Type-IIx
Well-known Member
Comparative Erythropoiesis (Increases to Hematocrit) by & between AAS Including What We Know about EQ & the Apparent Counterexample of Trenbolone
Author: Type-IIx
Comparative potencies to increase hematocrit (HCT) & hemoglobin (Hb)
Nandrolone (decanoate > phenylpropionate) > Anadrol (Oxymetholone) > Testosterone (propionate > cypionate > enanthate). [1].
Discussion
While Testosterone is modestly erythropoietic, this effect becomes significant at doses greater than peak myotrophic‡ & androgenic response. [2]. Methyltestosterone is not significantly erythropoietic and highly androgenic, the same goes for Cheque drops & Halotestin (potently androgenic and not significantly erythropoietic). [2].
Dianabol possesses ideal features as a hematinic agent: at doses equating to 0.6 mg per k.g. daily in man, significant myotrophic and erythropoietic activity is observed (in rodent) without androgenicity. [2]. Masteron's erythropoietic potency is significant in man [3] and rat [4]. This feature of Masteron is dissociated from its relatively weakened myotrophic potency.
Anadrol is consistently demonstrated as a potent stimulator of erythropoiesis in man [3] and rat [4], though is associated with considerable hepatotoxicity. In aplastic anemia cases, 80% of patients saw mild-to-marked alterations in liver function given 17AAs Dianabol & Anadrol versus a mere 26% given Masteron & Primo Ace (oral) at doses ranging from 0.25 - 3.0 mg/kg/day [3]. Noteworthy, however, is the high background of liver dysfunction comorbid with aplastic anemia (24%); as well as normalization of liver function in patients switched from the 17AAs (Anadrol & Dianabol) to non-17AA oral androgens Masteron & Primo Ace [3].
Is EQ is Particularly Erythropoietic?
From [2], we can say that there is no class effect of androst-1,4-dien-3-ones (e.g., EQ, Dianabol) in augmenting erythropoiesis. While the most potent hematinic agent assayed was of this class (Dianabol), 17β-hydroxy-2-methyl-androst-1,4-dien-3-one (a 2-methyl generally decreases androgenicity; an apparent exception to this, then, is present here) and 11β,17β-dihydroxy-17-methyl-androst-1,4-dien-3-one (an 11β-hydroxyl substituent added to an androst-1,4-dien-3-one serves only to hinder potency unlike in the 19-nortestosterone series or in the presence of a 9α-fluoro substituent) lacked any particular potency in this regard. [2]. See †, below.
General Rule (Androgenicity is Inversely Related to Hematopoietic Potency)
Nandrolone, Anadrol, Dianabol, Masteron, and Primobolan are more potent stimulators of erythropoiesis than Testosterone. Halotestin, Cheque drops, and Methyltestosterone, while potently androgenic, do not significantly stimulate hematinic activity.
If there is a general rule with respect to AAS’ hematopoietic potencies, it is that androgenic potency is inversely related to hematopoietic potency.
Still, if AAS are used at doses that are above those which are maximally stimulatory of N retention‡ (i.e., > peak myotropic response), one should expect that this general rule will not necessarily hold.
Trenbolone as an Apparent Exception to the Rule
The case of Trenbolone presents an illustration of this phenomenon of the general rule not applying at very high doses. To reiterate, AAS used at doses that are above those which are maximally stimulatory of N retention‡ (i.e., > peak myotropic response), one should expect that this general rule will not necessarily hold.
Trenbolone, as acetate, is according to bro-science, to be used at a 350 mg/w dose for a novice. This is, however, a remarkably high dose for this drug. On a molar (per-mg) basis, 350 mg of trenbolone acetate posesses approximately 5.5-fold the AR activation potency as 350 mg of testosterone enanthate. That is to say, 350 mg of trenbolone acetate is equivalent in AR potency to > 1,900 mg/w of testosterone enanthate. Since the hazards or health risks germane to trenbolone are mostly AR-mediated, but (e.g., cardiovascular risks, electrolyte disturbances and therefore renal/kidney risks) are also mediated by its antagonism of the MR (mineralocorticoid receptor). An often reported side effect by trenbolone users is appetite supression. This is indicative of acute toxicity. Since AAS (at therapeutic doses) increase appetite as a class effect, the experience of reduced appetite is indicative of excessive dosing and acute toxicity.
†: By this rule, EQ, being particularly well tolerated in practice by women, one might – speculatively – follow through on this line of reasoning to consider EQ as a candidate for inclusion into this class of weak (or “attenuated”) androgens, and by extension, potent hematinic agents.
‡: Maximal stimulation of N retention is not the only mechanism by which AAS exert their effects on muscle size (↑) and fat mass (↓).
______________________
References:
[1] Gorshein, D., Murphy, S., & Gardner, F. H. (1973). Comparative study on the erythropoietic effects of androgens and their mode of action. Journal of Applied Physiology, 35(3), 376–378. doi:10.1152/jappl.1973.35.3.376
[2] Molinari PF, Rosenkrantz H. Erythropoietic activity and androgenic implications of 29 testosterone derivatives in orchiectomized rats. J Lab Clin Med. 1971 Sep;78(3):399-410.
[3] Sanchez-Medal L, Gomez-Leal A, Duarte L, Guadalupe Rico M. Anabolic androgenic steroids in the treatment of acquired aplastic anemia. Blood. 1969 Sep;34(3):283-300.
[4] Duarte, L., Sanchez Medal, L., Labardini, J., & Arriaga, L. (1967). The Erythropoietic Effects of Anabolic Steroids. Experimental Biology and Medicine, 125(4), 1030–1032. doi:10.3181/00379727-125-32268
Author: Type-IIx
Comparative potencies to increase hematocrit (HCT) & hemoglobin (Hb)
Nandrolone (decanoate > phenylpropionate) > Anadrol (Oxymetholone) > Testosterone (propionate > cypionate > enanthate). [1].
Discussion
While Testosterone is modestly erythropoietic, this effect becomes significant at doses greater than peak myotrophic‡ & androgenic response. [2]. Methyltestosterone is not significantly erythropoietic and highly androgenic, the same goes for Cheque drops & Halotestin (potently androgenic and not significantly erythropoietic). [2].
Dianabol possesses ideal features as a hematinic agent: at doses equating to 0.6 mg per k.g. daily in man, significant myotrophic and erythropoietic activity is observed (in rodent) without androgenicity. [2]. Masteron's erythropoietic potency is significant in man [3] and rat [4]. This feature of Masteron is dissociated from its relatively weakened myotrophic potency.
Anadrol is consistently demonstrated as a potent stimulator of erythropoiesis in man [3] and rat [4], though is associated with considerable hepatotoxicity. In aplastic anemia cases, 80% of patients saw mild-to-marked alterations in liver function given 17AAs Dianabol & Anadrol versus a mere 26% given Masteron & Primo Ace (oral) at doses ranging from 0.25 - 3.0 mg/kg/day [3]. Noteworthy, however, is the high background of liver dysfunction comorbid with aplastic anemia (24%); as well as normalization of liver function in patients switched from the 17AAs (Anadrol & Dianabol) to non-17AA oral androgens Masteron & Primo Ace [3].
Is EQ is Particularly Erythropoietic?
From [2], we can say that there is no class effect of androst-1,4-dien-3-ones (e.g., EQ, Dianabol) in augmenting erythropoiesis. While the most potent hematinic agent assayed was of this class (Dianabol), 17β-hydroxy-2-methyl-androst-1,4-dien-3-one (a 2-methyl generally decreases androgenicity; an apparent exception to this, then, is present here) and 11β,17β-dihydroxy-17-methyl-androst-1,4-dien-3-one (an 11β-hydroxyl substituent added to an androst-1,4-dien-3-one serves only to hinder potency unlike in the 19-nortestosterone series or in the presence of a 9α-fluoro substituent) lacked any particular potency in this regard. [2]. See †, below.
General Rule (Androgenicity is Inversely Related to Hematopoietic Potency)
Nandrolone, Anadrol, Dianabol, Masteron, and Primobolan are more potent stimulators of erythropoiesis than Testosterone. Halotestin, Cheque drops, and Methyltestosterone, while potently androgenic, do not significantly stimulate hematinic activity.
If there is a general rule with respect to AAS’ hematopoietic potencies, it is that androgenic potency is inversely related to hematopoietic potency.
Still, if AAS are used at doses that are above those which are maximally stimulatory of N retention‡ (i.e., > peak myotropic response), one should expect that this general rule will not necessarily hold.
Trenbolone as an Apparent Exception to the Rule
The case of Trenbolone presents an illustration of this phenomenon of the general rule not applying at very high doses. To reiterate, AAS used at doses that are above those which are maximally stimulatory of N retention‡ (i.e., > peak myotropic response), one should expect that this general rule will not necessarily hold.
Trenbolone, as acetate, is according to bro-science, to be used at a 350 mg/w dose for a novice. This is, however, a remarkably high dose for this drug. On a molar (per-mg) basis, 350 mg of trenbolone acetate posesses approximately 5.5-fold the AR activation potency as 350 mg of testosterone enanthate. That is to say, 350 mg of trenbolone acetate is equivalent in AR potency to > 1,900 mg/w of testosterone enanthate. Since the hazards or health risks germane to trenbolone are mostly AR-mediated, but (e.g., cardiovascular risks, electrolyte disturbances and therefore renal/kidney risks) are also mediated by its antagonism of the MR (mineralocorticoid receptor). An often reported side effect by trenbolone users is appetite supression. This is indicative of acute toxicity. Since AAS (at therapeutic doses) increase appetite as a class effect, the experience of reduced appetite is indicative of excessive dosing and acute toxicity.
†: By this rule, EQ, being particularly well tolerated in practice by women, one might – speculatively – follow through on this line of reasoning to consider EQ as a candidate for inclusion into this class of weak (or “attenuated”) androgens, and by extension, potent hematinic agents.
‡: Maximal stimulation of N retention is not the only mechanism by which AAS exert their effects on muscle size (↑) and fat mass (↓).
______________________
References:
[1] Gorshein, D., Murphy, S., & Gardner, F. H. (1973). Comparative study on the erythropoietic effects of androgens and their mode of action. Journal of Applied Physiology, 35(3), 376–378. doi:10.1152/jappl.1973.35.3.376
[2] Molinari PF, Rosenkrantz H. Erythropoietic activity and androgenic implications of 29 testosterone derivatives in orchiectomized rats. J Lab Clin Med. 1971 Sep;78(3):399-410.
[3] Sanchez-Medal L, Gomez-Leal A, Duarte L, Guadalupe Rico M. Anabolic androgenic steroids in the treatment of acquired aplastic anemia. Blood. 1969 Sep;34(3):283-300.
[4] Duarte, L., Sanchez Medal, L., Labardini, J., & Arriaga, L. (1967). The Erythropoietic Effects of Anabolic Steroids. Experimental Biology and Medicine, 125(4), 1030–1032. doi:10.3181/00379727-125-32268
