Novaldex and gains

Very very interesting. What's the anabolic:androgenic ratio of DHT (I'm just curious because that way I'd be able to know to what extent you hinder gains if you take proscar)? Where can I find a list of anabolic;androgenic ratios?

Nicely put (if not succinct! ) THis just makes SO much sense that it should be a sticky! We can argue the studies all day and night long but at the end of the day you have gyno you lost big time! Take the Nolvadex!

JB

Posted by: Nandi12

First, binding affinity can effect the potency of a steroid, but a strong binding affinity is not essential for potency, either anabolic or androgenic. I was not clear in emphasising this earlier.

In truth, not enough is known about how steroids cause prostate growth or baldness to say definitively. But go back and look at the study about MENT:

Its anabolic/androgenic ratio is so high that a dosage that maintains muscle mass in castrated monkeys is barely enough to even maintain prostate weight, much less cause the prostate to enlarge. This can be seen by comparing figures 4 and 5. But bodybuilders take dosages much higher than those required simply to maintain body weight, so MENT "abuse" would lead to prostate enlargement. This is the case with all of the commonly used AAS: their anabolic/androgenic ratio is not high enough so that prostate enlargement can be avoided at the dosages used by bodybuilders. There are experimental compounds I've seen discussed with anabolic/androgenic ratios as high as 25 to 1. Something like that could probably be used to build muscle with no effect on the prostate.

Here again, just not enough is known. My original point is that if a person had to decide between a high liklihood of getting gyno versus a possible but unproven effect on gains, I would do everything possible to avoid gyno, and take the risk of a possible loss in some gains.

IMO that is an extreme position. I would experiment and see. You are going to make gains using nolva and/or proscar. Countless bodybuilders do. There is nothing wrong with making a potential compromise (and there may not even be a compromise) to help preserve health. That is just common sense.

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What's the anabolic:androgenic ratio of DHT

DHT is generally considered about 10 times as androgenic as it is anabolic, but you will see a range of values based on the assay. People used to measure the weight of the rat levator ani muscle compared to prostate and seminal vesicle weight to get a ratio. Unfortunately, later people realized the levator ani is more responsive to androgenic agents than is other skeletal muscle, calling into question a lot of early ratios. The best assay is one like they used in the MENT study: carcass muscle weight v. prostate weight.

Bill Roberts has some discussion here giving some sample ratios:

Since DHT is rendered inert in skeletal muscle it has little if no direct effect on muscle anabolism. People attribute its effects to things like driving aggression, leading to more intense workouts, or somehow improving neuronal control of muscle, thus increasing strength. You may notice no effect whatsoever though on drive; this is the case with many who have used it during a test cycle, myself included.

If you are worried about the prostate though, I would use it, just like I would use nolvadex if I were worried about gyno.

Here we can clearly see BigCat's defense of estrogens and DHT as active agents in muscle anabolism:

"Structurally, clostebol is simply Testosterone with an added chloro group at the 4-position. In itself quite ingenious. I mean you see all sorts of structural alterations to prevent a steroid from interacting with enzymes, but none as simple as this. By putting a structural alterations right on top of the 4-position, it cannot be 5-alpha reduced to dihydrotestosterone, thereby limiting a more androgenic form in androgen specific tissue like scalp, prostate and skin. And so of course, avoiding all problems associated with DHT formation like extreme cases of acne and serious hair loss. But it also prevent aromatization, so no estrogen is formed. That limits fat gain, bloat and the risk of breast growth in men (gyno). Needless to say of course that eliminating the stronger androgenic and all of the estrogenic components, this steroid is nowhere near as potent as its parent, testosterone. But you have to admit the beauty of it. Why use testosterone if you are only going to stack it with fortunes worth of Arimidex and finasteride to block estrogen and DHT, if you can just take clostebol and be done with it? I mean if you are going to screw around and mess up the strongest anabolic, do us all a favour and just use this stuff. If you really can't take the side-effects and still want to use a steroid. Although I must say I loathe such people. Either you take it like man and accept the risk, go for the gains and get from it what you can, or you can't tolerate the risk, and then you should just stay away from all steroids. Period. I hate those "I want it all and don't want to pay for it" type of people. "

That's bigCat's opinion. Why the hell should we want so bad 5-alfa-reduced DHT from testosterone especially taking into account that its "superior" stimulation of the AR is gonna be exerted in skin,scalp and prostate, for these are the tissues where 5AR is most active. In any case, taking into consideration that we wanted DHT for AR stimulation wouldn't it make more sense directly injecting DHT because it would spread evenly in the whole body (and within that muscle tissue) as opposed to testosterone 5-alfa-reduced DHT which would exert his effect just in prostate,scalp,skin and not in muscle androgen receptors, which is what we want in any case? Am I right or am I missing something? Would it even make some sense to inhibit 5AR by means of Proscar and at the same time inject DHT so that it evenly reaches muscle tissue and prostate and not just prostate?

By the way, if DHT is ten times androgenic as it is anabolic people taking Proscar is not especially hindering gains at the gym, are they? In any case they might be hindering strength gains and agressivity at the gym because of the 5AR present in the nervous system.

Nandi12:

How can we know whether or not non-AR mediated anabolic mechanism which are represented in the anabolic:androgenic ratio are not largely dependant upon estrogen or progestin activity or enven 5-alfa-reduced forms of the given steroid?
For instance, let's say that we have a compound with an anabolic:androgenic ratio of, let's say, 6:1, now how can we know for sure that all those non-AR mediated mechanisms don't completely rely on estrogenic activity and that if we were to take nolvadex in conjunction with the steroid we are not going to be left busted with a ratio of 1:1?

To me, the big question which arouses now, after the previous discussion about as to whether or not we should use nolvadex+Proscar during a cylcle is to what extent you improve safety and reduce gains, if you improve safety by 300% and reduce gains by 100% you are on the right track. On the contrary, if your reduce gains and imporve safety by the same percentile is just as if you are taking products which counteract each other and you are better off not taking anything, don't you think?

Your username is apt ;you are overanalyzing this stuff. There are not enough data to attach any kinds of numbers to how things like estrogen blockers, aromatase inhibitors, of finasteride will affect your gains, if at all. Plenty of guys use these things on cycles and plenty don't. Most get good results either way.

I think it is a mistake to take ANY medication without proven need. But "proven need" exists for, for instance, at a gram a week, IMPO. We know estrogen levels will rise substantially, and so I prophalactically control it with an AI. I also like to keep some SERM around, because "nipple issues" develop even when E is within physiological range (it's the accelerations of serum androgen levels that does it then, methinks).

Anyway, back to the original point. I do not prophalactically prevent rises in DHT. If you are suffering MPB, that's one thing. But to take it under the misconception that it will somehow prevent prostatic morbidity later in life is ill-conceived. The same goes for saw palmetto. DHT is our friend!

Posted by: SWALE

I think it is a mistake to take ANY medication without proven need. But "proven need" exists for, for instance, at a gram a week, IMPO. We know estrogen levels will rise substantially, and so I prophalactically control it with an AI. I also like to keep some SERM around, because "nipple issues" develop even when E is within physiological range (it's the accelerations of serum androgen levels that does it then, methinks).

Anyway, back to the original point. I do not prophalactically prevent rises in DHT. If you are suffering MPB, that's one thing. But to take it under the misconception that it will somehow prevent prostatic morbidity later in life is ill-conceived. The same goes for saw palmetto. DHT is our friend!

Correct me if I'm wrong but I don't believe DHT is the primary cause of BPH. Don't most men with BPH have a high E/T ratio?

Bingo! I don't think it is a coincidence men suffer prostatic morbidity at precisely the time when T/E is lowest. Also, the nodules of BPH form in the periurethral transition zone--where the highest concentration of aromatase is found.

I really am coming to believe that estrogen is the real culprit here.

Posted by: SWALE

Bingo! I don't think it is a coincidence men suffer prostatic morbidity at precisely the time when T/E is lowest. Also, the nodules of BPH form in the periurethral transition zone--where the highest concentration of aromatase is found.

I really am coming to believe that estrogen is the real culprit here.

True and false at the same time. Yeah, you are right estrogen "fucks" your prostate... but how? Upgrading the androgen receptors, and these receptors are, in turn, activated by androgens, being DHT the most powerful. Which is to say that androgens and estrogen work synergically to produce BPH and, possibly but not proven, prostate cancer. DHT without estrogen and estrogen without DHT would probably almost harmless, for one propably needs the other in order to screw your prostate. It's sort of a simbiosis.

In truth nobody knows how BPH develops. Estrogens may be involved via production of growth factors, cross reactivity with the androgen receptor, AR upregulation, or some combination of the above or other as yet undetermined pathways. Alpha adrenergic signaling is important, as are androgens. Antiestrogens and aromatase inhibitors have been unsuccessful at treating BPH, so clearly estrogen in not crucial.

finasteride and alpha1 inhibitors used together probably have the best track record (this is the combination my urologist prescribed). Ironically at the time it was thought alpha 1 blockers simply improved voiding by relaxing the muscles at the base of the bladder. Now it is known that they shrink the prostate itself, often with dramatic improvement in symptoms.

I really believe that in the future we will be abandoning 5-AR control to treat prostate morbidity. Urologists prescribe for it because that is what they all do at this time.

I can't find it, but I did see an abstract from an article where tamoxifen had a positive effect on rat prostate tissue (perhaps it was protective of cancer?). Oh, to be composed entirely of rat prostate tissue!

To be sure, it is a complicated issue. But why should that surprise us?

I have not seen the research on rats and tamoxifen. The few studies I have seen in humans did not show much promise for the use of antiestrogens. My impression of the data is sort of summarized in this review:

"These data suggest that in the medical treatment of BPH, antiestrogens or aromatase inhibitors may be used: however, up to now the clinical results of this treatment are not promising and the improvement of the obstructive symptoms does not exceed that of placebo."(1)

(1) Arch Androl 2000 May-Jun;44(3):213-20

Role of estrogens in human benign prostatic hyperplasia.

Sciarra F, Toscano V.