2016年1月4日星期一

Can I Avoid Polycythemia while on TRT?

Q: Is there any way to avoid Polycythemia when doing TRT? I know that injections are more prone to causing this. I recently switched from shots and am currently doing 25mg T cream and 100iu HCG every day, but I am still getting elevated hematocrit and RBC. It looks like I might need to do a therapeutic phlebotomy twice in the next month for my numbers to come back within the normal range. Is there anything to be concerned about with doing frequent phlebotomies?

A: This is something that is sure to come up with testosterone replacement therapy (TRT). This is an additional reason why I suggest individuals who are on TRT for low normal testosterone come off once every 12-18 months. This not only ensures the functionality of the HPTA but if polycythemia is a problem this will ameliorate or fix it. I was referred a patient who had polycythemia and the referring doctor was unable to stop TRT due to symptoms.

Comparison of transdermal nonscrotal testosterone patch with intramuscular injections of testosterone enanthate observed that 15.4 percent and 43.8 percent of patients, respectively, had at least one documented elevated hematocrit value (defined as over 52 percent) during the course of ~1 year. Erythrocytosis was associated with supraphysiologic levels of bioavailable testosterone and estradiol, and it occurred more frequently in the group that received intramuscular injections of testosterone.

There has been demonstrated a direct relation between testosterone dosage and the incidence of erythrocytosis. Erythrocytosis occurred in 2.8 percent of men receiving 5 mg per day by nonscrotal patches and in 11.3 percent and 17.9 percent of men treated with gel preparations of 50 mg per day (delivering 5 mg per day) and 100 mg per day (delivering 10 mg per day), respectively.

Phlebotomy is on the whole a safe procedure, the frequency of side effects being low and their severity weak. Although untoward events are unlikely with mild erythrocytosis of relatively short duration, the hematocrit or hemoglobin level should be monitored in men receiving testosterone-replacement therapy so that appropriate measures, such as dosage reduction, the withholding of testosterone, therapeutic phlebotomy, or blood donation, may be instituted if erythrocytosis develops. It is reassuring that as far as we can determine, no testosterone-associated thromboembolic events have been reported to date.


Trenbolone for Androgen Replacement Therapy

The use of the anabolic steroid trenbolone has a long history in the bodybuilding but it has never really been considered a steroid suitable for therapeutic use in medicine. The U.S. Food and Drug Administration has not approved tren for use in humans. The media has often demonized it as a dangerous veterinarian steroid never intended for human use. However, the perception of trenbolone may soon change with the publication of a favorable study in a major scientific journal.

Joshua Yarrow and his colleagues at the University of Florida feel that trenbolone may be a viable alternative to testosterone for androgen replacement therapy. They are set to publish their study results in the February 2011 issue of the American Journal of Physiology – Endocrinology and Metabolism.

The researchers report that trenbolone enanthate may have certain advantages over testosterone that may make it an appealing treatment option for some individuals. Bodybuilders may be familiar with many of these findings.

Trenbolone is not adversely affected by the aromatase or 5-alpha reductase enzymes that metabolize testosterone into estradiol and dihydrotestosterone, respectively. Bodybuilders have enjoyed tren for years precisely because they are able to avoid steroid side effects related to estrogen and DHT.

Yarrow reports that low-dose trenbolone enanthate effectively produces anabolic effects in muscle size and partially maintains bone mineral density without causing prostate enlargement or polycythemia in castrated laboratory rats.

Supraphysiological dosages of testosterone enanthate were required to produce anabolic effects similar to low-dose trenbolone administration. However, negative side effects of prostate enlargement and elevated hemoglobin became problematic at this dose of testosterone.

Selective androgen receptor modulators (SARMs) may be the current darlings of scientific research into alternative options for androgen replacement therapy, but University of Florida researchers are excited by the “SARM-like potential” of trenbolone.

They suggest that the actions of trenbolone are similar to selective androgen receptor modulators (SARMs). Low-dose trenbolone is called “SARM-like” because of the positive anabolic effects in muscle and bone without negative side androgenic side effects of prostate enlargement or polycythemia.

Trenbolone may have benefits over testosterone in terms of androgen receptor activation, the upregulation of growth factors such as IGF-1 and fibroblast growth factor, and anticatabolic mechanisms.

Competitive bodybuilders have often preferred using trenbolone in the weeks prior to a bodybuilding competition due to its purported effects at accelerating fat loss.

The current study confirmed that trenbolone has more potent lipolytic effects on visceral adipose tissue than testosterone milligram per milligram. Furthermore, visceral fat loss increased in a dose-dependent manner with trenbolone. In other words, the more tren used, the greater the fat loss.

Trenbolone’s lack of aromatization, while generally desirable, has often been problematic for bodybuilders who have used trenbolone as the only steroid in a cycle. Therefore, most bodybuilders include an aromatizable steroid such as testosterone or Dianabol in their trenbolone steroid stacks.

Researchers also recognize that the lack of aromatization could be a potential problem if trenbolone is used alone in androgen replacement therapy. In their study, trenbolone only provided a partial bone protective effect when administered to castrated rats. The authors attribute this to the non-aromatizable nature of trenbolone.



They conclude that low-dose trenbolone enanthate treatment has SARM-like effects on muscle/fat body composition. Androgen replacement therapy with low-dose trenbolone could potentially produce anabolic gains comparable to supraphysiological testosterone treatment without the associated side effects. The therapeutic risk-benefit profile of low-dose trenbolone appears superior to supraphysiological testosterone treatment; however, additional research into this treatment option is necessary.

The researchers should be applauded for dispassionately and objectively researching the potential of trenbolone in androgen replacement therapy. Trenbolone is an anabolic steroid that has been demonized more than others due to its limited use (in pellet implants used by veterinarians to increase muscle growth in livestock). Fortunately, they looked past the political stigma associated with trenbolone to revisit a therapeutic use for an old steroid.

The Amazing History of Anabolic Steroids in Sports

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” preceded 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 Ružička 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 1939 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 (from 1935 to 1965) truly began.

Nobel Prize winner Ružička 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.

Leopold Ružička also synthesized androstenedione which, several decades later, 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.

Ružicka 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, synthetic steroids 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.

TRT and Steroid Side Effect Management – Interview With Dr. Michael Scally

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.

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.

2015年12月29日星期二

Best Way to Use Oral Anabolic Steroids Within an Eight-Week Steroid Cycle

Q: “I’m planning on a bulking cycle at a dosing level of about a gram of steroids per week. I have testosterone enanthate 250 mg/mL and plenty of Dianabol, and I have a little oxandrolone too. I don’t want to use orals for more than 6 weeks total. Week by week, how would you dose these for an 8-week steroid cycle?”

A: Because you’re doing a bulking cycle and you’ll need more help for gains in the later weeks than in the earlier weeks, I’d schedule the orals for the last 6 weeks.

I’d start the first two weeks with only testosterone, plus an anti-aromatase for estrogen control.

A convenient ongoing dosing would be 200 mg intramuscularly via an insulin needle five days per week. The two off days would be 3 or 4 days apart. In one example, the off days could be Tuesday and Saturday.

If you prefer less frequent though larger injections, then I’d do 500 mg twice per week.

In either case, I’d frontload the first day’s injection to be 700 mg larger than your ongoing injections. So for example if your ongoing injections are 200 mg at a time, your first injection would be 900 mg.

The reason is that during a cycle, ordinarily your body will have not only what was just injected, but also an amount remaining from previous injections. On the first injection, you have nothing from previous injections. Frontloading gets the correct amount into your body on the first injection.

At the start of week 3, I’d add the Dianabol at 50 mg/day, and reduce the testosterone to 800 mg/week. The combination of the two is considerably stronger than 1000 mg/week testosterone; you can be confident in making this small reduction in testosterone dosage.

The only potential reason for not reducing the testosterone dosage at this point would be if at this time point you really aren’t satisfied with results at the higher dose. If you’ve done several cycles before at gram-plus per week doses, this could occur. If so, you could maintain the 1000 mg/week testosterone dosage while adding the Dianabol.



I’d end the testosterone injections in the middle of week 7. This is so by the start of week 9 or soon after, levels will be low enough to allow recovery to begin.

I’d strengthen week 8 with oxandrolone to compensate for falling levels of injected testosterone. I’d either use 50 mg/day oxandrolone throughout week 8, or start at 50 mg/day and go to about 75 mg/day in the final 3 or 4 days of the cycle. Which way to go would depend on how much oxandrolone you have, and personal preference. Your final outcome would be almost identical either way.

This cycle will remain effective throughout the entire 8 weeks, and then transition quickly to levels of exogenous androgen low enough to allow a fast recovery. This will be a very effective bulking cycle for anyone who has not already reached a plateau at this level of steroid usage.

Testosterone – The Good, the Bad, the Ugly

One of the most infamous hormones around is Testosterone. You hear Clueless news anchors about it on the evening news. You hear about it in the gym. You even read about it in the “growing older with style” magazines. Depending on who you talk to, it is both the good, the bad, and the ugly of hormones.

In bodybuilding it is hailed as the king of muscle builders. Among forward-thinking baby boomers it is considered the fountain of youth. In other circles it is pointed to as the cause of all men’s shortcomings including violence and sexual promiscuity. Finally, it has even been associated with potentially lethal diseases that threaten the lives of thousands of men each year. So how can one hormone be so many different things to so many different people? Taking a closer look at this complex hormone may shed some light on this question.

First, what exactly is testosterone? Testosterone is the principle male hormone and belongs to a class of steroid chemicals called androgens (andro = man, gen = to make). It is produced primarily in the testes but can also be made by enzymatically converting other androgens (e.g. androstenediol) secreted from the adrenal gland into testosterone. Testosterone plays a role in everything from growth and maintenance of the male sexual organs during puberty, to male pattern baldness in the later years. It also plays an important role in bone growth, sexual behavior, male fertility, muscle protein synthesis, as well as inducing the appearance of secondary male sexual characteristics such as facial hair, body hair, and deepening of the voice.

Research has shown that resistance exercise can significantly raise testosterone levels. (1) This is good news if you’re looking to build a more muscular body. When in comes to muscle growth, testosterone production is the key to success. Testosterone literally turns on the genetic machinery leading to bigger and stronger muscles. It works like this. Testosterone binds to receptors inside your muscle cells. These receptors then transport the testosterone molecule to the nucleus. The nucleus is where your DNA is located. Your DNA contains blue prints for every protein found in your body. This androgen receptor, once bound to testosterone, acts as a messenger that tells the DNA which proteins to make from the blue prints. In muscle tissue the whole process results in the production of contractile proteins, which are used to make your muscle contract more forcefully, as well as structural proteins that are used to make the cell larger to accommodate the new contractile proteins. In plain and simple terms, testosterone is a messenger that tells your muscles to grow! Still, this barely touches the surface of the many secondary roles testosterone plays in muscle tissue as well as in the brain.

Clearly, testosterone is important to both mind and body. Among the anti-aging crowd, testosterone stands as a symbol of youth and vitality. One of the signs of aging is a reduction in the circulating levels of testosterone. This in turn has been associated with a decrease in muscle mass and strength as the years go by. Doctors are now calling this “andropause”. (2) Through testosterone replacement therapy, many older patients express a sense of psychological well-being and vitality they haven’t experienced since they were 30 years younger. (3,4) If men desire it, in the near future hormone replacement for men will be just as common as it is for women today.



Unfortunately, testosterone is not free from negative effects on the body. One common undesirable effect of testosterone, which could be considered minor, is alopecia or male pattern baldness. The drug Propecia, a 5-alpha reductase inhibitor, prevents the conversion of testosterone into a more potent androgen called dihydrotestosterone (DHT). DHT, and a set of your parent’s genes, is responsible for male pattern baldness. In many men Propecia is effective at preventing further hair loss and even allowing some to grow back. (5) On a more serious note, DHT may also be a serious risk factor for some cancers such as prostate cancer. (6) Treatment of prostate cancer often involves a total elimination of circulating testosterone. Although this helps to reduce the growth rate of tumors, removing a man’s testosterone leaves him feeling emotionally disoriented, there is a complete loss of sex drive and sexual function, muscle is lost and fat patterning takes on a feminine characteristic, even hot flashes, usually associated with female menopause, are experienced.

All in all testosterone plays a very important role in a man’s sense of health and well-being. It is the major muscle-building hormone; it increases the strength of both muscles and bones, and even affects our brains. Certainly a man’s interest in keeping his testosterone levels optimized is justified despite the unavoidable risks and negative effects it may impart. A healthy lifestyle including proper diet and regular resistance exercise will ensure that you are getting all the benefits testosterone has to offer.

Growth Hormone vs. Testosterone, which one is better for bodybuilding?

I was one of the first private practitioners in the country to dispense growth hormone as part of an overall anti-program hormone replacement program for adults that fit the criteria of the “Adult Onset Growth Hormone Deficiency Syndrome”. Like many other anti-aging physicians, I was extremely impressed by the initial research on growth hormone showing dramatic improvements in body composition, kidney function, skin, mood, well being, etc. I have been a member of the Growth Hormone Research Society for many years and have closely followed all the latest research on growth hormone and other adult hormone replacement therapies. As the number of studies on growth hormone as well as testosterone has piled up since I first began prescribing testosterone, I believe now is the time to look back at the research and see if growth hormone and testosterone have lived up to their promises.

It is well established in bodybuilding circles that testosterone is superior to growth hormone for gaining muscle. However, growth hormone still is enormously popular and generally has a better reputation than testosterone both in bodybuilding and in anti-aging circles. The general impression is that testosterone will make you big, but at the price of acne, puffiness, temper tantrums, prostate enlargement, and possibly “gyno”. Well it is acknowledged that growth hormone is not as anabolic as testosterone, people still think of growth hormone as a hormone that will make you lean and toned with almost no side effects. Growth hormone also has a reputation as being the “fountain of youth” among anti-aging enthusiasts, whereas testosterone is still considered somewhat dangerous. The purpose of this article is to see how the research on testosterone and growth hormone from the last few years has supported or disputed the public’s view of these two hormones.

Which is Better for Body Composition?

New research has shed some light on the anabolic effects of growth hormone. Several studies in the past have shown an increase in lean body mass in subjects taking growth hormone. However, lean body mass does not necessarily mean muscle, but anything that is not fat and this includes water, organ tissue growth, bone mass, and connective tissue growth. My friend Michael Mooney (author of Built to Survive and editor of the Medibolics Newsletter) has helped publicize the fact that not much, if any, of the lean mass gained while on growth hormone is actually muscle. One recent study on HIV positive test subjects showed no significant change in skeletal muscle mass after taking six milligrams (about 18 units) per day of growth hormone for 12 weeks.(1) Another study, also on HIV positive test subjects, also showed a lack of muscle growth when doses of nine milligrams (roughly 27 units) per day were given.(2) Keep in mind that HIV positive individuals are often suffering from muscle wasting conditions, which should make themmore responsive to any possible anabolic effects of growth hormone. Growth hormone is probably equally ineffective in healthy individuals.

One study on young (aged 22-33), highly trained athletes did show a significant increase in lean mass after six weeks of taking 2.67 milligrams (about 8 units) per day.(3) However this increase was only 4%, and may have not included any muscle mass at all. It seems overwhelming clear that growth hormone is either non-anabolic or very weakly anabolic for skeletal muscle when taken by itself, and it definitely not worth the large price if you are taking it solely for gaining muscle. The only real use in gaining muscle may be as a synergistic agent with testosterone. A synergistic effect of taking growth hormone with testosterone has been reported for increases in lean mass, but further research needs to be done to see if this synergistic effects holds for skeletal muscle. Keep in mind that some increases in lean mass are not desirable. Growing some organs too big such as kidneys can produce some embarrassing effects seen in some professional bodybuilders. You do not want your “guts” sticking blatantly out of your body.

But enough on growth hormone for muscle gain. For information, see Bryan Haycock’s article in this issue or go to Michael Mooney’s web site. If you are going to spend the money on growth hormone to try to improve your body, your best bet is to use it as a fat loss or “sculpting” agent. The previously mentioned study with growth hormone on trained athletes did show an impressive 12% decrease in bodyfat. So well it is well established that testosterone is far, far better for building muscle than growth hormone, is growth hormone the better choice for fat loss? The research on this issue is mixed, and there is no easy answer to this question.

One recent study put growth hormone head to head with testosterone and measured its effects on fat loss. In this study, men on growth hormone lost an average of 13% of their bodyfat compared to 5.8% in the group taking testosterone.(4) But before you jump to conclusions, there are a couple of reasons why this study doesn’t settle the question. For one thing, this study was on very old individuals (aged 65 to 88) who had low IGF-1 and testosterone levels. Another problem is that the doses of the hormones haven’t been reported yet (the study is only in abstract form right now) which also makes the comparison difficult to make. Most interesting about this study was that a synergistic effect was found in a group taking both testosterone and growth hormone, as they lost an average of 21% of their bodyfat. This is more than the averages of the testosterone alone and growth hormone alone groups combined.

Not all studies have shown this dramatic of an effect on body fat. One study using fairly large doses (adjusted by weight, but roughly 5 mg per day) on obese women failed to show any significant effects on body fat.(5) The growth hormone group lost less than two pounds more than the placebo group over a one month period. The main significant result was that the growth hormone group lost much less lean mass (an average loss of 1.52 kg compared to 3.79 in the placebo). While this may seem impressive, the same results could be achieved with a caffeine/ephedrine formula at a fraction of the price. While there are a good number of studies showing growth hormone to be effective for fat loss, testosterone may be almost as good for this purpose.

Testosterone was recently found to be effective for fat loss in young men even in small doses. One recent study showed that men given only 100 milligrams per week of testosterone enanthate lost an average of six percent of their bodyfat after eight weeks.(6) 100 mg per week is generally considered a very low dose by bodybuilding standards. Most impressive about this study was that the result was obtained in young, normal healthy men (aged 18 to 45), not obese or testosterone deficient. Most of the studies showing positive effects with hormone replacement therapy are on subjects who are obese or hormone deficient – i.e. the very subjects most likely to respond. While the amount of muscle gain reported in this study was not reported (it is still just in abstract form), another study showed 100 mg per week of testosterone enanthate was not anabolic.(7) It appears that testosterone has a strong mechanism for fat loss other than increased metabolic rate from increased muscle. Considering how much cheaper testosterone is than growth hormone, it may well be the cost-effective choice for burning fat even if it is slightly less effective overall.

Safety of Growth Hormone and Testosterone



Testosterone is widely believed to be far more dangerous than growth hormone. However, recent research is rapidly showing that much of these dangers have been exaggerated. For instance, the hypothesis that testosterone causes prostate cancer has never been established. In fact, one study even showed a slight negative correlation between testosterone levels and prostate cancer! A study on young men given supraphysiologic doses of testosterone showed no change is prostate specific antigen (PSA), which is one measure of prostate cancer risk.(8)

Growth hormone may also be less dangerous to the prostate than previously believed. One study showed strong positive correlation with prostate cancer and IGF-1 levels.(9) Since growth hormone stimulates IGF-1 synthesis in the liver, this study and others bring up the possibility of a link of growth hormone and prostate and breast cancer. Keep in mind that statistical correlations do not necessarily prove causality, i.e. IGF-1 has not yet been proven to be a cancer-causing villain. Actually IGF-11 may be one of the culprits in the cancer story, and not IGF-1. At the Serano sponsored Symposia on the Endocrinology of Aging in October, 1999 and at the Endocrine Society Meeting in June, 1999 there was an informal consensus that patients on growth hormone did not increase their risk of breast or prostate cancer. Several other recent studies have also cast doubt on the role of growth hormone as a cancer-causing villain.

Testosterone may have also gotten a bad rap for its effects on blood lipids. Since testosterone and otheranabolic steroids have been shown in some studies to lower HDL cholesterol levels, it was believed that testosterone may increase the risk for heart disease. This was refuted in one recent study on testosterone that showed some positive results. A study on 21 hypogonadal men (aged 36 to 57) showed a replacement dose of testosterone using the Androderm transdermal patch to reduce blood clotting.(9) While HDL levels did drop slightly, blood coagulability is believed to be the more important marker of heart disease risk. Another study showed a very strong negative correlation with testosterone levels and heart disease.

Growth hormone has shown mixed results on its effects on heart disease risk. One study on elderly men and women (aged 65-88) showed that growth hormone administration to lower LDL levels, but raised triglyceride levels.(10) Since high LDL and triglyceride levels are considered measures of heart disease risk, growth hormone’s effects on heart disease risk are ambiguous. However, long-term use of growth hormone as been shown to decrease the thickness of the carotid artery lining – i.e. increased room for blood flow.

While much more research needs to be done, I am convinced right now that testosterone replacement therapy in hypogonadal men may be safer than excessively large doses of growth hormone. The long-term studies have not yet been done to test the true long-term effects of these hormones, but the research seems quite clear at the moment. Michael Mooney has reported similar results on safety and side effects of these hormones:

While none of the studies on testosterone or anabolic steroids used for HIV have documented any significant health problems associated with their proper therapeutic use, Dr. Gabe Torres’ data on his patients who experienced a reduction in symptoms of HIV-related lipodystrophy with Serostim growth hormone showed that at the standard 5 and 6 mg doses, 80 percent of his HIV patients experienced significant side effects, that included elevated glucose, elevated pancreatic enzymes, or carpal tunnel syndrome. (1)

Conclusion

Don’t get me wrong – I still use both growth hormone and testosterone as part of overall anti-aging programs in my patients. This article is not meant to say one hormone is “good” and another is “bad”. It is just my opinion at the moment that the overall benefit/cost ratio for improving body composition is higher with testosterone than growth hormone. By cost, I mean both the monetary price – testosterone is far cheaper than growth hormone, and the side effect/safety profile – testosterone is safer than high-dose growth hormone use.

Since growth hormone is extremely expensive and perhaps riskier than testosterone, I screen patients very carefully and only recommend it to those who either have very low IGF-1 levels and fail growth hormone stimulation tests, or those who have failed to respond to testosterone or other therapies. The new research has also made me confident in encouraging more and more patients to go on testosterone. However, we must keep constant track of the new research to better refine both anti-aging and bodybuilding programs. The science of hormone supplementation is still in its infancy, and there is still a lot more questions that need to be answered.