Iron Game

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[h=2]ANABOLICS 101 - ORAL STEROID FLUOXYMESTERONE[/h]
Written by William Llewellyn


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[h=1]Anabolics 101 - Fluoxymesterone[/h]
Description
Fluoxymesterone is an oral anabolic steroid derived from testosterone. More specifically, it is a methyltestosterone derivative, differing by the addition of 11-beta-hydroxy and 9-alpha-fluoro groups. The result is a potent orally active non-aromatizable steroid that exhibits extremely strong androgenic properties. Fluoxymesterone is considerably more androgenic than testosterone, while at the same time the anabolic effects of this agent are considered to be moderate in comparison. This makes fluoxymesterone a great strength drug, but not the most ideal agent for gaining muscle mass. The predominant effects seen when taking fluoxymesterone are increased strength, increased muscle density and increased definition, with only modest size increases.
How Supplied
Fluoxymesterone is an oral medication, typically prepared in tablets or capsules containing 2 mg, 2.5 mg, 5 mg or 10 mg of steroid.

Side Effects
Estrogenic: Fluoxymesterone is not aromatized by the body, and is not measurably estrogenic. An anti-estrogen is not necessary when using this steroid, as gynecomastia should not be a concern even among sensitive individuals. Since estrogen is the usual culprit with water retention, this steroid instead produces a lean, quality look to the physique with no fear of excess subcutaneous fluid retention. This makes it a favorable steroid to use during cutting cycles, when water and fat retention are major concerns.
Androgenic: Fluoxymesterone is classified as an androgen. Androgenic side effects are common with this substance, and may include bouts of oily skin, acne and body/facial hair growth. Anabolic-androgenic steroids (AAS) may also aggravate male pattern hair loss. Those genetically prone to male pattern hair loss may wish to opt for a milder, less androgenic, anabolic steroid. As a potent androgen, this steroid may also increase aggressiveness. Women are additionally warned of the potential virilizing effects of AAS. These may include a deepening of the voice, menstrual irregularities, changes in skin texture, facial hair growth and clitoral enlargement.
It is of note that Halotestin has been shown to possess usual androgenic properties. In human studies published back in 1961, the steroid displayed a much stronger tendency to promote phallic enlargement compared to other androgenic effects such as hair growth, libido and changes in vocal pitch. Fluoxymesterone was offering a somewhat different androgenic profile compared to testosterone, and as such demonstrated that it was possible, at some level, to actually tailor drug effect within the broad category of androgenic action. Fluoxymesterone remains considered an androgen, but studies like the above suggest that it may not offer a complete biological equivalent to testosterone where androgenicity is concerned.

Liver Toxicity: Fluoxymesterone is a c17-alpha alkylated compound. This alteration protects the drug from deactivation by the liver, allowing a very high percentage of the drug entry into the bloodstream following oral administration. C17-alpha alkylated AAS can be hepatotoxic. Prolonged or high exposure may result in liver damage. In rare instances, life-threatening dysfunction may develop. It is advisable to visit a physician periodically during each cycle to monitor liver function and overall health. Intake of c17-alpha alkylated steroids is commonly limited to six to eight weeks, in an effort to avoid escalating liver strain. Studies administering 20 milligrams of fluoxymesterone to a group of nine male subjects for two weeks resulted in most patients (6/9) noticing abnormal sulfobromophthalein (BSP) retention, a marker of liver stress. The use of a liver detoxification supplement such as Liver Stabil, Liv.52 or Essentiale Forte is advised while taking any hepatotoxic AAS.
Cardiovascular: Anabolic-androgenic steroids can have deleterious effects on serum cholesterol. This includes a tendency to reduce HDL (good) cholesterol values and increase LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a direction that favors greater risk of arteriosclerosis. The relative impact of an AAS on serum lipids is dependant on the dose, route of administration (oral versus injectable), type of steroid (aromatizable or non-aromatizable) and level of resistance to hepatic metabolism. Fluoxymesterone has a strong effect on the hepatic management of cholesterol due to its structural resistance to liver breakdown and route of administration. Anabolic-androgenic steroids may also adversely affect blood pressure and triglycerides, reduce endothelial relaxation and support left ventricular hypertrophy, all potentially increasing the risk of cardiovascular disease and myocardial infarction.
To help reduce cardiovascular strain, it is advised to maintain an active cardiovascular exercise program and minimize the intake of saturated fats, cholesterol and simple carbohydrates at all times during active AAS administration. Supplementing with fish oils (four grams per day) and a natural cholesterol/antioxidant formula such as Lipid Stabil or a product with comparable ingredients is also recommended.
Testosterone Suppression: All AAS, when taken in doses sufficient to promote muscle gain, are expected to suppress endogenous testosterone production. Without the intervention of testosterone-stimulating substances, testosterone levels should return to normal within one to four months of drug cessation. Note that prolonged hypogonadotrophic hypogonadism can develop secondary to steroid abuse, necessitating medical intervention. Studies administering 10 milligrams, 20 milligrams or 30 milligrams of fluoxymesterone to nine healthy male subjects for up to 12 weeks have demonstrated the strong suppression of endogenous testosterone levels, with inconsistent effects on gonadotropin levels. Although not fully understood, fluoxymesterone is proposed to have a direct suppressive effect on testicular steroidogenesis that is not mediated by the suppression of gonadotropins.
The above side effects are not inclusive.
Effective Dosages
For physique- or performance-enhancing purposes, an effective oral daily dosage for most men falls in the range of 10-40 milligrams, taken in cycles lasting no more than six to eight weeks to minimize hepatotoxicity. This level is sufficient for measurable increases in muscle strength, which may be accompanied by modest increases in lean muscle mass. Halotestin is commonly used by athletes in weight-restricted sports like wrestling, powerlifting and boxing, due to the fact that strength gained from the drug is usually not accompanied by great increases in bodyweight. It is also commonly used for bodybuilding contest preparation. When the competitor has an acceptably low body fat percentage, the strong androgen level (in absence of excess estrogen) can elicit an extremely hard and defined (“ripped”) look to the muscles.
Halotestin is not recommended for women for physique- or performance-enhancing purposes, due to its strong androgenic nature and tendency to produce virilizing side effects.

Availability
Pharmaceutical preparations containing fluoxymesterone remain scarce. The drug has largely associated with Western medical markets, where it has been falling out of favor for most clinical application. The bulk of the supply presently comes from underground steroid manufacturers.

References:
Herr ME, Hogg JA, Levin RH. J Am Chem Soc. 78, 500 (1956).
Lyster SC, Lund GH and Stafford RO. Endocrinology 58, 781 (1956).
Testing for fluoxymesterone (Halotestin[SUP]®[/SUP]) administration to man: Identification of urinary metabolites by gas chromatography-mass spectrometry. Kammerer R, Mardink J, Jangels M, et al. J Steroid Biochem 36 (1990):659-66.
Eisenberg, E. Modern Trends in Endocrinology (H. Gardiner-Hill, ed) p 46. Hoeber, NY (1961).
Methyltestosterone, related steroids, and liver function. deLorimier A, Gilbert G, et al. Arch Intern Med v116 (1965):289-94.
The effects of fluoxymesterone administration on testicular function. Jones TM, Fang VS, et al. J Clin Endocrinol Metab 1977 Jan;44(1):121-9.
 
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