
Originally Posted by
BigCat
In defense of Boldenone
Boldenone differs from testosterone only in that it has an extra double-bond on it’s a-ring at the 1 position. This changes the conformation of the A-ring and its affinity for certain structures. As such it is only half as androgenic as testosterone because of lower affinity to the androgen receptor, and it does not form a more potent androgen in androgen-specific tissue, because it has particularly low affinity for the 5-alpha-reductase enzyme (10) (that converts test to DHT). Even though its conversion product is quite potent (1-testosterone).
Boldenone’s affinity for the aromatase is roughly reduced by the same percentage, and so it only creates about half as much estrogen. So in essence, boldenone offers us many of the same characteristics that testosterone does, but because of its lessened affinity poses less of a threat for the acute, visible side-effects. So by dividing our doses over testosterone and boldenone, we can reduce both acute and long-term side-effects.
Boldenone is patented as a veterinary drug, but the high demand has made a wide range of affordable human grade products available to us and the use of boldenone is now quite wide-spread among recreational athletes. It is touted as the successor to the mighty Deca-Durabolin. Deca is nandrolone decanoate. Nandrolone has the benefit of being deactivated by the 5-alpha-reductase enzyme and being even less of a threat for acute androgenic side-effects. But alas, it is a very suppressive hormone that severely interferes with endogenous production of testosterone and it has been concluded that both nandrolone (11) and several of its metabolites (12) exhibit progestagenic activity (which causes gyno through estrogen mediated pathways) and seems to cause more bloat because it acts as an aldosterone agonist (13), resorbing more salts from the urinary tract. On top of that it seems to have a terrible effect on our libido (can you say limp dick ?).
Boldenone gives us none of the aforementioned problems, and despite being a much, much weaker androgen than nandrolone, it seems to exhibit the same level of anabolism in vivo. Which again points in the direction of the non-AR and non-ER mediated pathways to muscular hypertrophy we discussed with testosterone. Boldenone offers two other distinct benefits that have been noted by many a user, despite lack of scientific backing so far. The first is that boldenone seems to increase the appetite. This too is most likely a non-AR mechanism, since many of its inactive metabolites like androstadiendione exhibit the same property and to the same extent, but in low doses. This could be crucial since we steroids can build our muscles, but they need something to build with. That something is amino acids derived from our protein intake, hence our high-protein diets. But to have ample amino acids left to build muscle, we must first eat sufficient calories, more calories than our maintenance of metabolism requires. And in that case it can be of huge benefit to increase your appetite.
The second advantage is that it causes an uncharacteristic rise in aerobic fitness. It is well known that androgen binding increases Erythropoetin release from the kidneys, which increases red blood cell count. Red blood cells carry oxygen through the blood stream, so we have a greater aerobic capacity. But boldenone seems to exhibit an increase in aerobic capacity, far greater than its androgenic affinity would allow us to suspect. This is probably why this veterinary hormone gained so much human attention in the first place. Along with the increase in respiratory capacity from beta-adrenrgic stimulation (discussed later in this article) could lead us to new heights in any type of sports we practice that require endurance.
So in light of its safety and efficacy, the choice for boldenone as our secondary drug is a quite easy one.