Whats the overall deal with this product? Is it effective and does it do what it claims?
Thanks alot,
Josh
There was a study done by Thomas Incledon that showed 6-OXO does work. They used 300 mg in the morning and 300 mg in the evening over the course of 3 weeks. The only bad thing is that this dosing schedule would give you only 10 servings per bottle.
The study showed that 6-OXO indeed increased free Testosterone while actually decreasing LDL and total cholesterol as well as triglycerides. That would seem to be a nice side-effect.
WV
I’ve read the clinical study ot…and it might be the one referred to…but as with most non-Biotest products…the product doesn’t completely work. If you read the data, you’ll notice that estradiol levels actually stay the same! They theorized that since the testosterone levels doubled over a 4 weeks period more of it was converted via aromatase back to estrogen (testosterone is the precursor to estrogen). So it works, but it sort of backfires.
Proteinpowda is correct on the research findings.
This can also be seen by stopping and thinking about it.
There are aromatase inhibitors that actually are effective… and with quite reasonable doses, you can make them every bit as effective as you want them to be. An example is Arimidex.
So we know what happens with aromatase inhibitors. With doses sufficient to increase testosterone much, estradiol levels drop dramatically, in some cases to near zero. And there is no great, if any, benefit to performance enhancement from aromatase inhibitors – that is a very important point – with certainly no substantial muscle gain and no “muscle-hardening” effect. (There may be an effect on subcutaneous fat depending on the individual, and on water retention.)
Do the results from Arimidex and 6-OXO sound alike or even similar? No. Not remotely. 6-OXO is not like low-dose or any dose of Arimidex or any aromatase inhibitor. And the reason is simple enough: it’s because 6-OXO, contrary to marketing claims, is not an effective oral aromatase inhibitor in man.
Which actually is a good thing by the way, except for your pocketbook: for about 99% of younger and middle-aged individuals not taking aromatizing anabolic steroids, aromatase inhibitors first are not beneficial, and second, can be quite problematic with regard to side effects particularly if blood testing is not done, which one cannot reasonably expect of those buying the product.
The data also doesn’t support the supplement 6-OXO acting as an effective aromatase inhibitor. If it were, estrogen levels would decrease significantly. The excuse that they don’t at all is because 6-OXO “really” decreases estrogen, but that in turn increases testosterone, which in turn increases estrogen as much as it was first decreased and thus totally masks the alleged significant anti-aromatase effect, makes no sense. That just does not happen with aromatase inhibitors.
Actually, I absolutely expect that what you will see with 6-OXO, and we’re quite likely to do though frankly our own research has greater priority, is that it does not increase testosterone at all. Zero, zip, nada.
Rather the claimed results are in error.
The reported results to the contrary are likely similar to when we first introduced Androsol, a topical 4-AD delivery system, and initial lab findings gave “testosterone” readings beyond what I found credible. I hypothesized that 4-AD was being falsely detected as being testosterone… and that proved to be the case. (Androsol still did increase testosterone greatly, but within the range of rational possibility, as opposed to the original extreme apparent results.)
Due to that concern, we expressed that possibility on our initial report on Androsol, and promptly did GC/MS and obtained the correct data and reported it. That’s just basic good science.
This sort of problem actually is endemic to testing by immunologic methods such as ELISA or RIA. Molecules of similar structural shape can be bound by the same immunoglobulin, and therefore differing molecules can be “mistaken” for what one intends to be assaying.
Until you see GC/MS (gas chromatography / mass spec) demonstrating that 6-OXO increases testosterone, don’t believe it.
This supplement is a product of error in three regards:
-
Expecting it to be an effective aromatase inhibitor in man when taken orally – it isn’t,
-
Mistake in the research being done in mistaking 6-OXO or more likely its metabolite 6-oxotestosterone as being testosterone, thus yielding wrong marketing claims that it increases testosterone, and
-
The completely “off” theory that it really does decrease estrogen despite test results showing no change.
What 6-OXO is, is a poor prohormone.
Our research in this area has led to much better things for performance enhancement and acquisition of muscle, incidentally.
Sweet, always good to hear from you Bill. Is this Carbolin-19?
Nope, totally different!
Thanks for the kind words… glad to be back on the Forum. I won’t be able to be on as often as before – which though I enjoyed it really was too much and reduced time spent in research and development of products – but I’ll definitely not make it as long a gap between posts in the future! 
What causes the acne and increased libido in 6OXO then Bill?
Bill, a friend of mine is planning on starting a cycle of 1 and 4-AD in a few weeks. He has been thinking of taking 6-OXO, but from the sounds of it you wouldn’t recommend it. I am trying to convince him not to take it, but what else can he take post cycle or during his cycle to limit estrogen during the cycle? I figure if I have another product to replace his 6OXO, he may be more likely to believe me
[quote]BodyIQ wrote:
What causes the acne and increased libido in 6OXO then Bill?
[/quote]
As both Bill and I have said, 6-oxo is actually a weak androgen and that can easily explain why you may have experienced some acne and an effect upon libido.
Well, during the cycle, neither 1-AD nor 4-AD converts to estrogen, and estrogen levels don’t rise during such cycles. So an anti-estrogen isn’t of value.
While in principle one might think that since 4-AD increases testosterone this might result in a concurrent increase in estrogen, in practice that is not so. I expect that is because of the weak antiaromatase activity of 4-AD that one would expect from its structure – so weak as to only keep estrogen levels essentially the same rather than decreasing them at all.
But in any case it’s just not an issue for a cycle such as your friend is doing: an anti-estrogen is called for only if aromatizing steroids are used, and that’s not the case here.
And after the cycle, again elevated estrogen is not an issue in this case. Further, just to discuss other situations, even if aromatizing steroids had been taken, there’s no evidence, as mentioned above, that 6-OXO can do anything to block elevated estrogen.
In terms of actually increasing production of testosterone post-cycle, Alpha Male is by far the better choice.
Damn, Bill…
That was one hell of an educational post, and I just wanted to say thanks for taking the time to report all that.
Just another reason this place kicks so much ass.
So Bill or Cy, what’s the story with M1T and it’s conversion to estrogen. Based on the clinical data you have from M, how effective will this be against an androgen of that magnitude?
And to comment on what you said ealier about the 4-ad…I’m guessing a lot of people have forgotten the original articles on androsol or MAG-10. There are actually higher circulating levels of 4-ad in our body than actual testosterone. It’s just not exactly (not as well as testosterone) how the 4-ad exert it’s effects. Also looking at the clinical data for the original 4-ad (before Biotest riced it out), it was very non-bioavailibe and had a conversion rate to test of less than 5% and I think the conversion to estrogen was either 0 or .1% or something in that range. If you need I can look it up and be a bit more precise and reference the data.
But realize that a hormone doesn’t need to be EXACTLY testosterone to exert effects; in fact the main purpose of many prohormones based on their claims wasn’t their converstion ratio to testosterone, it was rather the increased effectiveness of the hormone they converted to (or in some cases the state they were in). For example 1-test is supposed to 700% (if I remember right) more anabolic than testosterone while 4ad was 98% I think. Now don’t skew up these numbers. What they actually mean based on the test method relates to the AMOUNT you need to take to get a certain result (aka 7x less 1-test to get the effect testosterone).
Ok, enough for now.
Wow, Bill, I honestly want to thank you for that post. It’s the first post regarding this topic that has actually had some sort of explanation rather than just a “go read something.” So, if I am right, you believe that during the 1-AD and 4-AD nothing should be taken, and Alpha Male should be taken once the original cycle is done? Do you have any suggestions for someone who already has developed a bit of gyno, not through the use of any drugs, but simply genetics/whatever? Should they be taking anything else if they were to take the same cycle? Should they not do it at all?
It’s possible he could get a benefit, just not the intended one of reducing estrogen.
Now if 1-AD and 4-AD are being used only moderately, to get more effect I’d just add more of those myself rather than add 6-OXO as a third thing.
But if the plan already is to be using them pretty heavily, then adding 6-OXO, while not as efficient as previously-available approaches like MAG-10 or even any 1-testosterone product, seems to add some results with this maybe being more efficient than adding more of the diols. It doesn’t necessarily compete too severely with the diols in terms of enzymatic conversion, and adds some benefit as an androgen prohormone.
(BTW, if wondering why I said not necessarily competing “too severely” as opposed to not at all – which is the common belief given the fact that the enzymatic pathways are different – it is because there is binding of 3-ketosteroids (including the diones) to 3b-hydroxysteroid dehydrogenase, the enzyme responsible for conversion of diols to testosterone or related compounds, and therefore competitive inhibition; as well as binding of 17-hydroxysteroids (including the diols) to 17b-HSD, the enzyme responsible for conversion of diones to testosterone or related compounds. If there is a study showing the extent of this competition, I’m not aware of it, but beyond doubt it does occur and could be the explanation of why “stacking” of diols and diones has been generally been of only moderate added effectiveness rather than doing anything at all like doubling results. Nonetheless there can be some added effectiveness.)
With regard to gyno, non-aromatizing androgens are OK, while taking an aromatizing androgen can aggravate it. Mostly it’s a question of avoiding those problems – to some extent flax seed oil and Vitex agnus castus can be of benefit but neither is capable of overcoming the adverse effects of the above. They can have some good effect just generally dealing with problems from aromatization of natural testosterone though.
Proteinpowda, with regard to methyl-1-testosterone, it doesn’t convert to estrogen, so there’s no problem in that regard. It does have the issue of liver toxicity, as with any 17-alkylated steroid, but as a general rule for these compounds if use is limited to preferably no more than 1/3 the weeks of the year (not that that can’t be somewhat exceeded) and no more than 8 weeks at a time and preferably less, it can be gotten away with. As further issues though, it’s one of those steroids with much more noticable and frequent adverse side effects, much moreso than I consider acceptable for a supplement. Ill-effect on sense of well-being which can include lethargy isn’t uncommon; neither are headaches and considerably elevated blood pressure, moreso than typical for pharmaceutical androgens.
There are a great number of steroids that were synthesized and tested by the pharmaceutical companies: those that passed every test are obviously more likely to be good choices than those that did not, and also more likely than those which were perhaps dropped for no particular reason. We don’t have access to the proprietary data of these companies, but pretty clearly to me methyl-1-T is one that would not have passed human trials.
Bill-
GREAT stuff! I really, really appreciate your time and energy. Question though: any idea why do so many T-Nation members appear to be encouraging anti-estrogen drugs post-cycle for non-aromatizing PH/steroid use??? I know very few on here are educated enough to truly understand all that goes into PH/steroid use, but there are a few that appear to be veterans of these drugs that are encouraging this constantly. It would seem they are pushing post-cycle therapy with an anti-E because they are thinking the body will over-compensate and secrete too much E:T on the “rebound”. When in fact, in one of your posts above, you mention that there is no need for an anti-E during NOR post cycle with a non-aromatizing PH/steroid! I’m trying to clear up this rumor as it’s all over the steroid forum and elsewhere. I could have missed it, but I didn’t see Cy or any other very credible source stepping in to squelch this supposed fallacy.
Thanks much!
TopSirloin
Awesome to see Bill back on the forum. He definitley answered some questions I had.
Can’t wait to see what kind of supplements he has in the works.
Thanks!
On the anti-estrogen thing, there is a value to using an anti-estrogen (or more precisely, a selective estrogen receptor modulator) like Clomid post-cycle, because it helps boost natural T production. If one has access to this, I recommend it.
It actually is more effective in increasing testosterone than an antiaromatase can be. First that’s from observation, and then second there are physiological reasons for this.
First, one can use Clomid at a dose giving maximal possible antiestrogenic benefit, whereas antiaromatases need to be limited to only moderately reducing estrogen – as driving estrogen too low is a bad thing – which only moderately increases testosterone.
Further, Clomid has the remarkable property of being anti-estrogenic where estrogenic activity is undesirable for our purposes, and estrogenic where estrogenic activity is desirable. (It’s a pretty amazing drug!)
Estrogen has both positive and negative feedback aspects in the hypothalamic/pituitary/testicular axis (HPTA), in addition to other functions. Clomid capitalizes each way in this, rather than in just one direction as an antiaromatase does. So this is another reason it works better.
I think a lot of the “myth” you see about “need” for antiestrogens post-cycle, regardless of the type of cycle, is that ever since the theory that estrogen controlled HPTA feedback was put out back in I think the 80’s by a noted innovator and thinker in the area, it’s been generally accepted as if estrogen were all there is to it – and often with neglect of whether given cycles raised estrogen or not. But in fact estrogen is only one of many factors involved in inhibition of the HPTA.
For example, androgenic inhibition is an even greater factor.
In any case, with a non-aromatizing cycle anti-estrogens, whether Clomid or antiaromatases, aren’t needed post-cycle for the purpose of blocking some unusual bad post-cycle effect of estrogen. There can be a use, particularly with Clomid, in terms of enhancing HPTA recovery. In fact that’s an excellent thing to do for any cycle, although I’ve found in the past TRIBEX plus Vitex to be remarkably close in effect and therefore I expect that Alpha Male should be as well (and there are reports that it is.) I don’t really recommend an antiaromatase for that purpose: problems seem more common than genuine benefits in that situation.
With conservative dosing, blood testing, and cases where an individual is known to do well with a given antiaromatase then such use can make sense for them. But even then, an antiaromatase would be an inferior choice to Clomid, unless they are one of the relatively few who do not do well with Clomid, suffering either from depression or from visual disturbances.
Thanks so much, Bill for the education!
I’ve been wanting the lowdown on this product. Finally got expert info.
Bill-
Again thanks for that quite in-depth look at anit-E’s and PH/steroids.
I was also quite interested to know just how much a PH like M1T or the like can help a trainee when cutting?
For bulking we know that it can be very beneficial, but I’m wondering if the anabolic properties of the drug interfere/enhance in any way with the lipolytic functions of the body when calories are decreased through diet and exercise?
Much appreciated!
TopSirloin
This a great thread, especially with the bottom line explanation on 6 OXO – explains why T-Nation doesn’t have a 6 OXO product.