About Steroids

Provided dosing is sufficient, a steroid user can expect to make the most significant progress during their first cycle. Although this will vary from person to person, it is not uncommon for someone to gain 20 pounds of weight or more during a first cycle of AAS use. Some of this may be water retention, although a solid gain of more than 10-15 pounds of muscle mass is possible.

Yes, and no. Steroids can help you do two basic things with regard to muscle growth. First, they can allow you to more rapidly reach your genetic limits for muscle growth. Provided you continue to train actively, eat properly, and use an effective PCT program, you should be able to maintain at your genetic limit indefinitely. So in this regard, the early gains do not have to be temporary.

Later, steroids can allow you to push well beyond your genetic limits. It is important to emphasize this, as extreme physical development cannot be maintained long-term without the repeat administration of anabolic substances. The body will always revert back towards its normal metabolic limits once AAS are removed. In this context, some of the gains will not be permanent.

Steroids do permanently alter the physiology of your muscles by adding more cellular nuclei. With higher nuclei content, each muscle cell can manage its volume more efficiently, which allows more rapid expansion. Even after a long period of complete abstinence from training and AAS, the nuclei remain. This may provide a “muscle memory” effect, allowing you to reach your genetic limit (perhaps a slightly extended limit) faster than if you had never used AAS in the past. So in this regard, there are lasting benefits beyond the temporary increase in muscle size itself.

If you have the underlying genetics to allow for this extreme muscle growth, this may be possible with a lot of hard work and dedication. Genetics are a big factor in determining the ultimate limits to your physique, even in an enhanced state. Many people use steroids and look very big and impressive because of it, but very few users are able to make it to the stage of a professional bodybuilding show.

Anabolic/androgenic steroids are among the safest drugs available, at least in a short-term sense. Fatal overdose is not reasonably possible, and the negative health changes such as alterations in cholesterol, blood pressure, hematocrit, and blood clotting (among other things) are very unlikely to manifest in serious bodily harm or death after an isolated cycle. There are rare deaths from such things as stroke and liver cancer in short-term abusers, but such occurrences are statistically extremely rare in light of the millions of people that use these drugs. If you had to comparatively rate the acute risks of AAS abuse, they would be slightly higher than marijuana, but far less than virtually all other illicit narcotics.

The long-term use of steroids for non-medical reasons can be a unhealthy practice. It has been difficult, however, to quantify the exact risk. The main issue is the fact that AAS abuse can promote heart disease, the number one killer of men. Heart disease is a slow progressive disease, which may build for decades without symptoms. Steroid abuse may accelerate the silent process of plaque deposition in the arteries, and also induce other changes in the cardiovascular system that can increase susceptibility to stroke or heart attack. If death finally occurs, however, it will be difficult for a medical examiner to pinpoint AAS as the cause; too many variables play a role in the etiology of cardiovascular disease. The vast majority of deaths where AAS have contributed go unreported for this reason. The exact mortality rates of long-term steroid abusers have, likewise, been difficult to calculate. It is especially important to closely monitor cardiovascular disease and other health risk factors if long-term steroid use is a practice you will follow.

The non-medical use of AAS by definition cannot be defined as a safe practice. However, it can be argued that anabolic/androgenic steroids can be used with high relative safety, even over a period of many years. The guidelines of steroid harm reduction are important to minimizing the negative health effects of these drugs. Provided an individual follows these guidelines and is careful with drug selection, dosages, and durations of intake, follows a diet low in saturated fats, cholesterol, sugar, and refined carbohydrates, actively trains with both resistance and cardiovascular exercise, and uses cholesterol support supplements such as fish oils and others during all cycles, it may be difficult in many cases to argue high tangible health risks. It takes a great deal of involvement and planning to use AAS in this manner, which is always advised.

Testosterone, whatever the form, tends to be the safest steroid for men. When the dose remains within the moderately supratherapeutic range, alterations in cardiovascular risks factors are noticed, but not extreme. Some of this has to do with the beneficial cardiovascular effects of estrogen in men.

For those with a genetic predisposition to hair loss, all anabolic/androgenic steroids are capable of accelerating the process. Slowing the onset of this during AAS use requires a focus on reducing relative androgenicity in the scalp. This can be accomplished with the use of predominantly anabolic drugs. Alternately, moderate doses of testosterone can be used with finasteride, a drug that reduces DHT conversion (and androgenic amplification) in the scalp. Still, those genetically prone to hair loss can have problems with any steroid, and are always advised to limit dosing, drug intake durations, and monitor effects on the hairline closely.

Women are generally most concerned with the virilizing (masculinizing) effects of anabolic/androgenic steroids. The least virilizing agents are those with the highest relative anabolic to androgenic effect, such as nandrolone, oxandrolone, turinabol, and methenolone. Care must always be taken, however, as all AAS are based on male sex steroids, and as such can cause masculinizing effects in women.

There is no scientific evidence to support the popular view that AAS use might be expected to result in downregulation of the AR relative to receptor levels associated with normal androgen levels.

While there are no studies showing downregulation in human skeletal muscle resulting from high-dose AAS use, there are some studies in cell culture, and sometimes in vivo, which seem to indicate that downregulation can occur, though not as a result of increase in androgen from normal to supraphysiological.

All of these studies, however, are flawed from the perspective of the bodybuilder wishing to know if downregulation of the AR has ever been observed in any cell in response to increase of androgen from normal to supranormal levels.

Upregulation in human muscle tissue, in vivo, is not directly proven but seems to fit the evidence and to provide a plausible explanation for observed results.

These numbers come from early studies measuring the effect of each steroid on certain muscle and sex organ tissues of animals, usually mice. These numbers are useful for assessing the relative anabolic to androgenic balance of each drug in humans. They are not as accurate at assessing the total muscle building potential of each steroid, however, and should not be taken as absolute ratings of potency.

Answer: Gear can crash due to storing the product in colder than recommended temperatures (or in shipment)…or because the ratio of AAS to oil is out of balance (this can be either a manufacturer error or a personal error if home brewing). This does not damage the steroid. In order to correct the problem, simply run the vial under warm water until the products reverts back to its normal state. Clean with alcohol swab after drying off.

Answer: You can choose to either dispose of the product or you can re-filter it by using a Whatman filter. While opinions will differ on this subject, the opinion of re-filtering is still available and a suitable solution in many cases, assuming the product is not badly polluted. In cases where it is apparent that the product is very poor quality and contains a large amount of foreign material, it would be wise to dispose of the product. This should not occur with reputable UGL’s and will never occur with Pharm-grade versions, although an occasional speck may occur with UGL products here and there and is usually not a big deal.

Answer: A solution would be to switch over to testosterone Undecanoate. With a half life of 20 days, it makes for an excellent and risk free choice.

You could also frontload your choice of cypionate/enanthate ester for a shorted trip. Use steroidcalc to plan it out. However, the rapidly dropping levels of this choice make it difficult to manage estrogen properly.

The primary concerns for steroid users giving blood are infectious disease transmission. Given that users self-administer injections there is a concern about knowledge of proper needle handling and use. People with HIV / AIDS or Hepatitis should not give blood.

The first line of action should be:

• Taurine (3-10g pre-workout, you may also add 3-5g AM/PM depending on when you workout)

• Magnesium (200-500mg pre-workout, you may also add 200-500mg AM/PM depending on when you workout)

• Potassium (200-300mg pre-workout, you may also add 200-500mg AM/PM depending on when you workout)

• Upping your water intake (1-2 gallons ED)

If none of this helps, anecdotally, Cialis (10-15mg ED) has been known to help.

Answer: Get to a doctor for some antibiotics if it is red, itchy, or hot. If it is simply sore and/or swollen it is probably going to be okay see: Post Injection Pain (PIP). If in doubt, get some antibiotics; a common thing to tell your doctor is that you injected B12.

Answer: Yes, it is common to occasionally nick a vein close to the surface of the injection site, which will cause blood to leak from the surface. The amount of blood which can seep from an injection site can be anywhere from a drop or two, to a very light stream which slowly flows down that body part. Even in the event a larger vein is hit when doing an injection, this type of bleeding is relatively easy to stop and will not pose any harm to the individual.

Answer: Many AAS users do not aspirate when injecting. It is considered a bit of an out-dated methodology, but it never hurts to do it.

According to the CDC:

Aspiration - Aspiration is the process of pulling back on the plunger of the syringe prior to injection to ensure that the medication is not injected into a blood vessel. Although this practice is advocated by some experts, the procedure is not required because no large blood vessels exist at the recommended injection sites."

STTI International Nursing Research Congress Vancouver, July 2009:

"Aspiration is not indicated for SC injections."

"Aspiration is not indicated for IM injections."

Organizations which state aspiration is not necessary:

• Centers for Disease Control (CDC)
• Advisory Committee on Immunization Practices (ACIP)
• Department of Health Services (DHS)
• American Academy of Family Physicians (AAFP)
• U.K. Department of Health (DoH)
• World Health Organization (WHO)

References located at the bottom of the page.

Answer: Ampules can be aided in opening by scoring (some ampules come pre-scored). Scoring is a process in which in a fine line is ground away around the neck of the ampule. Scoring makes it much easier to snap the top of the ampule off without breaking the vial and spilling the oil. Normally, a scoring tool is used for this process, although sometimes knives or other objects can be used.

An amp opener can be used, which is the fastest and the least time consuming methods.

Lastly, the tape-method can be employed, as well. The tape method involves taping the entire vial all the way up to the neck line. Several layers of tape should surround the vial, so that it is properly secured. The point of taping the vial is two-fold. One purpose is to prevent the contents of the ampule from spilling, should the ampule break somewhere other than the neckline. The other purpose is to reinforce the ampule, so that it is more likely to break at the neckline. One can combine both the tape method and the scoring, which is the best way to ensure that the oil contained in the ampule will not be spilled.

Answer: Absolutely not. You should never take a needle which has entered the body and re-insert it back into a steroid product, as this can result in bacteria build-up and cause potential future infections.

How Fast Should I Inject?

Answer: As a general rule, 30 seconds per mL/cc.

Answer: No, a small amount of air will do no harm. Air bubbles injected into muscle tissue is of no concern. Even if the individual were to thread a vein and inject the entire contents of the syringe into the vein, the small air bubbles contained within it would be the least of that person’s worries. In reality, several cc’s of air would have to be injected directly into a vein all at once, in order to cause cardiac arrest. Even injecting 2-3 cc’s of air directly into a muscle would be largely inconsequential. Of course, such an action is not recommended, but you get the point.

A: Yes, they can when needed. Taking Arimidex with Nolvadex decreases the serum concentration of anastrozole by 27%, but has no effect on the pharmacodynamics of either.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2362190/

In conclusion, the results of this study confirm that anastrozole does not affect the pharmacokinetics of tamoxifen when the two drugs are given in combination to post-menopausal women with early breast cancer. In addition, the oestradiol suppressant effects of anastrozole appear unaffected by tamoxifen.

As a result of (a) the lack of effect of anastrozole on tamoxifen and DMT levels and (b) the observed fall in blood anastrozole levels having no significant effect on oestradiol suppression by anastrozole, we conclude that the observed reduction in anastrozole levels by tamoxifen is unlikely to be of clinical significance when anastrozole and tamoxifen are administered together.

"...the observed fall in blood anastrozole levels having no significant effect on oestradiol suppression by anastrozole, we conclude that the observed reduction in anastrozole levels by tamoxifen is unlikely to be of clinical significance when anastrozole and tamoxifen are administered together."*

A: Yes, they can when needed. Just be aware that taking Letrozole with Nolvadex decreases the serum concentration of Letrozole by 35-40%.

https://pdfs.semanticscholar.org/e492/c9fb67a771779ac3be19faf14ea3b458e03a.pdf

Pharmacokinetic analyses of the combination of tamoxifen and letrozole have revealed that these drugs interact, resulting in letrozole concentrations approximately 35-40% lower than when letrozole is used alone.
...
...letrozole has no impact on tamoxifen concentrations.

A: It works better when taken with a high fatty meal, yes.

http://www.rxlist.com/aromasin-drug.htm

Exemestane is freely soluble in N, N-dimethylformamide, soluble in methanol, and practically insoluble in water.

http://www.rxlist.com/aromasin-drug/indications-dosage.htm

The recommended dose of AROMASIN is 50 mg once daily after a meal.

http://www.drugs.com/monograph/aromasin.html

High-fat meal increases plasma exemestane concentrations by approximately 40%.

http://www.drugs.com/monograph/aromasin.html

Dosages >25 mg daily not shown to provide substantially greater suppression of plasma estrogens but may increase adverse effects.

Answer:

The mechanism by which chronic exposure to hGH leads to tolerance, dependence, and a withdrawal syndrome is unclear and does not involve the suppression of hormone secretion. During the nadir of growth velocity, which follows the withdrawal of prolonged drug therapy, serum GH levels remain normal, as do serum IGF-I and IGF-binding protein-3 levels (4). Moreover, endogenous pulsatile secretion of GH resumes within days even after long-term hGH therapy (7).

Temporarily, yes, it does. However, not ejaculating will eventually decrease the levels even more. For peak levels, only ejaculate every seven days.

A research on the relationship between ejaculation and serum testosterone level in men.
http://www.ncbi.nlm.nih.gov/pubmed/12659241

The purpose of this study is to gain understanding of the relationship between ejaculation and serum testosterone level in men. The serum testosterone concentrations of 28 volunteers were investigated daily during abstinence periods after ejaculation for two phases. The authors found that the fluctuations of testosterone levels from the 2nd to 5th day of abstinence were minimal. On the 7th day of abstinence, however, a clear peak of serum testosterone appeared, reaching 145.7% of the baseline ( P < 0.01). No regular fluctuation was observed following continuous abstinence after the peak. Ejaculation is the precondition and beginning of the special periodic serum testosterone level variations, which would not occur without ejaculation. The results showed that ejaculation-caused variations were characterized by a peak on the 7th day of abstinence; and that the effective time of an ejaculation is 7 days minimum. These data are the first to document the phenomenon of the periodic change in serum testosterone level; the correlation between ejaculation and periodic change in the serum testosterone level, and the pattern and characteristics of the periodic change.

Steroids are not part of the standard drug panel. However, users should be aware that their superiors have the ability to order steroid-specific testing if an individual is suspected of using. PCT drugs will also not appear on the test.

hGH: It is very likely that it can and will with prolonged usage.

Effect of human growth hormone therapy on penile and testicular size in boys with isolated growth hormone deficiency: first year of treatment.

http://www.ncbi.nlm.nih.gov/pubmed/6406387

The response of genital and gonadal growth during the first year of treatment with human growth hormone (hGH) was studied in 20 boys with isolated growth hormone deficiency (IGHD) (11 of hereditary origin and 9 sporadic cases). Prior to hGH treatment, 13 of the 15 prepubertal boys had a penis length below the normal mean, 3 of which were more than 2 SDS below the mean. The boys with hereditary IGHD had a greater deficit in penile size than did the sporadic cases. hGH treatment improved the penile length in all but two boys aged 14 and 15 yr, and led to growth up to normal size in the three boys with very small penises. Three of the hereditary IGHD patients had subnormal testes and all of the other prepubertal boys had a testicular volume in the normal range. hGH treatment increased testicular size, particularly in the prepubertal boys. Of three additional untreated adults with IGHD, one had a subnormal-size penis and two had penises of low-normal size. Our findings constitute further evidence that hGH deficiency is associated with decreased penile growth and, to some extent, decreased testicular size, and that hHG treatment improves the growth of the genitalia and gonads. Since these effects were also observed in prepuberty, it seems that not all the hGH or, rather, somatomedin effect on sex organs is androgen mediated.

Testosterone: There is evidence that in infants and young children that it can increase size.

Congenital hypogonadotropic hypogonadism and micropenis: effect of testosterone treatment on adult penile size why sex reversal is not indicated.

http://www.ncbi.nlm.nih.gov/pubmed/10228293

Micropenis is commonly due to fetal testosterone deficiency. The clinical management of this form of micropenis has been contentious, with disagreement about the capacity of testosterone treatment to induce a functionally adequate adult penis. As a consequence, some clinicians recommend sex reversal of affected male infants. We studied 8 male subjects with micropenis secondary to congenital pituitary gonadotropin deficiency from infancy or childhood to maturity (ages 18 to 27 years). Four patients were treated with testosterone before 2 years of age (group I) and four between age 6 and 13 years (group II). At presentation, the mean penile length in group I was 1.1 cm (-4 SD; range, 0.5 to 1.5 cm) and in group II it was 2.7 cm (-3.4 SD; range, 1.5 to 3.5 cm). All patients received one or more courses of 3 intramuscular injections of testosterone enanthate (25 or 50 mg) at 4-week intervals in infancy or childhood. At the age of puberty the dose was gradually increased to 200 mg monthly and later to an adult replacement regimen. As adults, both group I and II had attained a mean final penile length of 10.3 cm 2.7 cm with a range of 8 to 14 cm (mean adult stretched penile length for Caucasians is 12.4 2.7 cm). Six of 8 men were sexually active, and all reported normal male gender identity and psychosocial behavior. We conclude that 1 or 2 short courses of testosterone therapy in infancy and childhood augment penile size into the normal range for age in boys with micropenis secondary to fetal testosterone deficiency; replacement therapy at the age of puberty results in an adult size penis within 2 SD of the mean. We found no clinical, psychologic, or physiologic indications to support conversion of affected male infants to girls. Further, the results of this study do not support the notion, derived from data in the rat, that testosterone treatment in infancy or childhood impairs penile growth in adolescence and compromises adult penile length.

Role of parenteral testosterone in hypospadias: A study from a teaching hospital in India

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183705/

Additionally, a father decided to treat his infant son with Testosterone for increased penis size.

The number of fat cells in your body is set in childhood and early adolescence. Those fat cells will shrink or expand to hold more fat as required.

http://www.ncbi.nlm.nih.gov/pubmed/18454136

Obesity is increasing in an epidemic manner in most countries and constitutes a public health problem by enhancing the risk for cardiovascular disease and metabolic disorders such as type 2 diabetes. Owing to the increase in obesity, life expectancy may start to decrease in developed countries for the first time in recent history. The factors determining fat mass in adult humans are not fully understood, but increased lipid storage in already developed fat cells (adipocytes) is thought to be most important. Here we show that adipocyte number is a major determinant for the fat mass in adults. However, the number of fat cells stays constant in adulthood in lean and obese individuals, even after marked weight loss, indicating that the number of adipocytes is set during childhood and adolescence. To establish the dynamics within the stable population of adipocytes in adults, we have measured adipocyte turnover by analysing the integration of 14C derived from nuclear bomb tests in genomic DNA. Approximately 10% of fat cells are renewed annually at all adult ages and levels of body mass index. Neither adipocyte death nor generation rate is altered in early onset obesity, suggesting a tight regulation of fat cell number in this condition during adulthood. The high turnover of adipocytes establishes a new therapeutic target for pharmacological intervention in obesity.