Tag Archives: testosterone

androgen receptor

A Word About Testosterone – Part 1: Androgen Therapy

by Ed Barillas, Staff Writer

Androgen drugs can be found in many places. Because they are popular among athletes and bodybuilders, androgen drugs can be found easily in the black market. Physicians also prescribe androgens, legally, for many conditions.

Despite the strong presence of legal and illegal androgen use, the science of androgen effects has greatly lagged behind the understanding of the biological effects of estrogen and indications for estrogen replacement therapy. Female oral contraceptives have been in use for many years, but only recently have we seen studies regarding hormone contraceptive agents in men. Although there are a few very well defined clinical syndromes of male hypogonadism, which requires androgen therapy, their use in other clinical situations, such as mild hypogonadism and hypogonadism associated with aging, is less well known.androgens chart 1

The following should be able to dispel some of the mystery of androgen therapy in older men:

As far as normal androgen physiology, we know that testosterone is present in very low levels in boys prior to puberty.   Once the boy hits puberty a pulsatile secretion of GnRH causes the anterior pituitary to produce LH and FSH. This circulating LH induces the Leydig cells of the testicles to produce testosterone, with the following development of secondary sex characteristics. As the level of testosterone rises in the blood circulation, there is a negative feedback on the production of GnRH at the hypothalamic level, and LH and FSH at the pituitary level.

androgens chart 2A high intra-testicular level of testosterone is an absolute prerequisite for sperm production. The levels in the seminiferous tubules stay high due to the proximity of production in the Leydig cells, and well as by binding in the tubules by androgen binding-protein or ABP. This binding to ABP probably also prevents fluctuation of the levels by maintaining a reservoir of hormone immediately available to buffer changes in production. Although testosterone is the only absolute requirement for sperm production, FSH has a promotional effect and quantitatively normal spermatogenesis requires the action of FSH on the Sertoli cell. When sperm production is proceeding in a quantitatively normal manner, a peptide hormone called inhibin is released into the circulation and by the Sertoli cell, which is responsible for negative feedback of FSH, but not LH production, by the pituitary.

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

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

androgen receptor

The androgen receptor bound to testosterone.

As far as changes in testosterone levels, with aging there is no corollary of the menopause seen in females as men age. The menopause in women is caused by ovarian failure. No such similar event of complete testicular failure occurs in men. However, it has been well established that mean T levels drop progressively with age, and the percentage of men with T levels in the abnormal range increases. So when one looks at the levels of bioavailable testosterone (a probably more accurate measure of the decreasing androgenic effects) more marked changes may be evident. Other evidence of a relatively hypogonadal state in older men includes elevated LH, as well as an exaggerated response of LH to the administration of GnRH is staged testing.

Although T levels drop with aging, it is less understood whether any of the generalized manifestations of aging such as osteoporosis, impotence, CNS changes are due to the decrease in circulating androgen. Because it is not established that these age-related changes are due to hormonal deficiencies, the simple presence of a decline in circulating hormones cannot be taken as de facto evidence that hormone replacement therapy will be beneficial in reversing or preventing these changes.


Benefits of Frontloading

by Ed Barillas, Staff Writer

In this article we will be discussing “frontloading” of long ester-based testosterone cycles. Frontloading is the term for loading the steroid compound in the first weeks to facilitate its access in the blood stream. As we all well know, when we are going to run an injectable steroid cycle with long esters (such as Primobolan, Deca Durabolin, testosterone Enanthate, Cypionate and Boldenone), it is best to wait from 3 to 6 weeks to get what is called the kick – a full peak of the compound’s activity in order to reach the maximum anabolic state and keep it until the end of the cycle.frontloading

Therefore, when we are in a high anabolic state and the protein synthesis is raised, this is the time to add some good calories to fully avail the massive transport of amino acids in the muscle cells. For a first timer, to have to wait for the chemicals to “kick in” is not easy, so its best to “kick start” the cycle through one of these three methods:

1. First off, add an oral in the first 4-5 weeks of cycle to get some gains, even from the beginning days, although these will be mostly water gains for the majority of cases.

2. Second, try substituting the long ester with a shorter one for the first 2-3 weeks. So in other words, use Test Propionate to start and Test Enanthate for the rest of the course.

Some intermediate users should also try adding a short ester in conjunction with the longer cousin and run both for the first 2-3 weeks, then keep just the long esterified substance for the entire duration of the therapy.

3. Frontloading the long esterified compound in the first week and doubling the dose. This is probably the most effective manner yet to get benefits from the first weeks of a long esterified steroid intake. Before you consider how this method works, take a good look at the most used long esterified compounds’ duration, which is referred to as the activity time:

Main Long Esters Active Lifefrontload chart

  • Cypionate: 15-16 days
  • Undecylenate: 7-9 days
  • Enanthate: 8 days
  • Decanoate: 14-16 days.

Let’s take a look at a 14 days-active ester. Since we know that any esterified compound is expelled from the body after its active-life duration, we will take into account a theoretic injection protocol of 1 shot per week (every 7 days, its half-activity, or half-life).

Standard injection protocol at 500mg/week for 4 weeks:

WEEK 1: 500mg; substance left at the end of the current week: 250mg

WEEK 2: 500mg + 250mg; substance left at the end of the current week: 375mg

WEEK 3: 500mg + 375mg; substance left at the end of the current week: 437.5mg

WEEK 4: 500mg + 437.5mg; substance left at the end of the current week: 468.75mg

This shows us that we won’t never get those 500mg we’re injecting every week all the time as the minimum amount of compound guaranteed in the blood.

To make sure that you will have at least the amount of testosterone you’re injecting every week regularly circulating in the blood you just have to add 1 more dosage of the substance in the first week. That’s it!

This concept will make a lot of sense if you look at the following example:

WEEK 1: 1000mg (2x500mg); substance left at the end of the current week: 500mg

WEEK 2: 500mg + 500mg; substance left at the end of the current week: 500mg

WEEK 3: 500mg + 500mg; substance left at the end of the current week: 500mg

WEEK 4: 500mg + 500mg; substance left at the end of the current week: 500mg

With this protocol, the compound is swiftly active from the first week, just for having frontloaded it with 1 more shot than the usual protocol, and this way the chemical levels are even more stable (=less sides) and higher in the blood.

This should help you out to get relatively quick results from a long esters cycle.


beginner steroids

Steroids Cycles and Stacks to Start With

by Ed Barillas, Staff Writer

The most important reason a testosterone cycle is recommended for first time users is because it is the building block for all future cycles. By using testosterone first you will have an idea of how you body will react to it. You will find out if you are prone to gyno, how much your blood pressure will raise with the use of anabolic steroids and how much fluid you can retain as part of your training and nutrition programs. To put it this way, if you’re doing a stack of testosterone enanthate and dianabol you will feel signs and have symptoms of gyno developing. So you can repair the issue with 110 mg of Clomid or 20-30 mg of Nolvadex every day until it goes away and still a few days afterwards to make sure it stays away and so the next time that you cycle you should use only testosterone enanthate to avoid the aromotization issues caused by the addition of Dianabol tabs the first time out. But you know what? It wasn’t the test that was aromatizing after all – it was the dianabol!beginner steroids

Now with testosterone only, you are still getting the signs and symptoms of gyno and you should once again control the substance with the use of an anti estrogen. If you would have known that you were gyno prone with the testosterone you could have better planned this second cycle and worked out a stack to your advantage and possibly even eliminated or greatly reduced the risks of re-occurring gyno. So if you start cycling with a stack, you won’t have any way of knowing which steroids are causing which side effects and that’s not a good start.

Another reason why testosterone only is a good first cycle is that it’s your first cycle so don’t over-do it. You’ll grow fast off testosterone only with correct training and nutrition. In a study recent study, men with no weight training at all made increases in fat-free mass, 8.8 lbs. There where increases in triceps mass around 1.6″ also increases in quadriceps mass 2.4″ and added 22.2 lbs. on their bench press and 44.4 to their squat. It is testosterone that did this so remember that you’re injecting hormones into yourself. Don’t let the quantity fool you. Your virgin androgen receptors will gobble them up. Remember that last thing you want to do is develop a tolerance so that you require more quantity in the future.

It’s also good to know that testosterone may be a strong androgen, but the side effects are very easily controlled for almost all of them with a few simple ancillaries. With any steroids you take you are going to shut down your natural testosterone production and this will lead to short term impotence and testicular atrophy. Deca and Trenbolone are not the only ones that cause this as any drug can do this when not accompanied by testosterone. Deca and Trenbolone are just the most common and most complained about for this type of thing.

There are lots of other good reasons for this. It is very obvious that Dianabol is a 17-alpha alkylated steroid, and as such will warrant short-term use. Since Dianabol has little Androgen receptor activity, it functions particularly synergistic with strong compounds that have strong androgen receptor activity as in the case for all the before mentioned so basically you should stack it. You should ask yourself if you want to make muscle, strength and water gains and end up feeling pumped and huge by the end of your cycle only to realize that the Dianabol mainly gained you water and a few weeks after the cycle you lose it all? That surely will pop your bubble.

Its good to know that Dianabol is a methylated compound with a certain toxicity, so it would not be wise to use it longer than 6 weeks on end, 8 weeks at the absolute maximum and only under supervision of a medical professional who can monitor your liver values.

Dianabol heavily aromatizes so its not very useful during cutting and with 6-8 weeks of use maximum, that leaves the option open, to stack it with another, injectable, compound that can be used for longer terms.




Phytoestrogens: Foods to Avoid as a Male Bodybuilder

by 3J, www.3jsdiet.com

The human body has a complex endocrine system that regulates hormones in correlation with the sex of the individual. One of the important regulations that the male endocrine system controls is the testosterone to estrogen ratio. The definitive characteristics males develop come from testosterone and dihydrotestosterone (aka DHT). Testosterone plays the main role in male characteristics while DHT plays the secondary role. The male human body statistically likes to keep a 10 to 1 ratio of testosterone to estrogen. When there is an imbalance between these two hormones the body will try its best to make adjustments to enforce such a ratio. If your testosterone gets too high your body aromatizes testosterone to estrogen in an effort to keep the ratio, hence why aromatization in steroid users occur and there is a strong need for a selective estrogen receptor modulator or aromatase inhibitor while on cycle.phytoestrogens

Phytoestrogens are estrogens that are not produced by the human body. They occur naturally in food sources that humans eat. Though Phytoestrogens are not truly “human estrogen,” they are xenoestrogens. Xenoestrogens are not chemically identical to human estrogen, but their similarities are so close that they can have an estrogenic effect on the human body.   It’s important to note that these naturally occurring phytoestrogens are weaker versions of our human body’s estrogen. They have a much milder impact on the body. For the natural bodybuilder, a little bump in estrogen is not a bad thing. It promotes muscle growth and helps prevent injury. Most of the foods I am about to list can safely be eaten regularly for the natural bodybuilder. The body’s endocrine system will easily regulate any xenoestrogens that have been consumed. Unfortunately, the same does not apply for the steroid user. One of the top priorities a steroid user has is estrogen control. High estrogen can cause a number of unwanted sides like bloat and erectile dysfunction. Here is a list of foods that naturally have higher phytoestrogens in them. Many of these foods have dense rich nutrients and should not be removed from your diet due to the fact that the good outweighs the possible rise in estrogen, I personally avoid soy and soy derived products due to its higher phytoestrogen content.

(list sourced from Wikipedia)

  • Soybeans and soy products
  • Tempeh
  • Linseed (flax)
  • Sesame seeds
  • Wheatberries
  • Fenugreek (contains diosgenin, but also used to make Testofen®, a compound taken by men to increase testosterone).
  • Oats
  • Barley
  • Beans
  • Lentils
  • Yams
  • Rice
  • Alfalfa
  • Mung beans
  • Apples
  • Carrots
  • Pomegranates
  • Wheat germ
  • Rice bran
  • Lupin
  • Kudzu
  • Coffee
  • Licorice root
  • Mint
  • Ginseng
  • Hops
  • bourbon
  • Beer
  • Fennel
  • Anise
  • Red clover (sometimes a constituent of green manure).

 To follow this topic in our forum, click here.

test prop peak value

Test Prop and Peak Value

by 3jsdiet.com

Let’s clear something up before we get into test prop itself – Testosterone is testosterone. The ester (oil) that is connected to testosterone does not change what testosterone is or does, but changes the rate of release the hormone undergoes in your body.   Common esters are cyphoinate, enanthate, propionate, and acetate. Each of these esters have a half-life. By definition, a half-life is is the time it takes for a substance (drug, radioactive nuclide, or other) to lose one-half of its pharmacologic, physiologic, or radiological activity. We are worried about the pharmacological definition here. So, the half-life of testosterone cyp is about 10 days. If you inject 250mg of cyp, in 10 days there would be 125mg of it left of it in your system. The benefit of running test prop is its short half-life. The half-life of test prop is about 3-4 days. If you were to inject 100mg of test prop, in 3 days it would be about 50mg left in your system. Now that we have cleared that up, lets move on.test prop peak value

So what’s the difference between running test prop and test e or c? The answer is two things – peak value and duration of cycle. With all cycles you inject in a frequency that overlays the half-life, increasing the dosage every week until you reach your peak-value, the highest amount of testosterone that can be active in your body with the dosage you have chosen. Statistically, average test prop cycles do not reach the peak levels of average test c or e cycles due to the very short half-life of prop. At the same time, test prop will reach peak values much quicker than test e or c. An average test e or c cycle will reach peak levels around week 4-6 which is why the minimum for longer ester cycles is 10 weeks. But with test prop the peak value is reach in less than half the time, allowing for shorter and faster cycles. Test prop cycles can be as short as 6 weeks and average 8 weeks. Test c or e cycles run from 10 weeks up, averaging 12 weeks for most users. Furthermore, if something were to go wrong with your cycle, prop would be out of your system much quicker than test e or c. Many users claim that there are less side effects with the use of prop. The claims cannot be ignored since the ester is fast acting and, usually, the peak values of a prop cycle are lower than e or c (unless the user is running a higher dosage of prop), yet no specific credible research on the matter has been found.

With the 3 day half-life of test prop the most optimal frequency for injection would realistically be every day. Since the idea of injecting yourself every day is not something pleasant to most people, every other day injections have become the standard. While not “optimal” every other day injections have shown to be acceptable since, technically, the injection frequency should be 1.5 days or less.   First time users of test prop should start with a moderate dosage of 50mg every other day. I have seen the safe use of test prop at up to 150mg eod or 75mg ed. Keep in mind that ancillary drugs like a-dex or armoasin should be kept on hand or ran to keep estrogen levels in check and proper post cycle therapy protocols should be ran to promote a speedy recovery after cycle.

To view the discussion on this subject in our forum, click here.

anabolic dn

Anabolic DN

Anabolic DN, otherwise known as Nandrolone Cypionate, is a powerful compound that promotes muscle mass and most people will start to take it for this purpose. It is most recommended for bodybuilders who are looking to enhance their image and improve their muscle mass.

Anabolic DN is a modified form of nandrolone, in which a carboxylic acid ester has been fused to the 17-beta hydroxyl group. Esterified steroids are not as polar as free steroids and are absorbed more slowly after the initial injection. Anabolic DN provides a spike in nandrolone and sustains for up to two weeks.

anabolic dn

Anabolic DN

Anabolic DN was developed during the 1960s and was sold for a short amount of time as a pharmaceutical. However, it did not last, and in recent years, Anabolic DN has only been sold as medicine for veterinarians, not for muscle growth for the public at large. Recently, Anabolic DN has been mostly used in the Australian veterinary drug market, and there was also a high-dose version of Anabolic DN sold in the Mexican veterinary drug market, which has since been withdrawn.

But while Anabolic DN builds muscles, it also has several side effects, including increase in appetite, water retention, and a possible breakout of acne. It can also increase your risk for cardiovascular disease, growth stunting, and poor cholesterol. In terms of cardiovascular disease, anabolic DN can place extra strain on the heart and cause a temporary rise in blood pressure. Arteries can become less elastic and cardiovascular stress will increase, making the heart pump more and more. Blood pressure can eventually turn into a long-term health issue if not treated properly.

Anabolic DN can lower the levels of “good” cholesterol, which is known as high-density lipoprotein. This picks up any fats and fat molecules that are stuck on the walls of arteries and cleans them out. Anabolic DN lowers the high-density lipoprotein and increases the chance of gradually developing arterial plaque, which can eventually block an artery or cause a stroke.

In adolescents, Anabolic DN can stunt growth. The steroid can arrest the growth process to the point where growth plates will prematurely close instead of closing naturally, which can ruin chances of the bones elongating any further.

Some people can also develop a psychological desire to be on steroids based on how Anabolic DN positively alters their bodies—in this sense, mental health can be affected when using this steroid, so it is important to check in with yourself to make sure you have a sense of mental and emotional balance. This is another reason why cycling properly is extremely important.

Some steroids can also be suppressive to a male’s testosterone. A single injection can cause testosterone deficiency to develop and result in loss of libido, impotence, and lethargy—again, another reason why cycling properly is so important. Testosterone levels can reduce by as much as 70%, and several doses will worsen the condition. This can wear on anywhere from six to twelve weeks and causes many men extreme discomfort, becoming a prominent reason as to why men never use it. While the benefits are strong, the consequences are equally as powerful.

This kind of drug cannot be found anywhere in the US, as there are no US manufacturers. Aside from promoting muscle growth, this drug is being researched for other uses as well, including help with osteoporosis.

But when buying Anabolic DN to promote your own muscle growth, take caution. Sometimes, what you get is not always what is advertised. Some people who obtain Anabolic DN and use it to add to their muscles without checking it end up sustaining bodily harm. The people in the black market who sell Anabolic DN sometimes substitute it with a cheaper drug and still charge the same price, and oftentimes, the buyer doesn’t notice a difference. Even if you think you’re getting real Anabolic DN, checking with someone who knows more than you about how it should be packaged, and other characteristics of Anabolic DN is a great way to ensure you’re getting what you intended to get. Also, if you do not get the results you expect after a certain amount of time, you may have gotten a substitute and not authentic Anabolic DN.

If you are looking for a steroid that will build muscle mass and enhance your figure, anabolic DN is something you should consider trying. While it is not sold in the United States as a legal substance, it is offered on the black market, but as they say, “buyer beware.” Check to make sure you have the right product and you will get the results you want.


A-Rod’s Advanced Drug Regimen

Although Alex Rodriguez finally waived the flag of surrender and dropped his lawsuit against the MLB for suspending him, we have learned quite a bit about the evidence the league had on the star player’s use of performance enhancing drugs.


Alex Rodriguz’ PED program created by Biogenesis was a high-priced mix of high-tech drugs.

According to documents the league obtained from Bioigenesis, the lab where Rodriguez and a slew of other baseball players went for their PEDs,  Rodriguez’s $12,000 per month drug regimen appears to utilize some of the most sophisticated drugs and diet programs in use today. In four distinct, month-long phases, Rodriquez’s cycle included hGH, GHRP, CJC, Testosterone cream, L-Glutathione cream, Melatonin, Testosterone Troche, Clomiphene, iGF-1, hCG and a host of other vitamins, omegas and other dietary supplements.

Tony Bosch, Biogenesis owner and the developer of this high-priced program, likely got most of the drugs for these programs from legitimate drug-makers through his father Pedro Bosch who is a family physician and was listed as Biogenesis’ medical director. However, some of the drugs in the list were likely procured through underground labs because investigational compounds like GHRP 2/6 are not available on any regulated market.

“My guess is that [Biogenesis] was getting them from [online sources] and administering and reselling it to [Rodriguez],” said Jose Garcia, MD, PhD, an endocrinologist at Baylor College of Medicine who has been involved in studies of GHRP 2/6 in an interview with MedPage Today. “You would never go to a site like this because there is no quality control so you never know if these products are contaminated or if they contain what they’re supposed to. Not even for animal experiments.”

Tony Bosch

In exchange for immunity from lawsuits brought on by the MLB against Biogenesis and its associates, Tony Bosch turned over the evidence that eventually sunk Rodriguez.

Despite Dr. Garcia’s adamant plea for people to stop taking these kinds of drugs, they are known to the bodybuilding community as some of the best advances in lowering unwanted levels of estrogen during a testosterone cycle. But just as the hefty price tag for Biogenesis’ PED program indicates, these drugs can be very expensive.

As for Rodriguez, the most expensive part of his drug program will be his 162-game suspension from MLB which will take him out of the 2014 season completely – without pay.

As for Tony Bosch, now that Rodriguez has dropped all of his lawsuits against MLB, his players’ union and everyone else he threatened to sue over his getting caught, it looks like MLB will drop its own lawsuit against the Biogenesis founder on the grounds that he and his associates committed “intentional and unjustified tortious interference” with contracts between MLB and its players by providing them with banned substances.

It was MLB’s threat of litigation that forced Bosch to hand over information on Rodriguez and other baseball players who were using PEDs from Biogenesis, which is how the information on Rodriguez’ drug regimen (see below) was released.

Alex Rodriguez’ Drug Regimen

arod drug regimen

steroid nutrition

The Beginner’s Guide to Steroids and Nutrition

by 3Js, www.3jsdiet.com

So I’m going to make this article as simple and straight forward as I possibly can.  This article’s purpose is to serve the mass population of amateur steroid users who lack the proper knowledge necessary to get the most out of their cycle and progressive instinct toward their individual goals. Having been on various steroid forums for years I have seen a countless number of members come and go asking the same questions; “I’m too skinny, what steroid can I use to get big?” or “I’m overweight, is there a steroid out there that can help me lose weight?”

pictue of fit man with pills in spoon

There are no magic pills to bulk you up. Steroid cycles also require proper training and nutrition to gain and keep gains.

The notion that there is a “magic pill” has been grossly over popularized through a mixture of misconceptions leaked by the mass media and the flawed human psychological necessity that is instant gratification.  Since there is great pressure applied socio-psychologically to have a certain “look” in our culture, many will resort to extremes without the proper knowledge of what, when, and why they should be taking steroids.  What comes secondary to such goofs is the steroid “myth” that you cannot keep the gains that you make on cycle.  We shall discuss and debunk such notions later in this article.

Having said all that, I am making a step by step program here with certain requirements that have to be met in order for one to move forward to the next step.  If at any point you have not met a requirement, you’re not ready for steroids.  Furthermore, once you are ready for steroids there will be certain requirements set for the cycle which I will discuss.  Simply speaking, this is a step by step for the use of steroids and proper nutrition.

Table of Content

  1. Age
  2. Training Experience
  3. Nutritional Set Up and Experience
  4. Basic Steroid Knowledge (including compound knowledge and PCT)


The first and most important requirement of running a cycle is your age.  Through my years as a nutritionist I have seen some very athletic young men with ages ranging from 18-23 who look more ready for a cycle then most who are at the proper age.  Regardless, someone who is young has a very high natural testosterone level of 800-1000ng/dl. Getting to the root of the issue, there are two major reasons why running a cycle at a young age is unacceptable and risky.  Running a cycle at that young of an age will only risk the recovery of those high levels of testosterone, even if the user runs a perfect PCT (we will discuss that later) one could end up with subpar levels of natural testosterone for life after the fact. Secondly, between the ages of 18 and 23 one still has room to grow in height. When a surge of testosterone runs through the body at a supra-physiological dose your growth plates fuse and you’re at the tallest you will ever be.


The worst thing someone can do is hop on a cycle when they have little training experience.  Besides the obvious fact that you cannot learn how to properly train overnight (this includes form), it also means that you have not brought yourself anywhere close to your genetic potential. Simply put, someone who has been training for a little amount of time has not primed his body for what steroids will do.  With that being said, many armature and first time steroid users bring upon themselves injuries due to the undeniable fact that joints and ligaments do not grow on cycle like your muscles will.  As these users  increase the amount of weight they can move in their exercises at an alarmingly fast rate, their tendons will start to wear and tear bearing a load that they are not used to.  This causes many injuries that are usually not repairable without surgery.  Separation of or degeneration of the cartilage in the acromioclavicular join (a.k.a the AC joint) is a perfect example of a very common injury that occurs to beginner cycle users who get bench press crazy and lift weights much higher than their body can handle.  So, if you don’t have years of training under your belt stay away from gear.  You simply are not ready.

picture of steroid nutrition

Nutrition is the most important factor in how well a steroid cycle will work.

Nutritional Set Up and Experience

By far, the most important part of your struggle in reaching the set goals you have in mind will be your diet.  Diet is everything, and I do mean EVERYTHING.  It’s the deciding factor in whether your body will change or not.  Anyone can get into a gym and, with a little help, get some type of basic training routine going on.  Over the years in multiple forums I have seen the same thing over and over again.  People seem to focus too much on anabolics and their training routines.  I see skinny guys jumping on a 5×5 or 5/3/1 workout routine only to find out that they stall in progress in a very short period of time.  The simple truth is that 80% of your goals will be met in the kitchen.  It won’t be met in the gym and it won’t be met in the needle that you are filling either. Because of a lack of nutritional experience, a lot of people end up right where they started or worse after a cycle.  This brings about the “myth” that you cannot keep your gains from a cycle.  It’s not that you cannot keep your gains, it’s that you have not eaten the correct amount to keep your gains.  As you grow, your bodies nutritional needs also grow. Nutrition is by far the most decisive factor in whether or not you really make the change your looking for.  Now there are a lot of different types of dieting philosophies out there and it can be extremely confusing.  People are using different weight to protein and carbohydrate ratios.  There are fad dieting prospects like IIFYM and IF dieting (both of which I don’t personally condone).  You can run a traditional bulk and cut or you can do more advanced dieting like carb cycling. Remember guys, being on cycle without proper nutrition is like sitting in a Ferrari without gas in the tank.  It feels amazing to sit in the car, but you’re never going to get anywhere.  My advice to those starting out is simple, keep it simple.  Here is a basic way to get started with dieting.

You need to figure out your BMR (this is the basal metabolic rate of your body… which means if you were to do nothing all day, your body would burn these many calories. Once you’ve figured out your BMR, you need your TDEE (this is your total daily energy expenditure, it’s based upon your activity level). In order to figure out your BMR, you need to know what your lean body mass is, so, in turn, you need to know what your body fat percentage is. If you don’t know your body fat percentage, go to your gym and get tested (please don’t use electronic scales to get your body fat checked, they’re horrible. If you cannot find a gym to get tested at, please post up a picture for estimates on the forum.

  • BMR (men and women) = 370 + (21.6 X lean mass in kg)
  • Total weight x bf in decimal form = total bf weight
  • Total weight – total bf weight = total lean body mass

If your total lean body mass is in lbs, you can divide it by 2.2 to get it in kilograms. For example:

  • I am 6’4 and 275l bs at 14% bf… so I would multiply 275 by .14 (converted from percent to decimal)= 38.5lbs
  • 275 – 38.5 = 236.5lbs lean body weight
  • 236.5 / 2.2 = 107.5 lean mass in kg
  • 370 + (21.6 x 107.5) = 2692 BMR (this is high for the average person, I’m a big guy)


Once you have you BMR, you need to calculate your TDEE, this is simply done with some multiplication. You can multiply it by an activity number to figure out your daily caloric expenditure, be honest here as this is the very cornerstone of your diet, if you are between two of the below activity levels then just multiply by a number in between them. To determine your total daily calorie needs, multiply your BMR by the appropriate activity factor, as follows:

  • If you are sedentary (little or no exercise) : Calorie-Calculation = BMR x 1.2
  • If you are lightly active (light exercise/sports 1-3 days/week): Calorie-Calculation = BMR x 1.375
  • If you are moderatetely active (moderate exercise/sports 3-5 days/week) : Calorie-Calculation = BMR x 1.55
  • If you are very active (hard exercise/sports 6-7 days a week) : Calorie-Calculation = BMR x 1.725
  • If you are extra active (very hard exercise/sports & physical job or 2x training) : Calorie-Calculation = BMR x 1.9 

Once you have your TDEE, we can make some simple choices. If you’re going to bulk start by adding 500 calories to your TDEE. So, if I had a TDEE of 3000 calories, I would start my bulk at 3500 calories. If you’re going to cut, you want to reduce your calories by 15 to 20 percent.

So, again if I had a TDEE of 3000 then I would start my cut at about 450 to 600 calories below my TDEE. Here are some simple tips for setting up correct macros. For bulking, you want to keep two things high, protein and carbs.  For example, at a 3000 calories bulk I would personally have my macros look like this:

  • 250-300g protein
  • 300-350g carbs
  • 70g fats

Now you have to fill out six meals a day.  Divide the protein by 6 and average each meal to that number, at 300g 6 meals would average about 50g per meal.

Divide your carbs into 5 meals; at 300g carbs you would need 60g carbs per meal.  The last meal of the day should never have carbs.  It reduces natural growth hormone production as you sleep.

If you want to cut the ideal rule of thumb is to follow a PRN or as needed basis on the carbs.  Carbs should be focused on breakfast, pre, and post workout. Ideally, your macros at a 2500 calorie cut should look like this:

  • 300g protein
  • 150g carbs
  • 80g fat

Again, divide the protein evenly throughout the day.  Divide the carbs evenly into breakfast, pre, and post workout. Fill the rest of the meals with fats to get the necessary 80g fats that you need.

Basic Steroid Knowledge (including compound knowledge and PCT)

picture of buff gym man

Before you take any steroid compound, learn about how to use it properly.

Here is a brief understanding of a beginner’s steroid cycle.  If you do not at the least have a basic understanding of how steroids work you should not be using them.  Reading the hundreds of pages of info on compounds can be confusing, so we are sticking to the basics for first time users.


Your body naturally creates testosterone.  Testosterone is the male dominant hormone.   In a healthy young adult about 77mg of testosterone will be produced a week.  As a steroid user, you inject synthetic testosterone into your system.  When your system sees that there is an abundance of testosterone it simply shuts down your natural production.


Now here is where a lot of inexperienced people get confused.  Testosterone is Testosterone.  What is different is what ester or oil the testosterone is mixed with.  For example, testosterone Propionate has a oil that breaks down faster in the body then Testosterone Cypionate.  When you inject testosterone, a  depot is created in your muscle.  The half life of the ester that you inject will dictate the rate in which your body will absorb the testosterone from the depot.  The term “half life” means the amount of time it takes for your body to absorb the testosterone.  For example, if you inject 250mg of testosterone enanthate, in 10.5 days 125mg will be left in the depot (or injection site).   The recommended frequency of injection is half the half life of the compound.  For that reason, Prop is injected every other day, while cyp an enanthate are injected twice a week, about 3-4 days apart from each other.  The list below gives the half lifes of the most popular blends.

  • Testosterone Cypionate 12 days 
  • Testosterone Enanthate 10.5 days 
  • Testosterone Propionate 4.5 days 
  • Testosterone Suspension 1 day 

As a beginning steroid user, Testosterone Cypionate or Enanthate is recommended to reduce injection frequency.  A first time user should inject between 400 and 500mg of testosterone a week.  Usually, the dosage is split up into two injections.  250mg on Monday and 250mg on Thursday is the most traditional injection frequency. The first time cycle should range from 10 weeks to 12 weeks.  Running a cycle any shorter than 10 weeks will reduce benefits unless its propionate that you are running.  Due to the half life of cyp and enanthate it takes about 4-5 weeks for testosterone to reach its peak levels in your body.

It is very important for a first time steroid user to start with just injectable test.  Stacking compounds the first time around makes it much more difficult to figure out which compound is causing problems if problems were to arise.  But, if you were to just start with test and see that the cycle went well, then you can add a second compound to your next cycle. If adverse sides arise you could be fairly sure it is the second compound causing it.  Also, as a first time user your beta receptors are very fresh and the need for a second compound is not justified.

So you have completed your first successful cycle, now it’s time to recover.  PCT (post cycle therapy) is one of the most important part of your whole cycle.  In PCT, we provide ancillary drugs which promote the body’s natural testosterone production to restart.  The ideal compound for restarting the natural testosterone of your body is clomid.  If using testosterone cyp or e, you start pct 14 days after your last injection. If it was prop, it would be about 5 days. Refer to the half life chart to better understand why we wait that period of time.  Pct with clomid is simple.  You take 50mg of clomid daily for 4 weeks.  While in pct, you must increase your calories above your TDEE by 200 calories at the least.  If you have been bulking, increase your calories by 200 calories from where your last intake was before you start pct.

If you plan to do another cycle, keep in mind that time off equals time on + pct. So if you had a 12 weeks cycle, expect to wait at least another 16-18 weeks before you cycle again.

Keep in mind guys, if you want to take your body to the next level, consider 3Js Nutrition Network and my personal professional services as a coach in mind.  If interested, contact me at 3jsdiet@gmail.com






Testosterone to Help Give Women the Big O

Women who find it difficult or cannot reach climax during intercourse are soon be getting help from a male sex hormone. Canadian pharmaceutical company Trimel Pharmacueticals is in the middle of clinical trials for a testosterone-based drug they call Tefina.

In an interview with the Website Medical Daily, lead researcher Susan Davis said, “We have previously shown that for women with low sexual interest, testosterone therapy not only improves sexual desire and arousal, but also enhances a woman’s ability to reach orgasm.” Trefina is in the midst of Phase II clinical trials in Australia, Canada and the United States. The drug is administered nasally and the effects are supposed to last for up to six hours.

While drug companies are obviously excited at a possible cash cow they could dub the “female Viagra,” there has been much debate centered around the true cause of sexual dysfunction in women. While Trimel Pharmaceuticals claims a 60 percent success rate in getting previously non-orgasmic women to reach climax, there are many researchers in the field of sex therapy who say any clinical trials should be weighted on the fact that there are so many variables at play that may be missing. For example, a woman may reach climax while using the drug, but would it have been just as possible if she used extra stimulation with a vibrator during sex? Other factors such as overall health and body issues should be weighed before green lighting the drug to the marketplace.

Detractors of Trefina have good cause to be wary of unleashing a testosterone-based drug for women out onto the global market. Regular readers of this Steroidology are aware of the potential side effects for women who take testosterone. There is potential for abuse and the development of male sexual characteristics, like deepening of the voice, growing facial and body hair, infertility and a host of other medical conditions related to hormonal imbalance.

Trefina isn’t the first testosterone-based drug marketed for women with sexual dysfunction. In 2009, a drug called Intrinsa was introduced to Europe after a lengthy trial by Britain’s National Health Service. Intrinsa is a testosterone patch that boasted it increased sexual satisfaction by 73 percent during clinical trials, compared to 19 percent of women who were given placebos. Intrinsa’s manufacturer Procter & Gamble took the drug before the FDA in 2004 and was rejected due to safety concerns.

It is unclear whether or not Trefina will suffer the same fate as Intrinsa by the FDA, although recent attitudes toward hormone therapies might help its cause. Testosterone therapy for women has been gaining acceptance and momentum among medical circles for over a decade. In Canada, women have been able to get testosterone replacement therapies approved by the government since 2002. In Australia, post-menopausal women can take a testosterone implant drug called Organon that lasts for six months. And in the United States, even renowned medical institutions like the Mayo Clinic have begun speaking in favor of testing testosterone replacement for women – and not just for sexual dysfunction.

In an interview with CNN, Mayo Clinic endocrinologist Dr. Paul Carpenter, M.D. said, “studies show that [testosterone] helps maintain muscle and bone and contributes to sex drive, or libido. There are also quality-of-life issues. If you give testosterone replacement to testosterone-deficient women, they often say they feel better, but they’re not specific as to how.”

Whether or not Trefina is approved by the FDA and makes it into our pharmacies (and our television commercials) as the breakthrough “Viagra-for-women” drug that can turn even the most prudest housewife into a raging cougar in the sack remains to be seen. One thing for sure is that research into testosterone’s many helath benefits for an aging population won’t be restricted to just men.

MONACO - July 4: Lance Armstrong of Team Astana finishes the last 150 meters of the 2009 Tour de France on July 4, 2009 in Monaco.

Armstrong gives up on legal race to keep his titles

The Tour de France is the word’s most famous and challenging bicycle race – a 21-day, 2000-mile ride through grueling mountains and picturesque towns in France and neighboring countries. But for US cyclist Lance Armstrong, who has won a record seven Tour de France titles, it was not the steep inclines of the race that proves to be the most grueling.

picture of lance armstrong in competition

MONACO – July 4: Lance Armstrong of Team Astana finishes the last 150 meters of the 2009 Tour de France on July 4, 2009 in Monaco.

Last week, Armstrong gave up his legal battle with the US Anti-Doping Agency, who for years had accused him of using performance-enhancing drugs to fuel his unprecedented seven titles. When Armstrong announced that he would give up his fight with the USADA, reaction was swift. He was permanently banned from competing and he was stripped of all his Tour de France titles.

“There comes a point in every man’s life when he has to say, “Enough is enough.” For me that time is now,” Armstrong said in a statement to the Associated Press. Although Armstrong was never caught doing drugs, had passed hundreds of tests for banned substances and still had support from the International Cycling Union, he cited the cost of the legal battle with the USADA’s “unconstitutional witch hunt” as his main reason for giving up on challenging the organization’s accusations. “I have been dealing with claims that I cheated and had an unfair advantage in winning my seven Tours since 1999,” he said. “The toll this has taken on my family and my work for our foundation and on me leads me to where I am today – finished with this nonsense.”

Armstrong leads a foundation he started in 1997 for cancer patients called Livestrong – a foundation he started after undergoing treatment for testicular cancer.

And here is where there charges of doping become strange. Armstrong has not been accused of using testosterone – a drug that would seem to make more sense because he had one of his testicles removed, making natural testosterone much more difficult for him to produce. Armstrong is being accused of using erythropoietin, or EPO – a glycoprotein hormone that controls red blood cell production. EPO is a useful drug for endurance athletes like cyclists because it oxygenates the blood and aids to quickly heal muscle tissue that is worn out from extensive workouts.

Although Armstrong has never tested positive for EPO, charges of him using the drug began when he allegedly told a nurse in the hospital where he underwent chemo for his testicular cancer that he used the drug extensively. Other cyclists on the Tour de France also made claims that they saw Armstrong having blood transfusions to mask his drug use.

Despite the instant media feeding frenzy that pounced on Armstrong as “disgraced” and a “cheater,” the fact still remains that he had never tested positive for any banned substances. And if an athlete can be removed from a sport based on heresy and accusation, rather than physical evidence from a positive test, it cheapens the entire process of testing. Tests are put in place to ensure that sports are fair to those who don’t use performance enhancers. But they are also put in place so athletes won’t have to be subjected to innuendo.

Whether you believe Armstrong’s accusers and the USADA, or you believe him, Lance Armstrong’s career in cycling is over, his reputation is tarnished and the record books will show seven gaping holes where once rode a champion.

baseball steroids2

Another Bay Area baseball player suspended for steroids

Bay Area baseball fans got hit with more bad news this week – this time from across the Bay Bridge. Oakland A’s right handed starting pitcher Bartolo Colon was suspended 50 games for testing positive for testosterone, the second player this month to receive the hefty suspension after Giant’s left fielder Melky Cabrera was suspended for the same thing last week.

picture steroids in baseball

steroids in baseball

Colon’s suspension will certainly affect the A’s post season chances as they were 6 games out of first and only 1 game out of a wild card birth for the American League playoffs. In a statement released by the players’ association, Colon apologized to fans and teammates and the A’s organization and accepted responsibility for his actions.

Minor league pitcher Tyson Ross, who was called up from Sacramento when the suspension was announced, will replace Colon.

Ross’ reaction to the suspension and his call up to the big leagues was somewhat ironic, considering the number of Bay Area players, both recent and historicly, who have been caught taking steroids.

“It shocked all of us just the fact someone got caught for that,” he said.

Perhaps Bay Area baseball players should stop being “shocked” about getting caught for steroids. After Canseco, McGuire, Bonds, BALCO, Tejada and now Cabrera and Colon, it seems that Major League Baseball is on to the fact that there isn’t just good weed in the Bay Area, but good steroids, too.



Cabrera suspension highlights steroids continuing allure in MLB

The recent suspension of San Francisco Giants left fielder Melky Cabrera brings the issue of steroid use in Major League Baseball, once again, to the forefront of our national discourse.

Cabrera is the first high-profile player to be suspended for steroid use since Milwaukee Brewers left fielder Ryan Braun was suspended last season, before having that suspension overturned by an arbitrator. Unlike Braun, Cabrera fessed up to using synthetic testosterone after failing two tests. Despite Cabrera’s admission, questions remain. How long was he using before he was caught? How reliable then are the tests for MLB players? And how many other athletes in the league are juicing?

Only Cabrera knows how long he’s been using PEDs and so far hasn’t offered up that information. The MLB commission in charge of testing players has assured the press, the teams and the fans that the random testing is more than reliable. And as for just how many players are using PEDs in baseball, there are conflicting opinions.

In an interview with USA Today following the Cabrera scandal, BALCO founder and admitted steroid distributor Victor Conte said there is “rampant use of synthetic testosterone in Major League Baseball.”

picture steroids in baseball

steroids in baseball


“I would say maybe as much as half of baseball,” Conte said, citing that he has talked with many of the sport’s top players.

Despite Conte’s apparent inside information, MLB isn’t quite sure about Conte’s estimate of steroid use in baseball.

“He is just making that up,” said MLB vice president Rob Manfred. “It’s a guess.”

But Conte disagrees citing his extensive knowledge of how steroids work. (In case you are unfamiliar, Conte was the man behind some of the biggest sports steroid scandals including Barry Bonds and Marion Jones.)

“To circumvent the system is like taking candy from a baby,” Conte said. “The only people that get caught are the dumb and the dumber.”

Testing for steroids is quite simple. Urine is tested for the body’s natural ratio of testosterone to epitestosterone, which is 1 to 1 in adult men. When an abnormality occurs, the sample is then subjected to an isotope ration mass spectrometry test to determine whether the excess testosterone is natural or synthetic.

This seems like a fairly easy system to “duck and dodge,” as Conte put it in his USA Today interview, however there are plenty of reasons to not take his “half of baseball” claim to seriously.

Testing for steroids in MLB started after the league and the players union finally agreed to a test run for random testing of sorts back in 2003. If fiver percent or less of players tested positive, the league wouldn’t make testing part of the contract agreement between the players and MLB. If there were more than five percent, the players would have to agree to random testing the following season. After 1200 players were tested, 104 came up positive, or almost eight percent, so MLB has been randomly testing players since 2004.

Supporters of Major League Baseball’s testing program point out that if only eight percent of players were using steroids before random testing took place, then that number should be less now that the tests are in place and therefore Conte’s assumption that “half of baseball” is juicing is just outrageous.

Conte, of course, would argue that testing has been flawed from the start and that the initial percent of players using steroids in 2003 was much higher, they just didn’t get caught.

Who is right? We may never know, unless MLB and other sports organization can develop a full-proof testing procedure (some argue that baseball doesn’t even want that because homeruns equal ticket sales). What we do know is that players like Cabrera continue to risk expensive suspensions, shame in the media and the ire of fans and still use steroids. They must think they can get away with it for some reason.


A recently discovered human enzyme has shown potential to speed metabolism in mice.

Top 5 fitness science breakthroughs of 2011

by Jeff Clemetson, Editor

As we start the New Year, Steroidology takes a look back at the important scientific studies of 2011 that will impact the way we get in shape in 2012 and beyond. Important studies into weight loss, anti-aging, muscle growth and supplements top this year’s list.

picture of protein powder

Whey powder is proven to build muscle according to a 2011 study.

 #1 Winning with whey’s protein power

In the September issue of the American Journal of Clinical Nutrition, two studies were published that proved what bodybuilders and gym rats have known for a long time – whey protein builds muscle.

The independent studies showed that subjects who ingested whey protein shakes immediately after workouts, showed significantly more muscle mass gains than those who took no protein. These studies also investigated how protein should be ingested after a workout, showing that a large single dose immediately after workouts is far superior to taking small doses over time after workouts. The results showed that consuming whey protein after workouts increased muscle protein synthesis by 33 percent.

#2 Gene tweaking creates mighty mice

The days of taking a pill to become fit without working out are nearly upon us. A joint study by the Salk Institute and two Swiss institutes found a way to manipulate the genome in mice, making them twice as strong without exercise. The scientists were able to locate a genetic inhibitor that may be responsible for deciding our strength. The genome NCoR1 regulates how large our muscles grow and by blocking it, the mice were able to grow muscles twice their normal size.

So far, the science has only worked by manipulating the genes of mice embryos, however the researchers have found no side effects from tweaking the NCoR1 inhibitor and are working on developing chemicals that will act to suppress it in grown adults. This research, besides making us all ripped, can also be used to treat muscular dystrophy and other muscle degenerating diseases.

picture of obese mice

A recently discovered human enzyme has shown potential to speed metabolism in mice.

#3 Human enzyme creates skinny mice

A recent study at Brown University found that the human IKKbeta enzyme increased metabolism and burned fat at prosing levels when introduced to mice. The mice that were engineered to express the human enzyme ate more but gained less weight than the control group of mice who did not receive the enzyme. In addition, the mice with the IKKbeta enzyme had improved insulin function. The study proved that obesity is the main cause of insulin resistance and that the IKKbeta enzyme aids in metabolism. It also discovered that IKKbeta might only effect unwanted fat tissue and not affect other important fat tissues such as the ones found in the liver. These finding are new and research into developing a weight loss drug based on the IKKbeta enzyme are a long way off, but for those seeking a pill to improve metabolism and prevent diabetes, this is a promising lead.

#4 Turning back the clock on your aging body

Two studies published last year backup the claims of many anti-aging experts and give hope and proof to men who want to stay fit for life. The first study looked into the effects of testosterone levels in aging men. The study, published in the Journal of Clinical Endocrinology & Metabolism, found that men over 65 who had more testosterone lost less muscle mass than those with low levels of testosterone. The study looked at 1,183 men over a period of four and a half years. Lead author of the study Erin LeBlanc, MD concluded that the study “adds evidence to the growing body of literature that suggests higher levels of endogenous testosterone may be favorably associated with some key components of healthy aging men.”

picture of older man working out

Working out and testosterone levels have greater impact on health and fitness than age.

The second study, by the KG Jebsen Center of Exercise in Medicine at Norwegian University, found that exercise plays a more important role in health than age. The study followed physically active 50-year-olds and inactive 20-somethings. The study concluded that by increasing exercise, older men could beat back the metabolic syndromes that lead to diabetes, stroke and heart problems. Other findings in the study show that workout intensity is more important than duration and that inactivity for periods of time as a young adult can affect future health greater than previously thought.

#5 Chew your way to loosing weight

A study done by Syracuse University chemist Robert Doyle found that a certain hormone that tells the body that it has a full belly could be ingested orally. The study, published in the online version of the Journal of Medicinal Chemistry, showed that the PYY hormone that is responsible for telling the brain when to stop eating can be ingested into the bloodstream when it is attached to molecules of vitamin B12. The next step is to make a chewing gum or oral tablet that can be used by people who need help loosing weight. And there you have it – possibly the first real fitness product

workout, cycle, stack

How to use steroids: Cycles, stacks, workouts, precautions, diet and more

workout, cycle, stackOne of the most commonly held myths that people have about steroids is that they are easy to use. The belief is that by simply popping a pill or taking an injection, the user will suddenly grow giant muscles. But just like all things in life, building muscles with steroids takes a good deal of hard work, sound information and routine discipline.

Cycles and stacks

The period of time that a person takes steroids is called a cycle. For safety reasons, users should carefully plan their cycles well in advance before starting them. Proper planning includes learning about and obtaining the steroids you will be using in the cycle. When more than one type of steroid is used in a cycle it is called a stack. Stacking different steroids is an effective way to maximize the muscle-building effect of steroids.

Besides learning about and obtaining the steroids you will use in a cycle, you should also learn about and acquire any supplements used to counteract their side effects, both during the cycle and during the post-cycle recovery period. The more steroids you stack into your cycle, the more side effects you will need to counteract. Along with planning what types of steroids you will use during a cycle, you must also plan what type of cycle to use. There are many ways to cycle steroids, and you may want to test them all and make adjustments until you find the ones that work best for you.

Beginner Cycles

For the steroid novice there are additional factors to consider before starting your first cycle. First, you should not take steroids unless your body has stopped growing. For most men, their bodies stop growing at about age 20. Next, you should already be in shape. You should be two to three years into a steady workout routine and you should also be able to dedicate at least another year and a half to your workout. Finally, you should be comfortable with your ability to obtain real steroids and the supplements you may need for their side effects.

Although there are many types of steroids available today, first-time users should always start with a pure testosterone. Since this is the active agent in most steroids, it is important to know how your body will react to it. A dose of 400 mgs per week should be sufficient to notice some real gains throughout a first cycle. Your first cycle should only be 12 weeks long and you should also spend just as much time to recover before starting another cycle.

After your first, you can begin slowly stacking more steroids into your cycles. You should keep the first several cycles at 12 weeks, however, and follow with a post-cycle recovery plan.

Other Popular Cycles *(charts are from pharmaeurope.com)

Once your body has become familiar with steroid intake and you’ve learned which compounds work well for you, you may want to experiment with some different types of cycles and stacks to see if you can maximize your results. Some of the most popular cycles are the three-week blitz, the double-mini cycle, the inverted-pyramid cycle and the diamond cycle.

Three-Week Blitz

In the three-week blitz, each steroid is taken for three weeks. Most blitzes will start with a dose of one steroid before moving on to a stronger dose of another. The first dose is taken for two weeks by itself and on the third week the second compound is started so that the two compounds overlap for one week. The next compound is started during the third week of the second compound and so on and so on until the cycle is complete. The cycle is followed by a two-week recovery with HCG 5000 I.U.

week of



a day (5mg)


250mg amp


2 mg tab


100mg amp


200mg vial

HCG 5000



4 tabs/day


5 tabs/day


6 tabs/day 1 amp/week


1 amps/week


2 amps/week 1 tabs/a day


1 tabs/a day


1 tabs/a day 1 amp/ week


2 amps/week


2 amps/week 1 vial/week


2 vials/week


2 vials/week


1 vial/week


1 amp/week


1 amp/week

Double Mini Cycle

In the double mini cycle, users stack two or three steroids for six weeks. After the first mini cycle, there is a two-week recovery period with HCG 5000 I.U. before the second mini cycle. The second cycle uses the same compounds as the first. After the second mini cycle, the user recovers for two months.

week of cycle


200mg vial


tabs 50mg tab


5000 I.U.


100mg amp


tabs 2mg tab


1 vial/week 1 tab/day


1 vial/week 2 tabs/day


2 vials/week 2 tabs/day


2 vials/week 3 tabs/day


2 vials/week 2 tabs/day


1 vial/week 1 tab/day


1 amp/ week


1 amp/ week


2 amps/week 4 tabs/day


2 amps/week 4 tabs/day


3 amps/week 5 tabs/day


3 amps/week 6 tabs/day


3 amps/week 5 tabs/day


2 amps/week 4 tabs/day

Inverted Pyramid

Because the inverted pyramid cycle begins with a large amount of steroids and decreases until there are very little steroids in the body, it is the cycle choice for many athletes who undergo urine testing. This cycle is not recommended for beginners because it is unsafe for anyone to start using steroids with high doses.

week of



200 mg vial


250 mg amps


2 mg tab


2 vials/week 2 amps/week 8 tabs/day


1,5 vials/week 1,5 amps/week 7 tabs/day


1,5 vials/week 1,5 amps/week 6 tabs/day


1 vial/week 1 amp/week 5 tabs/day


1 vial/week 1 amp/week 4 tabs/day


1 vial/week 1 amp/week 3 tabs/day


0,5 vial/week 0,5 amp/week 2 tabs/day


0,5 vial/week 0,5 amp/week 1 tabs/day

Diamond Cycle

The diamond cycle is the exact opposite of the inverted pyramid cycle. In the diamond cycle, the user begins with a small amount of steroids and increases the dose over time. The dose is then decreased over time until it is back to level it started at. This is a good cycle for users who are not complete novices but are ready to begin trying new cycles.

week of



(5mg tabs)


250mg / amp

HCG 5000

I.U./ 1 cc amp


3 tabs/day 1 amp/week


3 tabs/day 1 amp/week


4 tabs/day 2 amp/week


5 tabs/day 2 amp/week


5 tabs/day 2 amp/week


6 tabs/day 3 amp/week


6 tabs/day 3 amp/week


7 tabs/day 3 amp/week


5 tabs/day 2 amp/week


4 tabs/day 2 amp/week


3 tabs/day 1 amp/week


3 tabs/day 1 amp/week


1 amp/week


1 amp/week


Although the natural bodybuilding world would like you to believe that you can obtain the same amount of muscle mass as pharmaceutically enhanced bodybuilders without using steroids, this is completely false. The gains made by using steroids are far greater than what can be made naturally. However, steroids do not magically grow muscles you must dedicate yourself to a disciplined workout routine to obtain the desired buildup of muscle mass. In fact, working out is absolutely necessary because the steroids can cause excessive bloating and other more pronounced side effects unless you workout enough to burn the body fat and water retention associated with steroid use.

When planning your workouts, there are several factors to consider. First, to kick the body into muscle-building gear and out of its state of homeostasis, you need to plan a high intensity workout. This means you should plan for a workout with few sets that work the muscle until it fails. Large muscle groups will need more sets than small ones, but no more than eight sets are necessary to get the desired results. Your sets should also be consist of a small number of reps. Ten reps should be sufficient for any workout as long as you are using heavy weights. You should increase the weights you lift as you get stronger to keep the workouts stressful on the muscles. If you can easily get through a set and you are not lifting until muscle failure, increase the weight.

While stressful workouts stimulate the muscles, they do not grow until they are at rest. You should only workout one muscle group at a time about once a week and you should always workout every other day to allow the body enough rest time to grow the muscles. Also, after a period of intense training, you should take a few days off to rest and then start a plateau training program that is intended to keep you in shape but not necessarily to gain more mass.

Because it is very likely that you will make gains of 20 pounds or more in a relatively short time, it is important to keep up a regular cardiovascular exercise workout as well to keep the heart in shape to handle the new body mass. Three to four half-hour cardio workouts a week should be sufficient to keep your heart healthy for your new body.


While it is true that Using anabolic steroids will allow the body to grow larger muscles than what your natural genetics will allow, you are still bound by the basic rules of physiology you can not grow more mass unless you intake more mass in your diet. One of the most common reasons why bodybuilders show stagnate gains in their muscle mass is poor nutrition.

Most people have bad habits when it comes to eating, which is why obesity is such a problem today. For bodybuilders, especially those using steroids, a disciplined diet can mean all the difference in the world when it comes to gains in muscle mass. Changing eating habits is hard to do but if you follow these simple guidelines, you can maximize the results of your diet.

Eat more meals per day

Most of us have become indoctrinated to the thee-meal-a-day lifestyle  a large breakfast, hearty lunch and a dinner feast. Unfortunately, this is not an ideal eating schedule for the body and can lead to more unhealthy habits, like skipping lunch because of a large breakfast, for example. By consuming five to six meals throughout the day, the body will begin to release insulin continuously. Insulin carries amino acids, an essential building block of muscles.

Eat regularly

One of the most important aspects of a proper diet is not what you eat but when. The body reacts best when it is kept of a strict schedule. By eating at the same times every day, you will optimize the nutrition of your diet. Because most of us live fairly hectic lives, eating on schedule will require a lot of pre-planning. Be sure to pack brunches, lunches and afternoon snacks ahead of time on busy days and always eat your breakfasts and dinners at the same time.

Increase your caloric intake

The average diet consists of 2,000 to 3,000 calories per day. This is actually quite healthy for most people, and with a little exercise, this diet will keep a person in decent shape. But for those who are using anabolic steroids and are adhering to a strenuous workout regime, the recommended diet is around 5,000 calories per day.

Protein, protein, protein

The most essential part of any bodybuilder’s diet is protein. Because protein breaks down in the and turns into amino acids (the most essential building block for muscles), it is important to maintain a high intake of protein in order to continue growth. The best sources for protein come from meat, fish, eggs and milk. An effective diet for bodybuilders is a protein intake of one to one and a half grams of protein per pound of bodyweight per day. This amount should be adequate enough to maintain a positive nitrogen balance in the muscle cell meaning the cell takes in more protein than it gives out.

Carbs galore

Carbohydrates are an important factor to a proper diet for athletes because they are essential to giving the body energy, maintaining blood-sugar levels and burning fat. A recommended amount of 800 to 900 grams of carbohydrates should be consumed daily. Good sources of complex carbohydrates, which should be about 85 percent of your carbohydrate intake, are whole grains, rice, oats, noodles, pasta and vegetables. Simple carbohydrates, which should be the remaining 15 percent of your carbohydrate intake, come from fruit.

steroid effect on sports

Impact of steroids on sports

picture of steroid effect on sports

Doping scandals, the media would have you believe, will ultimately bring about the destruction of competitive sports. The truth is quite the opposite.

Stripped medals. Congressional hearings. The dreaded asterisk. More so than any single sport or athlete today, the sports world is infatuated with how the use of steroids has infected its ranks. From the homerun records of Bonds, McGuire and Sosa to the Tour de France feats of Lance Armstrong, stories of steroid use, rumored or true, dominate the headlines and cast a shadow over the credibility of today’s athletic achievements. Doping scandals, the media would have you believe, will ultimately bring about the destruction of competitive sports. The truth is quite the opposite.

There is no better example of how steroids have aided, if not saved, professional sports than our own National Pastime – baseball. Following the players strike of 1994, attendance for MLB games was at an all-time low and threatened to bankrupt the sport into oblivion. That was until, in 1998, two players began a well-publicized race to beat one of baseball’s most coveted records – most homeruns in a single season. The excitement over Mark McGuire and Sammy Sosa’s battle for the new record revitalized baseball and turned a corner for the sports future a future that would see more homerun records broken, faster pitching and an all-around elevation to the level of play that brought fans back to the park and kept them there for the new-and-improved, more exciting game of baseball.

For a while, baseball fans were happy to see their sport get bigger and more exciting  until the news that steroids were the fuel to baseballs new fire. In a testament to the old adage that there is no such thing as bad publicity, baseball is still thriving as a sport, despite the negative press that surrounds its biggest stars and their alleged or proven steroid use. Sports talk radio shows and newspaper columns are filled with comments about who’s on what and what should be done about it. The steroid controversy has created a sports soap opera of heroes and villains, and sports fans are eager to fuel the argument from either side. The overall effect of the controversy surrounding steroid use in baseball? Not much different from the overall effect of steroid use in baseball it makes the sport bigger and more exciting.

To those who adamantly oppose steroids in sports, the new game isn’t just bigger and more exciting  it is also unfair. Pointing to the physical advantages of steroid-using athletes, the steroid naysayers make a completely valid point  athletes who use steroids force others to use steroids in order to compete. This is true because of one undeniable fact  steroids work. Steroids allow the body to exceed its genetics and grow to become stronger and larger than normal. Anyone who trains and tries to compete at a natural level would be at a disadvantage if he/she competes with steroid-using athletes. But as pediatrician, medical ethics expert and steroid advocate Dr. Norman Frost said in a recent interview for steroidlaw.com, the answer to the unfair advantage issue with steroids is equal access.

It is not considered immoral to try to gain a competitive advantage, he said. I would put steroids in the long list of things that athletes do to try to win. Better shoes, better equipment, better training, better coaching than the opponent has. If such advantages were not available to all competitors, then the advantage would be unfair.

Equal access to steroids has been a reality for many years and is the very reason why we are now learning about steroid use by so many athletes as the controversy rages on in the media. In a recent NPR sponsored debate over the ethics of steroids in sports, University of Oxford ethics professor Julian Savulescu made the point that performance enhancement is not against the spirit of sport, it’s been a part of sport through its whole history, and to be human is to be better, or at least to try to be better.”

Like it or not, the truth is that better athletes are exactly what performance-enhancing drugs have produced. Since the advent of steroids in sports, athletes have run faster, grown stronger, hit further and jumped higher than any other time in sports history. And as a nation of sports consumers, we’ve come to expect our sports heroes to maintain this level of athleticism. Fans are used to ball games with multiple homeruns or bike races that finish in record time or football games with iron curtain front lines. A return to naturally-fit athletes could be very disappointing. Professional sports, like all businesses, compete for the almighty dollar. And when competing against the memory of the days when games would sometimes feature fie to six homeruns, games with only one or two would seem boring and, once again, clear the bleachers of fans as they seek out more exciting sports.

Although fans cheer when they see their heroes outperform themselves on the field, they cringe at the headlines about them suffering from health problems attributed to steroid use. The truth is that although all drugs contain some inherent risk when taken, the health risks of steroid use by athletes as reported in the media are largely exaggerated and in most cases completely unfounded. A 1996 study by the Harbo UCLA Research and Education Institute and the Charles R. Drew University of Medicine and Science found that subjects taking 600 mgs of injected testosterone over 10 weeks showed virtually no health differences from the control group, other than increased muscle mass and lowered body fat.

Despite the lack of scientific evidence to back up the claim that steroids cause a major health risk, the media still reports all claims of steroid-related health problems as fact. Take the famous interview with Lyle Alzado, the NFL player who developed a brain tumor and claimed … this is what happens when you use anabolic steroids, says Dr. Frost. Nowhere in the article was there a single reference or scientific source for any connection between steroids and brain tumors – because there is none. These stories appear in the leading journalistic media, creating the false impression that the claims are somehow supported by scientific studies.

Scientific studies aside, steroid use in competitive sports is currently banned, the athletes who get caught using them are ostracized and users and dealers of these drugs can face serious criminal charges. But despite the risk to their careers if they get caught taking performance enhancers, many athletes still do. This is because, just like the fans that cheer them, they are impressed by the results they bring. Unless the ban on steroid use is lifted from professional sports, a dark cloud of doubt will continue to hover over the honesty of our athletes. Perhaps we should, instead have an honest debate over whether adult athletes should be given the right to train their bodies as they see fit in order to bring us fans the best possible performance they can deliver.


History of Anabolic/Androgenic Steroids

picture of female swimmer on steriods

The first serious research into the creation of anabolic steroids began in the 1930s

Since their creation in the early 1930’s, steroids have been praised for their effectiveness by users, debated over their safety by medical professionals, outlawed by sport governing bodies, made illegal by governments and demonized by the press and public opinion. But despite steroids well-publicized, controversial history, few people really know a lot about what these substances are, how they work and how their use came to be a controversy in today’s sports.

Anabolic Androgenic Steroids are substances that cause muscles and other male hormonal traits to grow and develop beyond what the body would naturally develop on its own. The term anabolic refers to the buildup of tissue in cells. The term androgenic refers to producing male characteristics, such as large muscles, a deep voice and body hair.

Throughout history, many cultures have used a variety of substances they believed to make men stronger, more viral or even braver in battle. Rhinoceros horn, shark tooth and other various powders and extracts have all been thought to improve strength and ability. It was probably the study of some these ancient cultures use of animal testicles that led modern scientists to the discovery of steroids.

The first serious research into the creation of anabolic steroids began in the 1930s by German chemist Adolf Butenandt, who isolated the male hormone androstenone from thousands of liters of urine. Following the success of those early experiments with androstenone, several teams of scientists, backed by pharmaceutical companies, worked to synthesize the more powerful male hormone testosterone. By 1939, the world’s scientific community was already conducting human trials on the effects of injecting testosterone and the Nobel Prize that year was offered to Butenandt and another scientist, Leopold Ruzicka, for their work with testosterone. Unfortunately for Butenandt, the Nazis wouldn’t allow him to accept the honor.

During the 1940s and 1950s experiments with steroids continued and its use widened among athletes and body builders, especially in the Soviet Union and Eastern Bloc countries. The overwhelming domination by these countries in weightlifting events at the 1952 Olympics, prompted U.S. Olympic Team physician Dr. John Ziegler to begin issuing steroids to his athletes. Dr. Ziegler recruited the help of chemists to develop a compound that would achieve the same results for strength building as the Eastern Bloc countries steroids but with fewer side effects. The result was the first FDA approved steroid Dianabol, a.k.a Dbol.

Studies on the effects of Dianabol and other pharmaceutical anabolic steroid compounds for the next 30 years proved to be inconsistent and in some cases completely incompetent. While some studies would point to the dangerous side effects of steroid use, others would make it seem completely benign. One such study conducted in 1972 showed anabolic steroids as having little to no effect on the body because patients who were given a placebo showed no different results than those who were given real doses of steroids. The results of this study were widely cited as fact for almost two decades, despite the fact that the study only used low doses of steroids in people and had zero control over such aspects as diet, weight or health of the subjects involved.

By the 1960s and 1970s, steroid use by Olympic athletes prompted the ban of its use. A study by BYU faculty member and former world record holder for discus Jay Sylvester, showed that over 68 percent of the athletes at the 1972 Olympics were using or had used steroids. And in 1976, East Germany further created controversy with its women’s track and swim teams when it was discovered that their Wonder Girls (as they came to be known) were taking steroids given to them by their trainers who told them they were vitamins. The heavy use of steroids at these games created new rules and testing procedures for Olympic athletes. However, the testing often proved to be unreliable and athletes found avoiding detection of their steroid use easy.

At the same time steroid use was being condemned by the Olympics, other sports figures and even movie stars were making its use popular. The growing body building industry, fueled by Hollywood images like Arnold Schwarzeneger’s Conan the Barbarian made the muscled look hip and steroids became widely sought after by amateur athletes for the first time.

In professional sports, steroid use was also on the rise, especially in football where size and strength are essential to a player’s effectiveness. But just as in Olympic sports, the backlash to steroid use in professional sports prompted organizations lie the NFL and NBA to adopt anti-steroid rules and screening for players to try and keep their use out of those sports.

In 1991, the government stepped in and made steroids a Schedule III controlled substance, making their non-prescribed possession and distribution illegal and punishable by fines and prison terms. Public backlash to steroid use continued to grow throughout the 1990s, fueled by reports of doping scandals in America’s Pastime Major League Baseball. As reports of baseball’s biggest stars using steroids came to light in the press, the world learned more and more about steroid use and its many new forms.

Today, steroids have taken on new forms. No longer known as just roids, Arnolds, pumpers, stackers and juice the street names of yesterday’s DBol and other testosterone-based substances today’s steroids have taken on more sophisticated titles like performance enhancers and human growth hormone. As more science is put into the creation of these new compounds, testing to make sure professional athletes aren’t juiced has become more and more problematic.

Because steroids are effective in what they do, it may be an uphill battle for sports and society in general to fully regulate and stop their use. The more people are educated on the risks and proper use, however, the safer their use of steroids will become.

picture of pct protocol

PCT Protocol

picture of pct image

250IU or 500IU on two days each week isn’t enough to stave off testicular atrophy,

I advise my AAS patients to use small amounts of HCG (250IU to 500IU) two days each week, right from the beginning of the cycle. This serves to maintain testicular form and function. It makes more sense to me to keep the horse in the barn, so to speak, then to have to chase it across three counties later on. I am also a big fan of maintaining estrogen within physiological ranges. Both therapies have been shown to hasten recovery.

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

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

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

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

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

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

picture of nolvadex

A comprehensive look at modern AAS cycling

A comprehensive look at modern AAS cycling

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

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

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

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

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

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

after 6 weeks, 81 mg of esterified remain.

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

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

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

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

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

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

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


Andropen 275

picture of andropen-275-image



Testosterone Acetate, Testosterone Decanoate, Testosterone
Propionate, Testosterone Phenylpropionate, Testosterone Cypionate
Testosterone + 5 esters
[4-androstene-3-one, 17beta-ol]
Molecular Weight of base: 288.429
Molecular Weight of Acetate ester: 60.0524
Molecular Weight of Propionate ester: 74.0792
Molecular Weight of Phenylpropionate ester: 150.174
Molecular Weight of Cypionate ester: 132.1184
Molecular Weight of Decanoate ester: 172.2668
Formula (base): C19 H28 O2
Formula of Acetate ester: C2 H4 O2
Formula of Propionate ester: C3H6O2
Formula of Phenylpropionate ester:C9 H10 O2
Formula of Cypionate ester: C8 H14 O2
Formula of Decanoate ester: C10 H20 O2

Manufacturer: British DAndropen is a combination of five of testosterones. The presence of the acetate ester allows the testosterone to display a rapid initial physiological response. The other four esters, which release at slower rates, prolong the physiological response with a relatively flat absorption curve over the duation of the injection life-cycle. Testosterone is a male sexual hormone with pronounced, mainly androgenic action, possessing the biological and therapeutic properties of the natural hormone. It is normally produced in women in small physiological quantities. In addition to the specific action that determines the sexual characteristics of the individual, testosterone also has a general anabolic action, manifested in enhancement of protein synthesis. Under the effect of testosterone, body weight increases and urea excretion is reduced. High doses suppress the production of hypophyseal gonadotropin, while low doses stimulate it. It has an antitumor effect on mammary gland metastases

Comes in 10 ml multidose vials. Each vial contains 20 mg per ml of testosterone acetate, 90 mg per ml of testosterone decanoate, 45 mg per ml of testosterone propionate, 45 mg per ml of testosterone phenylpropionate, and 75 mg per ml of testosterone cypionate. Vials come with a purple coloured flip-off top.

Andropen 275 is mixture of five different ester compounds designed specifically for athletes and body builders. It is a great steroid to stack for bulking or cutting, as it will produce results in muscle gain, fat loss, etc. Expect the usual side effects associated with testosterone acne, water retention, gynocomastia, etc. Price wise, Andropen 275 is less expensive than other steroid cocktails but still more than single ester compounds.

Steroid Books

Testosterone for Life

Increased vitality. More muscle. Improved health. Greater mental agility. These are just a few of the life-enhancing benefits that men with low levels of testosterone can experience when they increase their testosterone level. If you’ve noticed a decrease in your sex drive; experienced erectile dysfunction; or felt tired, depressed, and unmotivated, this authoritative, up-to-date guide from an expert at Harvard Medical School will help you determine if you have low testosterone–a surprisingly common but frequently undiagnosed condition among middle-aged men.

The Testosterone Advantage Plan

Wide shoulders, narrow waist, thick chest, muscular arms and legs: today’s male ideal physique is the same as that of ancient Greece. Aerobics and the Food Pyramid just won’t yield that shape, argues Lou Schuler, certified strength-and-conditioning specialist and fitness director of Men’s Health magazine. For weight loss and the Greek physique, he proposes the “T” (testosterone) plan: weightlifting and a diet of 33 percent each carbs (mostly low-glycemic-index), fat (the “good” kind), and protein; no alcohol; and minimal sweets and processed food. The book includes a meal planner, grocery list, and recipes.

The Steroid Bible

The Steroid Bible also contains comprehensive information on Human Growth Hormone, Insulin, Clenbuterol, and other drugs used by bodybuilders and athletes. In addition, The Steroid Bible lets you in on some of the best kept secrets in bodybuilding by allowing you to examine personal training diaries of top bodybuilders that document drugs used, training routines, diets, and results.

Anabolic Steroids and Making Them

A comprehensive compilation of making anabolic steroids from their original patents. A do it yourself manual.

Anabolic Steroids: Ultimate Research Guide

This Anabolic Steroid Research guide will educate you on every aspect of anabolic steroid use. Whether you are a steroid user and need to know everything about how to use them effectively and safely, or you are a researcher who would like to know every thing there is about anabolic steroids in one book, this is the reference guide for you.

Legal Muscle: Anabolics in America

What’s inside? At well over 400 pages, EVERYTHING anyone could ever want to know about steroids and the law! Read the true details of recent anabolic steroid investigations, arrests and prosecutions from all across America.

Dope: A History of Performance Enhancement in Sports

Since the dawn of athletic competition during the original Olympic Games in Ancient Greece, athletes, as well as their coaches and trainers, have been finding innovative ways to gain an edge on their competition. Some of those performance-enhancement methods have been within the accepted rules while other methods skirt the gray area between being within the rules and not, while still other methods break the established rules. In modern times, doping – the use of performance-enhancing drugs – has been one method athletes and their trainers have used to beat their competition.

The Anabolic Steroid Handbook

The ‘Anabolic Steroid Handbook’ is a reference guide to the world of steroids and related topics. Learn first-hand how to chemically enhance your physique and build an awesome body like the pro’s. The information inside this book can turn a weekend trainer into an iron wielding bodybuilding warrior.

Anabolic Steroids Reference Manual

Anabolics 2007: Anabolic Steroids Reference Manual (Hardcover)

Demystifying Steroids

Demystifying Steroids uncovers the “other side” of anabolic steroids and their possible benefits using real case examples from thousands of patients and medical research. This book empowers the reader to discover a new truth about anabolic steroids for themselves. Dr. Jesse Haggard has organized the information into two sections. The first section is easy to read and discusses steroid use in medicine and sports. Popular beliefs about anabolic steroids are challenged, including the dangers of steroid use.


Steroids (Compact Research Series) (Library Binding)

Steroids and Other Performance-Enhancing Drugs

This brief entry in the new Drugs series argues persuasively against anabolic steroid use. Succinct paragraphs focus on popular and once-respected athletes destroyed by steroids, including examples of anonymous abusers who either succumbed to the fatal effects (by dying themselves or killing others because of “roid rage”) or recovered from their addiction.

Anabolic Steroids – A Question of Muscle

What does it mean when it is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgment of trusted physicians for their prescribing recommendations? Where are we to go and be forewarned of the dangers of these prescribing practices?

Anabolic Steroids and the Athlete

The first edition of this work, published in 1982, concentrated on the athlete’s use of and the physician’s knowledge of, anabolic steroids. This fully updated second edition discusses the continuing controversy over their use in competitive sports.


Anabolic Steroid side effects and addiction


Anabolic steroids (AS) are effective in enhancing athletic performance. The trade off, however, is the occurrence of adverse side effects which can jeopardize health. Since AS have effects on several organ systems, a myriad of side effects can be found. In general, the orally administered AS have more adverse effects than parenterally administered AS. In addition, the type of AS is not only important for the advantageous effects, but also for the adverse effects. Especially the AS containing a 17-alkyl group have potentially more adverse affects, in particular to the liver. One of the problems with athletes, in particular strength athletes and bodybuilders, is the use of oral and parenteral AS at the same time (“stacking”), and in dosages which may be several (up to 40 times) the recommended therapeutical dosage. The frequency and severity of side effects is quite variable. It depends on several factors such as type of drug, dosage, duration of use and the individual sensitivity and response.

AS may affect sexual desire. Although few investigations on this issue have been published, it appears that during AS use sexual desire is increased, although the frequency of erectile dysfunction is increased. This may seem contradictory, but sexual appetite is androgen dependent, while erectile function is not. Erectile dysfunction can be caused by many factors, and men who suffer from this condition should speak with their doctor. You may also order Viagra, Cialis and Levitra online without having a prescription in hand through eDrugstore.MD. Simply provide your medical information, and a U.S.-licensed doctor will consider your request for a prescription for FDA-approved, brand-name Viagra, Cialis and Levitra. Since sexual desire and aggressiveness are increased during AS use, the risk of getting involved in sexual assault may be increased.

Liver Function

AS may exert a profound adverse effect on the liver. This is particularly true for orally administered AS. The parenterally administered AS seem to have less serious effects on the liver. Testosterone cypionate, testosterone enanthate and other injectable anabolic steroids seem to have little adverse effects on the liver. However, lesions of the liver have been reported after parenteral nortestosterone administration, and also occasionally after injection of testosterone esters. The influence of AS on liver function has been studied extensively. The majority of the studies involve hospitalized patients who are treated for prolonged periods for various diseases, such as anemia, renal insufficiency, impotence, and dysfunction of the pituitary gland. In clinical trials, treatment with anabolic steroids resulted in a decreased hepatic excretory function. In addition, intra hepatic cholestasis, reflected by itch and jaundice, and hepatic peliosis were observed. Hepatic peliosis is a hemorrhagic cystic degeneration of the liver, which may lead to fibrosis and portal hypertension. Rupture of a cyst may lead to fatal bleeding.

Benign (adenoma’s) and malign tumors (hepatocellular carcinoma) have been reported. There are rather strong indications that tumors of the liver are caused when the anabolic steroids contain a 17-alpha-alkyl group. Usually, the tumors are benign adenoma’s, that reverse after stopping with steroid administration. However, there are some indications that administration of anabolic steroids in athletes may lead to hepatic carcinoma. Often these abnormalities remain asymptomatic, since peliosis hepatis and liver tumors do not always result in abnormalities in the blood variables that are generally used to measure liver function.

AS use is often associated with an increase in plasma activity of liver enzymes such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AP), lactate dehydrogenase (LDH), and gamma glutamyl transpeptidase (GGT). These enzymes are present in hepatocytes in relatively high concentrations, and an increase in plasma levels of these enzymes reflect hepatocellular damage or at least increased permeability of the hepatocellular membrane.

In longitudinal studies of athletes treated with anabolic steroids, contradictory results were obtained on the plasma activity of liver enzymes (AST, AST, LDH, GGT, AP). In some studies, enzymes were increased, whereas in others no changes were found. When increases were found, the values were moderately increased and normalized within weeks after abstinence. There are some suggestions that the occurrence of hepatic enzyme leakage, is partly determined by the pre-treatment condition of the liver. Therefore, individuals with abnormal liver function appear to be at risk.

Anabolic Steroids and the Male Reproductive System

AS are derivatives of testosterone, which has strong genitotropic effects. For this reason, it will not be surprising that side effects include the reproductive system. Application of anabolic steroids leads to supra-physiological concentrations of testosterone or testosterone derivatives. Via the feed back loop, the production and release of luteinizing hormone (LH) and follicle stimulation hormone (FSH) is decreased.

Prolonged use of anabolic steroids in relatively high doses will lead to hypogonadotrophic hypogonadism, with decreased serum concentrations of LH, FSH, and testosterone.

There are strong indications that the duration, dosage, and chemical structure of the anabolic steroids are important for the serum concentrations of gonadotropins. A moderate decrease of gonadotropin secretion causes atrophy of the testes, as well as a decrease of sperm cell production. Oligo, azoospermia and an increased number of abnormal sperm cells have been reported in athletes using AS, resulting in a decreased fertility. After stopping AS use, the gonadal functions will restore within some months. There are indications, however, that it may take several months.

In bodybuilding, where usually high dosages are uses, after stopping steroid use, often choriogonadotropins are administered to stimulate testicular function. The effectiveness of this therapy is unknown.

The various studies suggest that using more than one type of anabolic steroid at the same time (“stacking”) causes a stronger inhibition of the gonadal functions than using one single anabolic steroid. After abstention from anabolic steroids these changes in fertility usually reverse within some months. However, several cases of have been reported in which the situation of hypogonadism lasted for more than 12 weeks.

A well known side effect of AS in males is breast formation (gynecomastia). Gynecomastia is caused by increased levels of circulating estrogens, which are typical female sex hormones. The estrogens estradiol and estrone are formed in males by peripheral aromatization and conversion of AS. The increased levels of circulation estrogens in males stimulate breast growth. In general, gynecomastia is irreversible.

AS may affect sexual desire. Although few investigations on this issue have been published, it appears that during AS use sexual desire is increased, although the frequency of erectile dysfunction is increased. This may seem contradictory, but sexual appetite is androgen dependent, while erectile function is not. Since sexual desire and aggressiveness are increased during AS use, the risk of getting involved in sexual assault may be increased.

Anabolic Steroids and the Female Reproductive System

In the normal female body small amounts of testosterone are produced, and as in males, artificially increasing levels by administration of AS will affect the hypothalamic-pituitary-gonadal axis. An increase in circulating androgens will inhibit the production and release of LH and FSH, resulting in a decline in serum levels of LH, FSH, estrogens and progesterone. This may result in inhibition of follicle formation, ovulation, and irregularities of the menstrual cycle. The irregularities of the menstrual cycle are characterized by a prolongation of the follicular phase, shortening of the luteal phase or amenorrhea. Although these changes are generally more pronounced in younger women, large inter-individual responsiveness to anabolic steroids exists. The effects of AS dosages as generally used in sport, on the hypothalamic-pituitary-gonadal axis in females are hardly studied.

Other side effects of anabolic steroid use in females are increased sexual desire and hypertrophy of the clitoris. The few systematic studies that have been conducted suggest that the effects are similar to the effects in patients, treated with anabolic steroids.

Anabolic steroid use by pregnant women may lead to pseudohermaphroditism or to growth retardation of the female fetus. Anabolic steroid use may even lead to fetal death. However, these side effects have not been studied systematically. It is likely that the severity of the side effects is related to the dosage, duration of use and the type of the drug.

Additional side effects of anabolic steroids specifically in women are acne, hair loss, withdrawal of the frontal hair line, male pattern boldness, lowering of the voice, increased facial hair growth, and breast atrophy. The lowering of the voice, decreased breast size, clitoris hypertrophy and hair loss are generally irreversible. Females using AS may develop masculine facial traits, male muscularity, and coarsening of the skin.

When anabolic steroids are administered in growing children side effects include virilization, gynecomastia, and premature closure of the epiphysis, resulting in cessation of longitudinal growth.

Serum Lipoproteins and the Cardiovascular System

AS also affect the cardiovascular system and the serum lipid profile. Relatively few studies have been done to investigate the effect of anabolic steroids on the cardiovascular system. No longitudinal studies have been conducted on the effect of anabolic steroids on cardiovascular morbidity and mortality.

Most of the investigations have been focused on risk factors for cardiovascular diseases, and in particular the effect of anabolic steroids on blood pressure and on plasma lipoproteins. In most cross-sectional studies serum cholesterol and triglycerides between drug-free users and non-users is not different. However, during anabolic steroid use total cholesterol tends to increase, while HDL-cholesterol demonstrates a marked decline, well below the normal range. Serum LDL-cholesterol shows a variable response: a slight increase or no change. The response of total cholesterol seems to be influenced by the type of training that is done by the athlete. When a great deal of the exercise consists of aerobic exercise, the increasing effect of AS is counterbalanced by an exercise-induced increasing effect, which may result in a net decline in total cholesterol. Aerobic training does not seem to be able to offset the steroid-induced decline in HDL-cholesterol and its subfractions HDL-2, and HDL-3.

The precise effect of anabolic steroids on LDL-cholesterol is unknown yet. It appears that anabolic steroids influence hepatic triglyceride lipase (HTL) and lipoprotein lipase (LPL). Males usually have higher levels of HTL, while females have higher LPL activity. HTL is primarily responsible for the clearance of HDL-cholesterol, while LPL takes care of cellular uptake of free fatty acids and glycerol. Androgens and anabolic steroids stimulate HTL, presumably resulting in decreased serum levels of HDL-cholesterol.

The effect of anabolic steroids on triglycerides is not well known. It is suggested that relatively low doses do not affect the serum triglyceride levels, while it cannot be excluded that higher doses elicit an increase.

No unanimity exists about the influence of anabolic steroids on arterial blood pressure. The response is most probably dose dependent. There is some data suggesting that high doses increase diastolic blood pressure, whereas low doses fail to have a significant effect on diastolic blood pressure. Increases in diastolic blood pressure normalize within 6-8 weeks after abstinence from anabolic steroids. It appears that repeated intermittent use of anabolic steroids does not affect diastolic blood pressure during drug free periods.

There is evidence that the use of anabolic steroids does elicit structural changes in the heart and that the ischemic tolerance is decreased after steroid use. Echocardiographic studies in bodybuilders, using anabolic steroids, reported a mild hypertrophy of the left ventricle, with a decreased diastolic relaxation, resulting in a decreased diastolic filling. Some investigators have associated cardiomyopathy, myocardial infarction, and cerebro-vascular accidents with abuse of anabolic steroids. However, a possible causal relationship could not been proved, because longitudinal studies that are necessary to prove such a relationship, have not been conducted yet. There is convincing evidence that oral administration of anabolic steroids has stronger adverse effects on the mentioned variables than parenteral administration.

Although the effects of anabolic steroids have an unfavorable influence on the risk factors for cardiovascular disease, no data are available about the long term effects. Most of the mentioned effects appear to reverse within 6-8 weeks after abstention. It is unknown, however, whether the structural changes as reported in the heart, are reversible as well.

Psychological Effects

Administration of AS may affect behavior. Increased testosterone levels in the blood are associated with masculine behavior, aggressiveness and increased sexual desire. Increased aggressiveness may be beneficial for athletic training, but may also lead to overt violence outside the gym or the track. There are reports of violent, criminal behavior in individuals taking AS. Other side effects of AS are euphoria, confusion, sleeping disorders, pathological anxiety, paranoia, and hallucinations.

Anabolic steroid users may become dependent on the drug, with symptoms of withdrawal after cessation of drug use. The withdrawal symptoms consist of aggressive and violent behavior, mental depression with suicidal behavior, mood changes, and in some cases acute psychosis. At present it is unknown which individuals are particularly at risk. It is likely that great individual differences in responsiveness may exist. Some individuals try to minimize the withdrawal affects by administration of human choriogonadotropins (hCG), in order to enhance endogenous testosterone production. However, it is unknown in how far the hCG administration is successful in ameliorating the withdrawal effects.

* ROID RAGE (extreme uncontrollable aggression due to high levels of testosterone)
* Irritability..
* Aggressiveness…
* Depression…
* Mood swings…
* Altered libido…
* Psychosis…
* Mental addiction…

Additional Physical Effects
* Cancer…
* Liver Damage…
* Feminizing effects in males (growth of breast tissue)…
* Male attributes in females (deepening of voice, excessive hair growth)…
* Enlarged clitoris…
* Shrunken testicles…
* Limb loss…
* Heart disease/heart attacks…
* Physical addiction…
* HIV/AIDS from the sharing of needles…
* Reduced sperm count…
* Impotence…
* Infertility…
* Baldness…
* Pain and difficulty urinating…
* Enlarged prostate…
* Baldness…
* Smaller Breast in women…
* Menstrual cycle stops…
* Adolescents experience premature closure of the growth plates (stunted growth)…

Possible unwanted side effects (more on http://en.wikipedia.org/wiki/Anabolic_steroid#Possible_unwanted_side_effects)

Many androgens are capable of being metabolized to compounds which can interact with other steroid hormone receptors including the estrogen, progesterone, and glucocorticoid receptors, producing additional (usually) unwanted effects:

* Possible elevated blood pressure
* Cholesterol levels –Some steroids can cause a increase in LDL, and decreased HDL levels[7]. This can cause a increase in risk of cardiovascular disease[8] or coronary artery disease[9] in men with high risk of bad cholesterol.
* Acne– Due to the stimulation of sebaceous gland[10][11]
* Conversion to DHT (Dihydrotestosterone). This can accelerate or cause premature baldness and prostate cancer.
* Altered left ventricle morphology – AAS can induce an unfavourable enlargement and thickening of the left ventricle, which loses its diastolic properties with the mass increase.[12] However the negative relation of left ventricle morphology to decreased cardiac function has been disputed.[13]
* Hepatotoxicity – Caused particularly by oral anabolic steroid compounds which are 17-alpha-alkylated in order to not be destroyed by the digestive system.
* Gingival overgrowth – AAS is closely associated with significant levels of gingival enlargement.[14]

Additional Side Effects

In addition to the mentioned side effects several others have been reported. In both males and females acne are frequently reported, as well as hypertrophy of sebaceous glands, increased tallow excretion, hair loss, and alopecia. There is some evidence that anabolic steroid abuse may affect the immune system, leading to a decreased effectiveness of the defense system. Steroid use decreases the glucose tolerance, while there is an increase in insulin resistance. These changes mimic Type II diabetes. These changes seem to be reversible after abstention from the drugs.

There are some case reports suggesting a causal relationship between anabolic steroid use and the occurrence of Wilms tumor, and prostatic carcinoma. In the literature also sleep apnea has been reported, which has been associated with AS-induced increased in hematocrit, leading to blood stasis and thrombosis.

AS use may affect thyroid function. Administration of AS has been found to decrease thyroid stimulation hormone (TSH), and the products of the thyroid gland. In addition, thyroid binding globulin (TBG). These changes reversed within weeks after discontinuation of AS use.

A serious consequence of AS use may be the multiple drug abuse. On the one hand athletes use different kinds of drugs in an attempt to counterbalance the side effects: hCG, thyroid hormones, anti-estrogens, anti-depressants. On the other hand people try to support the anabolic effects of AS by using additional anabolic hormones as for instance: different types of AS at the same time, growth hormone, insulin, erythropoietine, and clenbuterol. Because most of this takes place outside the official medical circuit, it is likely that these practices may lead to serious conditions.

AS may affect sexual desire. Although few investigations on this issue have been published, it appears that during AS use sexual desire is increased, although the frequency of erectile dysfunction is increased. This may seem contradictory, but sexual appetite is androgen dependent, while erectile function is not. Erectile dysfunction can be caused by many factors, and men who suffer from this condition should speak with their doctor. You may also order Viagra, Cialis and Levitra online without having a prescription in hand through eDrugstore.MD. Simply provide your medical information, and a U.S.-licensed doctor will consider your request for a prescription for FDA-approved, brand-name Viagra, Cialis and Levitra. Since sexual desire and aggressiveness are increased during AS use, the risk of getting involved in sexual assault may be increased.

Other Sources PDF Downloads
Steroid Abuse and Addiction – Download
NIDA InfoFacts: Steroids (Anabolic-Androgenic) – Download

(not referred to in the above review)

1. Alen, M., P. Rahkila. Anabolic-androgenic steroid effects on endocrinology and lipid metabolism in athletes. Sports Med. 6: 327-332, 1988

2. American College of Sports Medicine. Position stand on the use of anabolic-androgenic steroids in sport. Med. Sci. Sports Exerc. 19(5): 534-539, 1987

3. Bahrke, M.S., C.E. Yesalis, J.E. Wright. Psychological and behavioral effects of endogenous testosterone levels and anabolic-androgenic steroids among athletes; a review. Sports Med. 10(5): 303-337, 1990

4. Cohen, J.C., R. Hickman. Insulin resistance and diminished glucose tolerance in power lifters ingesting anabolic steroids. J. Clin. Endocrinol. Metab. 64: 960-963, 1987

5. De Piccoli, B., F. Giada, A. Benettin, F. Sartori, E. Piccolo. Anabolic steroid use in body builders: an echocardiographic study of left ventricular morphology and function. Int. J. Sports Med. 12(4): 408-412, 1991

6. Haupt, H.A. Anabolic steroids and growth hormone. Am. J. Sports Med. 21(3): 468-474, 1993

7. Wilson, J.D. Androgen abuse in athletes. Endocr. Rev. 9(2): 181-199, 1988


Anabolic Steroids- News

picture of steroids_news

In light of these hazards, measures to curtail the use of anabolic steroids are escalating



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

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

What are anabolic steroids?

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

How are steroids taken?

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

Who takes anabolic steroids and why?

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

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

What are the health hazards of anabolic steroids?

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

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

Physical side effects

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

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

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

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

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

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

Special dangers to adolescents

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

Behavioral side effects

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

Are anabolic steroids addictive?

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



Clomid: Frequently Asked Questions

picture of clomid

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

by The Iron Game

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

Question: What is Clomid?

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

Question: Why Should Bodybuilders use Clomid?

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

Question: Does Clomid also work as an anti estrogen?

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

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

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

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

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

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

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

Anadrol/Anapolan: 8 – 12 hours after last administration

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

Dianabol: 4 – 8 hours after last administration

Equipoise: 3 weeks after last injection

Fina: 3 days after last injection

Primobolan depot: 10 – 14 days after last injection

Sustanon: 3 weeks after last injection

Testosterone Cypionate: 2 weeks after last injection

Testosterone Enanthate: 2 weeks after last injection

Testosterone Propionate: 3 days after last injection

Testosterone Suspension: 4 – 8 hours after last administration

Winstrol: 8 – 12 hours after last administration

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

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

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

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

Question: How cheap is Clomid?

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

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

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

Gynecomastia: Etiology, Diagnosis, And Treatment

by H. Hajdo Everything you need to know about gyno.BREAST DEVELOPMENT

Male breast development occurs in an analogous fashion to female breast development. At puberty in the female breast, complex hormonal interplay occurs resulting in growth and maturation of the adult female breast.

In early fetal life, epithelial cells, derived from the epidermis of the area programmed to later become the areola, proliferate into ducts, which connect to the nipple at the skin’s surface. The blind ends of these ducts bud to form alveolar structures in later gestation. With the decline in fetal prolactin, placental estrogen and progesterone at birth, the infantile breast regresses until puberty (13).

During thelarche, the initial clinical appearance of the breast bud, growth and division of the ducts occur, eventually giving rise to club-shaped terminal end buds, which then form alveolar buds. Approximately a dozen alveolar buds will cluster around a terminal duct, forming the type 1 lobule. Eventually, the type 1 lobule will mature into types 2 and 3 lobules, called ductules, by increasing its number of alveolar buds to as many as 50 in type 2 and 80 in type 3 lobules. The entire differentiation process takes years after the onset of puberty and, if pregnancy is not achieved, may never be completed (38).


The initiation and progression of breast development involves a coordinated effort of pituitary and ovarian hormones, as well as local mediators (see Figure).

<!–[if !vml]–><!–[endif]–>


Estrogen and progesterone act in an integrative fashion to stimulate normal adult female breast development. Estrogen, acting through its ER a receptor, promotes duct growth, while progesterone, also acting through its receptor (PR), supports alveolar development (13). This is demonstrated by experiments in ER a knockout mice which display grossly impaired ductal development, whereas the PR knockout mice possess significant ductal development, but lack alveolar differentiation (25,6).

Although estrogens and progestogens are vital to mammary growth, they are ineffective in the absence of anterior pituitary hormones (13). Thus, neither estrogen alone nor estrogen plus progesterone can sustain breast development without other mediators, such as GH and IGF-1, as confirmed by studies involving the administration of estrogen and GH to hypophysectomized and oophorectomized female rats, which resulted in breast ductal development. The GH effects on ductal growth are mediated through stimulation of IGF-1. This is demonstrated by studies of estrogen and GH administration to IGF-1 knockout rats that showed significantly decreased mammary development when compared to age-matched IGF-1- intact controls. Combined estrogen and IGF-1 treatment in these IGF-1 knockout rats restored mammary growth. (21, 36). In addition, Walden et al. demonstrated that GH-stimulated production of IGF-1 mRNA in the mammary gland itself, suggesting that IGF-1 production in the stromal compartment of the mammary gland acts locally to promote breast development (43). Furthermore, other data indicates that estrogen promotes GH secretion and increased GH levels, stimulating the production of IGF-1, which synergizes with estrogen to induce ductal development.

Like estrogen, progesterone has minimal effects in breast development without concomitant anterior pituitary hormones; again indicating that progesterone interacts closely with pituitary hormones. For example, prolonged treatment of dogs with progestogens such as depot medroxyprogesterone acetate or with proligestone caused increased GH and IGF-1 levels, suggesting that progesterone may also have an effect on GH secretion (29). In addition, clinical studies have correlated maximal cell proliferation to specific phases in the female menstrual cycle. For example, maximal proliferation occurs not during the follicular phase when estrogens reach peak levels and progesterone is low (less than 1 ng/mL[3.1nmol}), but rather, it occurs during the luteal phase when progesterone reaches levels of 10-20 ng/mL (31- 62nmol) and estrogen levels are two to three times lower than in the follicular phase (38). Furthermore, immunohistochemical studies of ER and PR showed that the highest percentage of proliferating cells, found almost exclusively in the type 1 lobules, contained the highest percentage of ER and PR positive cells (38). Similarly, there is immunocytological presence of ER, PR, and androgen receptors (AR) in gynecomastia and male breast carcinoma. ER, PR and AR expression was observed in 100% (30/30) of gynecomastia cases (37). Given these data and the fact that PR knockout mice lack alveolar development in breast tissue, it appears as if progesterone, analogous to estrogen, may increase GH secretion and act through its receptor on mammary tissue to enhance breast development, specifically alveolar differentiation (25, 16).

Prolactin is another anterior pituitary hormone integral to breast development. Prolactin is not only secreted by the pituitary gland but may be produced in normal mammary tissue epithelial cells and breast tumors. (39, 23). Prolactin stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobulo-alveolar differentiation only with concomitant progesterone.


Estrogen effects on the breast may be the result of either circulating estradiol levels or locally produced estrogens. Aromatase P450 catalyzes the conversion of the C19 steroids, androstenedione, testosterone, and 16-a-hydroxyandrostenedione to estrone, estradiol-17b and estriol. As such, an overabundance of substrate or an increase in enzyme activity can increase estrogen concentrations and thus initiate the cascade to breast development in females and males. For example, in the more complete forms of androgen insensitivity syndromes in genetically male (XY) patients, excess androgen aromatizes into estrogen resulting in not only gynecomastia, but also a phenotypic female appearance. Furthermore, the biologic effects of over expression of the aromatase enzyme in female and male mice transgenic for the aromatase gene result in increased breast proliferation. In female transgenetics, over expression of aromatase promotes the induction of hyperplastic and dysplastic changes in breast tissue. Over expression of aromatase in male transgenics caused increased mammary growth and histologic changes similar to gynecomastia, an increase in estrogen and progesterone receptors and an increase in downstream growth factors such as TGF-beta and bFGF (15). Thus, although androgens do not stimulate breast development directly, they may do so if they aromatize to estrogen. This occurs in cases of androgen excess or in patients with increased aromatase activity.

PHYSIOLOGIC gynecomastia gynecomastia, breast development in males, can occur normally during three phases of life. The first occurs shortly after birth in both males and females. This is caused by the high levels of estradiol and progesterone produced by the mother during pregnancy, which stimulates newborn breast tissue. It can persist for several weeks after birth and can cause mild breast discharge called “witch’s milk” (38).

Puberty marks the second situation in which gynecomastia can occur physiologically. In fact, up to 60% of boys have detectable gynecomastia by age 14. Although it is mostly bilateral, it can occur unilaterally, and usually resolves within 3 years of onset (38). Interestingly, in early puberty, the pituitary gland releases gonadotropins in order to stimulate testicular production of testosterone mostly at nighttime. Estrogens, however, rise throughout the entire day. Some studies have shown that a decreased androgen to estrogen ratio exists in boys with pubertal gynecomastia when compared with boys who do not develop gynecomastia (30). Furthermore, another study showed increased aromatase activity in the skin fibroblasts of boys with gynecomastia. Thus, the mechanism by which pubertal gynecomastia occurs may be due to either decreased production of androgens or increased aromatization of circulating androgens, thus increasing the estrogen to androgen ratio (26).

The third age range in which gynecomastia is frequently seen is during older age (>60 years). Although the exact mechanisms by which this can occur have not been fully elucidated, evidence suggests that it may result from increased peripheral aromatase activity secondary to the increase in total body fat, coupled with mild hypogonadism associated with aging. For instance, investigators have shown increased urinary estrogen levels in obese individuals, and have demonstrated aromatase expression in adipose tissue (32). Thus, like the gynecomastia of obesity, the gynecomastia of aging may partly result from increased aromatase activity, causing increased circulating estrogen levels (7). Moreover, not only does total body fat increase with age, but there may be an increase in aromatase activity in the adipose tissue already present, increasing circulating estrogens even further. Lastly, SHBG increases with age in men. Since SHBG binds estrogen with less affinity than testosterone, the bioavailable estradiol to bioavailable testosterone ratio may increase in the obese older male.


Since the development of breast tissue in males occurs in an analogous manner to that in females, the same hormones that affect female breast tissue can cause gynecomastia. The testes secrete only 6-10 mg of estradiol and 2.5 mg of estrone per day. Since this only comprises a small fraction of estrogens in circulation (i.e. 15% of estradiol and 5% of estrone), the remainder of estrogen in males is derived from the extraglandular aromatization of testosterone and androstenedione to estradiol and estrone, respectively (27). Thus, any cause of estrogen excess from overproduction to peripheral aromatization of androgens can initiate the cascade to breast development.


Testicular tumors can lead to increased blood estrogen levels by: estrogen overproduction; androgen overproduction with aromatization in the periphery to estrogens; and by ectopic secretion of gonadotropins which stimulate otherwise normal Leydig cells. Tumors causing an overproduction of estrogen represent an unusual but important cause of estrogen excess. Examples of estrogen-secreting tumors include: Leydig cell tumors, Sertoli cell tumors, granulosa cell tumors and adrenal tumors.

Interstitial cell tumors, or Leydig cell tumors constitute 1%-3% of all testis tumors. Usually, they occur in men between the ages of 20 and 60, although up to 25% of them occur prepubertally. In prepubertal cases, isosexual precocity, rapid somatic growth, and increased bone age with elevated serum testosterone and urinary 17-ketosteroid levels are the presenting features. In adults, elevated estrogen levels coupled with a palpable testicular mass and gynecomastia may develop. Though mostly benign, Leydig cell tumors may be malignant and metastasize to lung, liver, and retroperitoneal lymph nodes (34, 14).

Sertoli cell tumors comprise less than 1% of all testicular tumors and occur at all ages, but one third have occurred in patients less than 13 years, usually in boys under 6 months of age. Although they arise in young boys, they usually do not produce endocrinologic effects in children. Again, the majority are benign, but up to 10% are malignant. gynecomastia occurs in one third of cases, presumably due to increased estrogen production (34).

Granulosa cell tumors, which occur very rarely in the testes, can also overproduce estrogen. In fact, only eleven cases have been reported with gynecomastia as a presenting feature in half of them (28).

Germ cell tumors are the most common cancer in males between the ages of 15 and 35. They are divided into seminomatous and nonseminomatous subtypes and include embryonal carcinoma, yolk sac carcinoma, choriocarcinoma and teratomas. Elevated alpha fetoprotein (AFP) and b HCG function as reliable markers in some tumors. As a result of the increased b HCG, acting analogously to LH to stimulate the Leydig cell LH receptor, testicular estrogen production is also increased, which, in turn, can cause gynecomastia. Although germ cell tumors generally arise in the testes, they can also originate extra-gonadally, specifically in the mediastinum. These extragonadal tumors also possess the capability of producing b HCG, but they must be differentiated from a multitude of other tumors such as large cell carcinomas of the lung which can synthesize ectopic b HCG (31).

Some neoplasms that overproduce estrogens also possess aromatase overactivity. Sertoli Cell tumors in boys with Peutz-Jegher syndrome, an autosomal dominant disease characterized by pigmented macules on the lips, gastrointestinal polyposis and hormonally active tumors in males and females, for instance, have repeatedly demonstrated aromatase overactivity, resulting in gynecomastia, rapid growth and advanced bone age as presenting features (18, 44, 10). Feminizing Sertoli cell tumors with increased aromatase activity can also be seen in the Carney complex, an autosomal dominant disease characterized by cardiac myxomas, cutaneous pigmentation, adrenal nodules and hypercortisolism. Other than sex-cord tumors, fibrolamellar hepatocellular carcinoma has also been shown to possess ectopic aromatase activity, causing severe gynecomastia in a 17-year-old boy (2). Furthermore, adrenal tumors can secrete excess dehydroepiandrosterone (DHEA), DHEA-sulfate (DHEAS) and androstenedione which can then be aromatized peripherally to estradiol.

<!–[if !vml]–><!–[endif]–>



Besides tumors, other conditions have been associated with excessive aromatization of testosterone and androgens to estrogen, which results in gynecomastia. For instance, a familial form of gynecomastia has been discovered, in which affected family members have an elevation of extragonadal aromatase activity (5). As stated, obesity may cause estrogen excess through increased aromatase activity in adipose tissue. Furthermore, hyperthyroidism induces gynecomastia through several mechanisms, including increased aromatase activity (38).


Another cause of gynecomastia from estrogen excess includes steroid displacement from sex-hormone binding globulin (SHBG). SHBG binds androgens more avidly than estrogen. Thus, any condition or drug that can displace steroids from SHBG, will more easily displace estrogen, allowing for higher circulating levels of estrogen. Drugs can cause gynecomastia by numerous mechanisms besides displacement from SHBG. These drugs and their mechanisms will be addressed in a subsequent section.


Breast development requires the presence of estrogen. Androgens, on the other hand oppose the estrogenic effects. Thus, an equilibrium exists between estrogen and androgens in the adult male to prevent growth of breast tissue, whereby either an increase in estrogen or a decrease in androgen can tip the balance toward gynecomastia. Increased estrogen levels will increase glandular proliferation by several mechanisms. These include direct stimulation of glandular tissue and by suppressing LH, therefore decreasing testosterone secretion by the testes and exaggerating the already high estrogen to androgen ratio.

Besides increased estrogen production, decreased testosterone levels can cause an elevation in the estrogen to androgen ratio, producing gynecomastia. Primary hypogonadism, with its reduction in serum testosterone and increased serum LH levels increases testicular estradiol production and is associated with an increased estrogen to androgen ratio. Klinefelter’s syndrome, occurring in 1 in 500 males who possess an XXY karyotype and primary testicular failure, features gynecomastia as well, again presumably secondary to decreased testosterone production, compensatory increased LH secretion, overstimulation of the Leydig cells and relative estrogen excess. In addition, any acquired testicular disease resulting in primary hypogonadism such as viral and bacterial orchitis, trauma, or radiation can also promote gynecomastia by the same mechanisms (27). Lastly, enzyme deficiencies in the testosterone synthesis pathway from cholesterol also result in depressed testosterone levels and hence a relative increase in estrogen. Deficiency of 17-oxosteroid reductase, the enzyme that catalyzes the conversion of androstenedione to testosterone and estrone and estrone to estradiol, for example, will cause elevation in estrone and androstenedione, which is then further aromatized to estradiol (7).

Secondary hypogonadism, if severe enough, results in low serum testosterone and unopposed estrogen effect from increased conversion of adrenal precursors to estrogens (27). Thus, patients with Kallmann’s syndrome, a form of congenital secondary hypogonadism with anosmia, also develop gynecomastia. In fact, hypogonadism from whatever cause constitutes most cases of gynecomastia.

The androgen resistance syndromes, including complete and partial testicular feminization (e.g. Reifenstein’s syndrome) are characterized by gynecomastia and varying degrees of pseudohermaphroditism. Kennedy Syndrome, a neurodegenerative disease, is also associated with decreased effective testosterone due to a defective androgen receptor (38). The gynecomastia is the combined result of decreased androgen responsiveness at the breast level and increased estrogen levels as a result of elevated androgen precursors of estradiol and estrone. As such, androgens in these diseases are not recognized by the peripheral tissues including the breast and pituitary. Androgen resistance at the pituitary results in elevated serum LH levels and increased circulating testosterone. The increased serum testosterone is then aromatized peripherally, promoting gynecomastia. Thus, gynecomastia is the result of increased estradiol levels which arise due to unopposed androgen unresponsiveness.


Other disease states have also resulted in gynecomastia.

Men with end stage renal disease may have reduced testosterone, and elevated gonadotropins. This apparent primary testicular failure may then lead to increased breast development (16).

The gynecomastia of liver disease, particularly cirrhosis, does not have a clear etiology. Some have speculated that the gynecomastia is the result of estrogen overproduction, possibly secondary to increased extraglandular aromatization of androstenedione, which may have decreased hepatic clearance in cirrhotics. However, testosterone administration to cirrhotics causes a rise in estradiol, but decreases the prevalence of gynecomastia (11, 3, 33). Therefore, although the association of gynecomastia with liver disease is apparent, current data are conflicting and the mechanism by which this occurs remains unclear.

As previously stated, thyrotoxicosis is associated with gynecomastia. Patients often have elevated estrogen which may result from a stimulatory effect of thyroid hormone on peripheral aromatase. Testosterone may also be increased possibly due to thyroid-hormone-stimulated increase in SHBG, as free testosterone is usually normal. Since SHBG binds testosterone more avidly than estradiol, there is a higher ratio of free estradiol to free testosterone. Thus, with normal testosterone and increased estrogen, there is an elevated estrogen to testosterone ratio. In addition, LH is also increased, which may also stimulate testicular estrogen synthesis (16, 9). gynecomastia can also follow spinal cord disorders. Most patients with spinal cord disorders display depressed testosterone levels and, in fact, can develop testicular atrophy with resultant hypogonadism and infertility. Some have speculated that this may result from recurrent urinary tract infections, increased scrotal temperature, and a neuropathic bladder, which ultimately cause acquired primary testicular failure. The exact mechanism, however, remains elusive (17).

Refeeding gynecomastia refers to breast development in men recovering from a malnourished state (13). Although most cases regress within seven months, the etiology of this phenomenon has not been fully elucidated.

HIV patients can also develop gynecomastia. There is a high incidence of androgen deficiency due to multifactorial causes, including primary and secondary hypogonadism (27).


A significant percentage of gynecomastia is caused by medications or exogenous chemicals that result in increased estrogen effect. This may occur by several mechanisms: 1) they possess intrinsic estrogen-like properties, 2) they increase endogenous estrogen production, or 3) they supply an excess of an estrogen precursor (e.g. testosterone or androstenedione) which can be aromatized to estrogen. Examples of drugs that cause gynecomastia are listed in Tables 2 and 3. Contact with estrogen vaginal creams, for instance, can elevate circulating estrogen levels. These may or may not be detected by standard estrogenic qualitative assays. An estrogen-containing embalming cream has been reported to cause gynecomastia in morticians (4, 12). Recreational use of marijuana, a phytoestrogen, has also been associated with gynecomastia. It has been suggested that digitalis causes gynecomastia due to its ability to bind to estrogen receptors (16, 35). The appearance of gynecomastia has been described in body builders and athletes after the administration of aromatizable androgens. The gynecomastia was presumably caused by an excess of circulating estrogens due to the conversion of androgens to estrogen by peripheral aromatase enzymes (8).

Drugs and chemicals that cause decreased testosterone levels either by causing direct testicular damage, by blocking testosterone synthesis, or by blocking androgen action can produce gynecomastia. For instance, chemotherapeutic drugs, such as alkylating agents, cause Leydig cell and germ cell damage, resulting in primary hypogonadism. Flutamide, an anti-androgen used as treatment for prostate cancer, blocks androgen action in peripheral tissues, while cimetidine blocks androgen receptors. Ketoconazole, on the other hand, can inhibit steroidogenic enzymes required for testosterone synthesis. Spironolactone causes gynecomastia by several mechanisms. Like ketoconazole, it can block androgen production by inhibiting enzymes in the testosterone synthetic pathway (i.e. 17a hydroxylase and 17-20-desmolase), but it can also block receptor-binding of testosterone and dihydrotestosterone (40). In addition to decreasing testosterone levels and biologic effects, spironolactone also displaces estradiol from SHBG, increasing free estrogen levels. Ethanol increases the estrogen to androgen ratio and induces gynecomastia by multiple mechanisms as well. Firstly, it is associated with increased SHBG, which decreases free testosterone levels. Secondly, it increases hepatic clearance of testosterone, and thirdly, it has a direct toxic effect on the testes themselves (27). Unfortunately, besides the drugs stated, a multitude of others cause gynecomastia by unknown mechanisms (Table 3).

<!–[if !vml]–><!–[endif]–>

Table 3. Drugs that cause gynecomastia by uncertain mechanisms:
Cardiac and antihypertensive medications:
Calcium channel blockers (verapamil, nifedipine, diltiazem)
ACE Inhibitors (captopril, enalapril
b blockers

Psychoactive drugs:
Tricyclic antidepressants
Drugs for infectious diseases:

Drugs of Abuse:



Male breast cancer is rare and comprises only 0.2 percent of all male cancers. Although uncommon, it has been associated with gynecomastia and necessitates inclusion in the differential diagnosis. Other risks include Klinefelter’s syndrome, exogenous estrogen exposure, family history, and testicular disorders. It is unclear if these are specific risks for breast cancer are linked to the stimulatory process responsible for gynecomastia. New evidence suggests obesity and consumption of red meat may also raise the risk for the development of male breast cancer (19).



At presentation, all patients require a thorough history and physical exam. Particular attention should be given to medications, drug and alcohol abuse, as well as other chemical exposures. Symptoms of underlying systemic illness, such as hyperthyroidism, liver disease, or renal failure should be sought. Furthermore, the clinician must recall neoplasm as a possible etiology and should establish the duration and timing of breast development. Obviously, rapid breast growth that has occurred recently is more concerning than chronic gynecomastia. Additionally, the clinician should inquire about fertility, erectile dysfunction and libido to rule out hypogonadism, either primary or secondary, as a potential cause.

In our experience, the breast examination is best performed with the patient supine and with the examiner palpating from the periphery to the areola. The glandular mass should be measured in diameter. gynecomastia is diagnosed by finding subareolar breast tissue of 2 cm in diameter or greater. Malignancy is suspected if an immobile firm mass is found on physical examination. Skin dimpling, nipple retraction or discharge, and axillary lymphadenopathy further support malignancy as a possible diagnosis.

A thorough testicular exam is essential. Bilaterally small testes imply testicular failure, while asymmetric testes or a testicular mass suggest the possibility of neoplasm. Visual field impairment may suggest pituitary disease. Physical findings of underlying systemic conditions such as thyrotoxicosis, HIV disease, liver, or kidney failure should also be assessed.


All patients who present with gynecomastia should have serum testosterone, estradiol, LH and b HCG measured. Further testing should be tailored according to the history, physical examination and the results of these initial tests. An elevated b HCG or a markedly elevated serum estradiol suggests neoplasm and a testicular ultrasound is warranted to identify a testicular tumor, keeping in mind, however, that other non-testicular tumors can also secrete b HCG. A low testosterone level, with an elevated LH and normal to high estrogen level indicates primary hypogonadism. If the history suggests Klinefelter’s Syndrome, then a karyotype should be performed for definitive diagnosis. Low testosterone, low LH and normal estradiol levels imply secondary hypogonadism, and hypothalamic or pituitary causes should be sought. If testosterone, LH and estradiol levels are all elevated, then the diagnosis of androgen resistance should be entertained. Liver, kidney and thyroid function should be assessed if the physical examination suggests liver failure, kidney failure, or hyperthyroidism, respectively. Furthermore, if examination of breast tissue suggests malignancy, a biopsy should be performed. This is of particular importance in patients with Klinefelter’s syndrome, who have an increased risk of breast cancer.


Treatment of the underlying endocrinologic or systemic disease that has caused gynecomastia is mandatory. Testicular tumors, such as Leydig cell, Sertoli cell or granulosa cell tumors should be surgically removed. In addition to surgery, germ cell tumors are further managed with chemotherapy involving cisplatin, bleomycin and either vinblastine or etoposide (34, 14). Should underlying thyrotoxicosis, renal or hepatic failure be discovered, appropriate therapy should be initiated. Medications that cause gynecomastia should also be discontinued whenever possible based on their role in management of the underlying condition. Of course, if a breast biopsy indicates malignancy, then mastectomy should be performed.

If no pathologic abnormality is detected, then appropriate treatment is close observation. A careful breast exam should be done initially every 3 months until the gynecomastia regresses or stabilizes, after which a breast exam can be performed yearly. It is important to remember that some cases of gynecomastia, especially that which occurs in pubertal boys, can resolve spontaneously.


If the gynecomastia is severe, does not resolve, and does not have a treatable underlying cause, some medical therapies may be attempted. These include testosterone, dihydrotestosterone, danazol, clomiphene citrate, tamoxifen and the aromatase inhibitor testolactone. Testosterone treatment of hypogonadal men with gynecomastia often fails to produce breast regression once gynecomastia is established. Unfortunately, testosterone treatment may actually produce the side effect of gynecomastia by being aromatized to estradiol. Thus, although testosterone is used to treat hypogonadism, its use to specifically counteract gynecomastia is limited (42). Dihydrotestosterone, a non-aromatizable androgen, has been used in patients with prolonged pubertal gynecomastia with good response rates (22). Since dihydrotestosterone is given either intramuscularly or percutaneously, this may restrict its usefulness. Danazol, a weak androgen that inhibits gonadotropin secretion, resulting in decreased serum testosterone levels, has been studied in a prospective placebo-controlled trial, whereby gynecomastia resolved in 23 percent of the patients, as opposed to 12 percent of the patients on placebo (20). Unfortunately, undesirable side effects including edema, acne, and cramps have limited its use (27). Investigators have reported a 64 percent response rate with 100 mg/day of clomiphene citrate, a weak estrogen and moderate antiestrogen (24). Lower doses of clomiphene have shown varied results, indicating that higher doses may need to be administered, if clomiphene is to be attempted. tamoxifen, also an antiestrogen, has been studied in 2 randomized, double-blind studies in which a statistically significant regression in breast size was achieved, although complete regression was not documented (1). One study compared tamoxifen with danazol in the treatment of gynecomastia. Although patients taking tamoxifen had a greater response with complete resolution in 78 percent of patients treated with tamoxifen, as compared to only a 40 percent response in the danazol-treated group, the relapse rate was higher for the tamoxifen group (41). Although complete breast regression may not be achieved and a chance of recurrence exists with therapy, tamoxifen, due to relatively lower side effect profile, may be a more reasonable choice when compared to the other therapies. If used, tamoxifen should be given at a dose of 10 mg twice a day for at least 3 months (27). An aromatase inhibitor, testolactone, has also been studied in an uncontrolled trial with promising effects (45). Further studies must be performed on this drug before any recommendations can be established on its usefulness in the treatment of gynecomastia.


When medical therapy is ineffective, particularly in cases of longstanding gynecomastia, or when the gynecomastia interferes with the patient’s activities of daily living, then surgical therapy is appropriate. This includes removal of glandular tissue coupled with liposuction, if needed. In our experience, uses of delicate cosmetic surgical techniques are warranted to prevent unsightly scarring.


In summary, gynecomastia is a relatively common disorder. The causes of its development range vastly from benign physiologic processes to rare neoplasms. Thus, in order to properly diagnose the etiology of the gynecomastia, the clinician must understand the hormonal factors involved in breast development. Parallel to female breast development, estrogen, along with GH and IGF-1 is required for breast growth in males. Since a balance exists between estrogen and androgens in males, any disease state or medication that can increase circulating estrogen or decrease circulating androgen, causing an elevation in the estrogen to androgen ratio, can induce gynecomastia. Due to the diversity of possibly etiologies, including neoplasm, performing a careful history and physical is imperative. Once gynecomastia has been diagnosed, treatment of the underlying cause is warranted. If no underlying cause is discovered, then close observation is appropriate. If the gynecomastia is severe, however, medical therapy can be attempted and if ineffective, glandular tissue can be removed surgically.


1. Alagaratnam TT: Idiopathic gynecomastia treated with tamoxifen; a preliminary report. Clin Ther 9:483-7, 1987

2. Agarwal VR, Takayama K, Van Wyk JJ, Sasano H, Simpson ER, Bulun SE: Molecular Basis of Severe gynecomastia Associated with Aromatase Expression in a Fibrolamellar Hepatocellular Carcinoma. Journal of Clinical Endocrinology and Metab 83(5): 1797-1800, 1988

3. Bahnsen M, Gluud C, Johnsen SG: Pituitary-testicular Function in Patients with Alcoholic Cirrhosis of the Liver. European Journal of Clinical Investigation 11: 473-479, 1981.

4. Bhat N, Rosato E, Gupta P: gynecomastia in a mortician: A case report. Acta Cytol 34:31, 1990.

5. Berkovitz GD, Guerami, Brown TR, MacDonald PC Migeon CJ: Familial gynecomastia with Increased Extraglandular Aromatization of Plasma Carbon 19-Steroids. Journal of Clinical Investigation 75: 1763-1769, 1985.

6. Bocchinfuso WP, Korach KS: Mammary Gland Development and Tumorigenesis in Estrogen Receptor Knockout Mice. Journal of Mammary Gland Biology and Neoplasia 90: 323-334, 1997.

7. Braunstein: Aromatase and gynecomastia. Endocrine-Related Cancer 6: 315-324, 1999.

8. Calzada L, Torres-Calleja JM, Martinez N: Measurement of Androgen and Estrogen Receptors in Breast Tissue from Subjects with Anabolic Steroid-Dependent gynecomastia. Life Sciences 69 (2110): 1465-1479.

9. Chan WB, Yeung VT, Chow CC, So WY, Cockram CS: Gynaecomastia as a Presenting Feature of Thyrotoxicosis. Postgraduate Medical Journal 75(882): 229-231, 1999.

10. Coen P, Kulin H, Ballantine T, Zaino r, Frauenhoffer E, Boal D, Inkster S, Brodie A, Santen R: An Aromatase-Producing Sex-cord Tumor Resulting in Prepubertal gynecomastia. New England Journal of Medicine 324 (5): 317-22, 1991.

11. Edman DC, Hemsell DL, Brenner PF: Extraglandular Estrogen Formation in Subjects with Cirrhosis. Gastroenterology 69: 819, 1975.

12. Finkelstein J, McCully W, MacLaughlin D, et al.: The mortician’s mystery: gynecomastia and reversible hypogonadotropic hypogonadism in an embalmer. N Eng J Med 319:961, 1988.

13. Franz A, Wilson J: Williams Textbook of Endocrinology ninth edition, 877-885, 1998.

14. Gana BM: Leydig Cell Tumor, British Journal of Urology 75(5): 676-8, 1995.

15. Gill K, Kirma N, Tekmal RR: Overexpression of Aromatase in Transgenic Male Mice Results in the Induction of gynecomastia and other Biochemical Changes in Mammary Gland. Journal of Steroid Biochemistry and Molecular Biology 77(1):13-18, 2001.

16. Glass AR: gynecomastia. Endocrinology and Metabolism Clinics of North America. 23(4): 825-837, 1994.

17. Herito RJ, Dankner R, Berezin M, Zeilig G, Ohry A: gynecomastia Following Spinal Cord Disorder. Archives of Physical Medicine and Rehabilitation 78(5): 534-537, 1997.

18. Hertl MC, Wiebel J, Schafer H, Willig HP, Lambrecht W. Feminizing Sertoli Cell Tumors Associated with Peutz-Jeghers Syndrome: An Increasingly Recognized Cause of Prepubertal gynecomastia. Plastic Reconstructive Surgery 102(4):1151-57, 1998.

19. Hsing A, McLaughlin J, Cocco p, Chen H, Fraumeni JF: Risk factors for male breast cancer. Cancer Causes and Control 9; 269-275, 1998.

20. (Jones DJ, Holt SD, Surtees P, et al: A comparison of danazol and placebo in the treatment of adult idiopathic gynaecomastia: results of a prospective study in 55 patients. Ann R Coll Surg Engl, 72:296-8, 1990.)

21. Kleinberg DL, Feldman M, Ruan W: IGF-1: An Essential Factor in Terminal End Bud Formation and Ductal Morphogenesis. Journal of Mammary Gland Biology and Neoplasia 5(1):7-17, 2000.

22. Kuhn JM, Roca R, Laudat MH, et al: Studies on the treatment of idiopathic gynecomastia with percutaneous dihydrotestosterone. Clin Endo 19: 513-20, 1983.)

23. LeProvost F, Leroux, C, Martin P Gaye P, Djiane, J, Prolactin Gene Expression in Ovine and Caprine Mammary Gland, Neuroendocrinology 60: 305-313, 1994.

24. Leroith D, Sobel R, Glick SM: The effect of clomiphene citrate on pubertal gynaecomastia. Acta Endocrinol (copenh). 95:177-80, 1980.

25. Lubahn, DB, Moyer JS, Golding TS: Alteration of Reproductive Function but not Prenatal Sexual Development after Insertional Disruption of the Mouse Estrogen Receptor Gene. Proc Soc Natl Acad Sci USA 90:11162-11166, 1993.

26. Mahoney CP: Adolescent gynecomastia. Differential Diagnosis and Management. Pediatric Clinics of North America 37(6): 1389-1404, 1990.

27. Mathur R, Braunstein: Gynecomastia: Pathomechanisms and Treatment Strategies. Hormone Research 48:95-102, 1997.

28. Matoska J, Ondrus D, Talerman A: Malignant Granulosa Cell Tumor of the Testes Associated with gynecomastia and LongSurvival. Cancer 69(7): 1769-72, 1992.

29. Mol JA, Van Garderen E, Rutteman GR, Rijnberk A: New Insights in the Molecular Mechanism of Progestin-induced Proliferation of Mammary Epithelium: Induction of the Local Biosynthesis of Growth Hormone in the Mammary Gland of Dogs, Cats, and Humans. Journal of Steroid Biochemistry and Molecular Biology 57 (1-2): 67-71, 1996.

30. Moore DC, Schlaepfer, LP, Sizonenko PC: Hormonal Changes During Puberty: Transient Pubertal Gynecomastia; Abnormal Androgen-Estrogen Ratios. Journal of Clinical Endocrinology and Metabolism 58:492-499, 1984.

31. Moran CA, Suster S: Primary Mediastinal Choriocarcinoma: A Clinicopathologic and Immunohistochemical Study of Eight Cases. American Journal of Surgical Pathology 21(9): 1007-1012, 1997.

32. Niewoehner CB, Nuttall FQ: gynecomastia in Hospitalized Male Population. American Journal of Medicine 77: 633-638, 1984.

33. Olivo J, Gordon GG, Raifi F: Estrogen Metabolism in Hyperthyroidism and in Cirrhosis of the Liver. Steroids 26: 47-56, 1975.

34. Richie J: Campbell’s Urology 7th Edition, 2439-2443, 1998.

35. Rifka SM, Pita JC, Vigersky RA, et al. Interaction of digitalis and spironolactone with human sex steroid receptors. J Clin Endocrinol Metab 1977; 46:228-244.

36. Ruan W, Kleinberg DL: Insulin-like Growth Factor I is Essential for Terminal End Bud Formation and Ductal Morphogenesis during Mammary Development. Endocrinology 140(11): 5075-81, 1999.

37. Sasano H, Kimura m, Shizawa s, Kimura N, Nagua H, Aromatase and Steroid Receptors in gynecomastia and Male Breast Carcinoma: an Immunohistochemical Study. Journal of Clinical Endocrinology and Metabolism 81 (8): 3063-7, 1996.

38. Santen R: Endocrinology fourth edition vol. 3: 2335-2341, 2001

39. Steinmetz R, Grant A, Malven, P: Transcription of Prolactin Gene in Milk Secretory Cells of the Rat Mammary Gland. Journal of Endocrinology 36: 305-313,1993.

40. Thompson DF, Carter J: Drug-induced gynecomastia. Pharmacotherapy 13(1): 37-45, 1993.

41. Ting AC, Chow LW, Leung YF: Comparison of tamoxifen with danazol in the management of idiopathic gynecomastia. Am Surg 66(1):38-40, 2000.

42. Treves N: Gynecomastia: the origins of mammary swelling in the male: and analysis of 406 patients with breast hypertrophy, 525 with testicular tumors, and 13 with adrenal neoplasms. Cancer 11: 1083-102, 1958.

43. Walden PD, Ruan W, Feldman M, Kleinberg DL: Evidence that the Mammary Fat Pad Mediated the Action of Growth Hormone in Mammary Gland Development, Endocrinology 139 (2): 659-62, 1998

44. Young S, Gooneratne S. Straus FH 2nd, Zeller WP, Bulun SE, Rosenthal IM: Feminizing Sertoli Cell Tumors in Boys with Peutz-Jehgers Syndrome. American Journal of Surgical Pathology 19 (1):50-58, 1995.

45. Zachmann M, Eiholzer U, Muritano M, et al: Treatment of pubertal gynaecomastia with testolactone. Acta Endocrinol supple (copenh) 279:218-26, 1986.

Nandrolone Phenyl Propionate (NPP) Explained

NPP was never really all that popular simply because of availability issues. Many of the pharmacy grade NPP products range between 25mg-50mg/ml and are extremely expensive. Naturally, this limited its use among the bodybuilding crowd. Mexico and the underground did not bother producing it.

The recent increase in popularity of NPP can be attributed to the introduction of BM’s Dubol-100; the first affordable pharmacy grade 100mg/ml NPP. Eventually, more and more Underground Labs started producing the forgotten drug.

PhenylProp vs Decanoate.

pictute of man participates in Amateur bench press championship in Professors GYM January 29, 2011 in Pecs, Hungary.

These numbers apply to reasonable use of Nandrolone Decanoate; between 200-400mg a week.

Here is some interesting information from Andy13:

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

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

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

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

after 6 weeks, 81 mg of esterified remain.

After 8 weeks, 32mg of esterified remain.”

Nandrolone Decanoate is a long acting depot; it takes quite a while for it to “kick in” and clear out of the system. Depending on how much is used; it will take at least 4-6 weeks after the last shot for Deca to clear out. It also takes about 4 weeks for active blood levels to stabilize. This can easily add up to 8-10 weeks of “dead time” i.e. periods of time when blood levels are not consistent. These numbers apply to reasonable use of Nandrolone Decanoate; between 200-400mg a week. The more you use, the worst it gets. So a 10-week cycle of Deca can easily end up been a 16-week cycle when you account for clearance time (active blood levels). The first 4 weeks are also somewhat of a waste of time.

So that 10-week cycle ends up been 16 weeks; 6 weeks of optimal blood levels and 10 weeks of dead time. Not a very effective way to cycle.

With NPP, you can bypass all that dead time.
19-Nortestosterone based drugs are known to shutdown HPTA very easily – think Trenbolone. Most bodybuilders will use Tren for around 6 weeks at the beginning of a cycle. NPP should be used in a similar manner.

Here’s an example of a balanced cycle consisting of NPP

W1-6: Dbol
W1-6: NPP
W1-8: Test Prop

It is a good idea to run Test 2 weeks past the NPP, however; NPP can be used as a stand-alone.

Earlier, I compared NPP to Tren. They are similar in some ways but Tren is much more androgenic and stronger in general.

NPP shares some of the same sides associated with Deca (they are after all the same base compound). It should be noted that most of the sides that come with Deca are a result of its long ester. Decanoate ester is very hard to control and Nandrolone side effects are not easily countered like Testosterone related sides (Tamoxifen, Anastrozole, finasteride…)

Overall, Nandrolone is a milder compound than Testosterone and is better mg for mg (but that’s a matter of opinion)

Nandrolone PhenylProp should be injected at least every 3 days. A typical dose is 350mg-700mg a week for 5-8 weeks.

It stacks very well with Winstrol, Dbol, Test, EQ, Anavar

It does not stack well with Tren and especially Anadrol

Here are some good cycle suggestions:

Fast Acting Classic Test/Deca/Dbol cycle:

W1-6: Dbol 30mg ED
W1-6: NPP 150mg EOD
W1-8: Test Prop 150mg EOD

Highly Anabolic cycles

W1-6: NPP: 200mg E3D
W1-8: Anavar: 30mg ED

W1-6: NPP: 200mg E3D
W1-8: Winny: 50mg ED

A good First cycle:

W1-6: NPP: 150mg E3D
W1-4: Dbol: 25mg ED
(W5-8: Anavar: 30mg ED – optional)

NPP in a typical cycle

W1-10: EQ 400mg a week
W1-9: Test Cyp 600mg a week
W1-8: NPP 200mg E3D
W10-13: Test Prop 150mg EOD

Nandrolone got a very bad rap with many bodybuilders; there is no reason to use Nandrolone Decanoate if NPP available aside from year-round juicer using it for joint pain. Nandrolone is a tremendous bodybuilding drug that can take your physique to a whole different level but many people shy away from it because of what they have heard or experienced with Deca.


Nolva vs. Clomid for PCT

picture of nolva_clomid

This misconception originates from their
completely different uses

by liftsiron

It seems like everyday questions concerning PCT pop up, and weather one should
use either Clomid or nolva or a combo of both. I hope that this article written
by BigCat may help to clear up some misconceptions.

While practically similar compounds in structure, few people ever really consider
Clomid and nolva to be similar. Its not just a common myth in steroid circles,
but even in the medical community. This misconception originates from their
completely different uses. Nolvadex is most commonly used for the treatment
of breast cancer in women, while Clomid is generally considered a fertility
aid. In bodybuilding circles, from day one, Clomid has generally been used as
post-cycle therapy and Nolvadex as an anti-estrogen.

But as I intend to demonstrate this is in essence the same. I believe the myth
to have originated because nolva is clearly a more powerful anti-estrogen, and
the people selling Clomid needed another angle to sell the stuff, so it was
mostly used as a post-cycle aid. But few users really understand how Clomid
(and also Nolvadex, logically) works to bring back natural testosterone in the
body after the conclusion of a cycle of androgenic anabolic steroids. After
a cycle is over, the level of androgens in the body drop drastically. The body
compensates with an overproduction of estrogen to keep steroid levels up. Estrogen
as well inhibits the production of natural testosterone, and in the period between
the return of natural testosterone and the end of a cycle, a lot of mass is
lost. So its in everybody’s best interest to bring back natural test as soon
as humanly possible. Clomid and Nolvadex will reduce the post-cycle estrogen,
so that a steroid deficiency is constated and the hypothalamus is stimulated
to regenerate natural testosterone production in the body. That’s basically
how the mechanism works, nothing more, nothing less.

Both compounds are structurally alike, classified as triphenylethylenes. Nolvadex
is clearly the stronger component of the two as it can achieve better results
in decreasing overall estrogen with 20-40 mg a day, than Clomid can in doses
of 100-150 mg a day. A noteworthy difference. Triphenylethylenes are very mild
estrogens that do not exert a lot, if any activity at the estrogen receptor,
but are still highly attracted to it. As such they will occupy the receptor
and keep it from binding estrogens. This means they do not actively work to
reduce estrogen in the body like Proviron, Viratase or arimidex would (by competing
for the aromatase enzyme), but that it blocks the receptor so that any estrogen
in the body is basically inert, because it has no receptor to bind to.

This has advantages and disadvantages. The disadvantage is that when use is
discontinued, the estrogen level is still the same and new problems will develop
much sooner. The advantage is that it works much faster and has results sooner
than with an aromatase blocker like Proviron or arimidex. Therefor, when problems
such as gynocomastia occur during a cycle of steroids one will usually start
20 mg/day of nolva or 100 mg/day of Clomid straight away, in conjunction with
some Proviron or arimidex. The proviron or arimidex will actively reduce estrogen
while the Clomid or Nolvadex will solve your ongoing problem straight away.
This way, when use is discontinued there is no immediate rebound.

So which one should you use? Well personally, I’d have to say Nolvadex. Both
as an on-cycle anti-estrogen and a post-cycle therapy. As an anti-estrogen its
simply much stronger, demonstrated by the fact that better results are obtained
with 20-40 mg than with 100-150 mg of Clomid. For post-cycle, this plays a key
role as well. It deactivates rebound estrogen much faster and more effective.
But most importantly, Nolvadex has a direct influence on bringing back natural
testosterone, where as Clomid may actually have a slight negative influence.
The reason being that tamoxifen (as in Nolvadex) seems to increase the responsiveness
of LH (luteinizing hormone) to GnRH (gonadtropin releasing hormone), whereas
Clomid seems to decrease the responsiveness a bit1.

Another noteworthy fact about Nolvadex is that it acts more potently as an
estrogen in the liver. As you remember, I mentioned that clomiphene and tamoxifen
are basically weak estrogens. Well, tamoxifen is apparently still quite potent
in the liver. This offers us the positive benefits of this hormone in the liver,
while avoiding its negative effects elsewhere in the body. As such Nolvadex
can have a very positive impact on negative cholesterol levels2 in the body,
and therefore too should be considered a better choice than Clomid. It will
not solve the problem of bad cholesterol levels during Steroid use, but will
help to contain the problem to a larger degree.

Another reason why I promote the use of Nolvadex over Clomid post-cycle (as
if being 3-4 times stronger and having more of a direct effect on restoring
natural test wasn’t enough) is because it’s a lot safer. Not just because it
improves lipid profiles, but also because it simply doesn’t have the intrinsic
side-effects that Clomid has. Clomid causes more acne for sure, but that’s mainly
because you need to use a 3-4 times higher dose. But Clomid seems to also affect
the eyesight. Long-term Clomid therapy causes irreversible changes in eyesight3
in users. Irreversible. For me that alone is reason enough to prefer Nolvadex.

Lastly, one should be aware that use of these compounds can reduce the gains
made on steroids. Nolvadex more so than Clomid, simply because it is stronger.
Estrogen is responsible for a number of anabolic factors such as increasing
growth hormone output, upgrading the androgen receptor and improving glucose
utilization. This is why aromatizing steroids like testosterone are still best
suited for maximum muscle gain. When reducing the estrogen levels, we therefore
reduce the potential gains being made. For this reason one may opt to try Clomid
during a cycle instead of Nolvadex. Although I would imagine that the problem
that needed solved would be of more concern, in which case nolva remains the
weapon of choice. It’s a plain fact that there is a high correlation between
gains and side-effects. Either you go for maximum gains and tolerate the side-effects,
or you reduce the side-effects, and with it the gains. That’s life, nothing
is free.

Stacking and Use:

If problems of Gynocomastia or other estrogen related symptoms tend to pop
up during a cycle the use of 20-30 mg of Nolvadex or 100 mg of Clomid daily
should easily contain the problem, and be used until a few days after the problem
subsides. For best results and the least amount of problems upon cessation it
is best stacked with Proviron (50 mg) or arimidex (0.5 mg) for this duration
as well. Its not advised that these products be ran concomitantly with the steroid
for the entire duration of the stack, as this will reduce your gains. Instead
cease the usage of anti-estrogens once the problem is contained, and should
the problem resurface, simply recommence the use of the products in the same
manner as described above.

Once a cycle of steroids is concluded one should always initiate a post-cycle
therapy to help bring back natural testosterone as soon as possible. This will
help you to retain the mass you gained. How this is done depends highly on the
type of steroid used. If only orals were used, therapy should start immediately,
even the last day of the stack. If short-acting esters or water-based injectables
were used, therapy should commence within 4-7 days after last injection, and
if long-acting esters were used then it should commence 1.5 to 2 weeks after
the last injection was given. The length of the therapy will vary as well, from
3-5 weeks. The longer acting the product was, the longer therapy should be continued
to make sure all suppressive factors are cleared before use of Clomid/Nolvadex
is discontinued.

For best results, it is best stacked with HCG (Human Chorionic gonadotrophin),
which functions as an LH analog and can help bring testicle size back up. HCG
use starts the last week of a cycle, and on from there every 5-6 days (usually
1500-3000 IU) and discontinued 1.5 to weeks prior to the cessation of Nolvadex/clomid.
The reason being that HCG itself is also suppressive of natural testosterone
and should be out of the body before therapy is over, or it will inhibit natural
testicle function. But I can not stress enough that HCG possibly plays a more
important role in post-cycle therapy than clomid/Nolvadex. For Clomid and Nolvadex,
doses are usually tapered down. Its best to start with 40-50 mg of Nolvadex
or 150 mg of Clomid for the first week or the first two weeks, and then finish
the program with 20-25 mg of Nolvadex or 100 mg of Clomid for an additional
two weeks.


Arimidex (anastrozole)

picture of arimidex diagram

Many anabolic steroids will convert, or aromatize, in the body into estrogen


Tetramethyl-5-(1H-1,2,4-triazol-1ylmethyl) 1,3-benzenediacetionitrile

Molecular Formula C17H19N5
Molecular Weight 293.37
CAS Registry Number 120511-73-1
Melting point
81-82 ºC

Although Arimidex does increase testosterone levels slightly in the body, it is more often used in conjunction with other steroids to lower estrogen in the body. Many anabolic steroids will convert, or aromatize, in the body into estrogen, which causes many of the unwanted side effects like bloating and acne. Arimidex is one of the best compounds to lower the aromatizing effect of steroids.

Arimidex® (generic name is anastrozole) is a newer drug developed for the treatment of advanced breast cancer in women. It is manufactured by Zenica Pharmaceuticals and was approved for use in the United States at the end of December 1995. Specifically, Arimidex is the first in a new class of third-generation selective oral aromatase inhibitors.. It acts by blocking the enzyme aromatase, subsequently blocking the production of estrogen. Since many forms of breast cancer cells are stimulated by estrogen, it is hoped that by reducing amounts of estrogen in the body the progression of such a disease can be halted. This is the basic premise behind Nolvadex, except this drug blocks the action and not production of estrogen. The effects of Arimidex can be quite dramatic to say the least. A daily dose of one tablet (1 mg) can produce estrogen suppression greater than 80 % in treated patients. With the powerful effect this drug has on hormone levels, it is only to be used (clinically) by post-menopausal women whose disease has progressed following treatment with Nolvadex (tamoxifen citrate). Side effects like hot flushes and hair thinning can be present, and would no doubt be much more severe in pre-menopausal patients.

For the steroid using male athlete, Arimidex shows great potential. Up to this point, drugs like Nolvadex and Proviron have been our weapons against excess estrogen. These drugs, especially in combination, do prove quite effective. But Arimidex appears able to do the job much more efficiently, and with less hassle. A single tablet daily (1 mg), the same dose use clinically, seems to be all one needs for an exceptional effect (some even report excellent results with only 0.25 mg daily). When used with strong, readily aromatizing androgens such as Dianabol or testosterone, gynecomastia and water retention can be effectively blocked. In combination with Propecia (finasteride), we have a great advance. With the one drug halting estrogen conversion and the other blocking 5-alpha reduction , related side effects can be effectively minimized. Here the strong androgen testosterone could theoretically provide incredible muscular growth, while at the same time being as tolerable as nandrolone. Additionally the quality of the muscle should be greater, the athlete appearing harder and much more defined without holding excess water.

There are some concerns with using an aromatase inhibitor such as this during prolonged steroid treatment however. While it will effectively reduce estrogenic side effects, it will also block the beneficial properties of estrogen from becoming apparent (namely its effect on cholesterol values). Studies have clearly shown that when an aromatase inhibitor is used in conjunction with a steroid such as testosterone, suppression of HDL (good) cholesterol becomes much more pronounced. Apparently estrogen plays a role in minimizing the negative impact of steroid use. Since the estrogen receptor antagonist Nolvadex is shown not to display an anti-estrogenic effect on cholesterol values, it is certainly the preferred from of estrogen maintenance for those concerned with cardiovascular health.

Arimidex has another principle drawback, namely the great price of this drug. Tablets can easily sell for $10 each, becoming quite costly with regular use. Clearly the price of an ancillary drug can be much greater than the steroids themselves, a situation destined not to be popular with recreational bodybuilders. Competitors on the other hand are likely to welcome this item. It can ward off the side effects of strong androgen therapy much better than Nolvadex and/or Proviron, making heavy cycles much more comfortable. As the number of countries manufacturing this drug increases, we may be able to look forward to a reduction in price. Privately compounded versions of “liquid Arimidex” have also been formulated “for research purposes” are also available. Generic tabs are also available and these two forms represent a very cost-effective alternative for buying the brand name drug.



Aromasin (exemestane)

picture of aromasin

Developed to help fight breast cancer, Aromasin is one of the most powerful estrogen suppressing compounds


6-Methylenandrosta-1,4-diene-3,17-dione; 10,13-Dimethyl-6-methylidene-7,8,9,10,11,12,13,14,15,16-decahydrocyclopenta[a]phenanthrene-

Molecular Formula C20H24O2
Molecular Weight 296.40
CAS Registry Number 107868-30-4
Melting point 155.13 ºC

Developed to help fight breast cancer, Aromasin is one of the most powerful estrogen suppressing compounds available for body builders taking anabolic steroids. Additionally, it also raises testosterone in the body, which is a bonus for bodybuilders during post-cycle-therapy.


Testoviron is a testosterone blend of long and short acting esters that is very popular among bodybuilders. Its high cost and its scarcity make it one of the most sought after steroid compounds on the market today. Its short esters cause a spike in testosterone levels and the long esters keep testosterone in the plasma for several days, giving users a well-balanced anabolic effect.

picture of man working out

ts short esters cause a spike in testosterone levels and the long esters keep testosterone in the plasma for several days,

As with any testosterone, Testoviron will give the user more mass to the muscle, burn fat in the body, enhance libido, increase immunity and increase energy. All the usual side effects of testosterone can also be expected conversion to estrogen and DHT, gynocomastia and water-retention.



diagram of cyclophenil

Unfortunately, Cyclfenil is not as effective and requires higher doses and more frequent injections as its two counterparts that are less expensive and more available.


Fertodur; (Cyclohexylidenemethanediyl)dibenzene-4,1-diyl diacetate; [4-[(4-Acetyloxyphenyl)-cyclohexylidenemethyl]phenyl] acetate
Molecular Formula C23H24O4
Molecular Weight 364.44
CAS Registry Number 2624-43-3
EINECS 220-089-1

Like Clomidand Nolvadex, Cyclofenil is used in post-cycle-therapy to increase testosterone and prevent gynocomastia. Unfortunately, Cyclfenil is not as effective and requires higher doses and more frequent injections as its two counterparts that are less expensive and more available.