Anyone Tried Superdrol Yet?

so general concensus PCT cycle is: Alpha Male/M, Red yeast rice with CoQ10 (or is there another similar thing that I can take rather then the rice?) and is that it? What about a something for the liver?

If this has already beem asked I apologize, but where can I pick this stuff up at? I’m very interested. Also, how would it compare to M1T? Thanks.

[quote]WhiteFlash wrote:
If this has already beem asked I apologize, but where can I pick this stuff up at? [/quote]

Google.

[quote]Gnostic wrote:
trailer36 wrote:
Gnostic,
be careful on this, Cy has said that these types of PCT supps do not work as they are touted to. if i was you i would add the ergomax and stick to the tried and true nolva/clomid for PCT.

Thx for the headsup, Trailer. It appears that Novedex XT has some descent supporting data behind it.

Poster 43
Ziegenfuss T.N., Mendel R.W., and Hofheins J.E. Safety and Efficacy of a Commercially-Available, Naturally-Occurring, Aromatase Inhibitor in Healthy Men. Ohio Research Group of
Exercise Science and Sports Nutrition. Wadsworth, Ohio 44281, USA.
tim@ohioresearchgroup.com
Rationale: In healthy eugonadal men, it is known that blocking estrogen formation stimulates the hypothalamic-pituitary-testicular (HPT) axis to increase in vivo androgen production. Recently, a new class of dietary supplements has appeared that claim to inhibit the aromatase enzyme (i.e.,
decrease the transformation of aromatizable androgen[androstenedione, DHEA, testosterone] into estrogens [estriol, estrone, estradiol]), leading to an increase in androgen and testosterone formation.

Purpose: As the first step in a series of experiments on a popular, over-the-counter aromatase inhibitor, the purpose of this pilot study was to examine the effects of Novedex XT?
(NOV-XT) administration on selected hormonal responses (total testosterone [TT], bioavailable testosterone [BT] and estradiol [E2]), as well as serum and plasma markers of renal, hepatic, and hematological function.

Methods: Using an open-label, proof-of-concept design, five eugonadal men (mean ? SD age, height, weight, body fat: 31.0 ? 5.3 yr, 177.0 ? 3.8 cm, 86.6 ? 8.7 kg, 15.2 ? 5.4 %) ingested 4 capsules of NOV-XT prior to bed for 28 consecutive days. According to the manufacturer, each capsule of NOV-XT contains 60 mg of a proprietary blend of three naturally occurring aromatase inhibitors: 6, 17-keto-etiocholene-3-ol tetrahydropyranol ether, 3, 17-ketoetiochol-triene, and 3?,5,7-trihydroxy-4?-methoxyflavone (supplements were provided by an FDA registered, pharmaceutically licensed manufacturer; confirmation by an external laboratory is pending). Blood samples obtained at baseline (prior to supplementation), and at weekly intervals the reafter for 28 days, were analyzed for TT, BT, and E2 by radioimmunometric and chemilluminetric assays.

Subjects were required to maintain their normal dietary and training patterns during the study. All blood samples were obtained at the same time of day (0700-0900) to
minimize diurnal variation. Hormone concentrations were statistically analyzed by ANOVA and Journal of the International Society of Sports Nutrition. 2 (1):1-30, 2005.

(www.sportsnutritionsociety.org)
29 Tukey?s HSD post-hoc test. Dependent t-tests were used to compare changes in blood chemistries.
Statistical significance was accepted at p<0.05. Results: Compared to baseline, NOV-XT administration rapidly and significantly increased TT and BT. Mean changes from baseline for TT(Figure 1) after one, two, three, and four weeks of NOV-XT administration were: +145%
(p<0.006), +183% (p<0.0005), +232% (p<0.0002), and +240% (p<0.0002), respectively. Mean changes from baseline for BT (Figure 2) after one, two, three, and four weeks of NOV-XT
administration were: +300% (p<0.01), +402% (p<0.0009), +511% (p<0.0002), and +528%(p<0.0002), respectively.

Despite these large increases in TT and BT, no significant aromatization
to estradiol was observed (i.e., E2 concentrations remained 3-6 pg/mL below baseline at all time
points). No statistically significant changes in clinical blood chemistries (fasting glucose, BUN,
creatinine, bilirubin, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase,
sodium, potassium, chloride, calcium, albumin, globulin, CO2, total protein, total cholesterol,
triglycerides, HDL-cholesterol, LDL-cholesterol, VLDL-cholesterol) or systemic hemodynamics
(heart rate, systolic blood pressure, diastolic blood pressure) were observed, nor were any adverse events reported in the study.

Conclusions: Within the framework of the current experimental design, these preliminary data indicate that four weeks of NOV-XT administration significantly elevates serum TT and BT, likely via the inhibition of estradiol formation and the shifting of the HPT axis towards androgen/testosterone production. In healthy, eugonadal men, supplementation with NOV-XT does
not appear to result in any deleterious effects on blood chemistry or systemic hemodynamics.
Ongoing research is being conducted to confirm and refine these results in a larger sample size, as well as examine the impact of NOV-XT on androgenic and estrogenic metabolites, body
composition, and muscular performance.

[/quote]

This data actually doesn’t make any sense. Just as with another similar study, the methods used for hormone quantitation aren’t sufficient. RIA is great if the compound you’re administering isn’t anything remotely similar to a targeted hormone which you’re trying to measure, but in cases where there is a significant similarity, there tends to be cross-reactivity. I think this study demonstrates this perfectly. If you look at it, there are reported increases in total endogenous testosterone levels, well beyond the physiological range. This just doesn’t happen. No aromatase inhibitor or estrogen antagonist allows one to have testosterone levels increased to where they are in the supraphysiological range, especially this far. Not even letrozole, which is arguably the most potent aromatase inhibitor available. When men were given large doses of letrozole (30 mg), an amount most would shudder thinking about, pushing estradiol to around 1-3 pg/ml, there is still no such increase in endogenous testosterone levels, as seen in these studies.

So, essentially what this data is suggesting is that a minute decrease in serum estradiol of 3-6 pg/ml from baseline (if significant) resulted in an increase in testosterone beyond that seen even with those aromatase inhibitors that decrease estradiol below physiologic levels. Again, that doesn’t make any sense. The only thing that does make sense, is that both some of the steroids administered and endogenous testosterone were assayed, which would explain these enormous figures, despite little to no decrease in estradiol. To answer the real questions that need to be addressed, one needs to measure LH and when assaying testosterone, should use GC/MS, in order to ascertain exactly what is happening to endogenous testosterone levels. Unfortunately, in every one of these small pilot studies, neither is done.

On another note, one other point that everyone seems to miss, is that in nearly every one of these cases, these steroids that these companies are using as aromatase inhibitors, interact significantly with the AR. In short, you don’t want to be taking an androgen when the goal is to “recover” endogenous testosterone production. But in just about every one of these cases, that’s exactly what these steroids are.

If people are looking for an effective and safe aromatase inhibitor, anastrozole is your best bet. You’re not suppressing estradiol below the level of detection, which can have adverse effects upon cardiovascular function, muscle, adipose, etc., unlike letrozole. You’re still experiencing a moderate and confirmed increase in endogenous testosterone production. Last but not least, you’re not talking about a steroidal compound which interacts with the AR. There are really only a few exceptions.

Alternatively, one could use estrogen antagonists like tamoxifen or clomiphene as well.

Great insight, Cy. I’m FAR from a pharmacology expert, so it’s great to get an objective perspective from a credible source like yourself.

Unfortunately, for the common user, that doesn’t have expertise in this area, the conflicting views really make things ambiguous. That’s not necessarily a bad thing because it helps people make informed decisions.

I do know a few users that have had pre and post use blood-work done after using a few of these products, and the results were supportive of the claims. My biggest concern would be, as you mentioned, an acute drop in estrodiol, which might cause adverse effects. I guess the key would be short term usage (2-4weeks)between cycles only.

[quote]Gnostic wrote:
Great insight, Cy. I’m FAR from a pharmacology expert, so it’s great to get an objective perspective from a credible source like yourself.

Unfortunately, for the common user, that doesn’t have expertise in this area, the conflicting views really make things ambiguous. That’s not necessarily a bad thing because it helps people make informed decisions.

I do know a few users that have had pre and post use blood-work done after using a few of these products, and the results were supportive of the claims. My biggest concern would be, as you mentioned, an acute drop in estrodiol, which might cause adverse effects. I guess the key would be short term usage (2-4weeks)between cycles only. [/quote]

Hi Gnostic,

Well, again, even in the cases of your friends’ case reports, in respect to testosterone levels, it’s extremely important to differentiate between methods like LC/MS or GC/MS versus immunoassay as again, IA in these particular cases are going to give skewed figures. These figures of 1,500 and 2,000 ng/dl and greater just aren’t seen. These are the same figures one gets when using 300-600 mg/week of testosterone enanthate. These are not figures you get using aromatase inhibitors, even with letrozole.

Now, when you have a small pilot study demonstrating a significant decrease in estradiol, that is reflective of an effective aromatase inhibitors, but again, the figures given for testosterone levels are skewed, again, giving the false indication that the steroidal AI is allowing for increased endogenous testosterone production. Well, these compounds interact with the AR and that in and of itself is suppressive. That is again why LH needs to be measured and testosterone needs to be measured via more accurate methods.

So, for example, let’s take one of these which actually does decrease estradiol to a significant degree. We would expect it to increase endogenous testosterone production, via increased LH, right? However, if this steroid also acts as an AR agonist, which suppresses LH, you can get some suppression of testosterone production as well. Now, there’s no way to answer how effective the compound is unless you’re either measuring LH or assaying testosterone in a more accurate method. Hope that makes more sense. There’s generally a reason that pharmaceutical companies leave certain compounds alone, irrespective of whether it’s naturally occurring or not. In the case of an AI, you don’t want a compound which acts as an AR agonist or isn’t completely selective, as your target population is women, in which case the former isn’t desirable for women and the latter really isn’t desirable for any population.

It seems that no one here is concerned with detection times for dope test. Is there any way to determine it approximatly, looking at it’s peculiarities? Anyone had any experience with this stuff in conjunction with a doping test?

That’s a great breakdown, Cy. Much obliged. I do see your logic and it helped me glean some additional perspective on the science. Oh well, I think I will just stick with a lighter/shorter cycle for now, so PCT won’t be such an issue. At my age, I’m just too paranoid to get too agressive without feeling comfortable with PCT alternatives.

hey, i have stopped my Superdrol trial for a while, as i tore something (don’t know what yet-waiting on the MRI results) in my knee.

i did use Superdrol at 30mg/day in the Am for about 10 days and didn’t notice anything. as a whole, i generally don’t respond very well to prohormones, so take that for what it’s worth…

[quote]Gnostic wrote:
That’s a great breakdown, Cy. Much obliged. I do see your logic and it helped me glean some additional perspective on the science. Oh well, I think I will just stick with a lighter/shorter cycle for now, so PCT won’t be such an issue. At my age, I’m just too paranoid to get too agressive without feeling comfortable with PCT alternatives.[/quote]

Gnostic,

for what it is worth i am going to use superdrol at 10mg/day for the first two weeks and see how that goes. i will only up it to 20 if i feel no sides and am not making decent gains. i am 6’0" 185 with about 9% bf to give you an idea. i dont really see any reason to go above 20 mg as most users have had great gains at these levels (i’m sure you know that though from reading the logs). i might run an ergomax cycle first thought to see how that works.
i’ll make you a deal, you let me know how you do on your superdrol cycle and i will let you know about ergomax. when are you starting?

[quote]trailer36 wrote:
Gnostic wrote:
That’s a great breakdown, Cy. Much obliged. I do see your logic and it helped me glean some additional perspective on the science. Oh well, I think I will just stick with a lighter/shorter cycle for now, so PCT won’t be such an issue. At my age, I’m just too paranoid to get too agressive without feeling comfortable with PCT alternatives.

Gnostic,

for what it is worth i am going to use superdrol at 10mg/day for the first two weeks and see how that goes. i will only up it to 20 if i feel no sides and am not making decent gains. i am 6’0" 185 with about 9% bf to give you an idea. i dont really see any reason to go above 20 mg as most users have had great gains at these levels (i’m sure you know that though from reading the logs). i might run an ergomax cycle first thought to see how that works.
i’ll make you a deal, you let me know how you do on your superdrol cycle and i will let you know about ergomax. when are you starting?[/quote]

Hey Trailer,

Actually, I am going to test drive prostanozol (Starting Monday). I entertained the idea of coupling it with Ergomax, but after reading some of the side-effects other users have experienced, I opted against it. I ready that some guys experienced complete shutdown (testicular shrinkage) in as little as 3wks. Good luck with the SD cycle. I will report my P-zol results periodically over the next four weeks. Cheers!

[quote]Gnostic wrote:
That’s a great breakdown, Cy. Much obliged. I do see your logic and it helped me glean some additional perspective on the science. Oh well, I think I will just stick with a lighter/shorter cycle for now, so PCT won’t be such an issue. At my age, I’m just too paranoid to get too agressive without feeling comfortable with PCT alternatives.[/quote]

Any time, Gnostic. I agree. I think the shorter cycle and use of anastrozole or tamoxifen or clomiphene are the best bets.

Honestly, if the outlay of cash wasn’t so “wife rioting” extreme, my ideal cycle would be 12wks of double-dose Methoxy-7 concurrent with max dose Carbolin 19…That would probably rock!!

hey all,
what exactly is the deal with the lower back pain? christ, in a matter of two days, i went from feeling great to this nagging, dull throb in my lower left back. any ideas?

[quote]shady659 wrote:
hey all,
what exactly is the deal with the lower back pain? christ, in a matter of two days, i went from feeling great to this nagging, dull throb in my lower left back. any ideas?[/quote]

Try taurine at 2-3g per day. it should greatly reduce the pain.

TENPI i think the reason u did not gett an answer right away is 1.) the question you are asking is a little boring since the answer is so well known and easily answered yourself with a little reading 2.) the way you ar asking is alot like a 16 year old girl asking about piercing her ears rather than and 18 year old boy asking a question about bodybuilding and testosterone.

I mean if you know that suppressing T is a bad thing, and that at your age T is the main thing going on in your body- peak T years- then simple equation means that suppressing T at the most significant years of its production is pretty dumb right?? Your body now is adjusting and finding its correct T levels , so if you go and shut it down for six weeks, your body could very well say “ok, zero is a great level” becaus e there is all this exogenous stuff in your body doing what T does, so your body thinks it does not need nay more T…

Now you have reset your body to zero T production, then come off the cycle, and now your fucked- and for life!!! Hope you like ur new tits!!

Conversely, older guys with T levels already established by their bodies, can fiddle with things a bit more and not take such a risk resetting their T level so low, whereas you at your age can reset it pretty badly for the rest of your life. Older guys are past the key T years when t is dominant and establishig itself.

Sorry to have an attitude, but your initial “i know eveyrthing, and i am smarter than everyone sked so just answer my question” read more like “tell me what i want to hear”. just research and decide if you like your nuts- if you’re not that attached to them, them by all means use at your age, dry them up good, kill all your T production for life, and use one them as a hot new kind of key chain.
LOL

A while ago (a long while) when reading these boards about prohormones and side effects, I remember someone saying that hitting them short and hard would be the safest way to use them and help prevent/minimize any unwanted sides (testicular shutdown, drastically altered chol. levels, etc.).

So, since I will be going back to Korea this week and can’t take any 'scripts with me, I will not have any tax. or clo. to use with my superdrol. I will, however, have a bottle of M, 2 x Carbolin 19, and 2.5 x TRIBEX. Here are my two possible scenarios, please give me your 2 cents:

  1. Week 1 - 10mg SD/day with Milk Thistle, Red Yeast Rice, Fish Flax oils, Hawthorn Berry
    Week 2 & 3 - 20mg SD/day with same supp’s above
    Week 4 - 10 mg SD/day with same supp’s above
    Week 5 - 3 caps M ED, 4 caps TRIBEX twice/day, 1 cap Carbolin 19 twice/day, max. recommended dosage of Methoxy-7 ED (until I run out; 1 bottle left)
    Week 6 - same TRIBEX, same M, 2 caps Carbolin 19 twice/day
    Week 7-… use week 6 supps untill exhaustion

  2. Week 1 - 20 mg SD/day with other supps above
    Week 2 20 or 30 mg SD/day (depending on reaction to week 1) plus other supp’s above
    Week 3 - off, start PCT (shortened version)
    Alternate this scenario with 2 weeks on, four weeks off, until 3 cycles are completed

Any thoughts?