Type-IIx
Well-known Member
Symposium Announcement
Type-IIx's NEXT LIVE SYMPOSIUM and Q&A is this Saturday, July 6 @ 11:00 AM EST – Clenbuterol & Unique Anabolic Steroid Features per- Drug (12 AAS), Redux
Place & Time
Place: Join the Ampouletude: Home of Type-IIx Discord Server!
Time: Saturday, July 6, 2024 @ 11:00 AM (EST/New York Time)
Introduction
The first symposium and Q&A went off without a hitch, and was informative and enjoyable! I want to do it again!
Plus, since so many of you were disappointed that you missed it on short notice last time, I want to revisit the topics of last week’s, on the Unique Features and Effects of Anabolic-Androgenic Steroids per-Drug, reviewing twelve (12) different compounds that are all commercially available and in widespread use, besides one, Miotolon (furazabol) – notoriously associated with Ben Johnson’s Olympic medal, world record – and his coach, Charlie Francis.
TOPICS:
Part I: Clenbuterol
• Introduction & Basic Pharmacokinetics
• Effects on Body composition
• Effects on performance – strength, power, speed
• Desensitization (Tachyphylaxis) – see the Final Segment for Practical Cycle Design Overview
• Side Effects:
◦ Class Effects of B2R Agonists
◦ Cardiac Effects and Dealing with Them
◦ Muscle Cramps and Dealing with Them
◦ Effects on GH and Dealing with It
• Comparison versus Albuterol (Salbutamol)
• Practical Cycle Design Overview – Planning the Use of Clenbuterol for Bodybuilding
Part II: Revisiting Last Week’s Unique Effects of Different Steroids per-Drug
• Trenbolone: insulin sensitivity, augments muscle satellite cell proliferative response to IGF-I, tissue-level antiglucocorticoid effects (decreased GR number), atherosclerotic and pro-inflammatory (antagonizing MR).
◦ Insulin sensitizing by reducing:
▪ GH pulse amplitude and duration (resulting in decreased serum IGF-I)
▪ PPARγ expression (anti-adipogenic, anti-hyperglycemic), and
▪ TAT activity (analogously to THG: “The Clear”) thereby decreasing gluconeogenesis and hepatic glucose output (lowering blood glucose).
◦ Anabolic effects by increasing the proliferative responsiveness of muscle satellite cells to IGF-I.
◦ Anticatabolic effects by decreasing muscle tissue GR number.
◦ Relative cardiac harm derives from inhibition of cortisol oxidation and exerting MR action, aggravating atherosclerosis via MR activation and inflammatory processes in the vascular endothelium.
• Stanozolol (Winstrol): Drying-out effect, long biological half-life.
◦ Mitogenic and myogenic effects by likely increasing free IGF-I bioavailability by decreasing IGFBP-3. [1].
◦ Glucocorticoid modulation by directly, and indirectly via its 16β-hydroxylated metabolite 16β-ST, negatively regulating the LAGS (low affinity glucocorticoid-binding site) in the liver. [2].
◦ Antiprogestagenic effects by antagonizing PR (progesterone receptor). [3].
◦ Profoundly long biological activity (“half-life”) of > 24 h, remarkable among the 17α-alkylated AAS (17AAs). [4].
◦ Joint aching: Stanozolol, notoriously associated with joint pain (“achy, dry joints”) affects synovial fibroblasts, precursors to cells that comprise the synovial joints (e.g., hip, knees, shoulders), by inhibiting DNA synthesis [5], and perhaps secondarily by (particularly potently) stimulating C1-inhibitor (C1-INH) activity [6] – not unique to stanozolol but common to the 17AAs – that might plausibly decrease vascular permeability and affect joint lubrication and delivery of nutrients to joints. [7].
• Fluoxymesterone (Halotestin): [5α-reduction] Particularly reductive of fat mass, systemic antiglucocorticoid effect (competitive inhibition of GR).
▪ Biological half-life of 9.2 h, Usage (Androxy pamphlet) is 10 - 40 mg daily in 1 - 4 doses (Adults).
▪ President JFK was prescribed it for Addison’s Disease (adrenal insufficiency), and his reputation for sexual potency was legendary
◦ Both the 11β-hydroxyl & 9α-fluoro group are known to increase binding to the glucocorticoid receptor (GR). This imparts on fluoxymesterone a strong affinity for the glucocorticoid (cortisol) receptor, acting as an antagonist
◦ Dysregulates electrolytes in a different fashion than Tren, but still potently!
• Trestolone (MENT): [aromatization] Particularly suppressive (decreased LH, FSH).
• Testosterone: [aromatization & 5α-reduction] Bioidentical.
• Nandrolone (Deca durabolin; NPP): [aromatization & 5α-reduction] Joint benefits (increased type I collagen deposition), depression and learning, memory deficits (increased homovanillic acid).
• Oxandrolone (Anavar): A 2-oxasteroid. Particularly lipolytic, enhances hepatic ketosis.
• Methasterone (Superdrol): 2α-methylation dramatically increases anabolic and reduces androgenic potency, most toxic commercially available AAS (resistant to metabolism & potent 17AA).
• 1-Testosterone (Dihydroboldenone): Increases DHT (perhaps via 17β-HSD1 inhibition but not 5α-reduction), increases C-reactive protein either directly or by requiring guaiacol to hold in solution. Decreases E2, increases E1, too. All these features with its androgenicity potentially treat breast cancer.
• Metandienone (Dianabol): [aromatizable] Decreases ACTH (antiglucocorticoid effect), potently suppressive, potently hematopoeitic.
• Epistane: highly unusually lacking the 3-keto group (for which the O atom has a lone pair of electrons allowing its action as a H-bond acceptor, able to interact with polar or charged amino acids to form strong bond with the N-terminus/amino-group), acts partly as a prodrug to desoxymethltestosterone (Madol), potently antigynecomastic. ts non-methylated counterpart (epitiostanol) is used (or was used) clinically in Japan. At a 20 mg weekly dosage epitiostanol, considered an anti-estrogen agent, was more effective than Mast (at 50 mg weekly) in treatment of gynecomastia. Epitiostanol also has demonstrated efficacy in treatment-resistant, relapsing stage IV metastatic breast cancer, as an alternative form of endocrinotherapy faced with relapse.
Discord is kinda cool, actually. Come check it out! You can ask questions by typing, or by microphone.
Type-IIx's NEXT LIVE SYMPOSIUM and Q&A is this Saturday, July 6 @ 11:00 AM EST – Clenbuterol & Unique Anabolic Steroid Features per- Drug (12 AAS), Redux
Place & Time
Place: Join the Ampouletude: Home of Type-IIx Discord Server!
Time: Saturday, July 6, 2024 @ 11:00 AM (EST/New York Time)
Introduction
The first symposium and Q&A went off without a hitch, and was informative and enjoyable! I want to do it again!
Plus, since so many of you were disappointed that you missed it on short notice last time, I want to revisit the topics of last week’s, on the Unique Features and Effects of Anabolic-Androgenic Steroids per-Drug, reviewing twelve (12) different compounds that are all commercially available and in widespread use, besides one, Miotolon (furazabol) – notoriously associated with Ben Johnson’s Olympic medal, world record – and his coach, Charlie Francis.
TOPICS:
Part I: Clenbuterol
• Introduction & Basic Pharmacokinetics
• Effects on Body composition
• Effects on performance – strength, power, speed
• Desensitization (Tachyphylaxis) – see the Final Segment for Practical Cycle Design Overview
• Side Effects:
◦ Class Effects of B2R Agonists
◦ Cardiac Effects and Dealing with Them
◦ Muscle Cramps and Dealing with Them
◦ Effects on GH and Dealing with It
• Comparison versus Albuterol (Salbutamol)
• Practical Cycle Design Overview – Planning the Use of Clenbuterol for Bodybuilding
Part II: Revisiting Last Week’s Unique Effects of Different Steroids per-Drug
• Trenbolone: insulin sensitivity, augments muscle satellite cell proliferative response to IGF-I, tissue-level antiglucocorticoid effects (decreased GR number), atherosclerotic and pro-inflammatory (antagonizing MR).
◦ Insulin sensitizing by reducing:
▪ GH pulse amplitude and duration (resulting in decreased serum IGF-I)
▪ PPARγ expression (anti-adipogenic, anti-hyperglycemic), and
▪ TAT activity (analogously to THG: “The Clear”) thereby decreasing gluconeogenesis and hepatic glucose output (lowering blood glucose).
◦ Anabolic effects by increasing the proliferative responsiveness of muscle satellite cells to IGF-I.
◦ Anticatabolic effects by decreasing muscle tissue GR number.
◦ Relative cardiac harm derives from inhibition of cortisol oxidation and exerting MR action, aggravating atherosclerosis via MR activation and inflammatory processes in the vascular endothelium.
• Stanozolol (Winstrol): Drying-out effect, long biological half-life.
◦ Mitogenic and myogenic effects by likely increasing free IGF-I bioavailability by decreasing IGFBP-3. [1].
◦ Glucocorticoid modulation by directly, and indirectly via its 16β-hydroxylated metabolite 16β-ST, negatively regulating the LAGS (low affinity glucocorticoid-binding site) in the liver. [2].
◦ Antiprogestagenic effects by antagonizing PR (progesterone receptor). [3].
◦ Profoundly long biological activity (“half-life”) of > 24 h, remarkable among the 17α-alkylated AAS (17AAs). [4].
◦ Joint aching: Stanozolol, notoriously associated with joint pain (“achy, dry joints”) affects synovial fibroblasts, precursors to cells that comprise the synovial joints (e.g., hip, knees, shoulders), by inhibiting DNA synthesis [5], and perhaps secondarily by (particularly potently) stimulating C1-inhibitor (C1-INH) activity [6] – not unique to stanozolol but common to the 17AAs – that might plausibly decrease vascular permeability and affect joint lubrication and delivery of nutrients to joints. [7].
• Fluoxymesterone (Halotestin): [5α-reduction] Particularly reductive of fat mass, systemic antiglucocorticoid effect (competitive inhibition of GR).
▪ Biological half-life of 9.2 h, Usage (Androxy pamphlet) is 10 - 40 mg daily in 1 - 4 doses (Adults).
▪ President JFK was prescribed it for Addison’s Disease (adrenal insufficiency), and his reputation for sexual potency was legendary
◦ Both the 11β-hydroxyl & 9α-fluoro group are known to increase binding to the glucocorticoid receptor (GR). This imparts on fluoxymesterone a strong affinity for the glucocorticoid (cortisol) receptor, acting as an antagonist
◦ Dysregulates electrolytes in a different fashion than Tren, but still potently!
• Trestolone (MENT): [aromatization] Particularly suppressive (decreased LH, FSH).
• Testosterone: [aromatization & 5α-reduction] Bioidentical.
• Nandrolone (Deca durabolin; NPP): [aromatization & 5α-reduction] Joint benefits (increased type I collagen deposition), depression and learning, memory deficits (increased homovanillic acid).
• Oxandrolone (Anavar): A 2-oxasteroid. Particularly lipolytic, enhances hepatic ketosis.
• Methasterone (Superdrol): 2α-methylation dramatically increases anabolic and reduces androgenic potency, most toxic commercially available AAS (resistant to metabolism & potent 17AA).
• 1-Testosterone (Dihydroboldenone): Increases DHT (perhaps via 17β-HSD1 inhibition but not 5α-reduction), increases C-reactive protein either directly or by requiring guaiacol to hold in solution. Decreases E2, increases E1, too. All these features with its androgenicity potentially treat breast cancer.
• Metandienone (Dianabol): [aromatizable] Decreases ACTH (antiglucocorticoid effect), potently suppressive, potently hematopoeitic.
• Epistane: highly unusually lacking the 3-keto group (for which the O atom has a lone pair of electrons allowing its action as a H-bond acceptor, able to interact with polar or charged amino acids to form strong bond with the N-terminus/amino-group), acts partly as a prodrug to desoxymethltestosterone (Madol), potently antigynecomastic. ts non-methylated counterpart (epitiostanol) is used (or was used) clinically in Japan. At a 20 mg weekly dosage epitiostanol, considered an anti-estrogen agent, was more effective than Mast (at 50 mg weekly) in treatment of gynecomastia. Epitiostanol also has demonstrated efficacy in treatment-resistant, relapsing stage IV metastatic breast cancer, as an alternative form of endocrinotherapy faced with relapse.
Discord is kinda cool, actually. Come check it out! You can ask questions by typing, or by microphone.
