Boldenone finasteride

Superdrol Stack/Cycle: For men effective Superdrol dose to improve the physical form is in the range of 10-20 mg per day, no more than 6-8 weeks. This level provides a significant increase in muscles and is accompanied by the burning of fat and improved rendering. Do not expect to gain 30 pounds, most will be able to add only 10 pounds. Higher doses give more stress to the liver. Sometimes (20 mg) is combined with non-toxic drugs, Testosterone type, Deca 300 or Boldenone, which increases muscle growth. For drying it is often combined with Primobolan or Trenbolone.

Like other AAS, boldenone is an agonist of the androgen receptor (AR). [6] The activity of boldenone is mainly anabolic , with a low androgenic potency. Boldenone will increase nitrogen retention, protein synthesis, increases appetite and stimulates the release of erythropoietin in the kidneys. [7] Boldenone was synthesized in an attempt to create a long-acting injectable metandienone , for androgen deficiency disorders. Boldenone acts similar to metandienone with fewer adverse androgenic effects. [ medical citation needed ] Although commonly compared to nandrolone , boldenone lacks progesterone receptor interaction and associated progestogenic side effects.

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 aromatase inhibitors such as anastrozole. The use of a PCT 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.

Finasteride results in a decrease of circulating DHT levels by about 65 to 70% with an oral dose of 5 mg and of DHT levels in the prostate gland by up to 80 to 90% with an oral dose of 1 or 5 mg. [13] [14] [53] Unlike inhibitors of all three isoenzymes of 5α-reductase like dutasteride , which can reduce DHT levels in the entire body by more than 99%, [13] finasteride does not completely suppress DHT production because it lacks significant inhibitory effects on the 5α-reductase type I isoenzyme, with more than 100-fold less inhibitory potency for type I as compared to type II ( IC 50 = 313 nM and 11 nM, respectively). [23] [1] In addition to inhibiting 5α-reductase, finasteride has also been found to competitively inhibit 5β-reductase (AKR1D1), although its affinity for the enzyme is substantially less than for 5α-reductase (an order of magnitude less than 5α-reductase type I) and hence is unlikely to be of clinical significance. [54] As of 2012, the tissues in which the different isozymes of 5α-reductase are expressed are not fully clear, as different investigators have obtained varying results with different reagents , methods, and tissues examined. [11] However, the different isozymes appear to be widely expressed, most notably in the prostate gland and hair follicles. [11]

Boldenone finasteride

boldenone finasteride

Finasteride results in a decrease of circulating DHT levels by about 65 to 70% with an oral dose of 5 mg and of DHT levels in the prostate gland by up to 80 to 90% with an oral dose of 1 or 5 mg. [13] [14] [53] Unlike inhibitors of all three isoenzymes of 5α-reductase like dutasteride , which can reduce DHT levels in the entire body by more than 99%, [13] finasteride does not completely suppress DHT production because it lacks significant inhibitory effects on the 5α-reductase type I isoenzyme, with more than 100-fold less inhibitory potency for type I as compared to type II ( IC 50 = 313 nM and 11 nM, respectively). [23] [1] In addition to inhibiting 5α-reductase, finasteride has also been found to competitively inhibit 5β-reductase (AKR1D1), although its affinity for the enzyme is substantially less than for 5α-reductase (an order of magnitude less than 5α-reductase type I) and hence is unlikely to be of clinical significance. [54] As of 2012, the tissues in which the different isozymes of 5α-reductase are expressed are not fully clear, as different investigators have obtained varying results with different reagents , methods, and tissues examined. [11] However, the different isozymes appear to be widely expressed, most notably in the prostate gland and hair follicles. [11]

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