I hope that this communication finds you and yours in the best of health and spirit. Winstrol tabs have now become available in 50mg. and even 100 mg. dosages. I know you can't give specific recommendations but what if you had about 200 or 300 Winstrol 50 mg. tabs as the only anabolic to use. How would you use them, for how long, would the "the boys" shrink, any hair loss, libido increase or decrease? Also, how would you rate minstrel’s muscle building activity? Thanks for your time and information.
C. Graham
Thank you for your well worded communication. My family is well as am I...and thank you for your well wishes in our behalf. I do not know as to whether or not you have read Chemical Muscle Enhancement (BDR) or not but this is actually in the book. Nonetheless we can answer this without rewriting the entire text in an E-mail format and perhaps bring to light a few additional thoughts. By the way it is possible that your question and reply will appear in one of the Q & A columns I do for various magazines and possibly on one or more Internet sites.
Winstrol (stanozolol) is a c17 alkylated non-aromatizing AAS utilized both orally and as an injectable preparation. Oddly enough is that the only commercially available injectable is a non-hydrophilic (does not dissolve in water) veterinarian preparation in sterile water. I say odd due to the fact that an oil preparation is notably more effective due to a prolonged active-life and the lymphatic percentage absorption factor. More bang for your buck so to speak. The oral has the distinct advantage of possessing a surprising degree of IGF-1 stimulation as it passes through the livers hepatic passages and as a result of cellular interaction in lean mass tissues. This has failed to be validated in most clinical research due to the low dosages (about 10mg/d) administered. Oddly enough reviews of blood work performed upon several notable athletes administering stanozolol in excess of 40mg/d showed that IGF-1 was elevated significantly. The injectable preparations appear to induce some increase in natural localized MGF (Mechano Growth Factor), PGF-2, IGF-1 and IGF-2 production "site specifically". In that lies the key to a more synergistic approach to utilization.
One of the greatest down falls of AAS administration is the period of time in which AAS remain effective. I refer to effective at the cellular level, not actual active-life. Some old school mentality seems to embrace the ever ascending dosages and prolonged administration periods ideals. This is simply a matter of progressively trying to keep up with the body's anti-growth counter measures as they mount until at some point the protocol is ended and the AAS induced progress in lost unnecessarily. In short at that point "The boy's ain't doing nothing manly" and every other natural anabolic pathway has long since shut down as well. This is a physiological environment best for the better endowed females and certainly not for an athlete of any kind. So a progressive alternative is mandatory for continued progress.
The full body circulation of liver produced IGF-1 is full body effectual. This means that the extra IGF-! from oral stanozolol administration has an effect on the entire musculature as does the AAS itself. Unfortunately within a period of about 2 weeks this effect decreases significantly due to an adaptive response in the liver that shuts down the extra growth goodies and a decrease in IGF-1 receptor site sensitivity results as well due to various other hormone actuated events (Action/Reaction Factors). Less IGF-1 production and less receptor sensitivity means less muscle growth and poor chemical synergy.
Site specific administration of an injectable preparation of stanozolol has full body effects due to AAS induced androgenic and anabolic activity but only significant "localized" MGF, PGF-2, IGF-1 and IGF-2. MGF increases IGF-1 receptor sensitivity, PGF-2 increases androgen receptor count and sensitivity, and the localized IGF-1 production acts synergistically with the AAS. Oh, did I mention that the IGF-2 initiates an increase in vascular tissue growth for better nutrient supply?
Day 1-10 & 21-30 25-50mg 2xd (orally)
Day 11-20 & 31-40 50-75mg 2xd (site specifically)
Since stanozolol is a derivative of DHT (dihydrotestosterone) the occurrence of premature balding has been noted in individuals who are predisposed to MPB when administering this drug. For the same reason real stanozolol does not convert to estrogens and has a lesser degree of HPTA inhibition and the effects last for a shorter period post-cycle. However due to the peripheral nervous system and the presence of an abnormally high degree of androgenic activity some " shrunken nuts syndrome" can occur with prolonged use. The effect is greatest upon the testes themselves so most have realized minimal interruption in natural androgen production with intermittent HCG only administration.
Stanozolol has been a very effective drug employed to increase lean tissue mass with minimum increase in water retention thus providing a lean muscular appearance.
C. Graham
Thank you for your well worded communication. My family is well as am I...and thank you for your well wishes in our behalf. I do not know as to whether or not you have read Chemical Muscle Enhancement (BDR) or not but this is actually in the book. Nonetheless we can answer this without rewriting the entire text in an E-mail format and perhaps bring to light a few additional thoughts. By the way it is possible that your question and reply will appear in one of the Q & A columns I do for various magazines and possibly on one or more Internet sites.
Winstrol (stanozolol) is a c17 alkylated non-aromatizing AAS utilized both orally and as an injectable preparation. Oddly enough is that the only commercially available injectable is a non-hydrophilic (does not dissolve in water) veterinarian preparation in sterile water. I say odd due to the fact that an oil preparation is notably more effective due to a prolonged active-life and the lymphatic percentage absorption factor. More bang for your buck so to speak. The oral has the distinct advantage of possessing a surprising degree of IGF-1 stimulation as it passes through the livers hepatic passages and as a result of cellular interaction in lean mass tissues. This has failed to be validated in most clinical research due to the low dosages (about 10mg/d) administered. Oddly enough reviews of blood work performed upon several notable athletes administering stanozolol in excess of 40mg/d showed that IGF-1 was elevated significantly. The injectable preparations appear to induce some increase in natural localized MGF (Mechano Growth Factor), PGF-2, IGF-1 and IGF-2 production "site specifically". In that lies the key to a more synergistic approach to utilization.
One of the greatest down falls of AAS administration is the period of time in which AAS remain effective. I refer to effective at the cellular level, not actual active-life. Some old school mentality seems to embrace the ever ascending dosages and prolonged administration periods ideals. This is simply a matter of progressively trying to keep up with the body's anti-growth counter measures as they mount until at some point the protocol is ended and the AAS induced progress in lost unnecessarily. In short at that point "The boy's ain't doing nothing manly" and every other natural anabolic pathway has long since shut down as well. This is a physiological environment best for the better endowed females and certainly not for an athlete of any kind. So a progressive alternative is mandatory for continued progress.
The full body circulation of liver produced IGF-1 is full body effectual. This means that the extra IGF-! from oral stanozolol administration has an effect on the entire musculature as does the AAS itself. Unfortunately within a period of about 2 weeks this effect decreases significantly due to an adaptive response in the liver that shuts down the extra growth goodies and a decrease in IGF-1 receptor site sensitivity results as well due to various other hormone actuated events (Action/Reaction Factors). Less IGF-1 production and less receptor sensitivity means less muscle growth and poor chemical synergy.
Site specific administration of an injectable preparation of stanozolol has full body effects due to AAS induced androgenic and anabolic activity but only significant "localized" MGF, PGF-2, IGF-1 and IGF-2. MGF increases IGF-1 receptor sensitivity, PGF-2 increases androgen receptor count and sensitivity, and the localized IGF-1 production acts synergistically with the AAS. Oh, did I mention that the IGF-2 initiates an increase in vascular tissue growth for better nutrient supply?
Day 1-10 & 21-30 25-50mg 2xd (orally)
Day 11-20 & 31-40 50-75mg 2xd (site specifically)
Since stanozolol is a derivative of DHT (dihydrotestosterone) the occurrence of premature balding has been noted in individuals who are predisposed to MPB when administering this drug. For the same reason real stanozolol does not convert to estrogens and has a lesser degree of HPTA inhibition and the effects last for a shorter period post-cycle. However due to the peripheral nervous system and the presence of an abnormally high degree of androgenic activity some " shrunken nuts syndrome" can occur with prolonged use. The effect is greatest upon the testes themselves so most have realized minimal interruption in natural androgen production with intermittent HCG only administration.
Stanozolol has been a very effective drug employed to increase lean tissue mass with minimum increase in water retention thus providing a lean muscular appearance.
