffering from the syndrome are often ultimately subdued via physical or electrical measures at the hands of law enforcement agents (Grant et al., 2009). The cause of death among those who exhibit AD is usually cardiac-related and it has been plausibly suggested that the syndrome emerges from extreme catecholamine (e.g., adrenergic) activity (e.g., Otahbachi, Cevik, Bagdure, & Nugent, 2010). Consistent with this “over-arousal” of the sympathetic nervous system, AD is often related to the abuse of stimulants. In fact, a finding of sympathomimetics (drugs that stimulate the sympathetic nervous system) in the blood has traditionally been one criterion used for diagnosing AD after fatal rampages like Brothers’ (Vilke et al., 2012). Drugs that have been linked to occurrence of this syndrome include cocaine (most often), methamphetamine, lysergic acid diethylamide, and phencyclidine (PCP) (e.g., Sztajnkrycer & Baez, 2005; Takeuchia, Ahern, & Henderson, 2011). In fact, PCP’s undesirable effects of “…agitation, violent behavior, paranoid delusions, disorientation, delirium, and hallucinations… (p. 658; deRoux, Sgarlato, & Marker, 2011)” led to its abandonment as an anesthetic.

The Albany Times-Union covered the Chad Brothers rampage with the headline: “Officials: Man had steroids in system” (http://www.timesunion.com/local/article/Officials-Man-had-steroids-in-system-2390621.php). The DA’s spokeswoman was quoted that AD is “a condition that can result from steroid use.”

Is this an open and shut case of steroid-induced aggression – the infamous “’roid rage”? Did steroids cause Brothers’ AD? Although some experts have suggested that if “’roid rage” exists at all, it occurs rarely and only in a small fraction of predisposed steroid users (p. 60; Yesalis & Cowart), we will probably never know for sure what role, if any, the man’s apparent use of steroids may have played in this tragic incident. Human behavior is generally too complex to pin-point a single cause, although simple explanations are much more attractive. As we have seen before in such cases (e.g., Chris Benoit, David Jacobs), selectively blaming steroids for a tragedy, rather than presenting a fuller account of other possible causative factors, is a convenient way to sensationalize the news.

There’s no direct causal evidence or documentation linking steroids to AD. But that doesn’t stop the media from quickly accepting knee-jerk conclusions. The Times-Union relied on the District Attorney (DA) as a source, apparently doing no independent fact-checking. It should be noted that this DA is the same controversial Albany politician who catapulted himself into national headlines by his anti-steroid investigations of doctors and pharmacies located in Florida. Up for reelection next year, he currently faces a Democratic primary challenger who has criticized his grandstanding anti-steroid crusade against businesses located far beyond his state’s boundaries and with minimal ties to New York.

Had the paper conducted even minimal due diligence, it would have learned a critical fact: that PCP – more popularly known as Angel Dust – was also found in Brothers’ blood. It would also have learned that a man with Brothers’ Body Mass Index (31) would be at increased risk for fatal AD (Park, Korn, & Henderson, 2001). If the Times-Union had learned these things, the public could have learned them as well. Although at this point we do not know how much PCP was in Brothers’ blood (nor do we know what steroid concentrations or types were found), the simple fact is that science links PCP to AD (e.g., Takeuchi et al., 2011). Additionally, a similar fatal case of AD occurred in Michigan only one month previously. Bradford Gibson, 35, also died after being Tased by police; autopsy reports showed he had PCP in his system (http://blogs.phoenixnewtimes.com/valleyfever/2011/12/taser_off_the_hook_for_two_dea.php). The relationship between the use of such “Electronic Control Devices” and AD remains a subject of investigation (e.g., Jauchem, 2011).

One would like to think there was no intent or collusion by the Times-Union and the DA to cherry-pick which facts to report, even though Times-Union reporters have had a virtual partnership with the DA’s press office in disseminating information about the anti-steroid investigations to the public. One would also like to think that the core of such investigations, whether by DAs or reporters, is the desire to know the truth, to understand what actually happened and why. But it’s hard to not be skeptical when the goal appears to be manipulation rather than knowledge. Once again, the media falls short on its obligations to report the important facts or help the public understand, choosing instead to blindly rely on sources that appear far from objective. The media’s role seems to have morphed from presenting and evaluating information to merely passing along what others say as fact. The public was misled into thinking that the only possible cause of the rampage was steroids. And if not for other news sources, the public would have never been the wiser.

In the midst of such abrogation of duty, is it any wonder that today’s public runs from one panic to another? This unfortunate situation emerges when “…a condition, episode, person or group of persons emerges to become defined as a threat to societal values and interest; its nature is presented in a stylized and stereotypical fashion by the mass media; the moral barricades are manned by editors, bishops, politicians, and other right-thinking people (p. 9; Cohen, 1972)”. With steroid headlines like this one, and steroid reporting in general, do mainstream media sources serve as bulwark against such panic … or its facilitator?

Photo credit: YNN [http://www.ynn.com/]

References

Cohen, S. (1972). Folk devils and moral panics: The creation of the mods and rockers. London: MacGibbon & Kee Ltd.

deRoux, S.J., Sgarlato, A, & Marker, E. (2011). Phencyclidine: A 5-Year retrospective review from the New York City Medical Examiner’s Office. Journal of Forensic Sciences, 56, 656-659.

Grant, J.R., Southall, P.E., Mealey, J., Scott, S.R., & Fowler, D.R. (2009). Excited delirium deaths in custody: Past and present. The American Journal of Forensic Medicine and Pathology, 30, 1-5.

Jauchem, J.R. (2011). Pathophysiologic changes due to TASER devices versus excited delirium: Potential relevance to deaths-in-custody? Journal of Forensic and Leal Medicine, 18, 145-153.

Otahbachi, M., Cevik, C., Bagdure, S., & Nugent, K. (2010). Excited delirium, restraints, and unexpected death: A review of the pathogenesis. American Journal of Forensic Medicine and Pathology, 31, 107-112.

Park, K.S., Korn, C.S., & Henderson, S.O. (2001). Agitated delirium and sudden death: Two case reports. Prehospital Emergency Care, 5, 214-216.

Sztajnkrycer, M.D., & Baez, A.A. (2005). Cocaine, excited delirium and sudden unexpected death. Emergency Medical Services, 34, 77-81.

Takeuchi, A., Ahern, T.L., & Henderson, S.O. (2011). Excited delirium. Western Journal of Emergency Medicine, 12, 77-83.

Vilke, G.M., Payne-James, J., & Karch, S.B. (2012). Excited delirium syndrome (EDS): Redefining an old diagnosis. Journal of Forensic and Legal Medicine, 19, 7-11.

Yesalis, C.E., & Cowart, V.S. (1998). The Steroids Game. Champaign: Human Kinetics.

© Darkes and Collins, 2011

Originally published at: “Of Course, It’s the Steroids!” (Here We Go Again…)

Four of my books can now be read for free on kindle

• Built to Survive: A Comprehensive Guide to the Medical Use of Anabolic Therapies, Nutrition and Exercise for HIV (+) men and women
• Fortalecete y Sobrevive el VIH (Spanish Edition)
• La Testosterona: La Mejor Guia Para Hombres (Spanish Edition)
• What You Need to Know About Your Man’s Testosterone

If you do not have a kindle unit or app, you can download kindle for free on iphone, ipad, blackberry, or your computer:

Happy Holidays!

Originally published at: Read Hormone Books for Free on Kindle

Rick Collins, the leading legal expert on anabolic steroids and sports nutrition, has been the go-to guy for sports nutrition companies targeted by the federal government for illegally selling prohormone and steroidal ingredients as dietary supplements.

Collins’ firm has represented numerous supplements companies, including “Anabolic Xtreme”, “Advanced Muscle Science”, “Culver Concepts”, “Bradley Asgard”, “Bjorklund”, “Axis Labs”, “IForce Nutrition” and “American Cellular Labs”, accused of engaging in such conduct.

In each and every case, Collins has successfully negotiated corporate plea agreements that kept the principals of the company from personally facing felony charges and imprisonment.

In a statement emailed to MESO-Rx, Collins shared his general thoughts about practicing in this area of law.

He also offered a somber warning to supplement companies that continue to distribute illegal steroidal compounds as dietary supplements.

Thanks for contacting me about this. As we discussed by telephone, I’m obviously very pleased with the resolutions of all the prohormone cases on which I’ve served as counsel. The pleas were the result of back-and-forth exchanges, conferences and negotiations I had with the various U.S. Attorney’s Offices over a span of many, many months. It’s been a long journey. I work hard, Millard, and I’m proud of what I do on behalf of my clients. Nobody went to jail or was convicted of a crime. But rather than speaking now on the clients’ behalf or detailing any particular matter, I’ll offer you instead my own general thoughts as the only lawyer I know of practicing extensively in this area. Look, any criminal defense lawyer worth his salt will tell you that whenever the federal government gets you in their sights, the potential for bad things to happen to you escalates exponentially. It’s a bad place to be. Most criminal defense practitioners will tell you that the deck is heavily stacked against the accused. Most targets who are prosecuted for felonies by the Department of Justice go to prison, plain and simple. Corporate pleas – without any individual people being convicted – are so rare in federal court that most criminal defense attorneys have never even handled one. But I have to admit that the investigative agents as well as the prosecutors I dealt with in these jurisdictions were reasonable. They were tough, but they listened and were fair. While in some cases we disagreed on certain legal points, they were smart and came to understand the unique realities and circumstances of the prohormone market as it existed several years ago, as well as the complexity of the overlapping and intermingled laws in the area of anabolic steroids, steroid precursors, dietary ingredients and misbranded and unapproved drugs. Holding the corporate entities accountable, rather than the individual company principals, was the totally appropriate way to dispose of these cases. The companies accepted full responsibility for their mistakes. Fines and money forfeitures were part of the deals. The Government was greatly interested in finally ending the market for these types of illegal products and in protecting consumers, so in many cases the Government insisted that the corporations and their principals agreed to implement third party testing protocols. When imposed at sentence, those protocols will mean that every future batch or lot of product ingredients will be tested to ensure that they are free of steroids. Moving forward, these companies will have an opportunity to reconfigure the sports nutrition industry and set new standards for quality control. I am also representing several additional companies who were engaged in similar conduct dating back to the same period. I hope to resolve those matters in a similar fashion. However, for the future, I strongly suspect that the Government will attempt to take a harder line, arguing that any entities which are today still selling illegal steroidal ingredients as supplements are sufficiently on notice for the company principals to be fair game for indictment. Be warned. That’s not a good place to be.

Companies:

Anabolic Resources, Inc., doing business as Anabolic Xtreme Superdrol (methasteron aka methyldrostanolone aka 17 ?-Hydroxy-2?, 17?-dimethyl-5?-androstane-3-one)

Axis Labs LLC “Monster Caps” ( Superdrol, Halodrol and Madol)

DCD, LLC dba Advanced Muscle Science – “Dienedrone” (Estra-4,9-diene-3,17-dione) and “Liquidrone” (Estra-4,9-diene-3, 17-dione)

Nutrition Distribution, Inc., which also did business as Anabolic Xtreme – Hyperdrol (6-Bromodione aka 6-Bromo-androstane-3,17-dione)

R & D Holdings, LLC dba Culver Concepts, Bradley Asgard, and Bjorklund – “Orafinadrol 50” (Estra-4,9-diene-3,17-dione) and “Microdrol” (methasteron) and “Methyldrostanolone” (methasteron)

Tribravus Enterprises dba iForce - 1,4 AD Bold 200 (androstenedione), 17a PheraFLEX (Madol), Dymethazine (Superdrol) and Methadrol (Superdrol)

VMG Global dba American Cellular Labs Inc. – Tren Xteme (Estra-4,9-diene-3,17-dione) and Mass Xtreme (desoxymethyltestosterone, “DMT” and 17a-Methyl-etioallocholan-2-ene-17b-ol.)

Originally published at: Rick Collins Warning to Supplement Companies Selling Illegal Steroidal Products

Sports nutrition companies that continue to sell Superdrol or similar illegal steroidal ingredients as dietary supplements have been put on notice by the federal government. The same federal prosecutors that pursued defendants in the BALCO steroid scandal have announced the entry of a guilty plea by one of the first distributors of Superdrol.

Anabolic Resources, Inc., doing business as Anabolic Xtreme, pleaded guilty to a felony charge involving the introduction of an unapproved new drug (Anabolic Resources Superdrol) into interstate commerce. The company was sentenced to a $500,000 fine.

The company admitted that Superdrol was fraudulently marketed as a dietary supplement when, in fact, it was a synthetic steroid known as methasteron. Methasteron is also known as methyldrostanolone.

Superdrol was not legally defined as an anabolic steroid under the Controlled Substances Act. However, Superdrol was never legal to sell as a dietary supplement under the Dietary Health and Supplement Education Act either.

Rick Collins, the leading legal expert on anabolic steroids and sports nutrition, knows very well how determined the government is to eliminate illegal steroidal products from the marketplace.

Collins served as legal counsel for Anabolic Resources, Inc. and has represented numerous other companies that have engaged in similar conduct.

The penalties for selling unapproved new drugs can be severe. In an email to MESO-Rx, Collins explained that selling illegal steroidal products as supplements can have serious consequences for the individuals involved.

“Most targets who are prosecuted for felonies by the Department of Justice go to prison, plain and simple,” said Collins. “Corporate pleas – without any individual people being convicted – are so rare in federal court that most criminal defense attorneys have never even handled one.”

The possibility that the principal owners of supplement companies could be individually prosecuted, convicted of felonies and sent to prison should be a terrifying prospect for many people in the sports nutrition industry.

Rick Collins has argued that imposing fines and forfeitures on corporate entities rather than prosecuting individuals is the most expedient way for the government to handle these cases. He has successfully negotiated several settlements that resulted in a corporate plea.

“[T]he investigative agents as well as the prosecutors I dealt with in these jurisdictions were reasonable. They were tough, but they listened and were fair,” according to Collins. “While in some cases we disagreed on certain legal points, they were smart and came to understand the unique realities and circumstances of the prohormone market as it existed several years ago, as well as the complexity of the overlapping and intermingled laws in the area of anabolic steroids, steroid precursors, dietary ingredients and misbranded and unapproved drugs.”

“Holding the corporate entities accountable, rather than the individual company principals, was the totally appropriate way to dispose of these cases.”

The Anabolic Resources Superdrol case took over 5 years to reach its conclusion. The wheels of justice move slowly but the government has made its point loud and clear.

Collins noted that the illegal conduct (Superdrol sales) of Anabolic Resources stopped nearly 6 years ago, that the corporation is no longer manufacturing products, and that the corporation currently using the brand name of Anabolic Xtreme never sold Superdrol. He expressed concerned for companies that have continued to sell Superdrol and related illegal steroidal ingredients.

“For the future, I strongly suspect that the Government will attempt to take a harder line, arguing that any entities which are today still selling illegal steroidal ingredients as supplements are sufficiently on notice for the company principals to be fair game for indictment,” according to Collins. “Be warned. That’s not a good place to be.”

Originally published at: Superdrol and the End of Illegal Steroidal Ingredients Sold As Dietary Supplements

American bodybuilders have long been envious of their counterparts in the United Kingdom. British bodybuilders have been able to legally obtain anabolic steroids for personal use under the Misuse of Drugs Act 1971 (“MDA”). As a result British bodybuilders never had to worry about personal possession of steroids as long as they were solely for self-administration. It didn’t matter if they were used to increase muscle mass or to enhance performance. They have been free to buy steroids on the internet from the numerous internet pharmacies without fear of criminal repercussions. Unfortunately, this is all about to change!

The British government has decided to “restrict importation of anabolic steroids for self administration to personal custody” acting upon the recommendations by the Advisory Council on the Misuse of Drugs (“ACMD”) made this summer.

What does this mean for steroid users in the UK?

Bodybuilders will no longer be able to order steroids over the internet or otherwise legally import them by mail into the country. Fortunately, it will remain legal to possess steroids for personal use; they simply can not be purchased over the internet. Bodybuilders will now be required to personally transport and import steroids into the country.

The United Kingdom Border Agency will be instructed to seize personal use quantities of anabolic steroids and human growth hormone (hGH) arriving via mail.

The second major change to the steroid laws in the United Kingdom involves a change in the requirement that steroids used by bodybuilders come in the form of a “medicinal product”. Previously, this requirement often made it illegal to possess steroids that were manufactured by “underground labs” (UGLs).

The government has decided to amend the Misuse of Drugs Regulations 2001 in order to remove references to “medicinal products”. This means that UGL steroids will be unambiguously legal to possess for personal use.

What impact will this have on steroid use in the United Kingdom?

The production of anabolic steroids by UGLs within the United Kingdom will likely explode accompanied by a concomitant increase in the use of UGL steroids by British bodybuilders. Bodybuilders will switch from pharmaceutical steroids to lower-quality UGL steroids.

Unfortunately, this seems largely at odds with the efforts at “harm reduction” by the government. The quality control standards of UGLs are generally inferior to those of legitimate pharmaceutical products (that have been legally obtainable over the internet prior to the current pending amendments.)

Here are the Advisory Council on the Misuse of Drugs (ACMD) recommendations for amending UK steroid laws:

Recommendation 3

13.4 The ACMD consider that although a small number deaths have been attributed to liver damage associated with steroid use, the health related harms associated with the use of anabolic steroids, are not of the severity of those associated with a number of other Class C drugs e.g. gammahydroxybutyrate, or ketamine –which can be life threatening in overdose, or benzodiazepines which carry dependence liability. For this reason the ACMD continues to believe that it should not be an offence under the Misuse of Drugs Act 1971 to simply possess anabolic steroids for personal use. Criminal prosecution should be limited to illicit steroid dealers, suppliers, manufacturers and traffickers who profit from this trade. Retaining the lack of a possession offence emphasises the ongoing need to focus on public health. The ACMD concludes that improved tailored intervention and education messages aimed at anabolic steroid users would be more effective than criminalising users and further pushing the issue underground

Restrict the method of importation to personal custody

13.5 The current legal framework permits imports (or exports) of steroids for self-administration. There is no requirement that the drugs have to be personally transported/ imported. This can pose problems where steroids are imported via post or courier (i.e. items are unattended in transit). Border force officials can be unable, in these circumstances, to determine whether the products are for personal use as they are unable to question the importer at point of entry and may not necessarily be able to identify the importer from the import declaration. To establish whether imported items are for personal use will necessarily involve a potentially costly investigation by UK Border Force officials as to the circumstances in which the drugs are being imported.

Recommendation 4

13.6 Further restriction should, after consideration in the context of the EU legislation, be placed on the importation, and exportation, exemption, namely personal custody on importation.

13.7 Anabolic steroids are currently freely available for on-line ordering by various web sites. There is no restriction on these and little or no quality control. Imposition of a personal custody requirement for importation would make such purchases illegal.

Here is the UK Government’s response to the recommendations by the ACMD:

Response to recommendations 1-4:

The Government accepts these recommendations. We will maintain the current classification (and exemption from the offence of possession) of anabolic steroids as Class C under the Misuse of Drugs Act 1971 based on the ACMD’s assessment of the latest available evidence. We will keep the list of steroids under review with reference to the World Anti-doping Agency Prohibited List as we approach London 2012 Olympics. The Government is committed to ensuring the legislative framework is clear, fit for purpose and supports enforcement partners. We therefore intend to amend the Misuse of Drugs Regulations 2001 to remove the reference to ‘medicinal product’ and restrict importation of anabolic steroids for self administration to personal custody. This will enable UKBA officials to seize imports of anabolic steroids through the post and via courier at the point of entry.

Subsequent to the ACMD’s letter of 26 July which advised that the ACMD’s legislative recommendations on anabolic steroids apply equally to human growth hormones, the legislative changes to remove the reference to ‘medicinal product’ and to restrict importation to personal custody will apply to all drugs in Schedule 4 Part II of the Misuse of Drugs Regulations 2001.

Originally published at: Bad News for British Bodybuilders – Buying Steroids on the Internet Soon to be Illegal

Q: Nelson, I am a HIV long term survivor, undetectable, all numbers great. Testosterone used to be high normal, is now right in the middle. Sex drive and sensation continues to go down hill..am in my mid 40′s(male) but it really seems to early for that to happen. Am in very good shape, very good health, but every year it gets less and less. Doc does think adding testosterone would increase my sex drive, but says it would in anyone… But its not time for me to do that she says.. Still being relatively young, and in great health, what are other options to increase my natural testosterone? I have heard of Tribulus terrestris a supplement may help..any other ideas? I am not on any new meds or anything i that i was not on years ago so its not that…

Response from Mr. Vergel: I wish having a sex drive was as simple as increasing testosterone blood levels.

Yes, testosterone replacement increases desire for sex and thoughts of sex in men who have low testosterone. But many factor can interfere with a healthy desire for sex:

1. Stress
2. Too busy of a schedule
3. Lack of attraction to the person you usually have sex with
4. Performance anxiety
5. Medications (blood pressure and antidepressant medications and others)
6. Fatigue
7. Sleep apnea
8. Diabetes
9. Having low free testosterone even in the presence of normal total testosterone blood levels
10. aving high estradiol blood levels (testosterone can convert into estradiol, a female hormone, in men)
11. Having thyroid dysfunction
12. Loss of sense of exploration to bring new experiences into our sex lives to prevent boredom

Some people take supplements hoping that they increase testosterone and/or sex drive.

Testosterone prohormones such as androstenedione, androstenediol, and dehydroepiandrosterone (DHEA) have been heavily marketed as testosterone-enhancing and muscle-building nutritional supplements for the past decade. Concerns over the safety of prohormone supplement use prompted the United States Food and Drug Administration to call for a ban on androstenedione sales, and Congress passed the Anabolic Steroid Control Act of 2004, which classifies androstenedione and 17 other steroids as controlled substances. As of January 2005, these substances cannot be sold without prescription. Contrary to marketing claims, research to date indicates that the use of prohormone nutritional supplements (DHEA, androstenedione, androstenediol, and other steroid hormone supplements) does not produce either anabolic or ergogenic effects in men.

Tribulus terrestris L. (Zygophyllaceae) have been used as an aphrodisiac both in the Indian and Chinese traditional systems of medicine. Administration of Tribulus terrestris extract (TT) increased sexual behavior and intracavernous pressure both in normal and castrated rats and these effects were probably due to the androgen increasing property of TT

In a study done in Bulgaria, twenty-one healthy young 2036 years old men were randomly separated into three groupstwo experimental (each n = 7) and a control (placebo) one (n = 7). The experimental groups were named TT1 and TT2 and the subjects were assigned to consume 20 and 10 mg/kg body weight per day of Tribulus terrestris extract, respectively, separated into three daily intakes for 4 weeks. No changes in testosterone, androstenedione and luteinizing hormone blood levels were observed with either dose.

Nelson Vergel Author Testosterone: A Man’s Guide

Originally published at: Boosting Testosterone Naturally

Excerpt from the second edition of Testosterone: A Man’s Guide available on www.testosteronewisdom.com or MESO-RX

Human Chorionic Gonadotropin (HCG)

Human chorionic gonadotropin (HCG) (not to be confused with human growth hormone, or HGH) is a glycoprotein hormone that mimics LH (luteinizing hormone), produced in pregnancy by the developing embryo soon after conception, and later by part of the placenta. Its role is to prevent the disintegration of the corpus luteum of the ovary and to maintain the progesterone production critical for pregnancy in women. It supports the normal development of an egg in a woman’s ovary, and stimulates the release of the egg during ovulation. HCG is used to cause ovulation and to treat infertility in women.

You’re probably asking yourself why you should care about this. But in men, HCG is also used in young boys when their testicles have not dropped down into the scrotum normally.  Additionally, HCG is used to increase testicular size after long-term testosterone or anabolic steroid use.

As mentioned at the beginning of the book, testosterone replacement therapy triggers the hypothalamus to shut down its production of GnRH (gonadotropin releasing hormone). Without GnRH, the pituitary gland stops releasing LH. Without LH the testes (testicles or gonads) shut down their production of testosterone. For males HCG closely resembles LH. If the testicles have shrunken after long-term testosterone use, they will likely begin to enlarge and start their testosterone production shortly after HCG therapy is instituted. HCG jump-starts your testes to produce testosterone and to increase their size.

HCG can be extracted from pregnant women’s urine or through genetic modification. The product is available by prescription under the brand names Pregnyl, Follutein, Profasi, and Novarel. Novire is another brand but it is a product of recombinant DNA. Compounding pharmacies can also make HCG by prescription in different vial sizes. Brand names of HCG in regular pharmacies cost over $100 per 10,000 IUs.  The same amount of IUs cost around $50 in compounding pharmacies. Many insurance policies do not pay for HCG since they consider its use for testicular atrophy while on TRT an off label use. So, most men using it pay for it themselves and get it from compounding pharmacies that sell it a lot cheaper.

HCG is dispensed as a powder contained in vials of 3,500 IUs, 5, 000 IUs or 10, 000 IUs. You can call compounding pharmacies and have them make vials for you with different IU amounts, though. These are usually accompanied by another vial of 1 mL (or cc) of bacteriostatic water to reconstitute the powder into a liquid solution. Bacteriostatic water (water with a preservative that is provided with the prescription) is mixed in with the powder to reconstitute, or dissolve, it before injection. This type of water can preserve the solution for up to 6 weeks when refrigerated. Some patients do not use the 1 mL water vials that come with the commercially (non compounded) available product and instead get their doctors to prescribe 30 cc bottles of bacteriostatic water so that they can dilute the HCG down to a more workable concentration that is more practical for men using lower doses of HCG weekly.

HCG is given as an injection under the skin or intramuscularly (there is still debate on which method is best). The number of IUs per injection will depend on how much bacteriostatic water you add to the dry powder vial. If you add 1 mL to a 5,000 IU powder vial, then you will have 5,000 IUs per mL, so 0.1 mL would be 500 IUs. If you add 2 mL to the 5,000 IU dry powder vial, then you will have 2,500 IUs/mL; 0.1 ml (or cc) in an insulin syringe will equal 250 IUs. If you need to inject 500 IUs, then you inject 0.2 ccs of this mixture. Table 3 provides dilution volumes at different HCG powder/water proportions.

Ultra-fine needle insulin syringes are used to inject HCG under the skin, making this very easy to take even for the needle-phobic. Typical sizes are:

• 1 ml, 12.7 mm long, 30 gauge and
• 0.5 ml, 8 mm, 31 gauge syringes.

Syringes require a separate prescription. Some compounding pharmacies will automatically include them with the shipment, but do not forget to ask them. Never use the syringe that you used for injecting the bacteriostatic water into the powder for injecting yourself; the needle will be dull (I usually use a regular 23 gauge, 1 inch, 3 ml syringe to load up the water). Remember that you also need alcohol pads to clean the injection area and the tip of the vial. Typical injection sites are the abdominal area close to the navel or in the pubic fat pad. Pinch a little of fat on your abdominals and inject into that pinched area, then massage with an alcohol pad. Discard syringes into the sharps container that can be provided by your pharmacy.

As I mentioned before, compounded HCG is a lot cheaper than the commercially available pharmaceutical products. Sometimes it is difficult to find commercially available HCG in regular pharmacies.

A review of the literature reveals a wide range of doses of HCG used and that there is very little agreement among physicians. For male infertility, doses range from 1250 IU three times weekly to 3000 IU twice weekly (these studies did not include men on testosterone replacement).

How long does the boost in testosterone last after an injection of HCG? A study looked into that and also tried to determine if high doses would be more effective at sustaining that boost. The profiles of plasma testosterone and HCG in normal adult men were studied after the administration of 6000 IU HCG under two different protocols. In the first protocol, seven subjects received a single intramuscular injection. Plasma testosterone increased sharply (1.6 ± 0.1-fold) within 4 hours. Then testosterone decreased slightly and remained at a plateau level for at least 24 hours. A delayed peak of testosterone (2.4 ± 0.3-fold) was seen between 72–96 hours. Thereafter, testosterone declined and reached the initial levels at 144 hours. In the second protocol, six subjects received two intravenous (IV) injections of HCG (5-8 times the dose given by injection to the first group) at 24-hour intervals. The initial increment of plasma testosterone after the first injection was similar to that seen in the first protocol despite the fact that plasma HCG levels were 5–8 times higher in this case. At 24 hours, testosterone levels were again lower than those observed at 2–4 hours and a second IV injection of HCG did not induce a significant increase. The delayed peak of plasma testosterone (2.2 ± 0.2-fold of control) was seen about 24 hour later than that in the first protocol. So, this study shows that more is not better when dosing HCG. In fact, high doses may desensitize Leydig cells in the testicles.  It also showed that testosterone blood levels peak not once but twice after HCG injections.  I wish they had studied a lower dose than 6000 IU since very few physicians prescribe this high dose.

HCG may not only boost testosterone but also increase the number of Leydig cells in the testicles. It is well known that Leydig cell clusters in adult testes enlarge considerably under treatment with HCG. However, it has been uncertain in the past whether this expansion involves an increase in the number of Leydig cells or merely an enlargement of the individual cells. A study was performed in which adult male Sprague-Dawley rats were injected subcutaneously daily with 100 IU HCG for up to 5 weeks. The volume of Leydig cell clusters increased by a factor of 4.7 during the 5 weeks of HCG treatment. The number of Leydig cells (initially averaging 18.6 x 106/cm3 testis) increased to 3 times the control value by 5 weeks of treatment (P<0.001), while the average volume of individual Leydig cells (initially  ~2200 µm3) enlarged only 1.6 times. They concluded that chronic treatment with HCG increases the number of Leydig cells in the testes of adult rats. We do not know if these results can be extrapolated to men.

Currently there are no HCG guidelines for men who need to be on testosterone replacement therapy and want to maintain normal testicular size. A study that used 200 mg per week of testosterone enanthate injections with HCG at doses of 125, 250, or 500 IU every other day in healthy younger men showed that the 250 IU dose every other day preserved normal testicular function (no testicular size measurements were taken, however). Whether this dose is effective in older men is yet to be proven. Also, there are no long-term studies using HCG for more than 2 years.

Due to its effect on testosterone, HCG use can also increase estradiol and DHT, although I have not seen data that shows if this increase is proportional to the dose used.

So, the best dose of HCG to sustain normal testicular function while keeping estradiol and DHT conversion to a minimum has not been established (I will explain why these two metabolites are important in TRT management).

Some doctors are recommending using 200–500 IUs twice a week for men who are concerned about testicular size or who want to preserve fertility while on testosterone replacement. Higher doses, such as 1,000–5,000 IUs twice a week, have been used but I believe that these higher doses could cause more estrogen and DHT-related side effects, and possibly desensitize the testicles for HCG in the long term. Some doctors check estradiol levels a month after this protocol is started to determine whether the use of the estrogen receptor modulators tamoxifen (brand name: Nolvadex) or anaztrozole (brand name: Arimidex), is needed to counteract any increases in estradiol levels. High estradiol can cause breast enlargement and water retention in men but it is important at the right blood levels to maintain bone and brain health (refer to the Gynecomastia section for more on this subject).

More to come in Part 2..stay tuned!

Originally published at: What You Need to Know about Human Chorionic Gonadotropin (HCG) (Part 1)

Dr. Michael Scally is a medical expert on testosterone replacement therapy (TRT) and anabolic steroid side effects. He is available for phone consultations.  Email him at mscally@hptaxis.com . I highly recommend anyone who cares about their bodies and health to pick his brain since he truly is one of the world’s experts on androgens.

The first part of the interview is found here.

NV: Can somebody on testosterone replacement become less fertile? If a man wants to impregnate his wife after, let us say, a year of testosterone replacement, is there any risk for that man to become less fertile to his wife?

MS: Testicular size and consistency often diminish, and men should be advised that fertility would be greatly compromised during testosterone replacement therapy because of downregulation of LH and FSH.

The general rule is they will become less fertile. But you cannot depend on its use as a fertility drug. And that is where we come in with contraceptive studies. We have many, many contraceptive studies that use testosterone cypionate at 200 mg a week and find that, yes, it decreases fertility. But there is still a subset of men that still produce sperm that are fertile.

NV: Are these men good candidates for a protocol to reset their HPGA?

MS: We have had many men who come to the clinic with the actual com­plaint that they were using anabolic steroids, or they were using testosterone, and they now want to get their wife pregnant. Although many will return to normal after stopping TRT, this period can be lengthy.

The amazing thing to me is that the number of people that come to me, who have seen the doctor, who are either non-prescription or prescription anabolic steroid users, testosterone with or without combination of anabolic steroids, who have the problem of infertility; and their doctors have no idea what to do, except to do nothing. But on top of this are all the psychological problems and effects that come along with doing nothing as a consequence of anabolic steroid-induced hypogonadism. The HPTA protocol has restored fertility as well as decreased the time substantially.

NV: Can you expand about resetting the HPGA?

The word resetting is a misnomer, though recent studies published in the New England Journal of Medicine (NEJM) do indicate this possible. In 2007, the NEJM reports on the resetting of the HPTA after TRT for adult onset idio-pathic hypogonadism. This is the first report demonstrating HPTA plasticity in adulthood. The term I prefer is HPTA functionality and restoration.

There are clear conditions under which testosterone requires adminis­tration for life-long treatment. However, there are increasing numbers of individuals being treated with TRT who do not fall under these disorders. TRT is being prescribed more and more for late onset hypogonadism. This is called by many other names, including andropause, androgen deficiency of the aging male, and others.

There are no consequences of the decline in serum testosterone with age that are known with certainty. Several parallels exist between the effects of aging and those of hypogonadism, which suggest that the decline in serum testosterone might be a cause of several effects of aging. Since the long-term effects of androgen treatment for late onset hypogonadism or andropause are not well-known, I discontinue therapy on an approximate annual basis to ensure HPTA normalization—functionality. This allows the patient the autonomy to stop therapy should the need arise.

What is clear is that upon stopping testosterone or anabolic steroids, a period of anabolic steroid-induced hypogonadism ensues. This occurs in one hundred percent of individuals stopping testosterone. The only variables are the duration and severity. The duration of hypogonadism, or the severity of hypogonadism, is typically related to the anabolic steroid drug, dose, and duration.

In other words, one person that is on testosterone for an entire year; they may come back to normal within 1 or 2 months. Another person may take 12, 18 months, or even 3 years to come back to normal. The best studies we have on this are contraceptive studies with testosterone for over a year. And what we find in those studies is that it may take up to three years for a person to return to normal.

If they have been taking those anabolic steroids to improve their body com­position, increase the lean body mass, and decrease the body fat, that all goes back to normal after stopping anabolic steroids. But you are also going to be exposed to the other adverse effects of hypogonadism, which include adverse psychological and cardiovascular effects. Some of the adverse psychological effects are depression, decreased cognitive abilities, insomnia, decreased libido, and erection dysfunction. More significantly, after cessation adds the comorbid condition of hypogonadism to their already existing chronic illness.

AAS, including testosterone, licit and illicit, administration induces a state of hypogonadism that continues after their cessation. All compounds classified as androgens or anabolic steroids cause a negative feedback inhi­bition of the hypothalamic-pituitary testicular axis, suppress endogenous gonadotropin secretion, and as a consequence serum testosterone.

The symptoms of AIH are identical to classical hypogonadism. This prob­lem prevents many of discontinuing testosterone or anabolic steroids. As we have said, there are many reasons for stopping testosterone, including polycythemia, gynecomastia, and other issue as compliance, affordability, and changing life style.

The accepted standard of care within the medical community for anabolic steroid induced hypogonadism is to do nothing with the expectation the individual will return to normal unassisted. But the literature shows this not to be the case.

AIH is critical toward any planned use of AAS or similar compound to effect positive changes in muscle mass and muscle strength as well as an understanding for what has been termed anabolic steroid dependency. The further understanding and treatments that mitigate or prevent AIH could contribute to androgen therapies for wasting associated diseases and stopping nonprescription AAS use.

NV: What is used for restoring the hormonal axis?

MS: A combination of three drugs. The individual use of HCG, clomiphene citrate, and tamoxifen is well-known, well-accepted, and well-tested standards of care treatments in peer-reviewed medical literature for diagnostic testing for underlying pathology of hypogonadism. The HPTA protocol uses the medications human chorionic gonadotropin, clomiphene citrate, and tamoxifen.

The first phase of the HPTA protocol examines the functionality of the testicles by the direct action of HCG. HCG raises sex hormone levels directly through the stimulation of the testes and secondly decreases the production and level of gonadotropin LH. The increase in serum testosterone with the HCG stimulation is useful in determining whether any primary testicular dysfunction is present.

This initial value is a measure of the ability of the testicles to respond to stimulation from HCG. Demonstration of the HPTA functionality is an adequate response of the testicles to raise the serum level of T well into the normal range. If this is observed, HCG is discontinued. The failure of the testes to respond to an HCG challenge is indicative of primary testicular failure. In the simplest terms, the first half of the protocol is to determine testicular production and reserve by direct stimulation with HCG. If one is unable to obtain adequate (normal) levels successfully in the first half, there is little cause or reason to proceed to the second half.

The second phase of the HPTA protocol, clomiphene and tamoxifen, examines the ability of the hypothalamic-pituitary axis to respond to stimulation by producing LH levels within the normal reference range. The clomiphene citrate challenge differentiates secondary hypogonadism. Clomiphene is an antiestrogen, which decreases the estrogen effect in the body. It has a dual effect by stimulating the hypothalamic pituitary area and it has an antiestrogenic effect, so that it decreases the effect of estrogen in the body. Tamoxifen is more of a strict antiestrogen, it decreases the effect of estrogen in the body, and potentiates the action of clomiphene. Tamoxifen and clomiphene citrate compete with estrogen for estrogen receptor bind­ing sites, thus eliminating excess estrogen circulation at the level of the hypothalamus and pituitary, allowing gonadotropin production to resume. Administering them together produces an elevation of LH and secondar­ily gonadal sex hormones. The administration of clomiphene leads to an appropriate rise in the levels of LH, suggesting that the negative feedback control on the hypothalamus is intact and that the storage and release of gonadotropins by the pituitary is normal. If there was a successful stimulation of testicular T levels by HCG, but an inadequate or no response in LH pro­duction, then the patient has hypogonadotropic, secondary, hypogonadism.

In the simplest terms, the second half of the protocol is to deter­mine hypothalamo-pituitary production and reserve with clomiphene and tamoxifen. The physiological type of hypogonadism—hypogonadotropic or secondary—is characterized by abnormal low or low normal gonadotropin (LH) production in response to clomiphene citrate and tamoxifen. In the functional type of hypogonadism, the ability to stimulate the HPTA to pro­duce LH and T levels within the normal reference range occurs.

There is a dearth of good studies in anabolic steroids, both while you are taking them and after you stop them, I think this is going to be something that we are going to need to look at in the future. In fact, we are going to plan on looking at it in our proposed clinical studies that we have with our company for the prevention of anabolic steroid-induced hypogonadism.

Dr Scally’s book  “Anabolic Steroids – A Question of Muscle: Human Subject Abuses in Anabolic Steroid Research” is available on Amazon.com

Nelson Vergel’s book “Testosterone: A Man’s Guide” is available on MesoRx : http://mesomorphosis.com/products/index.php/testosterone-by-nelson-vergel.html

Nelson Vergel’s book on the medical use of anabolic steroids:

http://www.amazon.com/Built-Survive-Wellness-Guide-Fourth/dp/1890772437/ref=sr_1_2?ie=UTF8&qid=1314889446&sr=8-2

To email Nelson : nelsonvergel@gmail.com

For more articles by Nelson Vergel : http://mesomorphosis.com/author/nelsonvergel/

Originally published at: TRT and Steroid Side Effect Management – Interview with Dr. Michael Scally – Part 2

Dr Michael Scally is a medical expert on anabolic steroid side effects and testosterone replacement therapy. He is available for phone consultations to anyone who needs help with hormone replacement and side effect management.  To contact him, email : mscally@hptaxis.com

His book “Anabolic Steroids – A Question of Muscle: Human Subject Abuses in Anabolic Steroid Research” is available on http://goo.gl/jaH05

Nelson Vergel (NV): Dr. Michael Scally is a well-known expert on men’s health in general, and specifically he’s an expert on hormone therapy and issues surrounding testosterone replacement. Dr. Scally, can you tell us a little bit about your background?

Michael Scally (MS): My education includes a double degree major in chemistry (1975) and life sciences (1975) from the Massachusetts Institute of Technology (MIT) Cambridge,MA. From 1975 to 1980, in the MIT division of Brain Sciences & Neuroendocrinology, I researched and published investigations on neurotransmitter relationships. During this time, I entered the prestigious Health Sciences & Technology Program, a collab­oration of the MIT and Harvard Medical School. In 1980, I was awarded by Harvard Medical School a Doctorate of Medicine, MD. In 1983, I completed a fellowship in anesthesiology at Parkland Southwest Memorial, in Dallas. From 1983 to 1994, I was a private practice anesthesiologist. In 1984, I set up the first ambulatory, outpatient, surgery center at Houston.

In 1994, I became interested in general and preventative medicine with a focus on endocrinology. I have been active in this area since that time.

In 1995, I inquired to Wyeth Pharmaceuticals about the association between primary pulmonary hypertension and pondimin (fenfluramine). I came to learn, this inquiry later was used as evidence in the class-action suit against Wyeth and was instrumental in showing that the known adverse effects were known to Wyeth but not revealed to the public.

During 1994, I competed in the Mr. Texas Bodybuilding Championship, placing second. While exercising, I was approached by a number of weightlifters on the medical treatment to restore the hypothalamic-pituitary axis (HPTA) after stopping anabolic steroids (AAS). Many of these same individuals also used over-the-counter (OTC) supplements.

As you might know, many bodybuilders are trying to decrease their body fat and increase their muscle mass as much as they can. And with these two specific goals in their mind, they were having a hard time because they were taking this over-the-counter supplement. Within a short time later, I dis­covered an over-the-counter weight loss supplement containing an ingredient, tiratricol, toxic to the thyroid. The reporting of this to the federal agency, MedWatch, was instrumental in the nationwide seizure of the supplement thus avoiding a disaster to the public health and welfare. We published our findings in the peer-reviewed literature, being the first to do so.

This spurred on my interest in the field of men’s health, particularly in the field of testosterone and anabolic steroids. I recognized the use of a treatment for stopping anabolic steroids, both prescription and nonprescription, was without any scientific support. The accepted standard of care within the medical community for anabolic steroid-induced hypogonadism is to do nothing with the expectation the individual will return to normal unassisted. This is proving not to be the case and now jeopardizes the health and welfare of countless individuals.

I developed a treatment for anabolic steroid-induced hypogonadism that has been published and presented before the Endocrine Society, the Amer­ican Association of Clinical Endocrinologists, American College of Sports Medicine, and the International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV. The condition of anabolic steroid-induced hypogonadism is found in nonprescription and prescription AAS alike. The failure of the medical community to recognize the importance of anabolic steroid-induced hypogonadism, particularly in the research setting, is the focus of my recently published book, “Anabolic Steroids—A Question of Muscle: Human Subject Abuses in Anabolic Steroid Research.”

NV: There are lots of misconceptions when it comes to testosterone replacement in men. Will you tell us, in your opinion, what are the main misconceptions? For instance, some doctors may think that giving testosterone to some­body with low testosterone may affect the liver, or may cause cancer of the liver or prostate.

MS: There are many misconceptions regarding anabolic steroids, which include testosterone. You mentioned two of the areas: liver and prostate cancer. Other areas are enlargement of the prostate or benign prostate hyper­trophy, anabolic steroid dependency, cardiovascular disease, and addiction.

I believe that many of the misconceptions come about by the politicization of anabolic steroids. As far as prescribed medicines are concerned, anabolic steroids are the only group of drugs with a law specifically aimed at their use. This has led to a lack or absence of good research. Instead, what the medical community has relied on are anecdotal and inflammatory reports.

This is probably most evident in the medical community’s steadfast refusal to accept that anabolic steroids increase muscle mass and strength. We now know that anabolic steroids conclusively do increase muscle mass and strength and athletic performance.

As far as liver effects, use of the oral anabolic steroids has been reported to cause liver dysfunction and cancer. These reports are primarily in individuals with a preexisting condition treated for extended periods. The intramuscular injections and transdermal preparations do not appear to be associated with liver problems, and routine monitoring is therefore unnecessary. In the thou­sands of patients I have treated with testosterone, I never even think about liver problems being a contraindication, because they just do not come up.

In non-obstructive benign prostatic hyperplasia (BPH), testosterone replacement therapy is not a concern. The prostate volumes increase in an inconsistent manner. As with any treatment, careful monitoring will alert one to a problem.

As far as prostatic cancer, there is no association. In 2004, a New England Journal of Medicine article review of over 60 studies on testosterone replace­ment therapy concluded that there is no causal or association with prostate cancer.

NV: But testosterone replacement seems to be getting more and more mainstream. Ever since the introduction of gels like Androgel and Testim, more and more doctors feel comfortable prescribing testos­terone. But yet, there are still a lot of fears, too. Another fear is changes in lipids and cardiovascular risks associated with testosterone. Can you expand on that a little?

MS: The available data indicate that testosterone replacement therapy within the physiologic range by transdermal or injectable testosterone prepa­ration is not associated with worsening of the lipid profile. Studies using physiologic replacement doses of testosterone show no change, or only a slight decrease, in HDL, often with a reduction in total cholesterol. The oral non-aromatizable anabolic steroids appear to lower high-density lipoprotein (HDL) levels.

The belief that testosterone is a risk factor for cardiac disease is based on the observation that men have both a higher incidence of cardiovascular events and higher testosterone levels than women do. There is little data for this idea. Many studies suggest the opposite. There are multiple studies showing a relation between hypogonadism and an increased cardiovascular risk.

There is evidence that testosterone replacement therapy may be beneficial for men with cardiac disease. In a small study, men with chronic stable angina who were treated with transdermal testosterone replacement therapy had greater angina free exercise tolerance. Importantly, testosterone replacement therapy has not shown an increased incidence of cardiovascular disease or stroke.

NV: There are some data on hypogonadism and increased risks of cardiovascular events. Is that what you mean? Some people actu­ally become so severely hypogonadal, they actually may be risking higher incidence of heart attacks and strokes?

MS: That is correct. There are numerous studies demonstrating the rela­tionship between low testosterone levels and adverse cardiovascular events, as well as stroke. Also, there are case study reports of people who stop anabolic steroids, and then suffer a heart attack.

In the book that I wrote, one of the studies in the published literature, looking at the effects of anabolic steroids in certain populations, for 12 weeks, did not look at the patients after they stopped the drug. If you want to look at the effects of these drugs, you need to see what happens when you stop them. I filed a Freedom of Information Act to obtain the patient records. One of the patients actually suffered a heart attack within four weeks of stopping the anabolic steroid. The details, including the original patient records, of this case are reported in my book.

NV: Should patients with an increased or elevated prostatic specific antigen (PSA) avoid testosterone? What role does testosterone replace­ment therapy (TRT) have on prostate cancer, if any? Is there a risk of worsening prostate cancer with TRT?

MS: You brought up a number of important and controversial issues. It is generally agreed that TRT with established prostate cancer is contraindicated.

It is known that suppression of testosterone levels causes regression of prostate cancer, and it is now commonplace for men with metastatic prostate cancer to undergo treatment designed to lower testosterone levels. The ques­tion becomes if lowering testosterone causes prostate cancer to regress, does elevating testosterone cause prostate cancer to appear?

There are case reports suggesting that TRT may convert an occult cancer into a clinically apparent lesion. These studies are wrong. One must be very careful in attributing causality to testosterone, since over 200,000 men are given a diagnosis of prostate cancer each year, and most of these cases are first detected by a rise in the PSA level unrelated to testosterone therapy. Studies have demonstrated a low frequency of prostate cancer in association with TRT. Despite extensive research, there is no compelling evidence that testosterone has a causative role in prostate cancer.

There appears to be no compelling evidence at present to suggest that men with higher testosterone levels are at greater risk of prostate cancer or treating men who have hypogonadism with exogenous androgens increases this risk. In fact, prostate cancer becomes more prevalent exactly at the time of a man’s life when testosterone levels decline.

Little evidence exists on the safety of TRT initiation after treatment for primary prostate cancer. In one very small case series, TRT after treatment of organ confined prostate cancer produced no adverse effects. There are no large, long-term studies proving that the risk of recurrence is not affected by TRT. Personally, I would be reluctant to provide TRT in prostate cancer; treatment should be left to strict research protocols.

PSA is a serum glycoprotein made by the normal prostate that is widely used as a tumor marker, because elevated PSA levels correlate with the risk of prostate cancer. A PSA value greater than 4.0 ng/mL has been the standard indication for prostate biopsy since the introduction of this test in the 1980s.

Testosterone trials have inconsistently shown a rise in PSA, typically between 0.2 and 0.5 ng/mL. A greater increase in PSA arouses concern that prostate cancer has developed. It is my practice to recommend a prostate biopsy in any patient with a yearly PSA increase of 1.0 ng/mL or more. If the PSA level increases by 0.75 ng/mL in one year, I repeat the PSA measurement in three to six months and recommend a biopsy if there is any further increase.

NV: Can you explain what polycythemia is and what it means when it comes to cardiovascular risk and other issues?

MS: In respect to anabolic steroid-induced polycythemia, polycythemia is a condition that results in an increased level of circulating red blood cells in the blood stream. Erythrocytosis is a more specific term that is used to denote increased red blood cells. People with polycythemia have an increase in hematocrit, hemoglobin, or red blood cell count above the normal limits. The reporting of polycythemia is typically in terms of increased hematocrit or hemoglobin.

Hematocrit is a blood test that measures the percentage of red blood cells found in the whole blood. This measurement depends on the number and size of red blood cells. Normally, for a male, the hematocrit raises up to a level of 52–54 depending on the reporting laboratory reference range. Polycythemia is considered when the hematocrit is greater than the upper limit of normal.

Hemoglobin is the protein molecule in red blood cells that carries oxygen from the lungs to the body’s tissues and returns carbon dioxide from the tissues to the lungs. The hemoglobin level is expressed as the amount of hemoglobin in grams (g) per deciliter (dl) of the whole blood, a deciliter being 100 mL, for adult males: 14–18 gm/dL. Polycythemia is considered when a hemoglobin level is greater than 18 g/dL in men.

It is a thickening of the blood. The blood becomes almost like sludge. You would think that with the increased number of red blood cells, it would carry more oxygen; but its oxygen-carrying capacity decreases markedly. Without treatment, polycythemia can be life threatening. Elevation above the normal range may have grave consequences, particularly in the elderly, since an attendant increase in blood viscosity could aggravate vascular disease in the coronary, cerebrovascular, or peripheral vascular circulation. However, with proper medical care, many people experience few problems related to this disease.

Symptoms of polycythemia can be none to minimal in many people. Some general and nonspecific symptoms include weakness, fatigue, headache, itch­ing, redness of your skin, bruising, joint pain, dizziness, abdominal pain, shortness of breath, breathing difficulty when you lie down; and numbness, tingling, or burning in the hands, feet, arms, or legs.

NV: Or when they work out, they turn purple.

MS: That can certainly be a symptom of polycythemia.

NV: Is the incidence of polycythemia related to the route of admin­istration, dose, duration, and age? Is polycythemia common in replace­ment doses?

MS: Yes. It occurs quite frequently in people who are just on replacement testosterone. Older men appear more sensitive to the erythropoietic effects of testosterone than young men do. Both testosterone dose and mode of delivery affect the magnitude of hematocrit elevation.

The incidence of testosterone-associated polycythemia may be lower in males receiving pharmacokinetically steady-state delivery of testosterone formulations, than it is in receiving intramuscular injections.

In patients using topical preparations, there is a 5–20 percent incidence of erythrocytosis. There is an apparent direct relation between testosterone dosage and the incidence of erythrocytosis. Erythrocytosis occurs in about 5– 15 percent by patches and in 10–20 percent with gel preparations depending on the use of 50 mg/day (delivering 5 mg /day) and 100 mg/day (delivering 10 mg/day) during the course of approximately 14 year.

The most commonly used forms of intramuscular-injectable testosterone esters are testosterone enanthate and cypionate. Injectable testosterone esters generate supranormal testosterone levels shortly after injection and then testosterone levels decline very rapidly, becoming subnormal in the days before the next injection.

Testosterone ester injections have been reported to be associated with a higher risk of erythrocytosis than transdermal testosterone. It is unclear whether the higher frequency of erythrocytosis observed with injectable testosterone esters is due to the higher dose of testosterone delivered by the injections or the higher peaks of testosterone levels. In one study, intramuscu­lar injections of testosterone enanthate produced an elevated hematocrit over 40 percent.

NV: Is therapeutic phlebotomy a good way to manage polycythemia?

MS: Untoward events are unlikely with mild erythrocytosis of relatively short duration. Therapeutic phlebotomy and blood donation are overall a safe procedure, the frequency of side effects being low and their severity weak. Other options include dosage reduction or the withholding of testosterone. However, these latter options can be problematic since the patient will expe­rience symptoms of anabolic steroid-induced hypogonadism.

This does present a catch-22 for many physicians. Because the half-life of the red blood cell is approximately 120 days, it might be a considerable length of time, more than three months or longer, to normalize the hemoglobin or hematocrit upon TRT cessation. But, the problem of anabolic steroid-induced hypogonadism symptoms complicated matters.

Many a times, an attempt will be to maintain TRT while simultaneously performing a therapeutic phlebotomy. Because of the increased erythro-poiesis, production of red blood cells, it feels like the proverbial chasing one’s tail. In a number of therapeutic phlebotomies, the units of the blood that have to be taken off are clearly quite excessive; and we do not want to do that too quickly. It may come to be three, four, or even five pints of blood that have to be taken off.

In order to get a good hold on the problem of polycythemia, it will be necessary to discontinue TRT. What we have done again, in our protocol, is that we have stopped the testosterone, thereby removing the cause of the increased red blood cell production, treat them with the HPTA protocol that prevents the hypogonadism, and have the therapeutic phlebotomy done. They are able to get the hemoglobin or hematocrit down to the normal level, do not go through the adverse effects of the hypogonadism; and then, at the other end, be able to start the testosterone therapy again. As far as we can determine, no testosterone associated thromboembolic events have been reported to date.

NV: I am actually surprised how many patients are out there that do not have their physician following up their hematocrit when they are put on testosterone or anabolics for wasting syndrome. It is something that the physician should be looking out for and measuring.

MS: The hemoglobin and hematocrit is part of the routine laboratory follow-up for anyone on TRT. If a patient complains of any of the symp­toms we describe for polycythemia, a hemoglobin and hematocrit should be checked. One of the confounding problems is the symptoms tend to be nonspecific.

NV: Can you say something about the prophylactic use of finasteride or dutasteride to avoid DHT-related problems like prostate enlargement or hair loss? Is there a role for the use of finasteride or dutasteride to prevent the possible increase of hair loss with TRT?

MS: Finasteride and dutasteride are 5-alpha reductase inhibitors. 5-alpha reductase comes in two forms, type 1 and type 2, and is responsible for the conversion of testosterone into DHT. Finasteride inhibits type 2 only while dutasteride inhibits both forms.

Finasteride comes in two doses depending on whether the indication is for hair loss or benign prostate hypertrophy. Propecia, 1 mg, is for hair loss. Proscar, 5 mg, is for prostatic hypertrophy.

DHT has been shown to be important in the development of hair loss or male pattern baldness. I am unaware any studies indicating a worsening of hair loss or male pattern baldness, though this possibility has not been carefully studied. There are anecdotal reports. The prophylactic use of these drugs is an individual decision after weighing the risks and benefits.

DHT is also important in prostate health. It is thought an overabundance of DHT may be important in benign prostatic hyperplasia (BPH) and prostate cancer. Dutasteride provides greater suppression of DHT than finasteride does, thereby underlying the hypothesis that inhibition of both type 1 and type 2 would provide correspondingly greater protection than inhibition of type 2 alone.

However, significant side effects of finasteride use include reduced volume of ejaculate, erectile dysfunction, loss of libido, and gynecomastia. This will prevent many from their use.

Some people think that DHT will affect lean body composition. DHT does have a higher affinity for the androgen receptor. But the enzyme that converts testosterone into DHT is not located in the muscle. There is no evidence for these drugs to effect muscle mass.

NV: What about other issues related TRT, such as to increased estro­gen levels and gynecomastia?

MS: A small number report breast tenderness and swelling. Fluid retention is uncommon and generally mild, but TRT should be used cautiously in men with congestive heart failure or renal insufficiency. After confirmation of elevated estrogen, estradiol, levels, this can be treated with either an aromatization inhibitor or estradiol receptor blocker. This must be done very carefully as any prolonged reduction in estradiol levels runs the risk of causing osteoporosis.

Exacerbation of sleep apnea or the development of sleep apnea has been associated with TRT who have other identifiable risk factors for sleep apnea. The mechanism appears to be central mediated rather than by means of changes in the airway. Other side effects include acne, oily skin, increased body hair, and flushing. Hypertension has rarely been reported.

Of course, the adverse effect I am most concerned with is androgen-induced hypogonadism, which occurs in one hundred percent of individuals stopping TRT, the variables being the duration and severity.

On testosterone replacement therapy, for those without organic hypogonadism, those with late onset of hypogonadism, the only thing that I always caution about is that people should not be on testosterone replacement therapy, year after year after year, without stopping every 12–18 months to restore the axis, to make sure the function is still there. The longer you are on testosterone, the harder it is going to be to come off testosterone.

NV: In your opinion, can you tell us a little bit about the different options for TRT? Have you seen any difference in using gels versus injections? Is there any advantage or disadvantage to using either one?

MS: Injectable, transdermal, buccal, and oral testosterone formulations are available for clinical use. These forms of treatment differ in several key areas.

Oral preparations include methyltestosterone and fluoxymesterone, which are rarely prescribed because of their association with substantial liver toxicity. InEurope, there is an oral preparation of testosterone undecenoate, Andriol. It has a poor history of bioavailability.

Recently, the FDA approved a buccal preparation of testosterone, Striant. Striant requires administration twice a day. It is used little at this time.

Transdermal testosterone is available as a patch, Testim, and gel, Androgel. Daily application is required for each of these. They are designed to deliver 5–10 mg of testosterone a day. The advantages include ease of use and maintenance of relatively uniform serum testosterone levels over time. Skin irritation in the form of itching and redness is a frequent adverse effect of Testim with reports as high as 60–70 percent. This is uncommon with Androgel. Inadequate absorption through the skin may limit the value of transdermal preparations in some persons. A common problem is the low dose preparations provide inadequate serum testosterone levels. This is also seen with the high dose.

The topicals have become, by far, the most-used products in the last decade or so, approaching a billion dollars in sales. Androgel is the biggest product of the topicals.

If the patient is not too scared of doing injectables, oil-based testosterone ester preparations are available. The most commonly used injectables are Delatestryl or testosterone enanthate and depo testosterone or testosterone cypionate. In my practice, the typical dose is between 100 and 150 mg/week. The peak serum levels occur in 2–5 days after injection, and a return to baseline is usually observed 10 days after injection. In this manner, adequate serum levels are maintained. Intramuscular injections of testosterone can cause local pain, soreness, bruising, redness, swelling, and possible infection.

NV: Most doctors prescribe 1-cc of 200 mL of testosterone every two weeks. Can you describe the problems with this schedule, if any?

MS: This is a problem that is seen much more often than necessary. Many doctors use a typical dose is 100 mg/week, or 200–300 mg every two to three weeks.

Within 7–10 days after injection, the serum testosterone levels are low to abnormally low. This is described as a “roller coaster” effect, characterized by alternating periods of symptomatic benefit and a return to baseline symp­toms, corresponding to the fluctuations in serum testosterone levels. This can be discovered by having the testosterone level checked within 24 hours prior to injection.

NV: Can you talk to us a little bit about compounding pharmacy prod­ucts? In particular, when using testosterone gels with concentrations higher than 1 percent for reaching total testosterone blood levels above 500 ng/L. Have you had any experience with the compounding industry?

MS: I have had some experience with the compounding industry. Com­pounding pharmacies are very capable at providing higher concentrations of transdermal testosterone preparations. Because of this, they are able to supply a transdermal product in small volumes. They also tend to be less expensive than commercially available pharmaceutical testosterone replace­ment options.

NV: Do you think it is advisable to get your testosterone levels rechecked after a few weeks of starting any of the therapies?

MS: My protocol is that once I start a patient on testosterone, I check the testosterone level 4–6 weeks after initiating TRT. In patients using topical preparations, I recommend testing within 4–6 hours after application. Those using injectables of testosterone esters, I recommend testing within 24 hours before their next scheduled injection.

NV: Do you have any preference between the free testosterone and total testosterone test?

MS: In the monitoring of the patient on TRT, I utilize the total testosterone. The initial evaluation of a patient might include the use of free testosterone or bioavailable testosterone. In a symptomatic individual, the total testosterone can be normal but the free or bioavailable testosterone abnormal.

Testosterone circulates in three forms. Testosterone circulates in a free or unbound state, tightly bound to SHBG, or weakly bound to the blood protein albumin. Bioavailable, non-SHBG, testosterone includes free testosterone and testosterone that is bound to albumin but does not include SHBG -bound testosterone.

Examined changes over time have demonstrated a decrease in the total testosterone and an increase in SHBG levels. Because of this, the total testosterone might be normal, whereas the free or bioavailable testosterone is abnormal. If these alternative methods are used to diagnose hypogonadism, their utility during TRT is limited.

I would caution about the assay methodology used to calculate the free or bioavailable testosterone. The methods used to conduct the measurements vary in their accuracy, standardization, the extent of validation, and the reproducibility of results.

Bioavailable testosterone is measured or calculated in several ways. SHBG bound testosterone can be precipitated with ammonium sulfate and the remaining testosterone is then taken as the bioavailable.

Measures of free testosterone (FT) are controversial. The only standard­ized and validated method is equilibrium dialysis or by calculating free testosterone levels based on separate measurements of testosterone and SHBG. Other measures of free testosterone are less accurate.

NV: And your goal is usually to have patients above what level?

MS: I like their total testosterone trough or lower level to be in the 500–700 range, normal being 300–1,000 ng/dL.

NV: Besides checking of the initial T level, can you elaborate on the monitoring during TRT?

I recommend a periodic follow-up of patients receiving replacement testos­terone therapy at the interval of three months during the first year of treatment. Afterward, patients are followed up every six months. It is important to do a review of systems to ensure the relief of the complaining symptoms as well as no worsening or new symptoms.

In addition to the serum total testosterone, I routinely monitor the basic chemistry profile, which includes liver function, kidney function, elec­trolytes, glucose, lipid panel, and hemoglobin or hematocrit. At three months, I will often include estradiol and DHT levels.

If the patient is older than 50 years, I include the PSA. The role of digital rectal examination (DRE) and PSA in detecting early, clinically significant, prostate cancer is controversial. I discuss this with each patient and allow them to decide on their use.

NV: How about the new non-steroidal androgens that are in the pipeline? Can you tell us what you have read about them?

MS: They are called SARM: selective androgen receptor modulators. They are going to become more and more popular. The closest SARM that is coming to the market, and it is years away, is called ostarine. It is being developed by GTx, Inc. Ligand Pharmaceuticals has a SARM in early phase of development. They are both traded on the NASDAQ Exchange.

The initial studies are being done in cancer patients. The data collected is change in muscle mass and strength. The clinical outcome being measured is the six-minute walk test.

My feeling on this is that we have a long way to go before these things come to market. If they come to market within the next 5–10 years, we will be lucky. As far as I know, these are the only SARMs in human clinical trials.

NV: I have also heard that SARMs may not have any influence on sexual function, only on lean body mass and maybe some functional capacity. They are really not replacement of testosterone. Are they?

MS: From the initial studies, these are meant to take the place of anabolic steroids, not testosterone. There are no indications SARMs are being devel­oped as TRT. The data from both animal and human studies is that they act similarly, if not identically, to anabolic steroids. They act through the androgen receptor. They do cause HPTA suppression.

Even though they have the same effect, they will be able to be marketed without that name “anabolic steroids.” This would be an obvious advantage in their marketing. It should be noted that these drugs, SARMs, have already found their way into the nonprescription or illicit market.

Please stay tuned for part 2 of this interview!

Nelson Vergel

Author, Testoserone: A Man’s Guide (available on http://goo.gl/Hqf4j )

To email Nelson : nelsonvergel@gmail.com

For more articles by Nelson Vergel : http://mesomorphosis.com/author/nelsonvergel/

Originally published at: TRT and Steroid Side Effect Management – Interview With Dr. Michael Scally – Part 1

Testosterone, Dianabol, Winstrol, Deca Durabolin, Anavar and Anadrol are some of the most popular anabolic steroids currently used by athletes and bodybuilders today. Few people outside the steroid subculture realize that these anabolic drugs have been available for over fifty years.

Many sports fans seem to be under the impression that widespread steroid use in sports is only a relatively recent phenomena. They are sorely mistaken. The truth is athletes have been experimenting with these drugs practically from the moment they became commercially available. The “secret” of steroids has been well-known among insiders for some time.

The First Injectable Anabolic Steroid Product

The testes have been known to be responsible for male-typical characteristics and behaviors since ancient times but it was not until 1849 that scientists learned how this happened. German scientist Arnold Adolf Berthold discovered that the testes influenced masculine behavior by secreting an unknown substance into the bloodstream.

A few decades later, French physiologist Charles-Édouard Brown-Séquard, the father of modern-day hormone research, sought to capture this essence of masculinity with a concentrated extract derived from guinea pig and dog testicles. He claimed that injecting the extract would increase physical strength and intellectual ability in humans.

The First Athlete to Use Steroids

Athletes looking for an edge have often looked to science as a means to improve their athletic abilities. Brown-Séquard’s hormone research intrigued future Major League Baseball pitcher and Hall of Famer “Pud” Galvin. Galvin wondered if injections of the Brown-Séquard Elixir would enhance baseball performance.

Since the extract undoubtedly contained trace amounts of as-of-yet-unidentified androgenic steroids, Galvin became the first known athlete to inject a steroid-based product when he became a regular user of the rejuvenating Brown-Sequard Elixir. The year was 1889. Galvin’s use of “steroids” preceding the recent steroids in baseball scandal by over 100 years.

Brown-Séquard’s research inspired several scientists to build on his research with testicular extracts.

Steroids Can Enhance Athletic Performance

A few years after “Pud” Galvin became baseball’s first “steroid user”, Austrian physiologist Oskar Zoth hypothesized that injections of steroid-based testicular extracts could enhance athletic performance.

Zoth published an 1896 paper proposing further research on performance be conducted with athletes. The idea that some mysterious substance in animal testicles could offer performance-enhancing benefits in athletes has been firmly planted in the research community ever since.

The next two decades saw scientists repeatedly confirm the androgenic effects of various testicular extracts.

In 1927, University of Chicago chemistry professor Fred Koch and research assistant Lemuel McGee derived 20 mg of a substance from 40 pounds of bovine testicles obtained from the Chicago Stockyards. The testicular extract re-masculinized castrated roosters, pigs and rats.

Still, the chemical structures of powerful androgens such as testosterone had not yet been elucidated and identified.

The Decade of Sex Hormones

Steroid hormone research exploded in the 1930s. The decade started off with the milestone discovery involving the isolation of the first androgenic hormone in 1931 by German biochemist Adolf Butenandt.

The discovery generated considerable excitement in the scientific community but researchers believed that a much more powerful anabolic-androgenic steroid hormone still existed. The race was on!

The “decade of sex hormones” would open a Pandora’s box with a far-reaching impact of sport and medicine.

The Horsemen of the Steroid Revolution

Three powerful pharmaceutical companies were highly involved in the rush to developed anabolic steroids. Not surprisingly, these three companies had a long and lasting effect on the history and development of anabolic steroids that continues until the present.

The development of steroids was big business even in the 1930s. Major pharmaceutical companies such as Organon, Schering and Ciba saw considerable potential in this emerging market. It is little surprise that the companies that launched the steroid revolution continue to be strongly associated with anabolic steroids among modern-day athletes.

The chemists working for these big pharma companies have changed the world perhaps not in ways that they could have imagined. They would become “steroid gods” in the annals of sports history. Athletes would soon make use of their creations during the next 75 years!

The Discovery and Identification of Testosterone

Organon, Schering and Ciba rushed to isolate and synthesize the powerful hormones contained in testicular extracts.

Karoly David and Ernst Laqueur of Organon (Netherlands) were the first pharmaceutical team to isolate and identify the chemical structure of testosterone when they isolated 10 mg from 100 kg of bull testicles. The discovery of testosterone was first announced in the classic paper entitled “On Crystalline Male Hormone from Testes (Testosterone): More Active Than Androsterone Preparations from Urine or Cholesterol” on May 27, 1935.

At this point, large quantities of animal testicles were required to extract testosterone which made the use of testosterone impractical for commercial use. However, competing research teams were only months away from publishing more efficient methods of synthesizing testosterone.

The Synthesis of Testosterone and the Nobel Prize in Chemistry

Schering and Ciba independently discovered less expensive methods of synthesizing testosterone in August 1935.

German biochemist Adolf Butenandt and G. Hanisch of Schering (Germany) published a paper entitled “On Testosterone Conversion of Dehydroandrosterone in Androstenediol and Testosterone: A Method for Preparing Testosterone from Cholesterol” on August 24, 1935.

Croatian organic chemist Leopold Ruži?ka and German chemist Alfred Wettstein of Ciba (Switzerland) published the paper entitled “On the Artificial Preparation of the Testicular Hormone Testosterone (Androsten-3-one-17-ol)” on August 31, 1935.

This steroid research was deemed so important that the lead researchers from the Schering and Ciba teams ultimately shared the 1938 Nobel Prize in Chemistry for their remarkable work on anabolic-androgenic steroid hormones.

The Golden Age of Anabolic Steroid Research

The discovery of synthetic methods of preparing the anabolic-androgenic steroid known as testosterone was a major breakthrough in the pharmaceutical world allowing steroid hormone research to flourish.

This is when the golden age of anabolic steroid research (1935-1965) truly began.

Nobel Prize winner Ruži?ka didn’t waste any time; he synthesized some pretty cool steroids back in 1935 including methyltestosterone, mestanolone and methandriol.

By 1937, the injectable anabolic steroid testosterone propionate and the oral steroid methyltestosterone were available in sufficient quantities to be used in human clinical research trials.

Ruži?ka also synthesized androstenedione which became one of the most infamous steroids in the history of steroids in baseball. Illinois chemist Patrick Arnold introduced androstenedione into the dietary supplement market in the United States in 1995 and it found its way into the controversy surrounding home run slugger Mark McGwire and steroids.

Testosterone Increases Muscle Mass

Charles Kochakian, a synthetic steroid pioneer, made a milestone discovery in the history of steroids. Kochakian’s animal research with testosterone acetate proved that testosterone was indeed an anabolic hormone in 1936. Kochakian’s research group was the first to scientifically document a connection between testosterone and increased muscle mass.

In 1938, Allan Kenyon’s research group confirmed that the anabolic muscle effects of testosterone propionate occurred in human subjects as well during steroid experiments on eunuchoidal boys, men and women.

The Use of Anabolic Steroids in World War II

Kochakian participated in a medical conference exploring methods to speed the healing process in injured American soldiers returning from combat during World War II. Kochakian promoted the muscle-building effects of testosterone for the post-surgical care of these soldiers.

There has been no evidence that steroids were ever used to enhance performance of soldiers on the battlefield.

Nazi Soldiers and Anabolic Steroids

The claim that German soldiers were injected with testosterone in World War II has often been repeated but Professor of Germanic Studies John Hoberman believes the use of steroid by Nazi soldiers is a myth. There has been no evidence in the German literature to support the use of anabolic steroids by soldiers in Nazi Germany.

Similarly, the rumor that German athletes used testosterone as an ergogenic aid during the 1936 Berlin Olympics is unsupported by literature published during this period.

Russell Marker Makes Steroid Use Affordable

The most significant discovery to facilitate the commercialization of pharmaceutical sex hormones was made by Pennsylvania State chemistry professor Russell Marker.

Ruži?ka and Butenandt may have won the Nobel Prize for their synthesis of testosterone but Marker made anabolic steroids a mass market phenomenon.

The cost of testosterone, progesterone and other important steroids fell dramatically in the 1940s when Marker recognized that the raw materials for steroid synthesis could be obtained from the naturally-occurring plant steroid diosgenin instead of the much more expensive method of converting cholesterol that existed at the time.

He developed a three-step chemical process by which diosgenin could be converted to progesterone. It became known as the Marker Degradation. Now, he only needed to find an inexpensive plant source of diosgenin.

The Indiana Jones of the Steroid Industry

In January 1942, the eccentric Marker became the Indiana Jones of the steroid industry when he left the ivory tower at Pennsylvania State College to explore the jungles of Mexico. He organized an expedition exploring the area surronding the city of Orizaba in the State of Veracruz.

Marker succeeded in locating the diosgenin-containing variety of Mexican wild yam known as the “cabeza de negro” (dioscorea mexicana). This variety of wild yam reached up to 100 kilograms in size.

Marker’s team continued searching for richer sources of plant steroids and eventually found the “barbasco” variety of wild yam (dioscorea composita) which contained four times the amount of diosgenin as the “cabeza de negro”.

The Mexican Steroid Industry Becomes International Player in Steroid Trade

The pharmaceutical company Parke-Davis funded Marker’s 1942 expedition to Mexico but rejected proposals to commercialize the discovery. The president of Parke-Davis didn’t consider Mexico a reliable investment given its instability and anti-American sentiment in the midst of World War II.

Marker resigned from Parke-Davis in 1943. He shopped his discovery to other American pharmaceutical houses which all rejected his proposal.

So, in 1944, Marker founded Syntex SA in Mexico City, with investments by the Mexican company Laboratorios Hormona SA, for the commercial production of steroid hormones.

The Mexican steroid industry, including “Syntex” and several other steroid companies, produced the bulk of sex hormones sold in the United States and became an international player in the field.

The price of anabolic steroids fell drastically setting the stage for their increased use in sport and society.

The Popularization of Testosterone Among West Coast Bodybuilders

In 1945, writer Paul de Kruif celebrated the anabolic properties of testosterone, testosterone propionate and methyltestosterone in the book entitled “The Male Hormone”. This widely-read book was rumored to have helped popularize the potential of testosterone (and future anabolic steroids) to increase muscle mass among West Coast bodybuilders in the late 1940s and early 1950s. This was only the beginning of bodybuilding’s fascination with anabolic steroids.

The bodybuilding community as a whole would soon start widely experimenting with anabolic steroids in the 1950s and become pioneers in steroid use. They would remain on the cutting edge of performance-enhancement drugs well into the next century.

IFBB Mr. Olympia Larry Scott admitted that he, and practically all of the top competitive bodybuilders, were also using anabolic steroids by 1960.

S.D. Searle Pharmaceuticals Creates One Thousand Different Anabolic Steroids in Laboratory

Searle initiated an unprecedented effort in steroid research to discover superior synthetic steroid hormones for use in medicine. Between 1948 and 1955, chemists at Searle had synthesized more than a thousand different testosterone derivatives and analogues with the specific goal of creating an orally active anabolic steroid with minimal androgenic side effects. Searle wanted to create steroids that avoided any virilizing effects.

Nilevar Becomes First Synthetic Oral Anabolic Steroid Approved by FDA (1956)

Of the thousand potential steroid profiles created by Searle during this period, Nilevar (norethandrolone) was the winning candidate selected for commercialization. Searle chemist Frank Colton synthesized norethandrolone in 1953.

Norethandrolone became the first orally-active, synthetic anabolic steroid when it was approved by the Food and Drug Administration (FDA) under the brand name Nilevar in 1956. The only other orally-active androgen available at the time was methyltestosterone which was simply a 17?-methylated version of testosterone to increase its oral bioavailability.

Bodybuilding Champion Bill Pearl Uses Nilevar

In 1958, West Coast bodybuilder and Mr. Universe champion Bill Pearl was one of the first bodybuilders to experiment with the new anabolic steroid created by Searle. Pearl did a 12-week cycle using 30 mg of Nilevar and increased his bodyweight by 25 lbs from 225 to 250 lbs.

Bill Pearl openly admitted using anabolic steroids in preparation for the 1961 National Amateur BodybBuilders Association (NABBA) Mr. Universe contest. He revealed that steroid use was no longer an underground practice among top bodybuilders corroborating Mr. Olympia Larry Scott’s assessment of the steroid scene in bodybuilding.

Pharmaceutical Companies Go Nuts Creating Anabolic Steroids

G.D. Searle was not the only pharmaceutical company to spend massive resources on developing new synthetic anabolic steroids. Several major pharmaceutical companies went absolutely nuts creating anabolic steroids during the 1950s and the early 1960s.

Between 1950 and 1965, practically all of the popular steroids currently used today had been developed. These included but are not limited to: Dianabol, Anadrol, Anavar, Winstrol, Halotestin, Equipoise, Durabolin, Deca Durabolin, Primobolan, Oral Turinabol, Masteron, Proviron and Trenbolone Acetate.

Even some of the more esoteric steroids to be used by future bodybuilders were developed during this period such as furazabol, Esiclene (formebolone), Oranabol (oxymesterone), Cheque Drops (mibolerone), Anatrofin (stenbolone) and Orabolin.

Organon Firmly Establishes Its Place in Steroid History

Organon created some incredibly popular injectable steroids during this period many of which are still widely used by bodybuilders and athletes. Organon will be forever linked to anabolic steroids in their minds due to the release of Durabolin and especially Deca Durabolin.

Organon released Durabolin (nandrolone phenylpropionate) in 1957 which became hugely popular. Its popularity was soon eclipsed when Organon released Deca Durabolin in 1962 over a decade after nandrolone decanoate was first created.

Deca Durabolin ultimately became one of the all-time most popular steroids in the history of performance-enhancement along with Dianabol, Anadrol, Anavar and Winstrol.

Syntex Continues Its Steroid Innovation

Russell Marker left his mark on the steroid industry with the founding of Syntex. Marker’s successors at Syntex continued its steroid research and released Anadrol (oxymetholone) in 1959 after it was synthesized by Howard Ringold and George Rosenkranz. Rosenkranz and Ringold had created Masteron (drostanolone acetate) for Syntex a couple of years earlier.

Many of Ringold’s creations were never commercially introduced by Syntex. However, at least one of his shelved anabolic steroid products – methyldrostanolone or methasteron – would become marketed as a widely successful “dietary supplement” named “Superdrol” during the era of prohormone supplement ushered in by the Dietary Health and Supplement Education Act of 1994.

Not only did Syntex create Anadrol, it provided the inspiration for Winthrop Laboratories to create stanozolol. Winthrop chemist was able to synthesize stanozolol from oxymetholone in 1959. Stanozolol was marketed as Winstrol and Winstrol Depot in the U.S. In 1962.

Anabolic Steroid Discoveries That Ended Up as “Dietary Supplements” Fifty Years Later

While Searle synthesized over a thousand anabolic steroids in the laboratory during this period, they unfortunately only published limited results of their research. Other major pharmaceutical companies, such as Synex, did not hesitate to publish many more of their steroid discoveries even though they only released a handful of steroids as commercially-available drugs.

These published steroid discoveries were long forgotten until supplement companies started pouring over the research looking for promising prohormones and prosteroidal products to be released as “dietary supplements” during the late 1990s and 2000s DSHEA regulatory environment.

Julius Vida’s Guide for Renegade Steroid Chemists

Fortunately, Julius Vida compiled the published results of some 650 anabolic-androgenic steroids discovered through 1967 in his seminal 1969 textbook “Androgens and Anabolic Agents: Chemistry and Pharmacology”. This later become an invaluable reference guide, not only for sports nutrition companies, but also for renegade chemists looking for undetectable designer steroids. It became a goldmine of information for supplement “entrepreneurs” during the late 1990s.

Designer Steroids Used by Future Athletes

Some of the anabolic steroids discovered during this period were later re-introduced, not as pharmaceuticals and not as “dietary supplements”, but as undetectable designer steroids used to evade anti-doping protocols in sports.

For example, Patrick Arnold used norbolothone, developed in 1963 by Wyeth, to help some athletes accomplish this goal. Methyltrienolone is another such steroid that was undetectable at one point in sports.

Dianabol – The Most Popular Anabolic Steroid Ever

The use of anabolic steroids by bodybuilders rapidly increased during the late 1950s. West Coast bodybuilders experimented with the steroids commercially available in the United States e.g. testosterone propionate, methyltestosterone and Nilevar. However, it wasn’t until Ciba Pharmaceuticals introduced Dianabol in 1958 that steroid use quickly went mainstream in bodybuilding and weightlifting before gradually spreading to other strength sports and eventually to all competitive sports.

As we have seen, many new oral and injectable anabolic steroids made it to the marketplace around this time in the late 1950s and early 1960s but it was Dianabol that clearly emerged as the steroid of choice among American bodybuilders and athletes.

While Dianabol would have eventually found its way into sports, there are certain individuals who helped facilitate the adoption of steroids in general, and Dianabol in particular, by American athletes. John Ziegler would probably be considered at the top of the list.

Dr. John Ziegler and the York Barbell Club

Physician John Ziegler was an avid weightlifter who became fascinated with the use of anabolic steroids to increase muscle mass and performance. In the early 1950s, he befriended bodybuilder John Grimek and other weightlifters associated with Bob Hoffman’s York Barbell Club. The United States weightlifting team trained in York, Pennsylvania and Ziegler soon became the team physician.

Hoffman suspected that Russian weightlifters were using steroids as early as 1952. At the 1954 World Championships in Vienna, Ziegler learned from a Russian coach that lifters on the Russian team were using testosterone as part of their training preparations.

Ziegler’s Association with Ciba Pharmaceuticals

Ziegler conveniently worked part-time at Ciba Pharmaceuticals laboratory in Summit, New Jersey during this time. Ciba generously provided Ziegler with a supply of testosterone propionate to be used for “research purposes”.

In 1954, Ziegler provided steroids to several weightlifters at York most notably Mr. America and Mr. Universe John Grimek. He injected Grimek, Jim Park and Yaz Kuzahara with testosterone propionate during the early days of steroid experimentation at York Barbell Club.

Ciba Pharmaceuticals Introduces Dianabol

Many bodybuilding websites erroneously credit John Ziegler with the discovery of Dianabol (methandrostenolone). While Ziegler worked at the Ciba lab and had access to the steroids developed by Ciba chemists, he did not synthesize Dianabol.

In actuality, a team of European researchers working for Ciba Pharmaceuticals in Switzerland first synthesized Dianabol in 1955. This team included several well-known steroid research pioneers including German chemist Alfred Wettstein who was on the Ciba team that first synthesized testosterone in 1935.

Steroid chemists Ernst Vischer, Alfred Hunger, Charles Meystre and Ludwig Ehmann were also members of the illustrious steroid research group who contributed to the revolutionary discovery of Dianabol while working for Ciba Pharmaceuticals in Switzerland.

Ciba Asks John Ziegler to Give Dianabol to Weightlifters

Ciba Pharmaceuticals in New Jersey purportedly asked Dr. John Ziegler to administer the newly developed Dianabol to Olympic weightlifters training at York Barbell in late 1959.

Dr. Ziegler prescribed 10 mg of Dianabol per day to John Grimek, Bill March, Tony Garcy and Louis Riecke in the spring and fall of 1960.

1960 Rome Olympics and Dianabol

Ziegler prescribed Dianabol to the entire U.S. Weightlifting team in preparation for the 1960 Rome Olympics. It wasn’t long before Schultz’ Drug Store in York, Pennsylvania was filling prescriptions for dozens of athletes from York Barbell Club as well as gyms around the country.

Alvin Roy – Founding Father of Modern Strength and Conditioning Profession

While John Ziegler is frequently credited as being the “father of steroids” and is undoubtedly one of the most notable individuals to facilitate the spread of steroids in sport, the role of strength and conditioning coach Alvin Roy is often overlooked.

Alvin Roy had watched and learned from the steroid experiments taking place at York Barbell throughout the 1950s.

He first met Bob Hoffman at the 1945 Weightlifting World Championships. Roy was enlisted in the Army’s 94th Infantry having fought in the Battle of the Bulge. He was assigned to look after the U.S. Weightlifting Team in post-war Paris for five weeks. Roy developed a close friendship with Bob Hoffman and several Olympic lifters during this time.

Alvin Roy was bitten by the “barbell bug” and opened his own gym in Baton Rouge, Louisiana upon his return to the United States in 1947.

Roy stayed in close contact with the guys at York Barbell and visited them often. He became the official trainer for the U.S. Olympic Weightlifting team at the 1952 Olympics.

Alvin Roy Learns About Dianabol at York Barbell

Alvin Roy kept close association with York Barbell and continued to collaborate with York fixtures Bob Hoffman, Dr. John Ziegler and Lou Riecke as late as 1962 and beyond. It seems obvious that Roy learned about the details of steroid experimentation at York including the little blue pills known as Dianabol.

Alvin Roy Introduces Dianabol to American Football

Alvin Roy was an evangelist for applying the strength and conditioning methods learned at York to the arena of team sports, specifically American football. He introduced the first strength and conditioning programs to teams at the high school, at the collegiate and at the professional level.

Alvin Roy was also somewhat of an evangelist for the use of anabolic steroids, specifically Dianabol, in football as well. Roy had become something of a steroid guru through his relationship with the York Barbell Club and his inside knowledge of the York Barbell Club “steroid experiments”.

As strength coach, Roy led Isotrouma High School and Louisiana State University to championships in the late 1950s. Many people suspect the introduction of steroids and weights may have been the secret combination responsible for the teams’ success yet it has never been documented that Dianabol or any other steroid was a part of Roy’s success at Isotrouma or LSU.

Yet, there is no doubt that Roy introduced the organized and systematic use of steroids to professional football as the strength and conditioning coach of the San Diego Chargers in 1963 with remarkable results.

Steroid Use by the San Diego Chargers in the 1960s

Professional football players were already using anabolic steroids by the time Alvin Roy became the first American Football League strength coach at San Diego in July 1963. San Francisco 49ers quarterback Bob Waters admitted being prescribed Dianabol by team physician Dr. Lloyd Millburn as early as 1962. If the quarterback was using steroids, you can imagine that the lineman were likely using steroids as well.

However, when Alvin Roy came to San Diego, he and head coach Sid Gillman introduced Dianabol to everyone in a more systematic manner. Gillman and Roy advised players to take one 5 mg tablet of Dianabol with each meal every day. Players were given cereal bowls full of Dianabol pills at training camp.

The San Diego Charger team became unstoppable winning the AFL national championship in 1963. Court testimony later revealed that Chargers team physician Paul Woodward and other physicians continued to write prescriptions for Dianabol for some players from 1965 until at least 1970.

Alvin Roy the Steroid and Strength Guru Goes to Kansas City, Dallas and Oakland

Alvin Roy left the Chargers to become the strength coach for the Kansas City Chiefs under head coach Hank Stram in 1968. The Chiefs won Super Bowl IV in 1970.

The strength-training and steroid guru then took his secrets to the Dallas Cowboys under head coach Tom Landry. The Cowboys won Super Bowl VI in 1972.

Alvin Roy finally ended up coaching for the Oakland Raiders until his death from a heart attack in 1979.

Roy’s influence on the sport of professional football was dramatic. His role in introducing systematic weight training programs and spreading the use of performance enhancing drugs (PEDs) throughout the NFL has largely been overlooked.

Additionally, one of Alvin Roy’s colleagues with the San Diego Chargers in 1963, assistant coach Chuck Knoll, ended up coaching the Super Bowl champion Pittsburgh Steelers. Knoll hired Alvin Roy’s friend from York, Louis Riecke. The 1970s Steelers had its own well-publicized issues with steroid use during this time.

Steroid Use Explodes Into Other Sports

The use of anabolic steroids was pervasive in the West Coast bodybuilding subculture and the East Coast weightlifting subculture by the early to mid-1960s. Steroid use rapidly spread to many other sports during this period. It has been estimated that most Olympic athletes at the 1968 Mexico City Olympics had experimented with some type of anabolic steroid. The systematic and organized use of steroids had already made its way into professional American football.

So many athletes in all elite athletic disciplines were using steroids by 1969 that Jon Hendershott, editor of Track and Field News, facetiously called anabolic steroids the “breakfast of champions”.

Systematic Use of Anabolic Steroids by the USSR and East Germany

Steroid use by elite athletes was no secret by this time but everyone was still wondering what the Russians and East Germans were doing. Athletes thought that there was some top secret steroid being used by athletes in these countries that accounted for their dominant performance in many international competitions.

It was widely suspected that the Soviet and German governments not only sanctioned steroid use by its athletes but spent considerable resources researching the use of steroids for increasing athletic performance.

Bob Hoffman of York Barbell publicly attributed the dominance of the Soviet Union weightlifting team in their very first Olympic appearance at the 1952 Helsinki games to hormone products. This suspicion was confirmed in 1954 when an intoxicated Russian coach admitted to Dr. John Ziegler that the Russian weightlifters were using large amounts of exogenous testosterone.

Russians Loved the Nerobol and Retabolil Stack

A top secret 39-page Russian doping report entitled “Anabolic Steroids and Sport Capacity” published by the State Institute of Physical Culture in Moscow in July 1972 confirmed and provided a rare glimpse into the ongoing state-sponsored research into performance-enhancement drugs during this period.

Dr. Michael Kalinski was one of the recipients of this document when he was the former chairman of the department of sport biochemistry of the Kiev Institute of Physical Culture. The document provided the results of studies conducted on Soviet athletes using various combinations of anabolic steroids.

Research studies involving “Nerobol” and “Retabolil” were conducted on athletes in a variety of disciplines such as biathletes, rowers and basketball players. “Nerobol” is the Russian brand name for methandrostenolone popularly known as Dianabol. “Retabolil” is the Russian brand for nandrolone decanoate also known as Deca Durabolin.

The Russians popularized the synergistic combination of steroids in a practice known as “stacking”. Steroid s tacks including a combination of Dianabol and Deca Durabolin seemed to be the most effective and popular combination used among Russian athletes during this period.

The document provided clear recommendations for steroid use for elite athletes in sports such as weightlifting, boxing, wrestling and even gymnastics.

State-Sponsored Steroid Use in the German Democratic Republic

The German Democratic Republic’s (GDR) top sports doctor Manfred Hoeppner and the GDR’s minister of sport Manfred Ewald sought to replicate the success in the 1950s and 1960s of the Soviet doping program. Hoeppner and Ewald are considered the architects of East Germany’s state-sponsored doping regime.

Hoeppner and Ewald met with the Communist Party leaders at the East German Sports Performance committee in order to devise a plan to best guarantee international glory through the winning of Olympic gold medals. The systematic doping devised by the duo was called “state plan theme 14-25″.

The plan involved a team of chemists and pharmacologists working at a secret laboratory researching the use of illicit performance-enhancing drugs in elite athletes. The program was supervised by the German secret police known as the Stasi.

Jenapharm Produces Oral Turinabol for East German Athletes

Ewald had strong ties to the state-owned pharmaceutical company Jenapharm Pharmaceutical Company that worked on behalf of the GDR to develop and provide advanced performance-enhancing anabolic steroids. Jenapharm synthesized Oral Turinabol in 1960. It became one of the most widely used anabolic steroids in the GDR’s doping program throughout the 1970s and 1980s.

The Americans loved their Dianabol. The Russians their Retabolil plus Nerobol stacks. And the East Germans loved their Oral Turinabol.

The doping by East Germany was advanced and sophisticated and undoubtedly helps explain their phenomenal Olympic success between 1972 and 1988.

State of the Art Doping in the GDR

Their use of performance-enhancing drugs was not just limited to Oral Turinabol but also involved other anabolic steroids such as Dianabol, Testosteron-Ampullen (testosterone propionate), Testosteron-Depot-Ampullen (testosterone enanthate), Turinabol-Ampullen (Durabolin) and Turinabol-Depot-Ampullen (Deca Durabolin).

The East Germans also experimented with nasal sprays containing various testosterone esters and androstenedione; testosterone-stimulating drugs such as human chorionic gonadotropic (hCG) and Clomid (clomiphene citrate); neuropeptides such as lysine-vasopressin, oxytocin and substance P; stimulants such as amphetamine and methamphetamine; neurotropics and psychotropics such as Piracetam, Nicergolin and Nivalin; and polypeptide hormones such as somatotropin (human growth hormone).

The GDR systematic doping program was sanctioned at the highest level of government which ordered that anabolic steroids be used in male and female athletes as “integral part” of the training process; directly controlled by the sports ministry with centralized distribution of steroids, further research into optimizing doping by athletes and avoiding detection at international meets; education classes to teach sports physicians and coaches about doping; and absolute secrecy with doping classified as Official State Secret.

The scope of the East German doping program was mind-boggling. It involved hundreds of chemists, physicians and coaches. Everyone was working together researching, creating and administering performance-enhancing drugs. Steroids were administered to over 10,000 elite GDR athletes, including children as young as 11 years old, over the three decades in which Hoeppner and Ewald oversaw the East German sports machine.

Originally published at: The History of Anabolic Steroids in Sports