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While the boss is away............Thread

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The Induction phase is the first, and most restrictive, phase of the Atkins Nutritional Approach. It is intended to cause the body to quickly enter a state of ketosis. Carbohydrate intake is limited to 20 net grams per day (grams of carbohydrates minus grams of fiber, sugar alcohols, or glycerin), 12 to 15 net grams of which must come in the form of salad greens and other vegetables. The allowed foods include a liberal amount of all meats, fish, shellfish, fowl, and eggs; up to 4 ounces (113 g) of soft or semi-soft cheese; salad vegetables; other low carb vegetables; and butter and vegetable oils. Alcoholic beverages are not allowed during this phase.[2] Caffeine is allowed in moderation so long as it does not cause cravings or low blood sugar. If a caffeine addiction is evident, it is best to not allow it until later phases of the diet.[2] A daily multivitamin with minerals is also recommended.

The Induction Phase is usually when many see the most significant weight loss — reports of losses of 5 to 10 pounds per week are not uncommon when Induction is combined with daily exercise.
 
The Induction Phase is usually when many see the most significant weight loss — reports of losses of 5 to 10 pounds per week are not uncommon when Induction is combined with daily exercise.

Read the article I posted on the other page.
 
that was bobo clearing it out, I think because with the steroid discussions on the board, he wants to be squeaky clean product wise
 
hmm he was just answering the question tho. could be something to it, most other sites still have all their PS/ph products for sale, and at normal prices
 
Cy,

What is your opinion of ATD (1,4,6-androstatriene-3,17-dione)?

Is it safe? Effective?

Thanks for your help.


I don't know that I can answer either of those questions. I will say this however. Likely limited by first-pass metabolism, and again something which it seems these companies which keep coming out with these products are forgetting, is that these steroidal aromatase inhibitors have two major drawbacks which is why you saw the shift in the pharmaceutical industry towards non-steroidal aromatase inhibitors, and those drawbacks are related to both lack of selectivity and in the case of someone who is using it post cycle in the hopes for increased recovery, these steroids, this one in particular, are androgenic. You can look in to the literature and find relatively easily, studies regarding this. One concluded that it may be an androgen antagonist, another concluding a likely metabolite binds to the AR acting as an agonist. Obviously, neither of these are what you want. Also, if it works as well in humans as it did in animal models, you could also expect a decrease in HDL.

If you're going to use an aromatase inhibitor, you're much better off using anastrozole.
 
How does it manage to restore the size of your testicles while on cycle, and not stop your gains? Sort of like HCG. Also I've seen people's blood work after using it along with other trib, or fenugreek type products for pct and their test levels aren't suppressed.

I'm not arguing, and you know that I know that you know you know alot more then me Cy ;-) I was just shocked at how quickly my nuts came back, and bigger then I ever remembered. On top of that aside from a slight decrease in sex drive (I could still get hard, just didn't have much of an urge) when I was on at 75 mg, I've never had a better pct.


WideGuy....why can't you take everything I say as fact?! It would be so much easier. :-) I'm kidding of course.

Well, I wouldn't speak of it restoring testicular size as such a matter of fact. I've had guys e-mail or tell me in person that they swear their testicles atrophied the day after they initiated a cycle with testosterone. Similarly I've had them tell me their testicles get larger during a cycle. As you know, the testicles aren't going to atrophy that quickly. I think the main part of confusion stems from guys evaluating the size of their scrotum, rather than actually palpating the testicles and getting a physical measurement. Just to give you an example of what I'm talking about, after 6 months of taking testosterone enanthate (normal men) at 300 mg/week, testicular size remained within 0.5 centimeters of pretreatment measurements. That is why I don't put much stock in to such reports as I've never met a guy who actually measured his testicles, nor was able to eye such small changes. Rather, they simply look down here and there.

I'm not sure what you mean about it not stopping gains. There's no data which supports the statement that any aromatase inhibitors decrease gains. I've heard of guys claiming that they use one drug over another because one doesn't affect IGF-1 levels, yet unbeknownst to them, there are just as many studies showing a decrease as there are showing no effect. Psychology plays a large role.

As for the effect upon testosterone levels. I don't doubt you there, but that's not what needs to be measured. Rather, LH needs to be measured. Depending upon which analytical method is used for testosterone, that steroid you're using or a metabolite thereof could be mistaken for testosterone. This is why it's so important to have LH assayed, yet, coincidentally or not, the highly publicized pilot studies for these steroidal aromatase inhibitor supplements lack an evaluation of LH. An evaluation of LH will truly allow one to know if "recovery" is taking place or if the steroid being administered is cross-reacting with the standard immunoglobulin. Bill Roberts has addressed this thoroughly.

Last, you said that these people were using other supplements when they had their blood drawn which really makes it difficult, if not impossible to differentiate which was responsible for what.

Keep in mind, I'm not saying you're imagining things or that you're wrong, I'm just pointing out why some people could be making such claims. In the end, if it worked for you, by all means, keep doing it.
 
Cy,

What is your opinion of ATD (1,4,6-androstatriene-3,17-dione)?

Is it safe? Effective?

Thanks for your help.


I don't know that I can answer either of those questions. I will say this however. Likely limited by first-pass metabolism, and again something which it seems these companies which keep coming out with these products are forgetting, is that these steroidal aromatase inhibitors have two major drawbacks which is why you saw the shift in the pharmaceutical industry towards non-steroidal aromatase inhibitors, and those drawbacks are related to both lack of selectivity and in the case of someone who is using it post cycle in the hopes for increased recovery, these steroids, this one in particular, are androgenic. You can look in to the literature and find relatively easily, studies regarding this. One concluded that it may be an androgen antagonist, another concluding a likely metabolite binds to the AR acting as an agonist. Obviously, neither of these are what you want. Also, if it works as well in humans as it did in animal models, you could also expect a decrease in HDL.

If you're going to use an aromatase inhibitor, you're much better off using anastrozole.

I was planning on running ATD on cycle and then switch up to 6-oxo or a clone for PCT. I guess that would still be basically the same issue since it's also steroidal,
 
6-oxo

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:

1) Expecting it to be an effective aromatase inhibitor in man when taken orally -- it isn't,

2) 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

3) 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.
 
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.
 
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.
 
right now I have 1 SNS superdrol, 2 revolt. So hmm yeah, maybe 3 bottles of an epi clone, 1 more superdrol, and hmm maybe 2 halodrol? I can always trade em off later :) how is the CEL halodrol clone?
 
I'm taking the ATD for the DHEA conversion. That's also interesting about the 4-AD not converting to Test...that's surprising compared to all I ever read on 4-AD.
 
Speaking of poopy, I am blowing hole like mad.

But yeah, poopy seemed like good peeps. I noticed SS hasn't been around much either. Maybe IBE is taking out their reps : O

Yeah, agreed on Poop. Maybe he's just overwhelmed w/ the family life right now.
 
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