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Equipoise FAQ



Oct 17, 2010
This one is by Realgains

EQ has been esterfied with the undecylenate ester making it a long acting steroid much like Deca.

EQ is almost identicle to d-bol. The only difference is EQ has been 17 beta esterfied while d-bol has been 17 alpha alkylated. This small change makes the two hormones act very differently in the body not to mention EQ is NOT liver toxic at sane doses.

EQ can convert to DHT via 5- alpha reductase but in reality very little is converted to DHT in humans and so it isn't particularily hard on the hair line in the sensitive, or the prostate. It must be stressed that one WILL loose hair on EQ IF one has the genetics for male pattern baldness.

EQ is said to increase hemaglobin and hematocrit(number of red blood cells and percentage of red blood cells) This, however, happens with steroid use in general and I don't think EQ does this more than average.

EQ is said to increase appetite but again all steroids do this. I have not noticed any difference myself but some say they have.

EQ is said to increase vascularity although again I have not noticed any difference from other roids in my experience.

EQ is a veterinary steroid used mainly in race horses. In horses it adds to their muscluar bulk and changes their disposition making then better race horses.
In humans it is noted as a steroid that gives slow steady and almost pure muscle gain with little water retention and few androgenic sides.

EQ is a mild androgen and good ananbolic. Most would agree that it is slightly more androgenic than nandrolone and at least as good at promoting muscle gain and probably a little better depending on the person. Not only that but it is usually cheaper than Deca. Recovery of HPTA seems to be better for many men than when using Deca as well.

EQ does aromatize to estrogen but not to a great extent. Most estimate have EQ converting to estrogen at 50% or less the rate of an equal amount of testosterone and as a result bloat , elevations in BP and gyno are not usually an issue with moderate doses of EQ.

EQ alone at 400-600mg for 10 weeks provides for a decent cycle that does not require estrogen control drugs, is NOT liver toxic, and will show few if any androgenic sides . Ones lipid profile will change for the worst, as with any steroid, but not to the same degree as with a strong androgen like test or tren, or with the 17aa oral like d-bol.

Have nolvadex on hand for gyno protection just in case.

Clomid therapy should begin about 18 days after the last shot. See my post on clomid.
HCG before the cycle ends would be a plus. See my post on HCG

For the ultimate in mass EQ can be stacked with testosterone at equal dose but I only recommend this for advanced users.
Some can safely use it in a cutting cycle with winstrol or trenbolone acetate although others experience a small amount of water retention from EQ and choose to omit it in favor of steroids that do not aromatize at all like primo.

I can't remember where I got this, so if it's yours let me know so I can give you credit.

Boldenone and its precursor 1,4-androstadienedione

Boldenone is a popular anabolic steroid, manufactured as boldenone undecylenate in several veterinary drug preparations including Ganabol, Equipoise, Ultragan, Maxigan and Equi-gan. Structurally boldenone (1,4-androstadiene-3-one,17b-ol) is a close derivative of testosterone (4-androstene-3-one,17b-ol), differing from this androgen only by the addition of a second double bond in the A-ring of the structure (between carbons one and two). Likewise its direct precursor 1,4-androstadienedione differs from testosterone's direct precursor 4-androstenedione only by this same alteration, and converts to active form via the same widely distributed body enzyme (17-beta hydroxysteroid dehydrogenase, which interconverts these hormones between inactive 17-keto and active 17-beta hydroxy form). Although similar in structure, boldenone's second double carbon bond creates a hormone with activity that differs from testosterone in a number of significant ways.

Rate of Aromatization

One such difference is manifest in the rate in which this compound will aromatize (convert to an estrogen). Upon incubation with human placental microsomal aromatase (a standard assay for aromatase activity), the ability of 1,4-androstadienedione to aromatize to estrogenic form appears to be roughly half that of androstenedione (1). An equal activity level is present with our active target hormones boldenone and testosterone, as our active 17beta hydroxyl group will not to alter aromatase activity toward the substrate (as is noted by the equal rates of aromatization between androstenedione and testosterone). As testosterone is the primary substrate for the synthesis of estradiol in men, cutting this ability in half amounts to quite a considerable reduction in the estrogenic activity of our 1,4-androstadien hormones. It is for this reason boldenone is usually not associated with estrogen related side effects such as gynecomastia, obvious subcutaneous water retention and enhanced fat deposition, and athletes likewise consider it to be more of a steroid to promote lean muscular growth than raw bulk.

5-alpha Reduction of Boldenone

Boldenone also differs from testosterone in its ability to interact with the 5-alpha reductase enzyme. This is the enzyme responsible for forming dihydrotestosterone from testosterone, which is a much more potent activator of the androgen receptor. The 5AR enzyme is predominantly found in androgen target tissues such as the skin, scalp, prostate, pituitary, hypothalamus, and other regions of the central nervous system, and as such causes a notable increase in the androgenic potency of testosterone in these tissues. Although the 5-alpha reduction of boldenone (to dihydroboldenone) also results in the formation a more potent androgen, the C1-2 double bond on this hormone almost completely inhibits such interaction in the human body (2). Dihydroboldenone is likewise produced in small amounts at best in humans, allowing this hormone to be much less androgenic in nature compared to testosterone. On the plus side we see why athletes using boldenone injectables usually find them much more tolerable in terms of not promoting androgenic side effects such as acne, body/facial hair growth and hair loss. On the minus, of course we pay for reduced androgenic potency in terms of expected strength and mass gains (androgens are known to support neuromuscular functioning and development), which will be lower (though probably of higher quality) compared to that achieved with testosterone.

Comparative effectiveness of nandrolone and boldenone

The closest steroid in appearance (obvious effect to the user) to boldenone would probably be nandrolone. Most athletes use these two drugs under similar conditions, typically when there is a need for lean muscle tissue gain or a drug with fewer side effects in general. For these purposes both are well suited, however there are still some noticeable variances in the effects of both hormones. For example, at promoting overall muscle and strength gains boldenone is often proported to be more effective than nandrolone. This may be because boldenone is somewhat more androgenic in nature than nandrolone, due to the fact that it goes primarily unaltered by the 5-alpha reductase enzyme whereas nandrolone is actually reduced to less active form (dihydronandrolone) (3). While this allows nandrolone to be slightly milder in terms of side effects (except for interfering with libido, which can be much stronger with nandrolone as it is too weak an androgen), the lack of strong activity in crucial areas of the central nervous system may also act to lessen its effectiveness as a muscle and strength promoting anabolic. As boldenone is almost fully resistant to 5-alpha reductase, it retains an equal level of potency in both muscle and androgen target tissues.

We also see that in their respective rates of estrogen conversion both nandrolone and boldenone are similar in that they aromatize much more slowly than does testosterone. That is not to say that are equally resistant to this process however. In fact we see than nandrolone actually converts to estrogen at an even lower rate than boldenone does (1). One might automatically think that this is a more beneficial trait, however this would be assuming estrogen serves us no purpose in terms of muscle growth. Indeed this would be ignoring quite a bit of evidence showing just the opposite. For example, we find Primobolan® (methenolone, a non-aromatizable steroid) and nandrolone activate the androgen receptor with near equal affinity (4), and more avidly than does testosterone. Yet we know that testosterone is more effective at building muscle size. Were 5-alpha reductase the only cause for this disparity, we would think methenolone would be a similarly or more potent steroid than nandrolone, as it is more androgenic (due to the fact that similar to boldenone, methenolone remains unaltered in the presence of the 5-AR enzyme).

But Primobolan is notably weaker as an anabolic compared to nandrolone, making one question if its inability to convert to estrogen is also a key factor mediating its ability to promote growth. We see an interesting trend here. Testosterone (easily aromatized and the least effective AR agonist of the group) is the most potent muscle builder, whereas nandrolone (weakly aromatized, strong AR agonist) is thought to be roughly half as effective. Methenolone (not aromatizable at all, AR agonist potency near equal to nandrolone) is further known to possess even lower anabolic potency next to nandrolone, to spite its near equal effectiveness at the level of the androgen receptor.

We do know a couple of important things about estrogen and muscle growth. This first is that its sodium and water retaining effects of estrogen can greatly enhance the size of muscle tissue. The bulk you see from highly estrogenic steroids is in large part due to intercellular and intracellular water retention, and makes agents like testosterone, Dianabol and Anadrol rapidly acting agents. We also know that the conversion of androgens to estrogens is responsible for enhancing glucose-6-phosphate-dehydrogenase enzyme levels in muscle tissue (5). G6PD is an important regulator of glucose utilization, and plays a vital role in muscle growth and recuperation (6). Clearly the athlete today knows that if you want to put on size, you don't want to get away from estrogen completely. Likewise the low rate of estrogen conversion we see with boldenone may be ideal in that it allows for enough estradiol buildup to help foster muscle growth, yet it should reach a point where we see strong side effects like gynecomastia and excess fat retention.

Boldenone and Dianabol

It is also interesting to point out that boldenone is also structurally almost identical to methandrostenolone (Dianabol), barring that the latter hormone contains an added c-17alpha methyl group to allow for optimal survival during oral administration. The principal achievement with both steroids was again the C1-2 double bond, which markedly increases the ratio of anabolic to androgenic effect in each case. Athletes however usually fail to notice the relationship between these two anabolics, the two drugs varying in outward appearance so much that use of methandrostenolone is usually isolated to bulking cycles while boldenone is accepted as a mild anabolic for cutting phases. Clearly the more active estrogenic nature of methandrostenolone is the cause for such discrepancy, a trait due to the added methyl group. Although we find that c-17 alpha methylation moderately decreases the affinity of this substrate for the aromatase enzyme, the product here is a different form of estradiol (17-alpha methylestradiol). When we look at testosterone for example, we find that a 17alpha-methylated version (methyltestosterone) represents a more potent form of this hormone. This is because the methyl group does not greatly interfere with the ability of the hormone to activate the androgen receptor, however it does allow it have a lower affinity for the serum binding protein SHBG and exist in a more free and active state (7). Sharing use of the same binding protein (SHBG is also referred to as Testosterone-Estradiol Binding Globulin) and knowing that 17-methylestradiol is near in potency to estradiol , it seems logical to conclude that 17-methylestradiol would be similarly more active (and explain the greater estrogenic potency of drugs such as methyltestosterone, methandrostenolone and norethandrolone). The structural and characteristic similarities between these two hormones however remain evident.

High Oral Efficacy and Legal Status:

Although one might think 1,4-androstadienedione would be a synthetic hormone at first glance, it has clearly been demonstrated to occur in nature (9). This allows it to be is protected by the Dietary Supplement Health and Education Act (DSHEA), and legal for sale as a nutritional supplement in the U.S. To support the belief that a 1,4-androstadienedione supplement really works as an effective precursor to boldenone in humans and not just on paper, we can take note of a 1971 study in which an unusually high amount of 17beta hydroxylated metabolites (as high as 22% of the given dose) were recovered in urine after oral administration of 100mg (10). Remember that in order to become active its 17-keto group must be converted to a 17-beta hydroxyl group. In fact 7.1% and 11.1% of the given dose was actually recovered in the form of intact boldenone in the two subjects of this investigation, indicating an extremely notable capacity for this hormone to convert to active form in the human body after oral dosing. It also demonstrates the ability for the C1-2 double bond to resist 17-ketosteroid reduction, a trait far different from testosterone, which produces 17-hydroxy metabolites in much smaller amounts.

Clearly boldenone has a firmly rooted place in the world of bodybuilding pharmaceuticals, standing out as a mild yet potent anabolic for the promotion of lean muscle tissue growth. It has likewise always been in high demand on the black market. The inclusion of a highly efficient steroidal precursor to this potent anabolic steroid in the world of legally available nutritional supplements will undoubtedly come to represent a welcome expansion in choices for the consumer.


1- Biosynthesis of Estrogens, Gual C, Morato T, Hayano M, Gut M and Dorfman R. Endocrinology 71 (1962) 920-25

2- Relative Importance of 5-alpha Reduction for the Androgenic and LH-Inhibiting Activities of Delta-4, 3-Ketosteroids. Steele R, Didato F, Steinets G. Steroids 1977 331-47

3- Relative Binding Affinities of Testosterone, 19-Nortestosterone and their 5-alpha Reduced Derivatives to the Androgen Receptor and to other Androgen-Binding Proteins: A Suggested Role of 5-alpha Reductive Steroid Metabolism in the Dissociation of "Myotropic" and "androgenic" activities of 19-Nortestosterone. Toth M. Zakar T. J. Steroid Biochem 17 (1982) 653-60.

4- Relative binding affinity of anabolic-androgenic steroids: Comparison of the binding to the androgen receptor in skeletal muscle and in prostate, as well as to Sex Hormone-Binding Globulin. Endocrinology 114 (1984) 2100-06

5- Aromatization of androgens to estrogens mediates increased activity of glucose

6-phosphate dehydrogenase in rat levator ani muscle. Endocrinol 106(2):440-43 1980
6- The pentose phosphate pathway in regenerating skeletal muscle. Biochem J 170: 17 1978

7- Binding of 17-alpha-Methyltestosterone In Vitro to Human Sex Hormone Binding Globulin and Rat Ventral Prostate Androgen Receptors. Wiita B, Althea A, Ackerman and Longcope C. Therapeutic Drug Monitoring 17 (1995) 377-80

8- Estrogen Receptor Binding Radiopharmaceuticals: II. Tissue Distribution of 17-alpha-Methylestradiol in Normal and Tumor-bearing Rats. Feenstra A., Vaalburg G., Nolten J., Reiffers A. et al. The Journal of Nuclear Medicine 24 (1983) 522-28

9- Identification of C19 Steroids in Bovine Feces. Miller, W.R., C.W. Turner, D.K. Fukushima and I.I. Salamon: J. Biol. Chem. 1956 220: 221

10- Metabolism of 1-dehydroandrostanes in man. I. Metabolism of 17-beta-hydroxyandrosta-1,4-dien-3-one, 17-beta-cyclopent-1-enyloxyandrosta-1,4-dien-3-one (quinbolone) and androsta-1,4-dien-3-one (1). Galletti F and Gardi R. Steroids 18 (1971) 39-50.


VIP Member
Sep 24, 2010
More good info...I've personally had the increased appetite from eq,mostly from the old ganabol.
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