Dismiss Notice
Join Physics Forums Today!
The friendliest, high quality science and math community on the planet! Everyone who loves science is here!

Steroids origin

  1. Aug 28, 2004 #1
    Looking at the "boom" (at least in Spain) that is happening with steroids these days, can anybody explain the origin of them and which was the first?

    Is there any trace of testoterone on animals?

    BTW, I dont consume steroids, just creatine... :biggrin:
    Last edited: Aug 28, 2004
  2. jcsd
  3. Aug 28, 2004 #2


    User Avatar
    Staff Emeritus
    Science Advisor
    Gold Member

    Steroids are naturally produced in all vertebrate animals. I'd have to look up whether there is are any steroids in invertebrates. They are all derived from the precursor cholesterol. Testosterone is important for many male characteristics, and estrogens and progesterone are important for many female characteristics, though all of those steroid hormones are found in both sexes and have functions in both males and females. We produce a number of other steroids too, such as cortisol (a variant of this, corticosterone, is found in some other species), that has functions in stress responses. This is not all the steroids we produce, or all their functions, just a sampling so you know they are normally present in our bodies.

    What athletes are using when they get caught breaking the rules are called anabolic steroids. These are in the class of steroids related to testosterone, known as androgens (andro is derived from the Greek word for man). These anabolic steroids build up muscle mass. Many of those used by athletes now are synthetic (i.e., manufactured to be similar to naturally produced androgens, but with slight modifications by chemists to make their effects last longer). There are some nasty side effects of using anabolic steroids, such as sterility and even shrunken testes, and most dangerous, thickening of heart muscle leading to heart attacks. And when women take these steroids, they develop male-like features, such as excessive hair growth, deeper voices.

    Steroid use by athletes gives an unfair competitive edge, but I think it was more because of the dangerous side effects that rules and laws started being put in place to ban their use to protect the health of athletes who didn't fully understand the dangers of using these steroids.
  4. Aug 28, 2004 #3
    First experimented with in the 1860 by Brown-Sequard, although he did not know what he was using. He would draw fluids from the testicles of animals and would inject these fluids into himself and his patients. He said that it made him stronger and he could run faster and jump higher.

    As far as your question. Is there any trace in animals? I guess I need to ask your level of understanding about animal anatomy and physiology. Do you know what testosterone is???

    It is found in every animal in both males and females. It has both anabolic as well as androgenic effects. Anabolic dealing with growth and repair and androgenic has to do with masculinization.

    As far as the boom with steroids. You are about 45 years behind. The boom came in teh 1960's. Which was when the phrase "breakfast of champions" was created. (No I am not talking about Wheaties). Pro football teams would have bowls of dianabol tablets in the eating area. The players would fix themselves a bowl of cereal and sprinkle these little pink pills over there bowl. Btw each of the pills contained approx 10 mg of dianabol and they would cover there cereal with them.

    The only reason you see a boom, is b/c the IOC wants to prove a point. Drug testing is very expensive ($15000-$2500 per person if it is a good test), so they target certain high profile individuals and claim they are cleaning up sports.

    The only reason and I repeat the only reason that most american athletes have tested positive recently is b/c a disgruntled coach send in a particular underground drug to the testing companies so that they could start testing athletes for this drug.

    There are many drugs that can be taken without detection. testosterone will not be detected so long as the t/e ratios are in line. Human Growth Hormone was not able to be tested for but supposidly now they can. IGF-1 can not be tested for. And I am sure that there will be a new designer drug with just a slightly different functional group that will alude testing agents in future.

    What I can't wait to see is when the viral delievery of IGF-1 comes on the seen. If the athletes can avoid detection, all current records will begin to fall.

    On the other hand, if the IOC and other oranizations such as MLB and NFL completely takes drugs out of the equation. Then athletics will suffer no records will be broken, home runs will go down.

    We all want to see sports cleaned up. Or do we. Personally, when I watch the Olympics I want to see a record broken. A record that most likely was created by an athlete that aluded drug test.
  5. Aug 28, 2004 #4

    I have to disagree with you on a few points.

    First of all most athletes are not looking for the anabolic effect so much as they are the androgenic effect. Drugs such as stanazole, oxandralone as well as many others are used by runners and jumpers who do not want to add bulk to their frame.

    As far as sterility and shrunken testes. They have actually tried to use testosterone as a means of birth control, but found that it does not work. The shrunken testes will only be after long term use when the body is no longer producing testosterone due to negative feed back mechanism. They will recover within a short time after usage has stopped.

    The unfair competitive advantage. You are showing your naivete here. I have been involved in College athletics, professional athletics, and international athletics. You would be completely amazed at the number of athletes who are on these performance enhancing drugs. It is the great equalizer and one can not compete unless they take them at least some time in their career. It may not be fair, but it is reality and they fan base expects these athletes to perform at levels which can only be achieved through the use of these drugs. Now don't get me wrong, I am not saying 100% of athletes are on these drugs, I am only saying it is a very large percentage.

    And as far as instituting these rules b/c athletes do not understand the dangers. Most of these athletes have doctors, trainers, nutritionist ect... that tell them exactly what they need to take how much, when, ect... in order to be competitive. They are extremely educated when it comes to what they put in their body.

    Look at some long tern studies to determine just how bad these side effects are that you speak of. Maybe they are not as bad as what the IOC once said.

  6. Aug 29, 2004 #5


    User Avatar
    Staff Emeritus
    Science Advisor
    Gold Member

    Actually, the reason it doesn't work as birth control isn't because it doesn't affect fertility, but because it doesn't block sperm production 100%. And it doesn't take that long term of use to affect the negative feedback mechanisms at the hypothalamic level. Those effects occur within hours. Instead, it just takes longer to physically see the effect on the gonads. With long-term usage, there is no guarantee of full recovery of function when you stop taking the steroids.

    All I can say is, sad, very sad. To need to be so competitive that athletes feel compelled to risk their health to break a record, that is a sad commentary on athletics. Well, I suppose the sociological pressures for athletic performance would belong in a different thread.

    Unfortunately, what I do have first-hand knowledge of is how little most MDs know of endocrinology. And it's hard to believe those counseling athletes to take steroids are necessarily acting in the athlete's best interest. I'm working with a reproductive endocrinology fellow who lacked some pretty basic understanding of feedback mechanisms when she first joined our lab, and you'd think of all the specialties out there, she'd be in the one to hammer that in over and over. Of course, that's why she's still in training, but if someone who already got through an OB/Gyn residency didn't have a solid understanding of those mechanisms, what makes you think someone who goes into sports medicine will?

    In this article:
    Sports Med. 2004;34(8):513-54.
    Effects of androgenic-anabolic steroids in athletes.
    Hartgens F, Kuipers H.

    the authors point out that laboratory studies probably underestimate the effects of anabolic steroids because they test doses far lower than those actually abused. The abstract is pretty long, so I'm not posting it here. You can look it up on pubmed though.
  7. Aug 29, 2004 #6
    Actually, it is closer to 10 days before the body stops shutting down production, but like I said before they well rebound after cestation.

    As far as sad. Yes, I completely agree. But, the athletes should not take all of the blame. They do what is expect of them by their fans. Besides, people go under the knife all the time for plastic surgery, for nothing other than looks. Maybe a Gold medal is worth minimal risk.

    And about the MD's not knowing. I agree 99.9999% of MD's no nothing of endocrinology. But, these doctors I speak of specialize in their use and are extremely knowledgeable. Don't expect to see any published studies, b/c if they are in this country they are not only cheating but also breaking the law. If they are in other countries they are cheating. And you can not imagine the amount of money that goes into R and D in order to gain a competitive advantage.

    The hundred meter will be won be .01 seconds and there are hundreds of athletes around the world that are within .2 or .3 seconds. The must shoot in order to be on top .01 seconds.

    One other comment about putting their health at risk. Compare the effects of long term alcohol use and then the effects of long term anabolic use. Not saying that I condone either but most who speak bad of anabolics are the same people who drink wine with diner and go outside for a smoke afterwards.

    What I would be interested in seeing is a survey of all ex athletes who used these substances. The football, baseball, and track athletes of the 70's and 80's. Then compare them to the average person of the same age. At that time we could have conclusive evidence one way or the other. But, maybe I need to stay in the real world.

  8. Aug 29, 2004 #7
    Effects of androgenic-anabolic steroids in athletes.

    Hartgens F, Kuipers H.

    Department of Surgery, Outpatient Clinic Sports Medicine, University Hospital Maastricht, and Sports Medicine Center Maastricht, Maastricht, The Netherlands. fhartgens@home.nl

    Androgenic-anabolic steroids (AAS) are synthetic derivatives of the male hormone testosterone. They can exert strong effects on the human body that may be beneficial for athletic performance. A review of the literature revealed that most laboratory studies did not investigate the actual doses of AAS currently abused in the field. Therefore, those studies may not reflect the actual (adverse) effects of steroids. The available scientific literature describes that short-term administration of these drugs by athletes can increase strength and bodyweight. Strength gains of about 5-20% of the initial strength and increments of 2-5 kg bodyweight, that may be attributed to an increase of the lean body mass, have been observed. A reduction of fat mass does not seem to occur. Although AAS administration may affect erythropoiesis and blood haemoglobin concentrations, no effect on endurance performance was observed. Little data about the effects of AAS on metabolic responses during exercise training and recovery are available and, therefore, do not allow firm conclusions. The main untoward effects of short- and long-term AAS abuse that male athletes most often self-report are an increase in sexual drive, the occurrence of acne vulgaris, increased body hair and increment of aggressive behaviour. AAS administration will disturb the regular endogenous production of testosterone and gonadotrophins that may persist for months after drug withdrawal. Cardiovascular risk factors may undergo deleterious alterations, including elevation of blood pressure and depression of serum high-density lipoprotein (HDL)-, HDL2- and HDL3-cholesterol levels. In echocardiographic studies in male athletes, AAS did not seem to affect cardiac structure and function, although in animal studies these drugs have been observed to exert hazardous effects on heart structure and function. In studies of athletes, AAS were not found to damage the liver. Psyche and behaviour seem to be strongly affected by AAS. Generally, AAS seem to induce increments of aggression and hostility. Mood disturbances (e.g. depression, [hypo-]mania, psychotic features) are likely to be dose and drug dependent. AAS dependence or withdrawal effects (such as depression) seem to occur only in a small number of AAS users. Dissatisfaction with the body and low self-esteem may lead to the so-called 'reverse anorexia syndrome' that predisposes to the start of AAS use. Many other adverse effects have been associated with AAS misuse, including disturbance of endocrine and immune function, alterations of sebaceous system and skin, changes of haemostatic system and urogenital tract. One has to keep in mind that the scientific data may underestimate the actual untoward effects because of the relatively low doses administered in those studies, since they do not approximate doses used by illicit steroid users. The mechanism of action of AAS may differ between compounds because of variations in the steroid molecule and affinity to androgen receptors. Several pathways of action have been recognised. The enzyme 5-alpha-reductase seems to play an important role by converting AAS into dihydrotestosterone (androstanolone) that acts in the cell nucleus of target organs, such as male accessory glands, skin and prostate. Other mechanisms comprises mediation by the enzyme aromatase that converts AAS in female sex hormones (estradiol and estrone), antagonistic action to estrogens and a competitive antagonism to the glucocorticoid receptors. Furthermore, AAS stimulate erythropoietin synthesis and red cell production as well as bone formation but counteract bone breakdown. The effects on the cardiovascular system are proposed to be mediated by the occurrence of AAS-induced atherosclerosis (due to unfavourable influence on serum lipids and lipoproteins), thrombosis, vasospasm or direct injury to vessel walls, or may be ascribed to a combination of the different mechanisms. AAS-induced increment of muscle tissue can be attributed to hypertrophy and the formation of new muscle fibres, in which key roles are played by satellite cell number and ultrastructure, androgen receptors and myonuclei. Copyright 2004 Adis Data Information BV

    PMID: 15248788 [PubMed - in process]

    I posted and read the study for you. I didn't say see anything that was conclusive about adverse effects. "aas did not seem to effect cardio structure and function". Unless you consider muscle mass and strength and adverse effect.

    Especially, considering that this may mean the difference in a multi-million dollar contract or a lifetime of chicken sexing at the local plant.

    As far as dosage. Most athletes do not take extreme amounts. The only ones that go nuts are bodybuilders, who will take 1000s of mgs per week. Actually, they stop measuring in mg's and start speaking of grams. Which, I completely agree is crazy. Although Arnold appears to be doing okay. At least after his heart valve replacement (lol). Of course, that could have been contributed to years of drinking and smoking his cigars.

  9. Aug 29, 2004 #8


    User Avatar
    Staff Emeritus
    Science Advisor
    Gold Member

    Did you read the entire article? There were plenty of other adverse consequences they spoke of.

    And, no, it takes far less than 10 days for steroids to start exerting negative feedback effects and shut down endogenous production of gonadotropins. The bold text is my emphasis.

    Clin Endocrinol Metab. 1996 Mar;81(3):896-901.
    Comparison between testosterone enanthate-induced azoospermia and oligozoospermia in a male contraceptive study. II. Pharmacokinetics and pharmacodynamics of once weekly administration of testosterone enanthate.

    Anderson RA, Wu FC.

    Medical Research Council Reproductive Biology Unit, Edinburgh, Scotland.

    Hormonal suppression of spermatogenesis is currently being investigated as a method of reversible male contraception. However, administration of exogenous testosterone (T) induces azoospermia in only 40-70% of Caucasian men, whereas the remainder suppresses to severe oligozoospermia (< 5 x 10(5)/mL). The reason(s) for the heterogeneity in the spermatogenic response is not clear. We have prospectively investigated the possibilities that higher plasma concentrations of T and/or differences in the extent and rate of gonadotropin suppression could maintain a low level of spermatogenesis in subjects taking part in a clinical efficacy trial of hormonal male contraception. Thirty-three healthy adult men, aged 21-41 yr, were given 200 mg T enanthate (TE), im, weekly for up to 18 months. Azoospermia was achieved in 18 men (55%) after 20 weeks of treatment, at which time the remaining 15 (45%) stabilized at a mean sperm density of 2.0 +/- 0.8 (+/- SD) x 10(6)/mL. These 15 subjects remained oligozoospermic for the rest of the efficacy study. To compare the pharmacokinetics and pharmacodynamics of TE between the azoospermic and oligozoospermic responders, plasma samples were obtained immediately before and 1, 2, 4, and 7 days after the 1st and 16th TE injections. Further samples were taken after 2, 4, 8, and 12 weeks of treatment. Plasma concentrations of total, free, and non-sex hormone-binding globulin (non-SHBG)-bound T, estradiol, LH, and FSH were measured. Compared to baseline, preinjection levels of total T increased 2.5-fold, reaching a steady state around 12 weeks of treatment. Peak concentrations of total T increased by 5-fold, but free and non-SHBG-bound T levels were increased by 10-fold after 16 weeks. The plasma levels of estradiol showed similar changes as T. However, neither T (bound or free) nor estradiol was significantly different between azoospermic and oligozoospermic responders. Plasma SHBG was reduced to a similar degree in both groups of men after 16 weeks of TE treatment. [bold]Plasma concentrations of both LH and FSH decreased rapidly after the first TE injection; a significant decline in LH was detectable after 24 h.[/bold] Mean levels of both gonadotropins decreased to less than 0.5 U/L by the end of 4 weeks and to below the limit of sensitivity of the assays (0.05 IU/L) by 12 weeks. There were no significant differences in plasma concentrations of LH or FSH or in the rates of suppression between azoospermic and oligozoospermic responders. We conclude that the polymorphism of spermatogenic suppression in response to exogenous T is unlikely to be due to differences in the pharmacokinetics or pharmacodynamics of TE or in the sensitivity of the hypothalamo-pituitary-testicular axis to sex steroid inhibition. Measurements of total plasma T considerably underestimate the increase in bioavailable T during the weekly TE regimen.

    PMID: 8772547 [PubMed - indexed for MEDLINE]

    The other danger that has not been brought up, and I'm not even aware if there are studies done on it since it would be hard to identify test subjects, are those who are abusing steroids while still teenagers. At that age, normal steroid production is already causing a lot of changes in things like brain structure that is part of the normal transition to adulthood. This is a very vulnerable age, and we all know the abuse starts that early for some (or many).
  10. Aug 29, 2004 #9


    User Avatar
    Staff Emeritus
    Science Advisor
    Gold Member

    After that last post, I thought of something else...androgen dependent prostate and/or testicular cancers. I only found one case study, but it may be too soon to see if exposure to such high steroid doses leads to higher incidences of prostate or testicular cancers later in life.

    Cancer. 1999 Oct 15;86(8):1571-5.
    Intratesticular leiomyosarcoma in a young man after high dose doping with Oral-Turinabol: a case report.

    Froehner M, Fischer R, Leike S, Hakenberg OW, Noack B, Wirth MP.

    Department of Urology, Universitaetsklinikum "Carl Gustav Carus," Technical University of Dresden, Dresden, Germany.

    BACKGROUND: Androgenic anabolic steroids have been suspected of activity as carcinogens in the development of carcinoma and angiosarcoma of the liver and adenocarcinoma of the prostate. Although the proliferation of smooth muscle cells is stimulated by sexual steroids, to the authors' knowledge a possible relation between androgenic anabolic steroids and the development of leiomyosarcoma has not previously been reported in humans. METHODS: A 32-year-old man underwent right radical orchiectomy for a tumor of the upper pole of the right testicle. Routine histopathologic examination and immunohistochemical staining were performed. RESULTS: The tumor was identified as an intratesticular leiomyosarcoma based on its typical growth pattern and the characteristic immunohistochemical staining profile. The patient reported a 5-year history of systematic use of high dose Oral-Turinabol (4-chloro-1-dehydro-17alpha-methylteststerone) that began at age 18 years and stopped approximately 9 years before presentation. CONCLUSIONS: The rarity of intratesticular leiomyosarcoma, the experimental induction of similar tumors in animals by androgens and estrogens, and the unusually young age at presentation of the patient in the current study support the hypothesis that high dose doping with androgenic anabolic steroids could have played a cocarcinogenic role in the development of the tumor in this case. Copyright 1999 American Cancer Society.

    Publication Types:
    Case Reports

    PMID: 10526287 [PubMed - indexed for MEDLINE]
  11. Aug 30, 2004 #10
    Biotech Week

    February 18, 2004


    LENGTH: 898 words

    HEADLINE: BETH ISRAEL DEACONESS: "No compelling evidence"of prostate
    heart disease risk found in study


    A retrospective analysis by researchers at Beth Israel Deaconess
    Center found no causal relationship between testosterone replacement
    prostate cancer or heart disease risk.

    The comprehensive review of 72 studies, addresses the current
    about testosterone replacement therapy and its potential health risks
    to men.

    "We reviewed decades of research and found no compelling evidence
    testosterone replacement therapy increases the incidence of prostate
    cancer or
    cardiovascular disease," said Abraham Morgentaler, MD, a urologist at
    BIDMC and
    associate clinical professor at Harvard Medical School. "Although it
    would be
    helpful to have data from long-term, large-scale studies, it must also
    recognized that there already exists a substantial body of research on
    effects of testosterone in men."

    The study was published in the New England Journal of Medicine.

    Low levels of testosterone affect an estimated 2-4 million men in
    the United
    States, a condition termed hypogonadism, and the prevalence of this
    increases with age. The symptoms include diminished libido and sense of
    vitality, erectile dysfunction, reduced muscle mass and bone density,
    depression, and anemia.

    The causes of hypogonadism may be classified as primary, meaning
    function of the testes; secondary, inadequate pituitary stimulation of
    testes; or a combination of primary and secondary causes, which is
    common in
    older men. Testosterone supplementation, in the form of injections,
    gels and a buccal tablet, is designed to elevate a hypogonadal man's
    testosterone levels into the normal physiologic range and alleviate

    "Testosterone is only for men who have symptoms of low testosterone
    with a confirmatory blood test. Testosterone therapy can be beneficial
    and safe
    for these men as long as they are appropriately monitored by their
    said Morgentaler.

    It has been known since the 1940's that severe reductions of
    testosterone can
    cause shrinkage of metastatic prostate cancer, and therefore there has
    been a
    concern that raising testosterone levels might cause growth of any
    prostate cancers. However, the study by Ernani L. Rhoden, MD, and
    found no connection between higher testosterone levels and prostate
    cancer, nor
    did they find evidence that testosterone treatment causes prostate

    In fact, they note that prostate cancer becomes more prevalent
    exactly at the
    time of a man's life when testosterone levels decline. To date,
    studies have demonstrated no difference in prostate cancer incidence
    hypogonadal men using testosterone therapy compared to men in the

    Regarding benign prostatic hyperplasia (BPH), multiple studies have
    failed to
    demonstrate consistent exacerbation of voiding symptoms during
    supplementation. "The impact of testosterone therapy on benign prostate
    appears to be mild," said Rhoden, "and rarely of clinical significance.
    testosterone therapy should be used cautiously in men with severe

    Monitoring the prostate during testosterone therapy is mandatory,
    given the
    theoretical concern that testosterone treatment may stimulate the
    growth of an
    occult cancer. Before and during treatment men should undergo regular
    evaluation, with a digital examination of the prostate, and a blood
    test called
    prostate-specific antigen (PSA). Patients with an abnormal prostate
    exam or an
    elevated PSA should undergo a prostate biopsy before initiating
    replacement to exclude the possibility that cancer is present. To
    monitor BPH,
    they recommend determining a base-line voiding history at the start of
    and assessing urinary symptoms at follow-up.

    The belief that testosterone may be a risk factor in cardiovascular
    is based on the observation that more men than women have
    cardiovascular events
    and men have higher testosterone levels than women. However, Rhoden and
    Morgentaler write that few, if any, data support a causal relation
    higher testosterone levels and heart disease.

    Indeed, several studies suggest that higher testosterone levels may
    have a favorable effect on atherosclerosis and heart disease. Studies
    testosterone replacement therapy have not demonstrated an increased
    incidence of
    cardiovascular disease, myocardial infarction, stroke, or angina,
    according to
    the retrospective analysis.

    Rhoden and Morgentaler describe other potential risks or side
    effects from
    testosterone replacement therapy as infrequent (acne or oily skin,
    sleep apnea);
    rarely of clinical significance (fluid retention); or reversible with
    of treatment (gynecomastia, testicular atrophy or infertility).
    treatment should be used cautiously or not at all in men with advanced
    disease. Skin reactions are commonly encountered in men being treated
    with the
    patch with a low incidence observed with testosterone gel (Rhoden EL,
    Morgentaler A. Risks of testosterone-replacement therapy and
    recommendations for
    monitoring. N Engl J Med, 2004;350(5):482-92).

    This article was prepared by Biotech Week editors from staff and
  12. Aug 30, 2004 #11


    User Avatar
    Staff Emeritus
    Science Advisor
    Gold Member

    Keep in mind, however, that testosterone replacement therapy to hypogonadal men is intended to restore testosterone to "normal" levels, not increase testosterone. A typical dose for steroid replacement therapy using Sustanon (a mixture of short- and long-acting forms of testosterone) is 100 mg once every 2 wk, or in a slightly longer acting formulation 250 mg once a month (most studies I've found have only used the 100 mg formulation) given to men with subnormal testosterone.

    It's amazing what you can find on the internet...apparently, for someone interested in "building mass and strength" the recommended dose is 250 mg weekly. I'm no expert on phamacokinetics, but this is MUCH higher than what is use for therapeutic treatment of hypogonadism, especially when you consider this is being given to men most likely starting out with normal testosterone concentrations.

    I don't know if it will result in higher incidences of prostate cancer in steroid abusers. And, since there is also a genetic predisposition to cancers, it may not happen in all abusers, just those who already had a predisposition to hormone-related cancers. I just don't think the studies are available on this to conclude one way or another.
  13. Aug 31, 2004 #12
    I believe the consensus is that it will only speed up the rate of cancer in those individuals who are predisposed, like you mentioned.

    As far as the dosage, you know as well as I do that you can believe 90% of the information on the net. The problem is most people do. Anyway a normal dosage for a professional bodybuilder is more like this.

    1-2 grams of testosterone per week (doesnt matter what kind b/c all test is the same after the ester is cleaved.
    350 mg's of dianabol per week (orally adminstered and aklylied at the 17th carbon position for passage through the liver)
    1 gram of deca or equipose per week (equipose is only made for animals but appears to have less side affects than deca)
    20-30 ius of insulin per day (Now this is really crazy - some have even starting injecting this on a zero carb diet. insulin is responsible for the differences in bb's today compared to that in the 70's)
    15 iu's of HGH per day.
    IGF-1 would be used also, if they can find some that is legit.

    That is a relatively mild cycle for these guys. Completely insane if you ask me. But the amazing thing about this is that if health problems do arise it is mostly due to the fact that this went on for 15-20 years. The few incidences of them being hospitalized are mainly due to the use of dieuretics. And as far as I have seen there has only been on steroid (anadrol - oxymetholone) that has ever been directly tied to any type of cancer (liver cancer).

    It is amazing what we as humans put our bodies through and survive.

  14. Aug 31, 2004 #13


    User Avatar
    Staff Emeritus
    Science Advisor
    Gold Member

    Well, in fairness, even estrogen and progesterone in the doses used in birth control pills can increase risk of cancer (not necessarily cause, but something that pushes someone predisposed to it over that edge). I work with steroids in my lab and they all come with a nasty carcinogen/teratogen warning label.

    Nah, I don't believe 90% of what I read on the net, but even though you suggest that at least professional athletes or serious athletes in training have doctors to help advise them on doses, we also both know there are amateur athletes (especially young, impressionable ones) who are going to be using the internet for their source of information on steroid use, as well as their source of information for suppliers. That dose I listed was recommended as a starting dose, so I wasn't sure if it goes up or down from there: start out slow and build up, or get a high loading dose and then back off.

    1-2 grams of testosterone per week?? And they aren't paying attention to the form? In a non-conjugated form, that's still excessive, but then if you get a form like testosterone enanthate, which is a very long acting form, you start getting a cumulative effect because each dose is being given on top of a baseline level that is increasing from the previous dose. On the other hand, they have little to no body fat, so less will be accumulating in fat (steroids accumulate in fat, so release dynamics are different if someone has a lot of fat than if they have little fat).

    So, are you a trainer or something, or do you just spend a lot of time in the gym that you know so much about what these guys are taking?
  15. Aug 31, 2004 #14
    You are exactly right about the young atheltes, it is scary.

    No, I don't spend alot of time at the gym. One time in my life I worked with college athletes, professional, IOC, and also bobybuilders to some extent. I quit mainly due to the fact that they were no longer interested in diet and training, only in drugs. The doses I gave are common knowlege.

    As far as the dosage. They do pay attention to the ester and they want the additive effect, unless of course they are drug tested. If they use enth or cyp, they will shoot 1 to 2 times per week. If they use prop, they will shoot everyday. If they use suspension they will shoot at least 2 x's per day. The suspension users are usually tested. They time the shoots so they can be below the 6 to 1 ratio if tested. They might also shoot some epitest before be tested to helf the ratio (although, epitest is now being tested for also.)

    And as far as starting doses. There are a couple of methods used. One is front-loading in order to get the blood concentration levels up as quickly as possible and then they stablize throughout the rest of their cycle.

    The other method is to gradually increase and then gradually decrease. I don't believe this method is used much anymore. Mainly b/c the athletes found out that as soon as they start they are shutting down naturaly production so they prefer to get levels high as soon as possible.

Share this great discussion with others via Reddit, Google+, Twitter, or Facebook