DISCLAIMER:

This information was gathered from sources including textbooks, medical journals, and pharmaceutical
reports, as well as interviews with athletes, steroid dealers, and medical experts. the author
assumes any liability for the information presented in this text. This blog is not intended to provide medical
advice. The purpose of this reference blog is only to provide a compendium of information for the reader, for entertainment purposes only. None of the information in this blog is meant to be applied.

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Thursday, April 28, 2011

testosterone/oxymetholone cycle (MASS)

testosterone/oxymetholone cycle (MASS)

Products: 20 mL 200 mg/mL testosterone (enanthate or cypionate)
100 tablets 50 mg oxymetholone

All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day).

Comments: A combination of testosterone and oxymetholone is generally regarded as the most potent 2-drug stack for gaining raw muscle mass. Both drugs will present significant estrogenicity, and will be likely to induce gynecomastia quickly unless an estrogen maintenance drug such as tamoxifen is used. Inexperienced steroid users have been known to gain over 25-30 pounds on a cycle such as this. Water retention will be very high with this stack, however, and a rapid loss of water weight (possibly up to 10 pounds or more) is expected soon after the cycle is discontinued.

week------------------testosterone-------------------------oxymetholone
1-----------------------200mg
2-----------------------400mg
3-----------------------400mg----------------------------------50mg/day
4-----------------------400mg----------------------------------50mg/day
5-----------------------400mg---------------------------------100mg/day
6-----------------------500mg---------------------------------100mg/day
7-----------------------500mg---------------------------------100mg/day
8-----------------------500mg---------------------------------100mg/day
9-----------------------500mg---------------------------------100mg/day
10----------------------200mg---------------------------------100mg/day

Wednesday, April 27, 2011

fish oil, recommended dosage for athletes


Fish oil
is a primary source of omega-3 fatty acids. These "healthy" fatty acids offer a number of benefits. If you don't enjoy fish or are unable to eat much of it, you can take fish oil capsules. Fish oil in dietary supplement form can provide the same benefits as eating fish if taken in proper dosages. Speak to your doctor before beginning a dietary supplement regimen of any type, and always read the dosage directions on supplement bottles.

Function of fish oil

Fish oil contains docosahexaenoic acid, or DHA, and eicosapentaenoic acid, or EPA, which have been specifically linked to a reduced risk of heart attacks. The acids also help correct abnormal heart rhythms, or arrhythmia, and lower the risk of stroke if you have cardiovascular disease. Fish oil can help slow the buildup of plaque in the arteries and encourage lower blood pressure . Taking fish oil supplements is helpful if you only eat fish that is fried. Frying fish eliminates fish oil's benefits.

Dosageof fish oil

Fish oil is considered safe for adults, including pregnant and breastfeeding women. According to MedlinePlus, you should not take more that 3 g of fish oil per day if you are healthy. Certain conditions may require a higher dosage. For instance, doctors may recommend you take 1 to 4 g of fish oil daily if you have high triglycerides. If you have rheumatoid arthritis, you should take 3.8 g per day of EPA. Up to 5.1 g of fish oil is the recommended dose to help prevent miscarriages in women with anti-phospholipid antibody syndrome. If you have a condition, speak to your doctor to determine if fish oil is appropriate for you to take

Side Effectof fish oil::

Taking more than the recommended dosage can lead to potentially dangerous side effects. Too much fish oil can increase your risk of bleeding. The acids in fish oil can keep blood from clotting, which can impede a wound from healing. Your immune system may also be adversely affected by fish oil doses that are too high and make you more susceptible to illness. A weakened immune system is especially dangerous for the elderly and people suffering from an immune deficiency disease.

Cautions

Fish oil capsules can be made with oil from various fish species. Certain species, including king mackerel, farm-raised salmon and shark, have a risk of containing mercury and other environmental contaminants. Use caution when taking fish oil if you also take birth control pills. The drugs in birth control can impede the fish oil from helping lower your triglyceride levels. You should also be cautious if you take medication for high blood pressure. Fish oil can promote low blood pressure. Coupled with your medication, the fish oil can force your blood pressure too low.
reference: livingstrong.com

Tuesday, April 26, 2011

deca/dianabol cycle 2 (MASS)

deca/dianabol cycle 2 (MASS)

Products: 20 mL 200 mg/mL nandrolone decanoate
-200 tablets 5 mg methandrostenolone
All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label recommended dosage).
- Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
- Estrogen Support: tamoxifen (20-40 mg/day).
Comments: A more popular manifestation of the Deca/Dianabol Cycle, with more commonly accepted dosages for a moderately experienced steroid user. Incidences of side effects are expected to be higher at these dosages, although overall this stack is likely to be less problematic than a combination of testosterone and oxymetholone.

week-----------------nandrolone----------------------methandrostenolone
1------------------------400mg
2------------------------400mg
3------------------------400mg-----------------------------10mg/day
4------------------------400mg-----------------------------10mg/day
5------------------------400mg-----------------------------20mg/day
6------------------------400mg-----------------------------20mg/day
7------------------------400mg-----------------------------20mg/day
8------------------------400mg-----------------------------20mg/day
9------------------------400mg-----------------------------20mg/day
10-----------------------400mg-----------------------------20mg/day

deca/dianabol cycle 1(MASS)

deca/dianabol cycle 1(MASS)

Products: 10 mL 200 mg/mL nandrolone decanoate
100 tablets 5 mg methandrostenolone

All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day).

Comments:This is an extremely old and widely repeated steroid combination, based on the predominantly anabolic steroid nandrolone decanoate. Methandrostenolone serves as the androgenic component of this stack, and is added durring 3 week, which is a time that side effects of reduced androgenicity (with the exclusive use of nandrolone decanoate) are commonly noticed, such as loss of libido and sexual dysfunction.The doses used in this cycle are not high by most bodybuilding standards, but are sufficient to impart a noticeable increase in muscle size and strength.

week---------------nandrolone-----------------methandrostenolone
1------------------------200mg
2------------------------200mg
3------------------------200mg-------------------------10mg/day
4------------------------200mg-------------------------10mg/day
5------------------------300mg-------------------------10mg/day
6------------------------300mg-------------------------15mg/day
7------------------------300mg-------------------------15mg/day
8------------------------300mg-------------------------15mg/day

stanozolol cycle 2 (LEAN MASS/CUTTING)

stanozolol cycle 2 (LEAN MASS/CUTTING)

Products: 200 tablets 5 mg stanozolol

All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Comments: This is a stronger version of a cutting/lean mass building cycle utilizing stanozolol. The dosage used here is substantially higher than the first stanozolol cycle, a fact that makes this cycle more properly suited for bodybuilding purposes than Stanozolol Cycle #1. Cardiovascular and hepatic strain will be I more notable, and visible side effects more pronounced, than the first cycle. There should be no need to addition an estrogen maintenance drug.
week----------------------stanozolol
1---------------------------20mg/day
2---------------------------20mg/day
3---------------------------25mg/day
4---------------------------25mg/day
5---------------------------25mg/day
6---------------------------25mg/day

stanozolol cycle 1(LEAN MASS/CUTTING)

stanozolol cycle 1(LEAN MASS/CUTTING)

Products: 200 tablets 2mg Stanozolol

All Weeks: Liver Support: liver Stabil, Liv-52, or Essentiale Forte (label recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).

Comments: This is a common first-cycle for an athlete looking for performance improvements or a bodybuilder looking for a lean mass or cutting steroid. This cycle was more common when stanozolol was widely available in 2 mg tablets. Such preparations are now uncommon except in Europe. The dosage used here is low by bodybuilding standards, although similar cycles have been the backbone programs for many athletic competitors, especially during the 1970s and 80's. Significant visible adverse reactions are unlikely at this dosage.

WEEK----------------------STANOZOLOL
1------------------------------8mg/day
2------------------------------8mg/day
3------------------------------10mg/day
4------------------------------10mg/day
5------------------------------10mg/day
6------------------------------10mg/day

Sunday, April 24, 2011

The Truth about Steroids


Why steroids are so powerful and so dangerous if abused


Steroids are natural substances with many different effects in the human body, which begin over several days. The primary use of steroids in health care is to reduce inflammation and other disease symptoms. Steroid inhalers have an important role in reducing deaths from asthma, local steroid injections are useful in treating painful joints and ligaments. Steroid creams are used extensively to treat eczema and other inflammatory skin conditions. Steroids make the whole immune system less active, which can be very useful in illnesses where there is an immune component - a huge number. Steroids are the ultimate anti-inflammatory drugs.

However steroid use in medicine is limited by very serious side effects in the body as a whole. That is why steroids tend to be used sparingly in local preparations such as sprays and creams, which ensure maximum steroid dose where it is needed, and minimum levels in the blood stream.


Steroid use in medicine and health care


Steroid skin creams for example cause thinning and weakness of the skin, while steroids also cause calcium to leak out of bones so that they weaken and fracture spontaneously. Steroids also make people feel very hungry and cause blood sugar to rise. People on steroids can gain weight and often develop a typical "moon face" as well as getting diabetes.

Another serious steroid problem is that we all need aggressive immune systems to fight infections and cancers, but steroids knock that out. People on high doses of steroids for medical reasons can die from chest infections and cancers of many kinds. We see these patterns in those who receive organ transplants, who need often need huge doses of steroids to stop the body from destroying the donated tissue. Cancers often develop, which shows us how important our white cells are in keeping us cancer-free, and how often all of us develop cancer in our daily lives. Most of us may have two or three tiny cancers inside us at any time. Taking high dose steroids makes it more likely one of these will develop rapidly.

People on high dose steroids are immune-deficient in every way so that many organisms that rarely cause problems can overgrow, totally upsetting the normal balance of mircobes in the body. An example is candida yeast which can grow rapidly in the mouth causing painful thrush.



Effects of steroids on brain and cancer


Steroids also affect the brain, and high doses can make people feel happy, euphoric, hyped-up, with disturbance of sleep and even serious psychiatric illness such as mania, very aggressive behavior and psychosis (delusions, pananoia, loss of touch with reality). If steroid users are also taking other drugs which affect mood or brain function, these side-effects can be far more common.

Steroids are really useful in the care of those with advanced cancer when short life expectancy from their condition means physicians are far more relaxed about long term side-effects.

Brain tumours often respond dramatically to steroids. The reason is that the brain is contained in a bony box inside the skull and pressure can build up inside the head, resulting in headaches, sickness, drowsiness and other problems. Brain scans often show that a tunour the size of a wallnut can be surrounded by a big immune reaction, with brain swelling and inflammation. Steroids reduce the additional swelling, often reversing symptoms and buying time - maybe a few weeks. The underlying cancer continues to grow and if the person finally begins to deteriorate death often follows rapidly as the steroid dose is reduced.

So steroids are really powerful, with wide ranges of actions, producing dramatic effects ranging from pain relief to mood elevation, and if it were not for the very serious side effects they would be used even more often.

The body becomes dependent on steroids and when used in health care, most physicians reduce dosage gradually, even though they may start in an acute illness with a very high dose.



Why do people abuse steroids?


So why on earth would anyone who is perfectly healthy want to take steroids? The reason is that one particular type, anabolic steroids, have another side effect which is to stimulate muscle growth. Sadly for the sports enthusiast, this effect only works well if steroid level in the body as a whole is quite high, and that guarantees problems with side effects.

Taking steroids won't increase muscle bulk without exercise but the normal response to exercise is exaggerated.

Often you will find underlying psychological reasons why people abuse steroids in muscle building. Some studies suggest up to 25% have been physically or sexually abused as children or attacked as adults and are highly motivated to make themselves powerful and resistant to future attack. Others have a body image problem similar to anorexia nervosa, so that they see a weak and feeble body in the mirror - muscle dysmorphia. In some, steroid abuse is just a part of a wider picture of risk-taking.



Anabolic and Androgenic steroids


Steroids can be divided into two types: anabolic and androgenic, but the distinction in some ways is artificial. Anabolic steroids mainly affect metabolism, immunity and muscle, while androgenic steroids have strong masculinisation effects on women and sometimes feminisation effects on men. But all anabolic steroids will increase masculine characteristics such as thick facial hair if the dose used is significant.

Steroid cycling is a regular pattern of steroid use and non-use by athletes or body builders, the aim being to get maximum action with minimum side-effects, often by using a wide variety of different steroid preparations at the same time (stacking), and perhaps to avoid detection by timing non-use to coincide with major competitions where steroids testing may be imposed.

Some steroid abuses use pyramidding - starting with low doses and building up over days or weeks to a peak dose and then tailing off.



Anabolic steroid side effects


Typical problems you will find in people who abuse anabolic steroids include liver tumors and cancer, jaundice (yellow skin from liver failure), retention of fluid, high blood pressure, heart attacks and strokes, increases in LDL (dangerous form of cholesterol), kidney cancer, acne and trembling.

Men may find their testes shrink, sperm count falls with increase of infertility, their hair falls out, breasts start to develop, and prostate cancer becomes more likely. More than half of body-builder sterod abusers will typically experience enlarged breasts and shrunken male organs.

Women can start looking like men: growing beards, going bald, voice breaking - while their menstrual cycle changes or stops, and the clitoris enlarges.

Steroid abuse is particularly risky for teenagers, because it forces the body rapidly to adulthood, bones stop growing - permanently - and they reach puberty early.

Adolescents--growth halted prematurely through premature skeletal maturation and accelerated puberty changes.

And of course, steroid injecting carries all the other risks associated with other injecting drug use, such as infection with HIV, and hepatitis B or hepatitis C.



How many people abuse steroids?

Some surveys suggest that 2.5% of high school pupils in the US will have taken illegal steroids at some time. This is particularly worrying considering the very high risks of steroid abuse in those under the age of 18.

source:globalchange.com

Saturday, April 23, 2011

Oxymetholone Post Cycle


Oxymetholone Post Cycle Therapy | Anadrol Post Cycle Therapy

Oxymetholone is the strongest and in the same time most effective oral steroid. First thing I want to underline is that Oxymetholone is 17-alkylated and it affects liver so better to use Liv52 during and after cycle.
If you can’t find Liv52 use Milk Thistle. Important thing here is to protect liver.

Also for the same reason I would not recommend using Oxymetholone longer than 6 weeks.

Now regarding post cycle therapy. Actually this will vary from case to case in dependency from other steroids used in combination with Oxymetholone.

I guess many of you will use it in combination with testosterone and in this case Oxymetholone Post Cycle Therapy would be next:


HCG used each fourth week at 250IU per week.

Nolvadex used 4 weeks after cycle at 20mg/day

source: steroidscycle.net

oxymetholone cycle 2(MASS)

oxymetholone cycle 2(MASS)

Products: 100 tablets 50 mg oxymetholone

All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day).
Comments: This is a more popular version of the oxymetholone only cycle. The doses here are more common with experienced steroid users, and more than sufficient to promote strong mass and strength increases. Side effects may be more noticeable than the lower dose cycle, of course, which may necessitate a higher dose of tamoxifen.

week---------------oxymetholone
1---------------------50mg/day
2---------------------50mg/day
3---------------------100mg/day
4---------------------100mg/day
5---------------------100mg/day
6---------------------100mg/day
7---------------------100mg/day
8---------------------100mg/day

oxymetholone cycle 1 (MASS)

oxymetholone cycle 1 (MASS)

Products: 50 tablets 50 mg oxymetholone

All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day).

Comments: Oxymetholone is commonly regarded as the most potent mass building steroid available. It is also prone to causing both strong estrogenic and androgenic side effects. A steroid novice may gain 15-20 pounds or more on this cycle, although a significant amount of this will be water retention, which will subside soon after drug discontinuance. Oxymetholone is also known for inducing strong cardiovascular and hepatic stress. While this drug may be more convenient to use than an injectable testosterone, it is not regarded as a safe alternative. Repeated use of c-17 alpha alkylated orals like this should be limited.

week-----------------oxymetholone
1-----------------------50mg/day
2-----------------------50mg/day
3-----------------------50mg/day
4-----------------------75mg/day
5-----------------------75mg/day
6-----------------------75mg/day

sustanon 250 cycle (MASS)

sustanon 250 cycle (MASS)

Products: 15 mL 250 mg/mL Sustanon (testosterone blend)

All Weeks: Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day) or anastrozole (.5-1 mg/day).

Comments: This mass building program is similar to the other testosterone cycles, but utilizes Sustanon 250, a form of blended testosterone more widely used in Europe and other regions outside the u.S.The total steroid dosage of this cycle is 3,750 mg, extremely close to the amount used in testosterone cycle #2. A similar level of cardiovascular strain and visible side effects are expected.

week---------------sustanon
1-------------------250mg
2-------------------250mg
3-------------------500mg
4-------------------500mg
5-------------------500mg
6-------------------500mg
7-------------------500mg
8-------------------500mg
9-------------------250mg

testosterone cycle :2(MASS)

testosterone cycle :2(MASS)

Products: 20 mL 200 mg/mL Testosterone (enanthate or cypionate)

All Weeks: Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day) or anastrozole (.5-1 mg/day).

Comments: This cycle is a common follow up to the first testosterone only cycle, with a higher dosage and 3 week longer duration of intake. The total testosterone dosage given is double in comparison, and is likely to produce more pronounced estrogenic and androgenic side effects. Cardiovascular strain may be slightly higher than the first cycle, but should remain substantially lower than cycles with oral AAS. Testosterone is arguably the safest, and at the same time one of the most effective, muscle-building steroids available.The exclusive repeated use of a cycle like this would be advised over more adventurous cycling/stacking if possible.

week---------------------testosterone
1---------------------------200mg
2---------------------------400mg
3---------------------------400mg
4---------------------------400mg
5---------------------------400mg
6---------------------------500mg
7---------------------------500mg
8---------------------------500mg
9---------------------------500mg
10--------------------------200mg

testosterone cycle :1(MASS)

testosterone cycle :1(MASS)

Products: 10 mL 200 mg/mL Testosterone (enanthate or cypionate)

All Weeks: Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4 g/day).
Estrogen Support: tamoxifen (20-40 mg/day) or anastrozole (.5 mg/day).

Comments: This mass building cycle is likely to yield simi,lar quantitative results as an early Dianabol cycle, but is favored over the oral for its lower cardiovascular and hepatic strain.The doses used are expected to cause mild shifts in the HDL/LDL cholesterol ratio, but not the substantial changes normally seen with oral anabolic steroids. This sample cycle is likely to present the least amount of health side effects of al listed in this section.
week-----------------testosterone
1-----------------------200mg
2-----------------------200mg
3-----------------------300mg
4-----------------------300mg
5-----------------------300mg
6-----------------------350mg
7-----------------------350mg

dianabol cycle :2(MASS)

dianabol cycle :2(MASS)

Products: 200 tablets 5 mg Methandrostenolone

All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day).

Comments: This is a common follow up to the first Dianabol cycle, utilizing a slightly higher dose and longer duration of intake.The dosages used here are more common for bodybuilding purposes. A slightly greater intensity of adverse reactions is likely.

week-------------------methandrostenolone
1---------------------------20mg/day
2---------------------------20mg/day
3---------------------------25mg/day
4---------------------------25mg/day
5---------------------------25mg/day
6---------------------------25mg/day

dianabol cycle :1(MASS)

dianabol cycle :1(MASS)

Products:100 tablets 5 mg Methandrostenolone

All Weeks:
Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4 g/day).
Estrogen Support: tamoxifen (10-20 mg/day).

Comments:
This is a very common first cycle for building muscle mass, and utilizes a single standard bottle of methandrostenolone. This cycle is likely to produce very noticeable muscle growth in a first-time steroid user, often in excess of 8-1 Olbs of weight gain.This is usually not accompanied by significant visible side effects such as gynecomastia and water retention. Although this is considered a beginner's cycle, methandrostenolone is a c-17 alpha alkylated oral steroid, and presents significant cardiovascular and liver toxicity. The repeated use of such drugs should be limited.

week----------------------
methandrostenolone
1 ------------------------------10MG/DAY
2 ------------------------------10MG/DAY
3 ------------------------------15MG/DAY
4 ------------------------------15MG/DAY
5 ------------------------------ 20MG/DAY

Friday, April 15, 2011

Stacking steroids


As individuals become more experienced with anabolic/androgenic steroid use they may begin experimenting with the use of more than one steroid at a time. This practice is referred to as stacking. Stacking is most common with advanced bodybuilders who find that at a certain level of physical development they begin hitting plateaus that are difficult to break with a previous single-agent approach. In many cases, however, it may simply be the greater cumulative steroid dosage that is necessary for the resumed progress. Stacking usually involves the combination of a more androgenic steroid with one or more primarily anabolic agents. On the anabolic side, common steroids of choice include boldenone, methenolone, nandrolone, oxandrolone, and stanozolol. Testosterone, oxymetholone, or methandrostenolone will serves as the androgenic base of most stacks .

The reasons for stacking androgenic and anabolic steroids together in this manner are two fold. On the one hand, high doses of testosterone, oxymetholone, or methandrostenolone are prone to producing strong androgenic and estrogenic side effects. Stacking first became very popular during the 1960s, a time when effective estrogen maintenance drugs were not widely availabl~.An anabolic-androgen stack allowed the use of a higher total steroid dosage than would be tolerable with a single androgen. Anabolic-androgen pairing also appears to offer efficacy advantages over the use of primarily anabolic agents alone, even when they are taken in higher doses. This conflicts with the original expectations for "anabolic" steroids, which were specifically designed to emphasize muscle-building properties, but is repeatedly noticed by users. The reason the basic androgenic steroids are more anabolically productive is not fully understood, but is believed to involve the interplay of estrogenic hormones, androgenic stimulation in the central nervous system, and potentially other unidentified synergisms necessary for optimal muscle growth.

Today, the availability of drugs that can reduce estrogenic activity makes the continued use of single agent cycles based on a strong androgen like testosterone enanthate or cypionate much more viable than it was decades ago, Side effects like gynecomastia and water retention car· now be effectively minimized with anti-estrogens 01 aromatase inhibitors, even when taking higher doses Individuals should be aware that stacking is, likewise, noi a necessary practice. It is likely to remain commonl) applicable in competitive bodybuilding circles, however or when an individual is sure they have progressed as fal as they possibly can with a single-agent approach Otherwise, for many athletes and recreationa bodybuilders, the periodic use of a single steroid will bE . more than sufficient to maintain optimal levels of musclE mass and performance, and it may never be necessary tc deviate from this approach.

Steroid Cycles


Anabolic/androgenic steroids are not medically approved to promote excessive muscle mass gains (bodybuilding) or improve athletic performance. Aside from early experimentation on athletes by a handful of sports physicians, an extensive effort to study the physique-and performance-enhancing properties of these drugs, specifically with an eye on developing strategies for using them to maximize benefits and minimize adverse effects, has not been undertaken by the medical community. Because of this, illicit users have been left to develop their own protocols for administering these drugs. The result has been a large variety of different approaches to using these agents, some safer or more effective than ,others. While it would not be possible to comprehensively evaluate all known approaches, this section will discuss some of the most fundamental and time-proven methods for using AAS

Steroid Selection
When first considering what steroid(s) to use, one will notice there are many different medications that fall under the category of anabolic/androgenic steroids. This has been the result of many years of development, where specific patients and needs are addressed with drugs that have specific characteristics. For example, some drugs are considered milder (less androgenic), and produce fewer side effects in women and children. Others are more androgenic, which makes them better at supporting sexual functioning in men. Some are injectable medications, and others made for oral administration. There are limits to this diversity, however. All AAS drugs activate the same cellular receptor, and as such share similar protein anabolizing properties. In other words, while different AAS drugs may have some differing properties, if your objective is to gain muscle mass and strength, this could be accomplished with virtually any one of the commercially available agents.

While all AAS drugs may be capable of improving muscle mass, strength, and performance, it would not be correct to say there are no advantages to choosing one agent over another for a particular purpose. Most fundamentally, the quantity and quality of muscle gained may be different from one agent to another. In a general sense, AAS that are also estrogenic tend to be more effective at promoting increases in total muscle size.These steroids also tend to produce visible water (and sometimes fat) retention, however, and are generally favored when raw size is more important than muscle definition. Drugs with low or no significant estrogenicity tend to produce less dramatic size gains in comparison, but the quality is higher, with greater visible muscularity and definition. In reviewing the most popular AAS drugs, we can separate them into these two main categories as follows.

Mass (Bulking):
Methandrostenolone -Oral
Oxymetholone -Oral
Testosterone (cypionate, enanthate) -Injectable

Lean Mass:
Boldenone undecylenate -Injectable
Methenolone enanthate -Injectable
Nandrolone decanoate -Injectable
Oxandrolone -Oral
Stanozolol -Oral

The early stages of AAS use usually involve cycles with a single anabolic/androgenic steroid. Building muscle mass is the most common goal, and usually entails the use of one of the more androgenic substances such as testosterone, methandrostenolone, or oxymetholone. Those looking for lean mass often find favor in such anabolic staples as nandrolone decanoate, oxandrolone, or stanozolol. First time users rarely welcome injecting anabolic/androgenic steroids, and will usually choose an oral compound for the sake of convenience. Methandrostenolone is the most co-mmon choice for mass building, and is almost universally regarded as highly effective and only moderately problematic (in terms of estrogenic or androgenic side effects). Stanozolol is the oral anabolic steroid most often preferred for improving lean mass or athletic performance.

The potential for adverse reactions should also be considered when choosing a steroid to use, especially if AAS use is to be regularly repeated. For example, the listed oral medications present greater strain on the cardiovascular system, and are also liver toxic. For these reasons, the injectable medications listed are actually preferred for safety (testosterone most of all). Potential cosmetic side effects may also be taken into account. For example, men with a strong sensitivity to gynecomastia sometimes prefer non-estrogenic drugs such as methenolone, stanozolol, or oxandrolone. Individuals worried about hair loss, on the other hand, may isolate their use to predominantly anabolic drugs, such as nandrolone, methenolone, and oxandrolone. A detailed review of personal goals, health status, and potential side effects of each drug is advised before committing to any AAS regimen.

Dosage
The dosage used is important in determining the level of
benefit received. Anabolic/androgenic steroids tend to be
most efficient at promoting muscle gains when taken at a
moderately supratherapeutic dosage level. Below this
(therapeutic), potential anabolic benefits are often counterbalanced, at least to some extent, by the suppression of endogenous testosterone. At very high doses (excessive supratherapeutic), smaller incremental gains are noticed (diminishing returns). In the case of testosterone enanthate or cypionate, for example, a dosage of 100 mg per week is considered therapeutic, and is generally insufficient for noticing strong anabolic benefits. When the dosage is in the 200-600 mg per week range, however, the drug is highly efficient at supporting muscle growth (moderate supratherapeutic). Above this range, a greater level of muscle gain may be noticed, but the amount will be small in comparison to the dosage increase. Below are some commonly recommended dosages for the steroids listed earlier.

-Boldenone undecylenate: 200-400 mg/wk
-Methandrostenolone: 10-30 mg/day
-Methenolone enanthate: 200-400 mg/wk
-Nandrolone decanoate: 200-400 mg/wk
-Oxandrolone: 10-30 mg/day
-Oxymetholone: 50-1 00 mg/day
-Stanozolol: 10-30 mg/day
-Testosterone (cypionate, enanthate): 200600 mg/wk

There are additional considerations other than the cost effectiveness of a particular dosage. To begin with, high doses of anabolic/androgenic steroids tend to produce stronger negative cosmetic, psychological, and physical side effects. In light of diminishing returns, the tradeoff between results and adverse reactions becomes less and less favorable. Gains made on lower doses also tend to be better retained after steroid discontinuance than those resulting from excessive intake. It is generally not realistic to expect that rapid double-digit weight gains induced by massive dosing will remain long after a cycle is over. Slower steadier gains are advised. It is also very important' to remember that higher doses aren't always what are needed to achieve greater gains. An individual more focused on his or her training and diet will often make better gains on lower dosages of AAS than a less dedicated individual taking higher doses. With this understanding, AAS should only be considered when alii other variables ,of training and diet have been addressed, and always limited to the minimum dosage necessary td achieve the next realistic training/performance goal.

Duration (Cycling)
The administration of anabolic/androgenic steroids at a given dosage will typically produce noticeable increases in muscle size and strength for approximately 6-8 weeks. After this point, the rate of new muscle gain typically slows significantly. A plateau may be reached soon after, where all forward momentum has ceased. To continue making significant progress beyond this point can entail escalating dosages, which is likely to coincide with a greater incidence of adverse reactions and diminishing anabolic returns. Even without dosage escalation, negative health changes are already likely to be apparent, and should be corrected fairly quickly. The practice of extended or continuous steroid administration is discouraged for these reasons. It is generally recommended to use AAS drugs for no longer than 8 weeks at a time (10-12 weeks at the maximum), followed by an equal or longer period of abstinence before another steroid regimen is initiated. This pattern of rotating between "on" and "off" periods is referred to as cycling.

off-Cycle(Recovery, Bridging, and Tapering)
The period immediately following steroid cession can involve a state of hypogonadism (low androgen levels), and as a result protein catabolism. In an effort to minimize muscle loss, the objective here is usually on restoring natural testosterone production, maintaining an optimal level of muscle stimulation, and remaining dedicated to proper nutrition. A hormonal recovery program is usually initiated, which may involve the use of HCG, tamoxifen, and clomiphene (see PCT: Post Cycle Therapy). A substantial off-cycle period is also advised, involving abstinence from anabolic/androgenic steroids for at least 8-12 weeks. Some AAS abusers have difficulties with complete drug abstinence, and will initiate "bridging" routines between full-dose cycles. This may involve the periodic low-dose administration of an injectable steroid, such as 200 mg of testosterone enanthate or methenolone enanthate every 2-3 weeks. Such practice is discouraged, however, as it can interfere with hormonal recovery, and prevent a return to metabolic homeostasis.

When concluding a cycle, some steroid users also follow a practice of first slowly reducing their dosages (tapering). This tapering may proceed for a 3-4 week period, and will involve an even stepping down of the dose each week until the point of drug discontinuance. It is unknown, however, if such tapering offers any tangible value. This practice has never been evaluated in a clinical setting, and is not widely recommended with steroid medications as it is with some other drugs such as thyroid hormones or antidepressants. Virtually every high-dose AAS administration study can also be found to end at the maximum dosage, with no time allotted to tapering. One flaw in the logic of using a tapering program is that they are ostensibly designed to aid hormone recovery. Recovery is not possible, however, while supraphysiological levels of androgens are present, and such levels are usually found during all weeks of a normal (nonmedical) steroid taper. Individuals remain cautioned that dosage tapering is not a proven way to reduce postcycle muscle catabolism.

Friday, April 8, 2011

The Endocrinology of Muscle Growth


The road to anabolic insight must include a biological understanding of what muscle growth actually entails. Often simplified by the term "protein synthesis': muscle growth is actually a highly complex process involving much more than just building proteins from amino acids. Muscle hypertrophy, the correct scientific term for the way we adult humans build skeletal muscle, actually requires the fusion of new cells (called satellite cells) with existing muscle fibers. Since this discovery of satellite cells in 1961, a great deal of research into the mechanisms of muscle hypertrophy has been undertaken. Scientists have come to understand that unlike normal muscle cells, these satellite cells can be regenerated throughout adult life. Furthermore, they serve not as functional units of their own, but provide some of the necessary components to repair and rebuild damaged muscle cells. These satellite cells are normally dormant, and sit resting in small indentations on the outer surface of the muscle fibers, waiting for something to trigger them into activation.

Injury or trauma will provide the stimulus necessary to activate satellite cells. Once activated, they will begin to divide, multiply, and form into myoblasts (myoblasts are essentially donor cells that express myogenic genes). This stage of hypertrophy is often referred to as satellite cell proliferation. The myoblasts will then fuse with existing muscle fibers, donating their nuclei. This stage of the process is usually called differentiation. Skeletal muscle cells are multinucleated, which means they possess many nuclei. Increasing the number of nuclei allows the cell to regulate more cytoplasm, which allows more actin and myosin, the two dominant contractile proteins in skeletal muscle, to be produced. This increases the overall cell size and protein content of the muscle cell. Incidentally, the number of nuclei in relation to cross-sectional area also helps to determine the fiber type of the cell, namely slow twitch (aerobic) or fast twitch (anaerobic)326 327. It is important to note that we are not increasing muscle cell number with muscle hypertrophy. We are only increasing cell size and protein content, even though we are using satellite cells to help accomplish this. It is possible for myoblasts to fuse together and actually form new muscle fibers.This is called muscle hyperplasia,and equates to the legitimate growth of new muscle tissue. This is, however, not the primary mechanism of muscle growth in adult life.

Monday, April 4, 2011

side sffects ;Testicular Atrophy


Anabolic/androgenic steroids may produce atrophy (shrinkage) of the testicles. Testosterone is synthesized and secreted by the Leydig cells in the testes. Its release is regulated by the hypothalamic-pituitary-testicular axis, a system that is very sensitive to sex steroids.When anabolic steroids are administered, the HPTA will recognize the elevated hormone levels, and respond by reducing the synthesis of testosterone. If the testes are not given ample stimulation, over time they will atrophy, a process that can involve both a loss of testicular volume and shape. This atrophy mayor may not be obvious to the individual. In some cases, the testes will appear normal even though their functioning is insufficient. In other cases, shrinkage is very apparent. Visible testicular atrophy is one of the most common side effects of steroid abuse, appearing in more than 50% of all anabolic/androgenic steroid abusers.

Although testicular atrophy is very common in frequency, it is also regarded as a temporary reversible side effect.296 The gonads, by their nature, will vary in size under hormonal influence. Atrophy should not produce permanent damage. Note, however, that it can be a somewhat persistent issue. It may take many weeks or months of sufficient LH stimulation after steroid discontinuance for original testicular volume to be restored. Likewise, testicular atrophy is usually the root cause of prolonged post-cycle hypogonadism. In extreme cases, full recovery can take more than 12 months, and may even require medical intervention. A post-cycle recovery program inclusive of HCG (which mimics luteinizing hormone activity) may be used to minimize this recovery phase.297 This drug is also frequently effective for maintaining testicular mass when used on a periodic basis during steroid administration.29B HCG must be used with caution, however, as overuse may cause desensitization of the testes to LH,299 complicating HPTA recovery.

Some of the more potent anabolic/androgenic steroids, including testosterone, nandrolone, trenbolone, and oxymetholone, appear to be more suppressive of testosterone release than many other AAS drugs.This may be explained in part by the additional estrogenic or progestational activity inherent in these steroids, as estrogens and progestins both also provide negative feedback inhibition of testosterone release.30o 301 It is important to note, however, that all anabolic/androgenic steroids are capable of suppressing testosterone secretion. This includes primarily anabolic compounds such as methenolone and oxandrolone, which are normally regarded as milder in this regard. While these compounds may be less inhibitive of testosterone synthesis under some therapeutic conditions, when taken in the supratherapeutic doses necessary for physique-or performance-enhancement, significant atrophy and suppression are common, and distinctions less pronounced.

side sffects :Prostate Cancer


Prostate cancer is dependent on androgens. This disease will not develop if androgens are eliminated from the body at a young age (as with castration), and abatement of androgenic activity in patients with active disease is regarded as a standard path of treatment. A complete picture of the involvement of androgens, however, remains unclear. Studies show there is no association between the testosterone level and likelihood of developing prostate cancer.273 On the same note, the administration of exogenous testosterone during androgen replacement therapy seems to have no effect on the risk for developing this disease. A review of the: available medical literature also does not support an increased risk of prostate cancer in steroid abusers,275 which typically endure excessive levels of androgenic: stimulation. The present model suggests that while' testosterone is a necessary component of prostate cancer/' it does not appear to be a direct trigger for its onset

New diagnoses of prostate cancer are sometimes reported during testosterone replacement therapy anq steroid abuse. Such reports may be the result of a previously undiagnosed condition or unrelate~ development of this disease, with androgen stimulation assisting the tumor growth rate. Many forms of prostatE cancer possess functional androgen receptors, and arJ highly androgen responsive. As such, they can bJ stimulated to grow under the influence of testosterone 01 other anabolic/androgenic steroids. Given this effect, AA~ drugs are usually contraindicated in patients with ~ history of prostate cancer. While steroid administratio~l appears unlikely to cause prostate cancer,

side effects :Libido/Sexual Dysfunction



Anabolic/androgenic steroids may alter sexual desire and functioning. The nature of this alteration, however, can vary depending on individual circumstances.Testosterone is the primary male sex steroid, and is responsible for increasing sexual desire and supporting many male reproductive-system functions.264 Since all anabolic/androgenic steroids influence the same primary receptor as testosterone, abuse of these drugs (characterized by high levels of stimulation) is usually linked to strong increases in sexual desire, as well as copulation and orgasm frequency.265 The effect of steroid abuse on erectile function is more variable. In many cases, a significant increase in the frequency and duration of erections is noted. In other instances, however, periodic issues with having or maintaining erections are reported, even when steroid levels are high and libido is significantly increased. Sexual issues are also common after steroid discontinuance, when endogenous androgen levels are low.

Studies with dihydrotestosterone and aromatase inhibition demonstrate that estrogen is not necessary for the support of male libido and sexual functioning.266 Many non-aromatizable steroids are, therefore, capable of sustaining male sexual functioning given the right level of androgenic stimulation. Difficulties remain possible in many instances, however, especially when primarily anabolic compounds such as methenolone, nandrolone, oxandrolone, and stanozolol are used alone. These drugs many not provide sufficient androgenicity to compensate for the suppression of endogenous testosterone.267 Given the diverse nature in which sex steroids influence human psychology, the existence of other influencing factors during steroid abuse cannot be excluded, including estrogenic activity.268 The addition or substitution of testosterone during a cycle is usually regarded as the most reliable way to correct issues with male sexual interest and functioning, as it supplements the full spectrum of sex steroid activity.

Priallism:
In very rare instances, anabolic/androgenic steroids have been linked to priapism.269 270 271 This is a condition characterized by the development of an erection that will not return to its flaccid state within four hours. Priapism is a potentially very serious condition, which can require medical or surgical intervention. If left untreated, priapism can lead to permanent penile damage, erectile dysfunction, or even gangrene, which may necessitate removal of the penis. When priapism is linked to steroid use, testosterone is usually responsible. Furthermore, this condition appears to be more frequent in younger patients undergoing treatment for hypogonadism. This may be due in part to a rapid increase in androgenicity, in a male reproductive system that has not yet been exposed to high levels of stimulation. Priapism is very unlikely to develop in adult steroid abusers.

Friday, April 1, 2011

Psycological side sffects


The effects of anabolic/androgenic steroids on human psychology are complex, controversial, and not fully understood. What is known for certain is that sex steroids influence human psychology. They play a role in an individual's general mood, alertness, aggression, sense of well-being, and many other facets of our psychological state.There are known psychological differences between men and women because of differences in sex steroid levels, and, likewise, altering hormone levels with the administration of exogenous steroids may influence human psychology. The exact strength of this association, however, remains the subject of much research and speculation. In reviewing some of the more substantial data that has been presented thus far, we find a better (though incomplete) understanding of the effects of AAS in several key areas of psychological health.

Aggression
Men tend to be more aggressive than women, a characteristic that has been partly attributed to higher androgen levels. Physiologically, androgens are known to act on the amygdala and hypothalamus, areas of the brain involved in human aggression. They also affect the orbitofrontal cortex, an area involved with impulse control.231 Steroid abusers commonly report increases in aggression (irritability and bad temper) when taking anabolic/androgenic steroids. In fact, among the illicit steroid-using community, these drugs are often differentiated from one another with regard to their aggression-promoting properties. Many athletes in explosive strength sports even specifically favor highly androgenic drugs such as testosterone, methyltestosterone, and fluoxymestero'ne due to their perceived greater abilities to support aggression and the competitive drive.232 Whil~ some association between steroid use and aggression is understood, the magnitude of this association remains the subject of much debate.

The psychological effects of escalating dosages of testosterone esters have been examined in a number of placebo-controlled studies. At therapeutic levels, no adverse psychological effects are apparent. If anything, testosterone replacement therapy tends to improve mood and sense of well-being. When used at a contraceptive dosage (200 mg per week), again, no significant psychological effects are seen.233 234 As the dosage reaches a moderate supratherapeutic range (300 mg per week), psychological side effects such as aggression began to appear in some subjects, but these reports remain mild and infrequent.235 At a dosage of 500 to 600 mg per week (5 to 6 times the therapeutic level), mild increases in aggression and irritability are frequently reported. Approximately 50/0 of subbbbjes displayed manic or hypomanic behavior in reaaaacn to this much testosterone, although the vast mmcrity of people still exhibited minor or no psychological ange.

Dependency Addiction
Anabolic/androgenic steroids are considered to be drugs of abuse. Although there is no universally accepted definition for this, abuse is commonly described as the continued use of a substance in spite of adverse consequences. Given the negative health consequences that are associated with supratherapeutic doses of AAS drugs, this cl.assification is a difficult one to dispute. Drugs of abuse are very often also drugs of dependency, which in this context describes an impaired ability to control the use of a substance. There has been a longstanding debate over whether or not anabolic steroids also fit the definition of drugs of dependency. Furthermore, among those that support the notion of an anabolic steroid dependency, there is a split with regard to the nature of this dependency (psychological or physical).

Physical dependency is usually regarded as the most serious form of drug dependency, although both types can be very extreme and troubling depending on the situation. Physical dependency is defined as the need to administer a substance in order for the body to function normally. A physical dependency is usually characterized by drug tolerance, and withdrawal symptoms if the drug is discontinued abruptly. The most well known examples of drugs of physical dependency are opiates such as morphine, hydrocodone, oxycodone, and heroin. Opiates can be very difficult drugs for dependant individuals to quit using, since stopping their use tends to produce extreme withdrawal symptoms including physical pain, sweating, tremors, changes in heart rate and blood pressure, and intense cravings for the drug. The physical symptoms may last for days to weeks after the drug is discontinued, while the psychological symptoms can persist for months longer.

Anabolic/androgenic steroid abuse could be associated with many of the DSM-IV criteria necessary for a diagnosis of both psychological and physical drug dependency. For instance, it is not uncommon for someone to take the drugs in higher doses or for longer periods of time then they had initially planned (criteria #1). Many abusers also have a desire to cut down on their use of these drugs, but concerns over lost muscle size, strength, or performance may prevent this decision (criteria #2). Individuals often continue to abuse steroids in spite of negative health consequences (criteria #5). Steroid abuse is also associated with a diminishing level of effect and escalating dosages (criteria #6). Lastly, steroid discontinuance has been associated with withdrawal symptoms (criteria #7), including reduced sex drive, fatigue, depression, insomnia, suicidal thoughts, restlessness, lack of interest, dissatisfaction with body image, headaches, anorexia, and a desire to take more steroids.

The physical benefits of anabolic/androgenic steroids complicate the matter of drug dependency a great deal. Unlike narcotics, the main motivator behind the use of steroids is their positive effect on muscle and performance. With this in mind, steroid addiction could actually be a misdiagnosis for muscle dysmorphia in many cases. This is a psychological disorder characterized by persistent feelings of physical inadequacy in spite of extreme muscular development. Steroid abuse (often extreme) is highly common in muscle dysmorphics, along with compulsive resistance training.243 But steroid abuse is regarded as a symptom of this disorder, not a cause. In a similar sense, the physique-, strength-, and performanceimproving qualities of anabolic/androgenic steroids could be driving much or all of the abuse. An analogy would be the so-called addiction to chocolate. Some individuals develop tangible psychological issues surrounding the consumption of chocolate, with uncontrolled binging and negative social and health consequences. But we do not regard chocolate itself as a substance that causes dependency. There is some evidence that the reinforcing qualities of steroid use go beyond an attraction to their physical benefits. Lab animals such as mice and hamsters will repeatedly self-administer testosterone and other anabolic/androgenic steroids for example, an effect that cannot be caused by a perception of physical change.245 Testosterone is also known to interact with the mesolimbic dopamine system, which is common with other drugs of abuse.246 247 Studies additionally suggest that anabolic/androgenic steroids influence dopamine transporter density and increase sensitivity of the brain reward system.248 Steroids are known to influence psychology, and abusers commonly report an increased sense of well ness, vitality, and confidence when taking AAS drugs. Some speculate this is due in part to an inherent psychoactive effect. Further research is needed to determine if anabolic/androgenic steroids are actually mild psychoactive drugs.

Depression/Suicide
Anabolic/androgenic steroids abuse may be associated with bouts of depression. This is most common after the administration of AAS drugs has been discontinued, especially following high doses or long cycles. During the time that steroids are being administered, natural hormone production is diminished because the body recognizes the excess hormone levels. When the steroid drugs are abruptly discontinued, however, the body can enter a state of temporary hypogonadism (low androgen levels). This may be associated with a number of psychological symptoms including depression, insomnia, and loss of interest.This condition is usually referred to as anabolic steroid withdrawal depression, and can persist for weeks or even months as the body slowly resumes normal hormone production The most common method of addressing anabolic steroid withdrawal depression in men is preemptively, with the implementation of an aggressive post-cycle hormone recovery program. These programs are typically based on the combined use of HCG (human chorionic gonadotropin) and anti-estrogenic drugs such as tamoxifen and clomiphene. They are used together in a way that can stimulate and sensitize the hypothalamic pituitary testicular axis, allowing natural hormone production to return more quickly. Alternately or concurrently, fluoxetine (or other antidepressant medications) may help alleviate symptoms of depression following steroid withdrawal, especially when this depression is prolonged or severe.251 These drugs must be used with caution, however, as they also have been linked with increased thoughts of suicide in some patients Although less common,depression is sometimes reported during the active administration of anabolic/androgenic steroids. This may be caused by an imbalance of sex steroid levels, particularly with regard to relative androgenicity or estrogenicity. In more cases than not, it' will involve a situation where sufficient androgenicity is' not present, usually when primarily anabolic drugs are', being taken alone. Given the diverse nature in which seXi' steroids interact with human psychology, however, it isi difficult to clearly outline the parameters necessary fo~ this type of depression to develop. Further confusing the issue is the fact that this depression can involve eitheri elevated or suppressed levels of certain sex steroids. Th~i addition of testosterone to an anabolic steroid cycle! causing depression may alleviate the problem in man(but not all) instances,as it can provide both supplemental' androgenic and estrogenic action.
Suicide has been linked to anabolic/steroid abuse in rare instances.253 Such reports are usually case studies, involving individuals that were believed to be psychologically stable before abusing AAS, and who committed suicide during or after use of the drugs. It is known that depression is a common complaint during anabolic steroid withdrawal. It is also known that a small percentage of users are especially sensitive to the psychological effects of anabolic/androgenic steroids,and notice dramatic mood swings, manic behavior, and/or severe depression with their use. It is unknown why these individuals have such extreme reactions, while the vast majority of users notice only mild or moderate changes to their psychological state. Further research is needed to identify and understand these individuals. Readers are cautioned that adverse psychological effects, including severe depression and suicidal thoughts, have been associated with steroid abuse in a small minority of users. Beyond this, there is no compelling evidence suggesting that anabolic/androgenic steroid abuse will lead to suicide in otherwise mentally stable users.

Insomnia
Anabolic/androgenic steroid use may be associated with insomnia. This adverse reaction appears to be related to an imbalance of hormone levels, and has been noticed during both excess and insufficient hormonal states. For example, insomnia is a common complaint among men suffering from low androgen levels (hypogonadism).254 It is also frequently reported by steroid abusers during the post-cycle refractory period, when endogenous androgen levels are also low due to steroid-induced suppression.255 At the same time, this side effect is also seen during active AAS administration,256 when androgen levels are very high. The full etiology of steroid-related insomnia is not fully understood, although increased cortisol or diminished estrogen is commonly blamed.257 258 Given the complex interactions between sex steroids and the human psyche, it is difficult to predict how and when this adverse reaction will appear. While insomnia may be frequently reported among steroid users, this side effect rarely reaches a clinically significant level.

Steroid Side Effects


While anabolic/androgenic steroids (AAS) are generally regarded as therapeutic drugs with high safety, their use can also be associated with a number of adverse cosmetic, physical, and psychological effects. Many of these side effects are often apparent during therapeutic-use conditions, although their incidence tends to increase profoundly as the dosages reach supratherapeutic ranges. Virtually everyone that abuses anabolic/androgenic steroids for physique-or performance-enhancing purposes notices some form of adverse effects from their use. According to one study, the exact frequency of tangible side effects in a group of steroid abusers was 96.4%. This shows very clearly that it is far more rare to abuse these drugs and not notice side effects than it is to endure them.88 In addition to the side effects that anabolic/androgenic steroids can have on various internal systems, there are others which may not be immediately apparent to the user. The following is a summary of the biological systems and reactions effected by AAS use.

Cardiovascular System
The use of anabolic/androgenic steroids in supratherapeutic (and often therapeutic) doses can have a number of adverse effects on the cardiovascular system.
\ This may be noticed in several areas including unfavorable alterations in serum cholesterol, a thickening of ventricular walls, increased blood pressure, and changes in vascular reactivity. In an acute sense these drugs are admittedly very safe. The risk of an otherwise healthy person suffering a heart attack from an isolated steroid cycle is extremely remote. The risk of stroke is also extremely low. When these drugs are abused for long periods, however, their adverse effects on the cardiovascular system are given time to accumulate. An increased chance of early death due to heart attack or stroke is, likewise, a valid risk with long-term steroid abuse. In order to better understand this risk, we must look specifically at how anabolic/androgenic steroids affect the cardiovascular system in several key ways.

Cholesterol/Lipids
Anabolic/androgenic steroids use can adversely affect both HDL (good) and LDL (bad) cholesterol values. The ratio of HDL to LDL cholesterol fractions provides a rough snapshot of the ongoing disposition of plaque in the arteries, either favoring atherogenic or anti-atherogenic actions. The general pattern seen during steroid use is a lowering of HDL concentrations, which is often combined with stable or increased LDL levels.Triglyceride levels may also increase.The shift can be unfavorable in all directions. Note that in some cases, the total cholesterol count will not change significantly. The total cholesterol level can, therefore, give a false representation of uncompromised lipid health. Almost invariably the underlying HDL/LDL ratio will decrease.While this ratio should return to normal following the cessation of steroid intake, plaque deposits in the arteries are more permanent. If unfavorable shifts in lipids are exacerbated by the long-term use of steroidal compounds, significant damage to the cardiovascular system can result.

Anabolic/androgenic steroids are most consistent in their lowering of HDL levels. This adverse effect is mediated through the androgenic stimulation of hepatic lipase, a liver enzyme responsible for the breakdown of HDL (good) cholesterol.89 With more hepatic lipase activity in the body, the favorable (anti-atherogenic) HDL cholesterol particles are cleared from circulation more quickly, and their levels drop. This is an effect that seems to be very pronounced at even modest supratherapeutic dosage levels. For example, studies with testosterone cypionate noted a 21 % drop in HDL cholesterol with a dosage of 300 mg per week.90 Increasing this dosage to 600 mg did not have any significant additional effect, suggesting that the dosage threshold for strong HDL suppression is fairly low.

Oral steroids, especially c-17 alpha alkylated compounds, are particularly potent at stimulating hepatic lipase and suppressing HDL levels. This is due to first pass concentration and metabolism in the liver. A drug like stanozolol may, therefore, be milder than testosterone with regard to androgenic side effects, but not when it comes to cardiovascular strain. A study comparing the effects of a weekly injection of 200 mg testosterone enanthate to only a 6mg daily oral dose of stanozolol demonstrates the strong difference between these two types of drugs very wel1.91 After only six weeks, 6mg of stanozolol was shown to reduce HDL and HDL-2 cholesterol levels by an average of 33 and 71 % respectively. HDL levels (mainly the HDL-3 subfraction) were reduced by only 9% in the testosterone group. LDL cholesterol levels also rose 29% with stanozolol, while they dropped 16% with testosterone. Esterified injectable steroids are generally less stressful to the cardiovascular system than oral agents.
It
is also important to note that estrogens can have a favorable impact on cholesterol profiles. The aromatization of testosterone to estradiol may, therefore, prevent a more dramatic change in serum cholesterol. A study examined this effect by comparing the lipid changes caused by 280 mg of testosterone enanthate per week, with and without the aromatase inhibitor testolactone.92 Methyltestosterone was also tested in a third group, at a dose of 20 mg daily, to judge the comparative effect of an oral alkylated steroid. The group using only testosterone enanthate in this study showed a small but not significant decrease in HDL cholesterol values over the course of the 12-week investigation. After only four weeks, however, the group using testosterone plus the aromatase inhibitor displayed an HDL reduction of an average of 25%. The group taking methyltestosterone experienced the strongest HDL reduction in the study, which dropped 35% after four weeks. This group also noticed an unfavorable rise in LDL cholesterol levels.

The potential positive effect of estrogen on cholesterol values also makes the issue of estrogen maintenance something to consider when it comes to health risks. To begin with, one may want to consider whether or not estrogen maintenance drugs are actually necessary in any given circumstance. Are side effects apparent, or is their use a preventative step and perhaps unnecessary? The maintenance drug of choice can also have a measurable impact on cholesterol outcomes. For example, the estrogen receptor antagonist tamoxifen citrate does not seem to exhibit anti-estrogenic effects on cholesterol values, and in fact tends to increase HDL levels in some patients. Many individuals decide to use tamoxifen to combat estrogenic side effects instead of an aromatase inhibitor for this reason, particularly when they are using steroids for longer periods of time, and are concerned about their cumulative cardiovascular side effects.

Enlarged Heart
The human heart is a muscle. It possesses functional androgen receptors, and is growth-responsive to male steroid hormones. This fact partly accounts for men having a larger heart mass on average than women.93 Physical activity can also have a strong effect on the growth of the heart. Resistance exercise (anaerobic) tends to increase heart size by a thickening of the ventricular wall, usually without an equal expansion of the internal cavity. This is known as concentric remodeling. Endurance' (aerobic) athletes, on the other hand, tend to increase heart size via expansion of the internal cavity, without significant thickening of the ventricles (eccentric remodeling). Even with concentric or eccentric remodeling, diastolic function usually remains normal in the athletic heart.The heart muscle is also dynamic.When regular training is removed from a conditioned athlete, the wall thickening and cavity expansion tend to reduce.

Anabolic steroid abusers are at risk for thickening of the left and right ventricular walls,94 known as ventricular hypertrophy. Hypertrophy of the left ventricle (the main pumping chamber) in particular is extensively documented in anabolic/androgenic steroid abusers.951 While left ventricular hypertrophy is, again, also found in natural power athletes, substance-abusing athletes tend to have a much more profound wall thickening. They also tend to develop pathological issues related to this thickening, including impaired diastolic function, and ultimately reduced heart efficiency.96 The level of impairment is closely associated with the dose and duration of steroid abuse. A left ventricle wall exceedinc 13mm in thickness is rare naturally, and may be indicativ~ of steroid-abuse or other causes.97 It may further sugges1 that pathological left ventricular hypertrophy ha~ developed. Additional testing of such patients d recommended.

Left ventricular hypertrophy (LVH) is an independenl predictor of mortality in overweight individuals with hig( blood pressure.98 It has also been linked to atri~ fibrillation, ventricular arrhythmia, and sudden collaps! and death.99 While LVH in non-steroid-using athlete' tends to be without clinical significance, pathologicc increases in QT dispersion are noticed in steroid abuse~i ~ith LVH ..100 The.se ch~nges ten.d to be si~ilar to th~ Increases In QT dispersion noted In hypertensive patientl with LVH.l0l Among other things, this could leave a steroi~ abusing individual more susceptible to a serious advers~ event, including arrhythmia or heart attack. Isolate~ medical case studies of longtime steroid abusers suppOr] an association between LVH and related pathologieJ including ventricular tachycardia (arrhythmia originatind in the left ventricle), left ventricular hypokinesil,(weakened contraction of the left ventricle), and decreased ejection fraction (reduced pumping volume and efficiency)

Heart mass can increase or decrease in relation to the current state of anabolic/steroid use, the average dosage, and duration of intake. Likewise, the heart usually begins to reduce in size once anabolic/androgenic steroids are no longer being used. This effect is similar to the way the heart will reduce in size once an athlete no longer follows a rigorous training schedule.103 Even with this effect, however, some changes in heart muscle size and function caused by the drugs may persist. Studies examining the effects of steroid use and withdrawal on left ventricular hypertrophy noted that athletic subjects who abstained from steroid abuse for at least several years still had a slightly greater degree of concentric left ventricular hypertrophy compared to non-steroid-using athletic controls.104 The disposition of pathological left ventricular hypertrophy following long-term steroid abuse and then abstinence remains the subject of investigation and debate.

Heart Muscle Damage
Anabolic/androgenic steroid abuse is suspected of producing direct damage to the heart muscle in some cases. Studies exposing heart cell cultures to AAS have reported reduced contractile activity, increased cell fragility, and reduced cellular (mitochondrial) activity, providing some support for a possible direct toxic effect to the heart muscle.10s 106 Furthermore, a number of case reports have found such pathologies as myocardial fibrosis (scar tissue buildup in the heart), myocardial inflammation (inflammation of heart tissue), cardiac steatosis (accumulation of triglycerides inside heart cells), and myocardial necrosis (death of heart tissue) in longterm steroid abusers.10? 108 109 110 A direct link between drug abuse and cardiac pathologies is assumed in these cases, but cannot be proven given the slow nature in which these cardiac pathologies develop, and the influence many other factors (such as diet, exercise, lifestyle, and genetics) can have on them. Individuals remain cautioned about the possibility of cardiac muscle damage with long-term steroid abuse.
taking steroids.112 Hypertension, or consistently high blood pressure at or above 140/90 for either systolic or diastolic measures, has been reported in steroid users/113 although in most cases the elevations are more modest. Increased blood pressure may be caused by a number of factors, including increased water retention, increased vascular stiffness, and increased hematocrit. Aromatizing or highly estrogenic steroids tend to cause the greatest influences over blood pressure, although elevations cannot be excluded with non-estrogenic anabolic/androgenic steroids. Blood pressure tends to normalize once anabolic/androgenic steroids have been discontinued.

Hematological (Blood Clotting)
Anabolic/androgenic steroids can cause a number of changes in the hematological system that affect blood clotting. This effect can be very variable, however. The therapeutic use of these drugs is known to increase plasmin, antithrombin 111/ and protein S levels, stimulate fibrinolysis (clot breakdown), and suppress clotting factors II, V, VII, and ,X.114 115 These changes all work to reduce clotting ability. Prescribing guidelines for anabolic/androgenic steroids warn of potential increases in prothrombin time, a measure of how long it takes for a blood clot to form.116 If prothrombin time increases too greatly, healing may be impaired. The effects of anabolic/androgenic steroids on prothrombin time are generally of no clinical significance to healthy individuals using these drugs in therapeutic dosages. Patients taking anticoagulants (blood thinners), however, could be adversely affected by their use.

Conversely, anabolic/androgenic steroid abuse has been linked to increases in blood clotting ability. These drugs can elevate levels of thrombin 11 ? and C-reactive protein,118 as well as thromboxane A2 receptor density,119 which can support platelet aggregation and the formation of blood clots. Studies of steroid users have demonstrated statistically significant increases in platelet aggregation values in some subjects.120 There are also a growing number of case reports where (sometimes fatal) blood clots, embolisms, and stokes have occurred in steroid abusers. Although it has been difficult to conclusively link these events directly to steroid abuse, the adverse effects of anabolic steroids on components of the blood coagulation system are well understood. These serious adverse effects are now regarded as recognized risks of steroid abuse among many that study these drugs. In therapeutic levels, the anti-thrombic effects of anabolic/androgenic steroids seem to dominate physiology, and decreases in blood clotting ability may be noted. At a certain supratherapeutic dosage point, however, the pro-thrombic changes appear to overtake the anti-thrombic changes, and physiology begins to favor fast and abnormally thick clot formation (hypercoagulability). The exact dosage threshold or conditions required to increase blood clotting has not been determined, and some studies with steroid users taking supraphysiological doses fail to demonstrate increased coagulability.126 Individuals remain warned of the potential increases in thrombic risk with anabolic/androgenic steroid abuse. Blood clotting tendency should return to the pretreated state after the discontinuance of anabolic/androgenic steroids.

Hematological {Polycythenlial
Anabolic/androgenic steroids stimulate erythropoiesis (red blood cell production). One potential adverse effect of this is polycythemia, or the overproduction of red blood cells. Polycythemia can be reflected in the hematocrit level, or the percentage of blood volume that is made up of red cells. As the hematocrit rises, so too does the viscosity of the blood. If the blood becomes too thick, its ability to circulate becomes impaired. This can greatly increase the risk of serious thrombic event including embolism and stroke. A high hematocrit level is also an independent risk factor for heart disease.127 The normal hematocrit level in men is 40.7 to 50.30/0, and in women it is 36.1 to 44.3% (numbers may vary very slightly depending on the source). For the sake of scale, while a hematocrit of 500/0 may be normal, a hematocrit of 60% or above is considered critical (life threatening).

Anabolic/steroid administration tends to raise the hematocrit level by several percentage points, sometimes more. As a result, many steroid-using bodybuilders will have hematocrit levels that are above the normal range. For example, one study measured the average hematocrit in a group of steroid abusing competitive bodybuilders to be 55.70/0.128 This level is considered clinically high, and would increase blood viscosity enough to raise the risk of serious cardiovascular event. Although not likely to be an isolated cause, high hematocrit is believed to have been a contributing factor in the deaths of a number of steroid abusers, usually paired with high blood pressure, homocysteine, and/or atherosclerosis. The average hematocrit level in bodybuilders not taking anabolic/androgenic steroids was 45.6%, well within the normal range for healthy adult men.

Many physicians that specialize in hormone replacement therapy consider a hematocrit level of 550/0 to be an absolute cutoff point. At or above this point, and anabolic/androgenic steroid therapy cannot be continued safely. Drug intake would be ceased at this point until the hematocrit issues have been corrected. Minor elevations in hematocrit may be addressed with phlebotomy. For this, 1 pint of blood may be removed periodically during steroid intake, often every two months. Proper hydration is also important, as dehydration can temporarily cause the hematocrit level to elevate, giving a false positive for polycythemia. The daily intake of aspirin is also commonly advised if the hematocrit is above normal, as this will reduce platelet aggregation, or the tendency for platelets to stick together and form clots. Individuals remain cautioned of the potential cardiovascular danger of high hematocrit levels associated with anabolic/androgenic steroid use.

Homocysteine
Anabolic/androgenic steroids may elevate homocysteine levels. Homocysteine is an intermediary amino acid produced as a byproduct of methionine metabolism. High levels of homocysteine have been linked to elevations in the risk for cardiovascular disease.129 It is believed to play a direct role in the disease, increasing oxidative stress, including the oxidation of LDL cholesterol, and accelerating atherosclerosis.13o Elevated levels of homocysteine may also induce vascular cell damage, support platelet aggregation, and increase the likelihood of thrombic event.131 132 133 The normal range for homocysteine levels in men aged 30 to 59 years is 6.311.2umoIlL. For women of the same age the average is 4.5-7.9umol/L. Increased risk of heart attack, stroke, o~ other thrombic event are noted with even modest elevations in homocysteine. According to one study, 2 homocysteine level exceeding 15umollL in patients wit~ heart disease is associated with a 24.70/0 increasec likelihood of death within five years .

Androgens' stimulate elevations in homocysteine,135 an~ men have an approximately 250/0 higher level on averag~ than women.136 Anabolic/androgenic steroid abuse hal been associated with hyperhomocysteinaemia, 0 consistent clinically high homocysteine levels.137 Oni study found that the average homocysteinJ concentration in a group of 10 men that had been sel~
I
administering anabolic/androgenic steroids (in a cyclij pattern) for 20 years was 13.2 umol/L.138 Three of thes\ men died of a heart attack during the investigation, an~ had homocysteine levels between 15umol/L an~ 18umollL. The average homocysteine level i~li bodybuilders who had never taken steroids wa 8.7umol/L, while it was 10.4umol/L in previous steroid· users (3 months abstinence). One study did show thai administering 200 mg of testosterone enanthate (Wit~ and without an aromatase inhibitor) for three weeks faile~ to produce a significant elevation in homocysteine.139 It il unknown if the moderate dosage, drug type (esterifie~')injectable vs. c17-aa), or short duration of intake were factors in the differing outcome from other studies. Individuals remain warned of the potential for elevations in the homocysteine level with steroid abuse.

Vascular Reactivity
The endothelium is a layer of cells that line the entire circulatory system. These cells are found on the inside of all blood vessels, and help increase or decrease blood flow and pressure by relaxing or constricting the vessels (referred to as vasodilation and vasoconstriction, respectively).These cells also he'lp regulate the passage of materials in and out of blood vessels, and are involved in a number of important vascular processes including blood clotting and new blood vessel formation. Having a more flexible (reactive) endothelium is generally considered desirable for health, and, likewise, the endothelium is often compromised in individuals with cardiovascular disease. Patients with endothelial dysfunction tend to notice greater vasoconstriction, restricted blood flow, higher blood pressure, local inflammation, and reduced circulatory capacity.140 This may place them at greater risk for heart attack, stroke, or thrombosis (blood clot).

Endothelial cells are androgen responsive, which may partly account for men exhibiting less vascular reactivity than women.141 Similarly, anabolic/androgenic steroid use has been shown to impair endothelial activity and vascular reactivity. Studies at the University of Innsbruck in Austria compared the level of endothelial dilation in 20 steroid users to a group of control athletes.142 Those individuals using anabolic steroids noticed slight but measurably impaired vascular dilation and endothelial function. Additional studies at the University of Wales in Cardiff comparing vascular dilation in active, previous, and non-steroid users, also demonstrated anabolic steroids to cause a decline in endothelial-independent vasodilation.143 These effects leave the steroid user with more relative "stiffness" in the vascular system, which could increase the chance of an adverse cardiovascular event. In both studies, vascular reactivity improved after the discontinuance of anabolic/androgenic steroids.

Immune System
The human immune system is responsive to sex hormones. This results in functional differences in immunity between the sexes. Women tend to have a more active immune system compared to men, and are slightly more resistant to bacterial infection and other types of infection.144 The female immune system is also more prone to developing autoimmune diseases, which may be linked to its higher level of activity.145 The day-to-day activity of the immune system can also fluctuate throughout the menstrual cycle, further demonstrating thestrong influence ofsexsteroids.146Theslightlyweaker resistance to infection of men appears to be caused by testosterone, which is an immunosuppressive hormone.147 Androgens may modulate the immune system directly, through their conversion to estrogens,148 or by modifying glucocorticoid activity.

Anabolic/androgenic steroids have displayed both immunostimulatory and immunosuppressive actions in animal models.15o Given that these drugs can influence the immune system through a variety of pathways, and anabolic steroids are a fairly diverse class of drugs, their effects on the immune system may vary depending on the particular conditions. When used therapeutically, changes in immune system functioning are usually minor, and have not amounted to strong immunostimulation or immunosuppression. Anabolic/androgenic steroids have also been used safely in many immunocompromised patients, such as those with muscle wasting associated with HIV infection, without any significant change in immune system or viral markers.

The use of anabolic/androgenic steroids in supratherapeutic doses may slightly impair immune system functioning, reducing an individual's resistance to certain types of infection. In one study, steroid abusers were shown to have lower serum levels of IgG, IgM, and IgA immunoglobulins (antibodies) compared to bodybuilding controls, consistent with immunosuppression.153 Although this may logically increase the chance of contracting certain types of illness a significant increase in the history of illness could not be established in these same steroid abusers. Given the very random nature of illness, however, it may be difficult to establish such a link without extensive study. The effect of hormone manipulation on immunity should also be temporary, and return to a normal state once pre-treated hormonal chemistry is restored. Individuals remain warned of the potential for minor immunosuppression and increased chance of illness with steroid abuse.

Kidlleys (Renal System)
Anabolic/androgenic steroids are generally well tolerated by the renal system.These drugs are largely excreted from the body through the kidneys, although there is no inherent strong toxicity in this process. In fact, there are many instances in which these drugs may be used as supportive treatment in patients with compromised kidney function. For example, anabolic steroids have been prescribed to increase the production of red blood cells in' patients with anemia related to various forms of kidney, disease.154 155 They have even been used as general anabolic (lean body mass) support, and to treat hypogonadism, in patients undergoing dialysis.156 157 While care must be taken with such patients, therapy maYl often be conducted very safely. In otherwise healthy: individuals, clinical renal toxicity caused by the short-term administration of anabolic/androgenic steroids is unlikely.

There have been isolated reports of severe kidney damage in steroid abusers. For example, a handful ot individuals have developed Wilms' Tumo~ (nephroblastoma),158 159 which is a rare form of kidne~ cancer usually found in children. Its appearance in adul1: steroid users is suspect, but not conclusive evidence tha1 drugs were the actual cause.There have also been isolate~ reports of renal cell carcinoma in steroid abusers.160 16] Since this is the most common form of kidney cance~ however, conclusive links are again difficult to draw.Ther~: have additionally been case reports of combined liver an~ renal failure with steroid abuse.162 163 In these casel kidney failure may have been subsequent to steroid induced liver toxicity, as cholestasis (bile duct obstructio~ is known to cause acute tubular necrosis and renal failure.

Kidney health should be a concern for long-term steroid! using bodybuilders and power athletes. To begin with excessive resistance training can produce some strain o~ the renal system. A condition called rhabdomyolysis i~ caused by the extreme damage of muscle tissue, whic~ releases myoglobin and a number of nephrotoxi1 compounds into the blood. In high levels this ca~ damage kidney tissue and even cause renal failure. Ther~' have been rare case reports of severe clinicarhabdomyolysis in bodybuilders, both with and without mentionofsteroid abuse. Steroid use mayalso cause hypertension, which can lead to kidney damage.17o While anabolic/androgenic steroids are generally not regarded as direct kidney toxic drugs, they may be used to support a lifestyle and long-term metabolic state characterized by extreme training, heightened daily muscle protein turnover, and elevated blood pressure. Over time this may compromise kidney health. Regular monitoring of kidney function is recommended.

Liver (Hepatic System)
Many oral anabolic/androgenic steroids (or injectable forms of oral steroids) are toxic to the liver (hepatotoxic). These compounds can cause serious and sometimes lifethreatening damage when abused, and occasionally even under therapeutic conditions. Those agents commonly associated with clinical hepatotoxicity include (but are not limited to) fluoxymesterone, methandrostenolone, methylandrostenediol, methyltestosterone, norethandrolone, oxymetholone, and stanozolol.171 172 173 174 175 These steroids all have either an ethyl or methyl group at carbon-17 (c-17alpha alkylation). All c-17alpha alkylated anabolic/androgenic steroids possess some level of hepatotoxicity. Liver strain, as assessed by elevated liver enzymes, has also been reported with non-alkylated esterified injectable steroids including nandrolone decanoate and testosterone enanthate in extremely rare instances.176 177 These steroids have never been associated with serious hepatic damage, however, and are not regarded as liver toxic.
Alkylation of c-17alpha specifically protects the steroid molecule from metabolism by the enzyme 17betahydroxysteroid dehydrogenase (17beta-HSD). This enzyme normally oxidizes a steroid's 17beta-hydroxyl (17beta-ol) group, which must remain intact for the drug to impart any anabolic or androgenic effect. Oxidation of 17-beta-ol is one of the primary pathways of hepatic steroid deactivation. Without protection from this enzyme, very little active drug will survive the first pass through the liver and reach circulation after oral dosing. Alkylation of c-17alpha effectively protects the steroid from 17beta-HSD by occupying a hydrogen bond necessary for the breakdown of 17beta-ol to 17-keto. The compound must be metabolized through other pathways as a result, and immediate hepatic deactivation is prevented. The process allows a very high percentage of the steroid dose to pass into the bloodstream intact, but it also places some strain on the Iiv~r in the process.

The exact mechanism of hepatotoxicity induced by alkylated anabolic/androgenic steroids remains unknown, but it is speculated to be due in large part to the natural activity of androgens in the liver. This liver possesses a high concentration of androgen receptors, and is responsive to these hormones.178 With physiological androgens such as testosterone and dihydrotestosterone, however, only a moderate level of activity is permitted in this organ. This is because the liver is normally very efficient at metabolizing steroids, which mutes their local activity. But with the liver unable to easily deactivate alkylated steroids, however, a far greater level of hepatic androgenic activity is allowed. The concentration of steroid in the liver is also very high after oral administration, as the digestive tract delivers the drug directly to this organ before it can reach circulation. The fact that the most potent steroid ever given to humans on a mg-for-mg basis is also the most liver toxic, also supports a close association between androgenic potency and hepatotoxicity.

Early liver toxicity is usually visible in blood test results for hepatic function before physical symptoms or dysfunction develop. This is most likely to include elevations in aminotransferase enzymes AST and ALT, also called serum glutamic-oxalocetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT), respectively. The cholestatic enzymes alkaline phosphatase (ALP) and gamma-glutamyltranspeptidase (GGT) may also be elevated, along with other markers (see: Understanding Blood Tests). Screening for abnormalities in hepatic markers is regarded as the most effective way of preventing liver damage from steroid administration. Should asymptomatic toxicity go unnoticed and without a change in drug intake, it is likely to progress to more severe hepatic strain, injury, or hepatic dysfunction. Immediate cessation of anabolic/androgenic steroid use and a full assessment of liver and full-body health is advised should any signs of unacceptable liver toxicity become apparent.

The most common form of actual liver dysfunction caused by the administration of oral anabolic/androgenic steroids is cholestasis.181 This describes a condition where the flow of bile becomes decreased, usually because of obstruction of the small bile ducts in the liver (intrahepatic). This causes bile salts and bilirubin to accumulate in the liver and blood instead of being properly excreted thorough the d'igestive tract. Inflammation (hepatitis) may also be present.182 Symptoms of cholestasis may include anorexia, malaise, nausea, vomiting, upper abdominal pain, or pruritus (itching). The stool may also change to a clay color (alcholic stool) due to the reduced excretion of bile, and the urine may become amber. Cholestatic jaundice may develop, which is characterized by a yellowing of the skin, eyes, and mucous membranes due to high levels of bilirubin in the blood (hyperbilirubinemia). Intrahepatic cholestasis may also coincide with hepatocellular necrotic lesions (death of liver tissue).

Intrahepatic cholestasis will usually resolve itself without serious injury or medical intervention within several weeks of discontinuing all hepatotoxic steroids. More serious cases may take several months before normal hepatic enzyme levels and functioning are restored. Hepatic lesions are likely to heal over time as well, at least partially. In some cases physicians have initiated supportive treatment with ursodeoxycholic acid (ursodiol), which is a secondary bile salt known to possess hepatoprotective and anti-cholestatic effects, in an effort to hasten recovery.183 The exact value of using this medication to treat steroid-induced cholestatic jaundice remains unknown, however. The liver is highly resilient, and intrahepatic cholestasis is unlikely to continue degrading after drug discontinuance unless additional pathologies are present.

More serious hepatic complications are rare, but have included peliosis hepatis184 (blood-filled cysts on the liver), portal hypertension with variceal bleeding 185 (bleeding caused by increased blood pressure in portal vein related to obstructed blood flow), hepatocellular adenoma186 (non-malignant liver tumor), hepatocellular carcinoma 187 (malignant liver tumor), and hepatic angiosarcoma 188 (aggressive malignant cancer of the lining of blood vessels inside the liver). Some of these pathologies can be very insidious at times, developing quickly and without clear early symptoms. Although many of these potentially life-threatening side effects have often been attributed to very ill patients receiving steroid medications, a growing number of case reports are now involving otherwise healthy young bodybuilders abusing these drugs.

Physical
Acne : Androgens stimulate the sebaceous glands in the skin to secrete an oily substance called sebum, which is made of fats and the remnants of dead fat-producing cells. Excess stimulation, as with steroid abuse, may also cause a significant increase in the size ofthe sebaceous glands.191 Sebaceous glands are found at the base of the hair follicles in all hair-containing areas of the skin. If the androgen level becomes too high and the sebaceous glands become overactive, the hair follicles may begin to clog with sebum and dead skin cells, resulting in acne Acne vulgaris (common acne) is frequent in steroid users, especially when the drugs are taken in supratherapeutic levels. This often includes acne lesions on the face, back, shoulders, and/or chest.
A mild incidence of acne vulgaris is usually addressed with topical over-the-counter acne medications and a rigorous skin cleaning routine that removes excess oil and dirt. More serious acne may develop in sensitive individuals, including acne conglobata (severe acne with connected nodules under the skin) or acne fulminans (highly destructive inflammatory acne). Such incidences may require medical intervention, which usually involves treatment with isotretinoin. Topical anti-androgen drugs are also under investigation for the treatment of severe acne, and have shown a great deal of promise in earl} trials.192 Acne is typically resolved with the cessation 01 steroid use, although the overproduction of sebum ma} persist until the sebaceous glands have had time tc atrophy back to original size. Serious forms of acne ma} produce lasting scars.

Hair Loss (Androgenetic Alopecia)
Anabolic/androgenic steroids may contribute to a form d, hair loss on the scalp known as androgenetic alopeci'\ (AGA). This disorder is characterized by a progressivl! miniaturization of hair follicles, and a shortening of th anagen phase of hair growth, under androgen influence The hair produced by affected follicles will progressivelj thin, covering the scalp less and less effectively. In meH the baldness produced is usually identified most simply aJ male pattern. This will initially include a receding hairlinJ . (fronto-temporal thinning) and thinning on the crowrl areas where androgen receptor concentrations are higH In women, the balding usually takes on a more diffuse pattern, with thinning throughout the top of the head. Most women with androgenetic alopecia do not have a receding hairline.

Androgenetic alopecia is the most common form of hair loss in men and women alike. It is especially common in males, and more than S09tb of the population will notice it by the age of 50.193 As its name signifies, androgenetic alopecia involves the interplay of both androgenic hormones and genetic factors. Individuals with this condition appear to be more locally sensitive to androgens, and have higher levels of androgen receptor protein and dihydrotestosterone in the scalp, in comparison to those unaffected.194 Although dihydrotestosterone is identified as the primary hormone involved in the progress of androgenetic alopecia, it does not possess a unique ability to influence this condition. All anabolic/androgenic steroids stimulate the same cellular receptor, and as a result are capable of providing the necessary androgenic stimulation. Baldness can result from steroid use, even in the absence of steroids that convert to, or are derived from, dihydrotestosterone.

The genetics of androgenetic alopecia are not fully understood. At one time it was believed this condition could be inherited solely from the maternal grandfather. More recent evidence contradicts this notion, however, showing strong support for father-to-son transmission in many cases.195 A number of genes have been identified as having a potential link to the disorder, including certain variants (polymorphisms) of the androgen receptor gene.l96 197 No single genetic variant alone has yet been able to explain all cases of androgenetic alopecia, however. AGA is now believed to involve several genes (polygenic).198 The way these genes combine, and the level of androgens in the scalp, may ultimately work together to control the onset and severity of androgenetic alopecia. Estrogen is also known to lengthen the anagen phase,199 and the pathogenesis of this condition may ultimately involve genes that alter both androgen and estrogen activity.
Treatment for androgenetic alopecia in men usually involves topical minoxidil and oral finasteride, as-alpha reductase enzyme inhibitor. Women are typically prescribed anti-androgens and estrogen/progestin drugs. The focus in both cases is on reducing relative androgenic action in the scalp, which may (at least temporarily) stall the condition. With this in mind, many steroid users concerned with hair loss will tailor their drug intake to minimize unnecessary androgenic activity. This usually involves moderate dosing and the careful selection of drugs with high anabolic-to-androgenic ratios, such as oxandrolone, methenolone, or nandrolone. Alternatively, some may choose to use injectable testosterone esters combined with finasteride to reduce scalp DHT conversion. These strategies are met with varying degrees of success.
There has been no study on the role of genetics in baldness linked to steroid abuse. Anecdotally, individuals with existing visible androgenetic alopecia appear to be those most susceptible to the effects of anabolic/androgenic steroids on the scalp. For many of these people, the loss of hair appears significantly accelerated when taking these drugs. On the other hand, this side effect is generally a much less significant issue with individuals that have not noticed thinning beforehand. Many go on to abuse steroids for years without any visible effect at all, making it clear that there is more to this disorder than local androgen levels. It is well understood that androgens play a role in the progression of androgenetic alopecia for those genetically prone. Steroid use can, therefore, coincide with the first noticeable onset of this condition. It is unknown, however, if anabolic/androgenic steroid abuse can cause baldness in an individual that does not carry any genetic susceptibility.

Water and Salt Retention
Anabolic/androgenic steroids may increase the amount of water and sodium stored in the body. This may include increases in both the intracellular and extracellular water compartments. Intracellular fluid refers to water that has been drawn inside the cells. While this does not increase the protein content of the muscles, it does expand the muscle cell, and is often calculated and viewed as a part of total fat free body mass. Extracellular water is stored in the circulatory system, as well as in various body tissues, in the spaces between cells (interstitial). Increases in interstitial fluid can be noticeable and troubling cosmetically. In strong cases this can bring about a very puffy appearance to the body (peripheral or localized edema), with bloating of the hands, arms, body, and face. This may reduce the visibility of muscle features throughout the physique. Excess fluid retention can also be associated with elevated blood pressure/os which can increase cardiovascular and: renal strain.
Estrogen is a regulator of fluid retention in both men and women.206 This effect appears to be mediated in part by: changes in hypothalamic arginine vasopressin (AVP), the: primary hormone involved in controlling water reabsorption in the kidneys.207 Increased levels 01 estrogen tend to increase AVP levels, which can promote the increased storage of water. Estrogen also appears td act on the renal tubes in the kidneys in an aldosterone~ independent manner to increase the reabsorption 01 sodium.20B Sodium is the major electrolyte in th~ extracellular environment, and helps to regulate thJ osmotic balance of cells. Higher levels can significantl)1 increase water in the extracellular compartmen~ Anabolic/androgenic steroids that either convert t~ estrogen, or possess inherent estrogenic activity, arei likewise, those steroids that are associated with increaseq extracellular water retention.20g

Estrogenic anabolic/androgenic steroids are generall) favored for mass gaining (bulking) purposes. A steroid\ user may ignore water retention during this phase o~ training, occasionally even finding the sheer increases in size to be a welcome benefit. Estrogenic steroids such aSl testosterone and oxymetholone are also regarded as theIl strongest mass-and strength-building agents, which may] be caused in part by anabolic benefits of elevated estrogenic activity.The excess water stored in the muscles'lll joints, and connective tissues is also commonly believed
to increase an individual's resistance to injury.With the use of many strongly estrogenic anabolic/androgenic steroids, water retention can account for a large portion (350/0 or more) of the initial body weight gain during steroid treatment. This weight is quickly lost once the steroids are discontinued or estrogenic activity is reduced.
Non-aromatizing steroids such as oxandrolone and stanozolol have also been shown to promote increased water retention, so this effect is not entirely exclusive to aromatizable or estrogenic substances.210 211 Anabolic steroids with low or no estrogenic action tend to produce modest increases in whole body water and intracellular fluid retention, however, and not in the visible extracellular compartment.212 213 These steroids are considered to be more cosmetically appealing, and are generally favored by bodybuilders and athletes when looking to improve lean mass and muscle definition. Popular anabolic/androgenic steroids that are associated with low visible water retention include fluoxymesterone, methenolone, nandrolone, oxandrolone, stanozolol, and trenbolone.
Excess water retention may be addressed with the use of ancillary medications such as the anti-estrogen tamoxifen citrate, or an aromatase inhibitor such as anastrozole. By minimizing the activity of estrogens, these drugs can effectively reduce the level of stored water. In most cases where an aromatizable steroid is used, aromatase inhibitors prove to be significantly more effective at achieving this goal. A common practice among bodybuilders during competition is to also use a diuretic, which can shed excess water by directly increasing renal water excretion. This is regarded as the most effective method for rapidly improving muscle definition, but it can also be one of the most acutely risky practices as well. Water retention is not a persistent side effect of steroid use. Excess water is quickly eliminated, and normal water balance returned, once anabolic/androgenic steroid administration is halted.

Dysphonia (Vocal Changes)
Although far less common than dysphonia in women, anabolic/androgenic steroids may alter vocal physiology in men. This may include a deepening of the voice. Dysphonia is most common when anabolic/androgenic steroids are administered during adolescence, as the deeper adult voice has not yet been established under the influence of androgens. The administration of anabolic/androgenic steroids before maturity can, likewise, cause a progressive lowering of the vocal pitch, and may trigger pubescent vocal changes in younger patients. Androgens have much less (often minimal) effect on vocal physiology in adulthood. Although a slight lowering of the voice may be noticed with androgen use in some cases, reports of clinically significant changes in the vocal quality of adult men are, likewise, very rare.There has also been an isolated report of stridor (vibrating noise when breathing) and vocal hoarseness in relation to anabolic/androgenic steroid abuse.214 This instance also involved smoking, however, making the direct influence of steroids more difficult to discern. In general, vocal physiology is well established by adulthood. Aside from very minor reductions in pitch, anabolic/androgenic steroids are not expected to have strong audible effects on the voice.

Gynecomastia
Anabolic/androgenic steroids with significant estrogenic or progestational activity may cause gynecomastia (female breast development in males). This disorder is specifically characterized by the growth of excess glandular tissue in men, due to an imbalance of male and female sex hormones in the breast. Estrogen is the primary supporter of mammary gland growth, and acts upon receptors in the breast to promote ductal epithelial hyperplasia, ductal elongation/branching, and fibroblast proliferation.215 Androgens, on the other hand, inhibit glandular tissue growth.216 High serum androgen levels and low estrogen usually prevent this tissue development in men, but it is possible in both sexes given the right hormonal environment. Gynecomastia is regarded as an unsightly side effect of anabolic/androgenic abuse by most users. In extreme cases the breast may take on a very female looking appearance, which is difficult to hide even Physical (Female) with loose clothing Gynecomastia tends to develop in a series of progressive Birth Delects
stages. The severity of this process will vary depending on the type and dose of drug(s) used, and individual sensitivity to hormones. The first sign is typically pain in the nipple area (gynecodynea). This may quickly coincide with minor swelling around the nipple area (Iipomastia). This is sometimes referred to as pseudo-gynecomastia, as it primarily involves fat and not glandular tissue. At this stage, it may be possible to address mild nipple swelling by reducing or eliminating the offending steroidal compounds, and administering an appropriate antiestrogenic medication for several weeks. If left untreated, however, this may quickly progress to clear gynecomastia, which involves significant fat, fibrous, and glandular tissue growth. The hard tissue growth may be easily felt in the early stages when pinching deeply around the nipple. Noticeable gynecomastia is likely to require corrective cosmetic surgery (male breast reduction).

Although gynecomastia is a very common side effect of steroid abuse, given its clear association with certain drugs or practices, it is also an easily avoidable one. Careful steroid selection and reasonable dosing are usually regarded as the most basic and reliable methods for preventing its onset. Many steroid users also frequently take some form of estrogen maintenance medication, which may effectively counter the effects of elevated estrogenicity. Common options include the anti-estrogen tamoxif~n citrate, or an aromatase inhibitor such as anastrozole. The use of a post-cycle hormone recovery program at the conclusion of steroid administration (which usually includes several weeks of anti-estrogen use) is also commonly advised, as gynecomastia is sometimes reported in the post-cycle hormone imbalance phase when steroids are not actually being taken.

It is important to note that progesterone can also augment the stimulatory effect of estrogen on mammary tissue growth.218 As such, progestational drugs may be able to trigger the onset of gynecomastia in sensitive individuals, even without elevating levels of estrogen. Many anabolic steroids, particularly those derived from nandrolone, are known to exhibit strong progestational activity. While gynecomastia is not a common compliant with these drugs, they are occasionally linked to this side effect in anecdotal reports. The anti-estrogen tamoxifen citrate is usually taken in such instances, as it can offset the effects of estrogen at the receptor, which are still necessary for progestins to impart their growthpromoting effects on the breast.




safe steroids use