Type-IIx
Well-known Member
There are an abundance of misconceptions about “EQ”; Equipoise (boldenone, as undecylenate) it seems. Let's address some of the primary misconceptions:
1. Misconception that boldenone is nonaromatizable, or that its use (in sufficiently high doses) permit abstaining from AI/SERM use in users that are not resilient against aromatizing effects (e.g., fluid retention/edema, growth of breast tissue, etc.)
Reality: Boldenone aromatizes (to estrone [E1] & estradiol [E2]) at 58% the rate of testosterone. This is significant. However, since Estrone (E1) is a weak estrogen, because lacks the 17β-OH group, it possesses only 2% of E2's potency to transactivate ERα (associated with aromatizing effects, many of which are negative side effects in men).
Practically, this means that moderate/moderately-high boldenone doses (used solo; or in combination with nonaromatizable drugs, and/or with low doses of exogenous testosterone) would tend to not require AI/SERM use in users that are not resilient against aromatizing effects, but: A) for those who principally aromatize to E2 rather than E1 (inter-individual differences are likely rooted in 17β-HSD1 isozyme expression, under the control of the A1-Q327 gene) particular; and/or B) where E1 blood concentrations start getting into the regions of > 50-fold above that at which E2 causes problems in the individual, then the aromatizing effects would be expected to predominate.
2. Misconception that boldenone is not intended for human use.
Reality: Boldenone has been manufactured by pharmaceutical companies for human therapeutic use (to wit, by Parke Davis) as Anabolicum Vister (Quinbolone; boldenone cyclopentenyl)… and yes, it was patented by Ciba as Parenabol (boldenone undecylenate) as well. Anabolicum Vister was an oral delivery drug that relied upon a 17α ether attachment and suspension in oil in order to increase its lipophilicity and therefore bioavailability. It was nontoxic; but had to be taken frequently (10 - 20 capsules daily were recommended, 100 - 200 mg of boldenone prodrug), and like oral testosterone undecanoate delivery, there was broad inter- (between) & intra- (within) individual and diurnal (between and within days) variability in blood concentrations achieved, affecting its efficacy & adherence (these are the primary reason that its manufacture was discontinued).
Rather than by 17α- alkylation (attachment of an angular methyl or ethyl group to the C-17 position), Anabolicum Vister relied upon attachment of a cyclopentenyl ether, 5 carbons in length to form a prodrug. The rationale for this was that by increased lipophilicity (in combination with suspension of the drug in oil vehicle), this polar oil could be ingested or swallowed and then, from the gut, absorbed by the lymphatic system, bypassing hepatic metabolism. The lymphatic system is a network of veins and arteries that only serve to reabsorb water. When blood is delivered to tissues, only ~85% of the fluid is recovered. The lymphatic system reabsorbes the excess (~85%) water and delivers it to the angulus venosus, where two large veins meet right before they empty out into the heart. In the digestive tract (where the capsules of Anabolicum Vister arrive after ingestion), the lymphatic system serves to transports fats. With a delivery system such as that of Anabolicum Vister, the lipid/fat contents are easily be absorbed into the lymphatic system, avoiding hepatic metabolism (and therefore, strain) and then are delivered via a fairly direct route into the bloodstream (for systemic delivery of active boldenone).
3. Misconception that boldenone is toxic, and particularly kidney & liver toxic.
Reality: Boldenone, when profiled for drug safety using ADME-Tox & GSK 400 standards, outperforms Metenolone enanthate (Rimobolan; “Primo”). Indeed, metenolone enanthate is deemed Rejected under these standards, hhence why it is not available for human medical use in many places that subject their medical drug supply to more scrupulous regulatory regimes and schemes. Conversely, boldenone is Accepted under these standards, and therefore suitable for human use according to industry and governmental regimes that enforce ADME-Tox & GSK 400 standards. Specifically, for those that are interested, metenolone enanthate fails by fully breaking the GSK 4/400 Rule, Pfizer 3/75 Rule (logP), & Lilly Med Chem Rules.
Boldenone has never been demonstrated to be particularly nephrotoxic in humans. While there is some fairly weak data that suggest that nonaromatizable AAS may pose a nephrotoxicity risk in animals (to wit, rodents; universally exposed to extremely high doses) under a fairly simple model that posits that AR activation per se poses some risk to nephrons that estrogens protect against. Well – boldenone aromatizes, so it’s not even a particularly good instance of a high risk compound under this model (unlike, e.g., metenolone, and certainly trenbolone).
The human data that does exist is totally & completely unreliable. There are two studies in particular that will be highlighted (as these are frequently used to defend the argument that boldenone is particularly hepato- and/or nephro- toxic).
The first study of note is Melick RA, Baird CW. The effect of "Parenabol" on patients with osteoporosis. Med J Aust. 1970 Nov 21;2(21):960-2. doi:10.5694/j.1326-5377.1970.tb63287.x. Hereafter, Melick.
This study (Melick) compared 2 doses of “EQ”: 50 mg Parenabol (boldenone undecylenate) every 2 weeks versus 25 mg Parenabol every 2 weeks.
Unsurprisingly, no anabolic or appetite-stimulative effects of the drug were noted. This is because both doses trialed are below the minimal effective dose in humans. Extrapolating from animal data and applying a human equivalence of dosing formula tells us that a minimal effective dose of boldenone undecylenate is 1.44 - 2.88 mg/kg e21d/e3w, or ~60 mg weekly for a 90 kg bodybuilder. Use of a human equivalent dose formula is the proper manner in which a trialworthy minimal effective dose should be arrived at.
And yet, despite these doses failing to induce any measurable anabolic or appetite-stimulatory effects, Melick is used to bolster the argument that boldenone is particularly ineffective and toxic.
Besides the doses being below that which could stimulate muscle anabolism, another problem with extrapolating from Melick is that its subjects were comprised of very sick individuals that were suffering from various maladies of long-term drug abuse, including alcohol (alcoholic cirrhosis), tobacco smoking (emphysema), and amphetamine addiction. Then, to draw any inferences about organic tissue damage from these data is totally incongruent to our population, not because bodybuilders never abuse street drugs, but because any instances of organic tissue damage from these subjects is not even fairly traceable to an ineffective drug dose trialed over the course of weeks versus the life-long abuse of toxic addictive substances on kidney and liver tissues in these elderly subjects with osteoporosis.
The second study of note is [2] Kantarci UH, Punduk Z, Senarslan O, Dirik A. Evaluation of anabolic steroid induced renal damage with sonography in bodybuilders. J Sports Med Phys Fitness. 2018 Nov; 58(11):1681-1687. doi:10.23736/S0022-4707.17.06763-9. This is trotted around the bodybuilding circles as the “Italian Human Use Comparator” study. Hereafter, Kantarci.
Basically, Peter Bond handily eviscerated Kantarci. Hopefully, he does not mind me quoting him (he has not reviewed any of my writings here or elsewhere); but I cannot do a better job with addressing this study than he has already done:
Conclusion: The undecylenate ester and its parenteral (intramuscular; I.M.) administration in a prodrug complex with boldenone cannot be more toxic than an oral delivery drug of the same in therapeutic doses of 200 mg daily (1.4 g/week). I.M. administration of boldenone and androgens generally form a depot in the applied tissues, where the rate of dissolution of the prodrug depends on the length of the esterified fatty acid attachment – its logP being inversely related to the rate of absorption. The direction of absorption is into the blood circulation, where active hydrolysis by esterase occurs only in human whole blood (and not the liver; despite some expression of PDE7B in liver). As an aromatizable AAS, boldenone contributed to both local muscle anabolic and total-body growth (by increasing systemic-circulating-liver-secreted IGF-I; unlike metenolone). It is less toxic than metenolone enanthate (Rimobolan; “Primo”).
1. Misconception that boldenone is nonaromatizable, or that its use (in sufficiently high doses) permit abstaining from AI/SERM use in users that are not resilient against aromatizing effects (e.g., fluid retention/edema, growth of breast tissue, etc.)
Reality: Boldenone aromatizes (to estrone [E1] & estradiol [E2]) at 58% the rate of testosterone. This is significant. However, since Estrone (E1) is a weak estrogen, because lacks the 17β-OH group, it possesses only 2% of E2's potency to transactivate ERα (associated with aromatizing effects, many of which are negative side effects in men).
Practically, this means that moderate/moderately-high boldenone doses (used solo; or in combination with nonaromatizable drugs, and/or with low doses of exogenous testosterone) would tend to not require AI/SERM use in users that are not resilient against aromatizing effects, but: A) for those who principally aromatize to E2 rather than E1 (inter-individual differences are likely rooted in 17β-HSD1 isozyme expression, under the control of the A1-Q327 gene) particular; and/or B) where E1 blood concentrations start getting into the regions of > 50-fold above that at which E2 causes problems in the individual, then the aromatizing effects would be expected to predominate.
2. Misconception that boldenone is not intended for human use.
Reality: Boldenone has been manufactured by pharmaceutical companies for human therapeutic use (to wit, by Parke Davis) as Anabolicum Vister (Quinbolone; boldenone cyclopentenyl)… and yes, it was patented by Ciba as Parenabol (boldenone undecylenate) as well. Anabolicum Vister was an oral delivery drug that relied upon a 17α ether attachment and suspension in oil in order to increase its lipophilicity and therefore bioavailability. It was nontoxic; but had to be taken frequently (10 - 20 capsules daily were recommended, 100 - 200 mg of boldenone prodrug), and like oral testosterone undecanoate delivery, there was broad inter- (between) & intra- (within) individual and diurnal (between and within days) variability in blood concentrations achieved, affecting its efficacy & adherence (these are the primary reason that its manufacture was discontinued).
Rather than by 17α- alkylation (attachment of an angular methyl or ethyl group to the C-17 position), Anabolicum Vister relied upon attachment of a cyclopentenyl ether, 5 carbons in length to form a prodrug. The rationale for this was that by increased lipophilicity (in combination with suspension of the drug in oil vehicle), this polar oil could be ingested or swallowed and then, from the gut, absorbed by the lymphatic system, bypassing hepatic metabolism. The lymphatic system is a network of veins and arteries that only serve to reabsorb water. When blood is delivered to tissues, only ~85% of the fluid is recovered. The lymphatic system reabsorbes the excess (~85%) water and delivers it to the angulus venosus, where two large veins meet right before they empty out into the heart. In the digestive tract (where the capsules of Anabolicum Vister arrive after ingestion), the lymphatic system serves to transports fats. With a delivery system such as that of Anabolicum Vister, the lipid/fat contents are easily be absorbed into the lymphatic system, avoiding hepatic metabolism (and therefore, strain) and then are delivered via a fairly direct route into the bloodstream (for systemic delivery of active boldenone).
3. Misconception that boldenone is toxic, and particularly kidney & liver toxic.
Reality: Boldenone, when profiled for drug safety using ADME-Tox & GSK 400 standards, outperforms Metenolone enanthate (Rimobolan; “Primo”). Indeed, metenolone enanthate is deemed Rejected under these standards, hhence why it is not available for human medical use in many places that subject their medical drug supply to more scrupulous regulatory regimes and schemes. Conversely, boldenone is Accepted under these standards, and therefore suitable for human use according to industry and governmental regimes that enforce ADME-Tox & GSK 400 standards. Specifically, for those that are interested, metenolone enanthate fails by fully breaking the GSK 4/400 Rule, Pfizer 3/75 Rule (logP), & Lilly Med Chem Rules.
Boldenone has never been demonstrated to be particularly nephrotoxic in humans. While there is some fairly weak data that suggest that nonaromatizable AAS may pose a nephrotoxicity risk in animals (to wit, rodents; universally exposed to extremely high doses) under a fairly simple model that posits that AR activation per se poses some risk to nephrons that estrogens protect against. Well – boldenone aromatizes, so it’s not even a particularly good instance of a high risk compound under this model (unlike, e.g., metenolone, and certainly trenbolone).
The human data that does exist is totally & completely unreliable. There are two studies in particular that will be highlighted (as these are frequently used to defend the argument that boldenone is particularly hepato- and/or nephro- toxic).
The first study of note is Melick RA, Baird CW. The effect of "Parenabol" on patients with osteoporosis. Med J Aust. 1970 Nov 21;2(21):960-2. doi:10.5694/j.1326-5377.1970.tb63287.x. Hereafter, Melick.
This study (Melick) compared 2 doses of “EQ”: 50 mg Parenabol (boldenone undecylenate) every 2 weeks versus 25 mg Parenabol every 2 weeks.
Unsurprisingly, no anabolic or appetite-stimulative effects of the drug were noted. This is because both doses trialed are below the minimal effective dose in humans. Extrapolating from animal data and applying a human equivalence of dosing formula tells us that a minimal effective dose of boldenone undecylenate is 1.44 - 2.88 mg/kg e21d/e3w, or ~60 mg weekly for a 90 kg bodybuilder. Use of a human equivalent dose formula is the proper manner in which a trialworthy minimal effective dose should be arrived at.
And yet, despite these doses failing to induce any measurable anabolic or appetite-stimulatory effects, Melick is used to bolster the argument that boldenone is particularly ineffective and toxic.
Besides the doses being below that which could stimulate muscle anabolism, another problem with extrapolating from Melick is that its subjects were comprised of very sick individuals that were suffering from various maladies of long-term drug abuse, including alcohol (alcoholic cirrhosis), tobacco smoking (emphysema), and amphetamine addiction. Then, to draw any inferences about organic tissue damage from these data is totally incongruent to our population, not because bodybuilders never abuse street drugs, but because any instances of organic tissue damage from these subjects is not even fairly traceable to an ineffective drug dose trialed over the course of weeks versus the life-long abuse of toxic addictive substances on kidney and liver tissues in these elderly subjects with osteoporosis.
The second study of note is [2] Kantarci UH, Punduk Z, Senarslan O, Dirik A. Evaluation of anabolic steroid induced renal damage with sonography in bodybuilders. J Sports Med Phys Fitness. 2018 Nov; 58(11):1681-1687. doi:10.23736/S0022-4707.17.06763-9. This is trotted around the bodybuilding circles as the “Italian Human Use Comparator” study. Hereafter, Kantarci.
Basically, Peter Bond handily eviscerated Kantarci. Hopefully, he does not mind me quoting him (he has not reviewed any of my writings here or elsewhere); but I cannot do a better job with addressing this study than he has already done:
(Peter Bond, Sep 28 2021)
Conclusion: The undecylenate ester and its parenteral (intramuscular; I.M.) administration in a prodrug complex with boldenone cannot be more toxic than an oral delivery drug of the same in therapeutic doses of 200 mg daily (1.4 g/week). I.M. administration of boldenone and androgens generally form a depot in the applied tissues, where the rate of dissolution of the prodrug depends on the length of the esterified fatty acid attachment – its logP being inversely related to the rate of absorption. The direction of absorption is into the blood circulation, where active hydrolysis by esterase occurs only in human whole blood (and not the liver; despite some expression of PDE7B in liver). As an aromatizable AAS, boldenone contributed to both local muscle anabolic and total-body growth (by increasing systemic-circulating-liver-secreted IGF-I; unlike metenolone). It is less toxic than metenolone enanthate (Rimobolan; “Primo”).
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