AAS Research Mega Thread (not pro hormones)

BeastFitness

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Similar or same study below (abstract?):

Trenbolone improves cardiometabolic risk factors and myocardial tolerance to ischemia-reperfusion in male rats with testosterone-deficient metabolic syndrome.
Donner DG1, Elliott GE1, Beck BR2, Bulmer AC1, Lam AK3, Headrick JP1, Du Toit EF1.
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Abstract
The increasing prevalence of obesity adds another dimension to the pathophysiology of testosterone deficiency (TD) and potentially impairs the therapeutic efficacy of classical testosterone replacement therapy (TRT). We investigated the therapeutic effects of selective androgen receptor modulation with trenbolone in a model of TD with the metabolic syndrome (MetS). Male Wistar rats (n=50) were fed either a control standard rat chow (CTRL) or a high-fat/high-sucrose diet (HF/HS). Following 8 weeks of feeding, rats underwent sham surgery or an orchiectomy (ORX). Alzet mini-osmotic pumps containing either vehicle, 2 mg/kg/day testosterone (TEST) or 2 mg/kg/day trenbolone (TREN) were implanted in HF/HS+ORX rats. Body composition, fat distribution, lipid profile and insulin sensitivity were assessed. Infarct size was quantified to assess myocardial damage following in vivo ischaemia-reperfusion, before cardiac and prostate histology was performed. The HF/HS+ORX animals had increased subcutaneous and visceral adiposity; circulating triglycerides, cholesterol and insulin; and myocardial damage, with low circulating testosterone compared to CTRLs. Both TEST and TREN protected HF/HS+ORX animals against subcutaneous fat accumulation, hypercholesterolaemia and myocardial damage. However, only TREN protected against visceral fat accumulation, hypertriglyceridaemia and hyperinsulinaemia; and reduced myocardial damage relative to CTRLs. TEST caused widespread cardiac fibrosis and prostate hyperplasia, which were less pronounced with TREN. We propose that TRT may have contraindications for males with TD and obesity-related MetS. TREN treatment may be more effective in restoring androgen status and reducing cardiovascular risk in males with TD and MetS.
 
BeastFitness

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^^^thanks for posting the abstract David!
 
yates84

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Good info. Subbed
 
BeastFitness

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I edited my post to reflect said. Very promising.
Very!

Good info. Subbed
Thanks! I plan on posting more of the research that I typically use as references or read in regards to AAS. I've been getting WAAY too many newbies coming into the gym and asking me about specific compounds with no regards to anecdotal or research based evidence about the compounds their using…hopefully this will help people!
 
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i saw an abstract posted elsewhere and assumed yours was another study and it looks like it's the same. It debunks the myths about Tren being so atrocious. The key is moderation. Excesses of even testosterone are unhealthy.
 
BeastFitness

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i saw an abstract posted elsewhere and assumed yours was another study and it looks like it's the same. It debunks the myths about Tren being so atrocious. The key is moderation. Excesses of even testosterone are unhealthy.
Completely agreed. Moderate dosages is key…something many seem to forget
 
BamBam0319

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Definitely subbed
 
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Cmon man when I came off I was a wreck and dick was broke maybe I didn't have enough exp at that time and didn't know wtf prolactin was however I love the way it makes me feel and think it's amazing stacked with test It's been awhile now can anyone remind me what libido and sex was like while on??
 
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There's a host of trouble that testosterone causes. Many find TRT and physiological ranges of test sufficient when running Tren. Let the Tren do its magic :D
 
datsthat

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Very!



Thanks! I plan on posting more of the research that I typically use as references or read in regards to AAS. I've been getting WAAY too many newbies coming into the gym and asking me about specific compounds with no regards to anecdotal or research based evidence about the compounds their using…hopefully this will help people!
Nice. I'd follow and I am sure MANY others will. When will you start?


Whats your thought on using beta blockers to combat sides from tren? I am only asking for education. I do not believe in adding another substance to combat a substance/compound. I believe in lower or stopping use (taper if needed).

I've heard that provirion complements tren....whats your thoughts?


osmotic infusion pumps...I want one
 
BeastFitness

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Definitely subbed
Right on!

Cmon man when I came off I was a wreck and dick was broke maybe I didn't have enough exp at that time and didn't know wtf prolactin was however I love the way it makes me feel and think it's amazing stacked with test It's been awhile now can anyone remind me what libido and sex was like while on??
If you don't know what your doing ANY compound will cause issues long term.

Typically tren is going to make libido sky rocket but I have had clients that it shut down their libido extremely rapidly…again, no 2 people are the same but I'd say 90% of people using tren, libido will explode

There's a host of trouble that testosterone causes. Many find TRT and physiological ranges of test sufficient when running Tren. Let the Tren do its magic :D
EXACTLY! Keep the whole protocol in mind and remember theres an upper limit to many compounds. Why only take 1 gram of test when there are synergies that exist amongst ALL these drugs.

Nice. I'd follow and I am sure MANY others will. When will you start?


Whats your thought on using beta blockers to combat sides from tren? I am only asking for education. I do not believe in adding another substance to combat a substance/compound. I believe in lower or stopping use (taper if needed).

I've heard that provirion complements tren....whats your thoughts?


osmotic infusion pumps...I want one
I'm not starting tren, simply trying to bring research to light to help keep people informed as half of my clients are enhanced athletes.

Honestly from a purely educational side of things, you would need to take into account all of the positive and negative side effects your experiencing while on tren and possibly change the dosage. I would rather have someone lower they dosage to manage the sides VS adding another drug on top of it to try and combat that drugs side effects as its not as simple as using X to cure Y…if that makes sense


In terms of tren and proviron, it will exert inhibitory actions on neurotransmission (pretty much acting as a potent positive allosteric modulator of the GABA receptor) AKA its going to produce better sleep to combat the tren-insomnia, reduce stress, and aid in an overall sense of well being…but again, depends on the person, their dosage, and the severity of their sides.







Quick question for everyone!

DOES EVERYONE WANT ME TO JUST KEEP POSTING MY AAS BASED RESEARCH IN THIS THREAD INSTEAD OF STARTING NEW ONES???
 
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Quick question for everyone!

DOES EVERYONE WANT ME TO JUST KEEP POSTING MY AAS BASED RESEARCH IN THIS THREAD INSTEAD OF STARTING NEW ONES???
Keep it here please. I can change the thread title afterwards to something appropriate if you like.

Tell me what you can about NPP please.
 
Gutterpump

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Mast perfectly complements tren. I'm planning on running that combo this spring, along with some trest. All in moderate doses, but with a very very low dose of test.
 
BamBam0319

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I really want to try tren/mast, but I'm going to try tren by itself first.
...in about 2 weeks ;)
 
BeastFitness

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Keep it here please. I can change the thread title afterwards to something appropriate if you like.

Tell me what you can about NPP please.
AWESOME! Lets change it to "AAS Research Megathread" or something catchy haha ;)


So NPP, tremendous in either cutting or bulking as its going to help you keep your muscles thick/full during a deficit and your going to grow mass and add strength like crazy during the offseason. OBviously its going to depend on the synergy of your other compounds but its a pretty "high result low side effect" drug. I've had people dieting for shows that reported their cloths fitting tighter as they got significantly leaner.

Overall, I'm a fan! I should note as well, I've seen many people respond well to either NPP or DECA…for whatever reason the majority seem to respond well to one and bad to another but this is all anecdotal

I really want to try tren/mast, but I'm going to try tren by itself first.
...in about 2 weeks ;)
Tren+Mast is going to give you a harder look than almost anything! If your diet and training is on point your going to look sick!

Mast perfectly complements tren. I'm planning on running that combo this spring, along with some trest. All in moderate doses, but with a very very low dose of test.
Agreed! Typically when using 2+ compounds, test should be kept low anyway…no need.

What kind of dosages do you plan on running?
 
datsthat

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Whats your thoughts on deca dick?....what causes it and how to prevent/avoid it?

Is it true that dopamine agonist shouldn't be needed as long as you can keep your e2 within desired range? Thanks
 
BeastFitness

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Whats your thoughts on deca dick?....what causes it and how to prevent/avoid it?

Is it true that dopamine agonist shouldn't be needed as long as you can keep your e2 within desired range? Thanks
SO I haven't seen ANY research to prove the exact cause of deca dick (someone please correct me if I'm wrong) but many believe its due to elevated prolactin levels (it could be that is has a neurosteroid-like activity, antagonist activity, etc.)

In terms of avoiding it your obviously going to want to look at your entire cycle which should include test (largely controls erectile function and libido) as 100mg of Deca is enough to completely suppress all testosterone production. I believe the recommended ratio was 150mgs of test for every 100mgs of deca


The increased Dopa output is auto-corrected by receptors desensitizing, essentially, its not permanent. BUT obviously your dosage, length, and genetics are going to play a huge role here. Typically as long as ranges are kept within their desired levels, there shouldn't be an issue. In general, I'm a big proponent of people utilizing the least amount of ancillaries needed at any time.
 
datsthat

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How does it take for NPP and Deca to "kick in"? And suggested cycle length for each? Do you know how nandrolone effect blood work...Which blood markers does it effect? Does it raises your TT?

Thank you

(I'll sit on my hands so I don't ask more questions...for now. I forget that this isn't about ME lol.)
 
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I really want to try tren/mast, but I'm going to try tren by itself first.
...in about 2 weeks ;)
I've never run tren before myself, but I did run dienolone ace at 100mg/day and f^&king loved it so much. Deca, not so much, but dien is more like tren, so I expect good things. The combo of tren/trest is going to require some serious ancillary business though. It's a good thing my body doesn't mind prami whatsoever.
 
BeastFitness

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How does it take for NPP and Deca to "kick in"? And suggested cycle length for each? Do you know how nandrolone effect blood work...Which blood markers does it effect? Does it raises your TT?

Thank you

(I'll sit on my hands so I don't ask more questions...for now. I forget that this isn't about ME lol.)
How does it take for NPP and Deca to "kick in"? And suggested cycle length for each? Do you know how nandrolone effect blood work...Which blood markers does it effect? Does it raises your TT?

Thank you

(I'll sit on my hands so I don't ask more questions...for now. I forget that this isn't about ME lol.)

DUDE! No keep asking questions I love it! Actually I like how this thread is turning into a Q&A type thing haha

In terms of NPP or Deca actually kicking in, no matter what anyone says, once you inject a compound, its going to peak in your blood levels within a few hours BUT in terms of that compound building up to the max level, its going to depend on how the person's genetics handle that compound.

Before I break down the length, remember this about Deca:

-Since it does a tremendous job at aiding the joints, immune function, and aids in collagen synthesis and bone density, its typically nice to use in a longer cycle when your body is under prolonged stress
-Remember, deca adds mass and strength without the androgenic/estrogenic sides

Typically both can be run longer within the 10-14 week range but will depend on the rest of your additions.


Nandrolone is going to raise TT and you'll wait to keep an eye out as it may decrease thyroxine-binding globulin (which results in decreased total T4 serum levels and increased resin uptake of T3 and T4.) Keep an eye on those blood sugar levels if you have a family history of diabetes.

I plan to run tren ace / trest ace / mast ace at around 50/50/50mg per day, but not sure if I should run the mast a bit higher, maybe 75mg/day.
Made a thread for it here but got no feedback in it really.

http://anabolicminds.com/forum/old-school-hormone/277534-tren-ace-trest.html
I've never run tren before myself, but I did run dienolone ace at 100mg/day and f^&king loved it so much. Deca, not so much, but dien is more like tren, so I expect good things. The combo of tren/trest is going to require some serious ancillary business though. It's a good thing my body doesn't mind prami whatsoever.
Honestly, I'm a fan of promoting using the lowest dosage possible to yield the greatest results as it typically will give you better long term progress + less sides. You can always increase.

HAHA! That is definitely going to be an interesting combo! Keep me updated man!
 
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SO I haven't seen ANY research to prove the exact cause of deca dick (someone please correct me if I'm wrong) but many believe its due to elevated prolactin levels (it could be that is has a neurosteroid-like activity, antagonist activity, etc.)

In terms of avoiding it your obviously going to want to look at your entire cycle which should include test (largely controls erectile function and libido) as 100mg of Deca is enough to completely suppress all testosterone production. I believe the recommended ratio was 150mgs of test for every 100mgs of deca


The increased Dopa output is auto-corrected by receptors desensitizing, essentially, its not permanent. BUT obviously your dosage, length, and genetics are going to play a huge role here. Typically as long as ranges are kept within their desired levels, there shouldn't be an issue. In general, I'm a big proponent of people utilizing the least amount of ancillaries needed at any time.
From what I heard/read somewhere recently, it's a myth perpetuated by people that thought to base their cycle off of either deca or test due to financial or knowledge limitations, not realizing they needed at least some test with the deca. So they crash hormones with no test base. Again, hearsay and I have no experience with the compound.
 
BamBam0319

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I ran 500 deca and 600 test per week for 15 weeks with a libido INCREASE.
 
datsthat

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I ran 500 deca and 600 test per week for 15 weeks with a libido INCREASE.
Nice. 2:1 or 1.5:1 test to deca ratio seems to be what most are running. How were your results? Did it meet/exceed your expectations? What did you use for AI and dose? thanks

EDIT: How was PCT? Did you recover? I've heard that Deca marinates for a very long time due to long ester 1/2 lift.
 
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BeastFitness in line with the opening post please provide reference literature to substantiate whenever possible. Although I'm not nor are others disputing anything being shared it is really cool and more importantly credible when there's data to support anecdotal findings.
 
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I find this article to be my most favorite in regards to cycles and most specifically androgenic compounds aka:trenbolone.

Some more thoughts on the topic. The info on esters is a little out of date since this is from 2002 and there are much more available today. Again, these are opinions and thoughts on the topic. This is long and I have cut some out from the original.


by MuscleTrainee
Background:
I began BBing with a trainer from Germany. In educating me, he related to me that, in his time BBing there, European BBers were relatively without American influence. Common practice called for the use of short halflife ester injectables, the variety of which was very much greater than exists today, combined with mild orals like Anavar and Winstrol and, sometimes, Dbol. Short cycles(2-4 weeks) were also the norm. Most interesting, use of test was very uncommon, and considered a horror. What was commonly used was Parabolan, what we, today, call Trenbolone. Eight week cycles were virtually unheard of, and the desire to pack on 20-40 pounds in such a short time was unthinkable. European BBers took a much more unhurried pace of growth. Young, competitive BBers were very much smaller than those found in the US, today, due to this orderly pace of growth. It was only the very rare, genetically unusual BBer who was big at a young age. Europeans simply had a different outlook and different standards.

Early on, my trainer lamented the situation he found in the US: heavy dependance upon test, long halflife esters used in long cycles, gross overeating, poor estrogen suppression, acceptance of high bodyfat percentages, and excessive lbm development in short timespans. He was horrified at what he envisioned would be the longterm consequences of widespread use of these practices. He was associated with IFBB pros, like Zhur, el Sonbaty, Schlierkamp, and Ruhl, while in Europe. He was well aware of the health complications associated with extreme muscularity. He kept reiterating "BBing is a sport for life".

While still a natural, I began to examine how an entire philosphy of AAS use might be developed, based upon the European experience. By the time it was appropriate for me to begin AAS, years later, I already had a plan. Initially, I quietly used myself as a lab rat. The results became quite visible, and, before too long, questions followed. My trainer asked that we work together, to develop a new way for his athletes to grow. And here we are.....

Characteristics of AAS:
There are two clearly discernable characteristics of interest to BBers. Anabolic: muscle growth/hypertrophy. and Androgenic: strength, aggression, fat burning. Most AAS possess these two characteristics in varying ratios, and in various strengths. For example, Halotestin may be seen to produce a pure androgenic response, but no anabolic response. Deca, on the other hand, will produce anabolism with no significant androgenic response. Test produces roughly a 50 percent anabolic response, and 50 percent androgenic response. Then there is strength of response. Winstrol is a moderate, pure anabolic. Anavar is a moderate, pure androgen. Trenbolone is a very powerful androgen(80 percent of total response), much more powerful than the androgenic characteristics of test. Tren's anabolic characteristic(20 percent of total response), is weaker than that of test. And so on. I have built a complete table of response characteristics of all the AAS components we use.

Site injection and localized growth:
Time and time again, we have seen localized growth response to site injected, esterless and short halflife AAS. I no longer accept that a positive response is anecdotal. It's just too commonplace, in my own work. Consequently, we no longer waste gear in glutes and quads. We identify and then site inject any and all lagging bodyparts, in a rotating injection program. And we have seen some startling responses. In nearly every case, we prefer tren and an esterless AAS, for the most powerful response. There must be weak-, or non-responders, but I have yet to find any. I owe much, in this particular area, to the work of Paul Borreson.

Cycle design:
Cycles are assembled by, first, determining the end response characteristics desired, and assembling components whose AAS characteristics interlock together to produce that end response with a minimum of overlap, over the cycle timespan desired. Consider this cycle: Nandrolone phenylpropionate(EOD), tren(EOD), Winstrol depot((ED), optional Anavar(ED). I've remarked, elsewhere, on the desireability of pairing tren with Winstrol. We require the use of a pure androgen for EVERY cycle, to insure strength, onging muscle definition, density, and post cycle androgenicity, so Anavar is our choice for this cycle. Here, Tren is our primary androgen, and nandrolone our primary anabolic. All of these agents are selected for their lack of water retention. All are either short acting or esterless, so that meets our requirements for site injection. And, yes, we do site inject it all. We begin by frontloading the estered injectables, up to three days before cycle day zero, and add the orals and esterless injectables at cycle day minus one. On cycle day zero, the AAS is already active, with blood levels increasing. We end the injectables and orals, suitably in advance of the end of the cycle, so that, on cycle day 15, the AAS is non-inhibitory, and HTPA recovery begins immediately. Add on 14 days further system recovery, and then a cycle can begin anew. Seven weeks, total. Over a year, this might be acccomplished seven times. When HCG, and an anti-e at suitable dosage, are added to the Clomid, the HTPA may be recovered in only 2 weeks. This shortens the next cycle availability point by one week.

Yes, it's a lot of injections. And the Winstrol hurts.

What might be expected, in the way of results? Bulking, we have seen as much as 10 pounds lbm. Average is five pounds. Over a year, that's 35 pounds. You say, "Hell, I can grow that much in 8 weeks". I say, let's see how many times a year you can accomplish that, and over how many years do you think you will continue to accomplish that? We have this steady, measured growing, going on and on. My guess is that this approach, using only a modest bulking diet, rather than the typical American pig-out bulking diet, can be accomplished for years and years. Due to short cycle length and rational diet design, there is very little fat gain. No pressing need to cut. No need to look like the typical big, smooth BBer, who only looks cut once a year. Our people are lean, defined, and feel healthy, all the time. They only spend two weeks out of seven(or six), cycling. And, since they get normalized quickly, they can train and grow natural, more quickly, because there is none of the weeks and weeks of getting that slow AAS out of their systems. The BBer doing the typical 8 week long acting ester cycle, exists for weeks in a kind of limbo, where the blood levels are not high enough for anabolism, but are still inhibitory, and he must wait all that extra time. My people are off, longer than they are on. Their bodies, free of drugs.

We tend to avoid test. Not completely; just most of the time. What we found is that, anytime you use test, it magnifies the sides of whatever you use with it. Tren, used in rational dosages, is relatively free of sides, and causes fewer overall sides during cycles. We use tren, like the typical BBer uses test. With tren, you get much more response, with much lower dosages, with greater androgenic intensity. Someone once wrote that tren was "the gear of the gods". Indeed, the Europeans brought to BBing AAS, a very great gift. We do use test, but only for very specialized purposes.

We only use one type of eight week bulk cycle. That for Boldenone, which now can only be obtained in a very long halflife ester. We are working with a supplier, and are patiently awaiting him to provide us with our first esterless Boldenone. Testing will begin immediately afterwords, to develop new dosage and protocols, following which, we expect to end our use of nandrolone phenylpropionate. Too many of our clients exhibit some degree of bloat from progesterone aromatization, emerging from the nandrolone. We consider any bloat, from any origin, entirely unacceptable, on health and esthetic grounds.

Bodyfat gain on cycles:
Ever notice how productive of muscle, a cycle usually is, during the first four weeks, and how it slows down and bodyfat accumulates, during the second four weeks? You end up eating more, in the attempt to return things to the former rate. More bodyfat. Finally, the whole process slows down for good. What's going on? The common explanation is that you are getting bigger, so that requires more nutrition. We say no. We say the body realizes what is going on, it exhausts and compensates, and body metabolism and developmental processes simply will no longer support this process. But you continue to eat. And that food has got no place else to go, but be turned into fat, with unproductive lbm production.

Our short cycle designs, whether for 2, 3, or 4 weeks features tren, as a foundation, which is a potent fat burner, due to powerful androgenicity, and will not aromatize to estrogen. And a diet, which is clean, and appropriately sized for rational lbm gain, while minimizing conversion to fat. Later, the body is clean of AAS, and primed for most sensitive and effective response, before the cycle begins. The conversion from nutrition to muscle takes place under optimum conditions, at low bodyfat levels. The AAS ramp-up is swift and full, and the cycle ends before the system can de-sensitize and cause spillover of nutrition to bodyfat.

Estrogen pileup is another cause of bodyfat accumulation, during the typical 8 week, long halflife ester cycle. I suggest that readers visit the AE zine Issue 46, and download the blood concentration calculator from the excellent article on blood concentration of various halflife esters of AAS. Then, plug in your long halflife ester cycle components, and witness the startling blood level concentrations of what you are injecting, late in the cycle. Using the typical paltry anti-e dosages of the typical BBer, is it any wonder that, late in the cycle, estrogen levels build up out of control, and bodyfat follows?

Estrogen and anti-e:
It is an obsolete belief that estrogen is necessary in any cycle. Indeed, ANY amount of estrogen is BAD in any cycle! There is not one study which supports the notion. But the idea lived on in yet another obsolete notion; that water weight is good weight, in a cycle. That, water introduced into the muscle, causes increased lifts, and by lifting heavier, greater growth is obtained. The experts would purposely advise minimal amounts of anti-estrogen drugs, only to minimize the chance of gyno, but to insure lots of this, supposedly, desireable water weight. On the AE boards, I have witnessed these experts advising NO anti-e's, but only to have some Nolvadex at hand, to deal with gyno, should it appear. Not only do you end up with fake strength and fake muscle size, but, at the same time, the estrogen buildup causes high blood pressure, electrolyte imbalance, and a host of health issues. There is water buildup in the lower back to the extent that posts frequently document BBers in pain, cramps, and difficulty, attempting deads. The champions of this approach say "Oh just take some ibuprofen, and you will be just fine". Try asking your liver what it thinks about that approach. Following the cycle, the water disappears, along with the strength and size it fooled the user into believing was real muscle. This often causes depression, and chases the user into a course of Creatine, to re-introduce that fake size and strength. The muscle character appears smooth, and the density is poor. When the BBer diets down, all this is lost, and the truth is seen. It's no wonder that certain other experts advise that BBers never come off AAS, so this scenario may never be exposed for what it is: a rollercoaster of reality versus water weight. I agree with them. It is not healthy to run back and forth between lost size and fullness caused by water weight. But it also is not a good thing to stay on AAS, all the time, either. This is a totally brain dead approach to AAS use. And the BBer who engages in it never attains the quality, defined physique he deserves. It's just alot of smooth water weight and high bodyfat.

And bodyfat. Everyone should know that the presence of excess estrogen causes fat deposition. The greater and the longer the exposure to elevated levels of estrogen, the greater the bodyfat accumulation. Endos, listen up; stay away from any situation which creates elevated estrogen levels. Everyone, listen up; it is OBSOLETE cycle technology to enable anything but minimal levels of estrogen, at any time. Estrogen is evil, and it is NOT your friend. Using anti-e's cannot reduce estrogen to levels below which the male body cannot function properly. It requires very little estrogen to function, and no anti-e removes it all.

What to do? Begin, with an entirely different approach. Say that ANY water weight is BAD weight. That estrogen must be banished, to the fullest rational extent. And that the muscle you grow and see is, in fact, muscle, and not water. That the muscle produced will be dense and well defined. A quality physique. How, then does one obtain that increased strength, which the water provided, to enhance growth during the cycle? As stated, we first kill off the estrogen and bloat. Second, we emphasize the introduction of powerful androgens into the cycle structure. I am speaking, once again, of tren and anavar. Together, these components make you VERY strong. And with NO bloat or estrogen required. The concentrated androgenicity encourages intense, aggressive workouts, while also encouraging fat burning. It is very commonplace to observe body recompositions during such cycles. In other words, you get big and lose bodyfat, simultaneously. The androgenicity also produces significantly increased muscle density and definition. At cycle end, what you end up with, is the real deal. Solid muscle, growth, and increased definition. No need to rush to the nearest container of creatine to stem your losses. And that strength is yours, to keep. And no test.....

Now, go back to that blood concentration calculator, and compare the blood concentrations of the typical 75 mg EOD of tren, to what you were subjecting yourself to, with that long halflife ester cycle. No stress caused by estrogen pileup, either. Now, you tell me which alternative is better.

What do we use to suppress Estrogen? Well, we formerly used grams of Arimidex per day. Arimidex is now an antique for us. We use Femara. We prefer one 2.5 mg tab ED. Our clients are kept dry as a bone. We will begin to study Aromasin, in mid-September. Aromasin utilizes a different approach to Estrogen control, which promises to be even more powerful than Femara. But research indicates that IGF-1 production is not suppressed by Femara, but may, in fact, be enhanced by it. We do not see that with Aromasin. Time and experimentation will tell.

Most importantly, we keep our people on anti-e, post cycle, during the HTPA recovery process, and later. This both speeds recovery of the HTPA, as well as minimizing fat buildup, while hormone levels fluctuate wildly.

Androgenicity and quality:
BBers commonly justify their long cycles by saying that they need the long cycle to enable "consolidation". They observe that this effect only occurs late in the cycle. Why is this? It's because the androgen level of the Sustanon test, typically used, takes that long to pile up and affect the muscularity of the BBer. But what about Trenbolone? Almost without fail, users commonly report density and hardening to appear within a few weeks. Why is this? Because the androgenic response of tren is so much more powerful than that of test. You can get this response to produce quality muscle at dosages of only 75 mg EOD, in less than a month. In a Sustanon test, it takes many weeks to accumulate an immense blood concentration, to achieve the same result. It is commonplace to observe tren users burning fat, while they cycle. Sust users never report this effect. Why? Once again, the androgenic response of tren is so much greater than that of test. Intense androgenicity induces fat burning. If Anavar is added, the androgenicity effect is intensified, still further.

Ever hear of the term "muscle maturity"? It describes muscle which is dense and defined. The commonly accepted belief is that it takes years and years to acquire this muscle characteristic. But why? Because, using test, the exposure to the muscle hardening androgenicity only occurs for about two weeks in the typical long cycle. And that cycle can only be repeated a few times a year. In the tren/anavar-based short cycle, the exposure to muscle hardening androgenicity occurs for longer periods, and the cycle can be repeated many times a year. "Muscle maturity", and quality, appears with rapidity, and not with years and years. I see muscle quality in only one year of regular short cycling, which I never see in the typical long cycle BBer, unless it occurs for years. Which would you prefer?

The issue of health:
There are those who say the typical American method of cycling, using long acting ester cycles, for 8 weeks or more, and eating 7-10,000 calories per day, for all that time, is no danger to health. To that, I say this: in the millions of years of human evolution, at no time, ever, has the male of our species been exposed to the barrage of hormonal, metabolic, and developmental pressure and manipulation, as occurs during the long acting ester eight week cycle. Do you really believe our bodies were engineered and evolved to deal with this attack, as well as the stress of being forced to add 20-40 pounds of lbm and bodyfat in this same timespan, over and over, again? Don't be a fool. If you believe so, then you are whistling past the cemetery. And there are additional fools, who would have you believe that staying on this course, continuously, can do you no harm. This is, currently, an unprecedented, uncontrolled lab experiment, taking place all over the world, with thousands of men as lab rats. The long term outcome cannot be predicted by anyone, today. True, every single one of us will die, someday. My people and I have no intention of hastening the arrival of that inevitable day, just to look big in a coffin, as we are laid to our eternal rest. What the hell is YOUR hurry? And, what if you don't die? What if you are forced to leave your beloved sport, and spend the rest of your days, living with hypertension and heart damage due to tachycardia. And kidney damage caused by the hypertension. And still other health issue possibilities. Is this any way to live? It's a personal value judgement and risk assessment process. Step back for a moment, and re-evaluate your position and priorities..............

Summary:
I have presented, above, only the most basic introduction to my philosophy and approach to short cycling, and offered only a simple example out of a program which I spent years developing. I have devised an entire series of special-purpose cycles, each of which embody most, if not all of the above principles.

The purpose of the short cycle is to employ moderate dosages of short halflife ester and esterless injectable and oral AAS, combined with moderate and healthy diet, to promote moderate stress anabolic growth, over time. This same process results in very high quality muscle production, which only increases with each cycle, and minimal health impact. It assumes a long term outlook. It is intended for the mature and rational BBer, who expects to remain in the sport for the rest of his life. If you truly love BBing, you never want to leave, and you want to keep your interest and grow, then consider how the short cycle might be what you need for your future in our beloved sport.
 
Gutterpump

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I ran 500 deca and 600 test per week for 15 weeks with a libido INCREASE.
I ran similar, 500 deca / 800 test, was feeling GREAT till the deca kicked in, then it's like I got depressed all of a sudden. Real strange. Not a fan. NPP doesn't have this effect though.
 
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Subbed for knowledge. I like this thread already.
 
BamBam0319

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Very good read David Dunn. I find the logic behind omitting test from cycles very interesting. I wonder in what situations they would actually include test?
I'd be interested in trying out a more brief, short ester only AAS cycle just to see the results for myself. Maybe even without test
 
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Nice. 2:1 or 1.5:1 test to deca ratio seems to be what most are running. How were your results? Did it meet/exceed your expectations? What did you use for AI and dose? thanks

EDIT: How was PCT? Did you recover? I've heard that Deca marinates for a very long time due to long ester 1/2 lift.
Results were good, I kept 15 pounds and at my heaviest, I was 25 pounds up from my start weight. A lot of water retention from the dbol kicker I used.
I would say it met my expectations, but it was hard to control estrogen. I think my aromasin was subpar quality. I was running up to 25mg ED, took a break to run 4 weeks of letro @ 2.5mg ED after I got off the dbol. I went to 12.5mg aromasin ED after I finished the letro.
PCT was alright. Strength went down considerably, but stayed above where I started out at. Libido was down for a while too but was returning by the time PCT finished. Also by the time PCT ended, my strength was starting to go back up and I was staying pretty lean.
Next time (if there is a next time I use deca), I will use HCG. However I'd rather try out other compounds first.
 

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That WAS an interesting read. Currently (as of the 31st) running a tren ph. So that is a startig point for me. Have always been interested in tren though.
 
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Anyone running a "tren ph" is likely running dienolone btw. Good stuff, but not tren. Never knew why that stuff was ever branded as a tren ph / trenavar etc.. Strange how marketing works
 
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Anyone running a "tren ph" is likely running dienolone btw. Good stuff, but not tren. Never knew why that stuff was ever branded as a tren ph / trenavar etc.. Strange how marketing works
Isn't trenavar the one that actually converts to trenbolone? I know trenazone, etc. convert to dienolone
 

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Youre right. It isnt. I assumed it was. So OL tr3n is in fact dienolone?
 
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From what I heard/read somewhere recently, it's a myth perpetuated by people that thought to base their cycle off of either deca or test due to financial or knowledge limitations, not realizing they needed at least some test with the deca. So they crash hormones with no test base. Again, hearsay and I have no experience with the compound.
Definitely agree. Pretty much hearsay but since we're discussing the two theres a pretty good study that I'll link below, pretty much shows that at the lower dosages, deca has fewer negative effects on the testes. There is less volume decrease and sperm cell production (stays nearer to the normal level.) You can pretty much see the non-homeopathic dosages you can expect more effect from testosterone than deca. If your mega dosing which I do not promote, test seems to be on the safer side than deca…THIS is why dosages need to be considered

Comparison of the effects of high dose testosterone and 19-nortestosterone to a replacement dose of testosterone on strength and body composition in normal men.

We examined the extent to which supraphysiological doses of androgen can modify body composition and strength in normally virilized men. In doubly blind tests, 30 healthy young men received testosterone enanthate (TE) or 19-nortestosterone decanoate (ND), at 100 mg/wk or 300 mg/wk for 6 weeks. The TE-100 mg/wk group served as replacement dose comparison, maintaining pretreatment serum testosterone levels, while keeping all subjects blinded to treatment, particularly through reduction in testicular volumes. Isokinetic strength measurements were made for the biceps brachii and quadriceps femoris muscle groups before treatment and 2-3 days after the 6th injection. Small improvements were noted in all groups but the changes were highly variable; a trend to greater and more consistent strength gain occurred in the TE-300 mg/wk group. There was no change in weight for TE-100 mg/wk but an average gain of 3 kg in each of the other groups. No changes in 4 skinfold thicknesses or in estimated percent body fat were observed. Of 15 circumferences, significant increases were observed only for men receiving TE-300 mg/wk (shoulders) and ND-300 mg/wk (shoulders and chest). The data suggest that high dose androgens increase body mass and may increase strength in normal men but, except for a consistent weight gain with greater than replacement doses, the detectable changes were highly variable and relatively small, especially in comparison to the significant alterations which were observed for other markers of androgen action.

http://www.ncbi.nlm.nih.gov/pubmed/1958561

I ran 500 deca and 600 test per week for 15 weeks with a libido INCREASE.
Definitely a synergistic combination!

BeastFitness in line with the opening post please provide reference literature to substantiate whenever possible. Although I'm not nor are others disputing anything being shared it is really cool and more importantly credible when there's data to support anecdotal findings.
Definitely whenever possible! It sucks that not everything is done in a clinical setting and its half anecdotal but the cominbation of anecdotal + research is honestly the best way to go!

I find this article to be my most favorite in regards to cycles and most specifically androgenic compounds aka:trenbolone.
LOVE it!

I ran similar, 500 deca / 800 test, was feeling GREAT till the deca kicked in, then it's like I got depressed all of a sudden. Real strange. Not a fan. NPP doesn't have this effect though.
Thats the anecdotal part haha. You didn't respond well to deca but more favorably to NPP…funny haha. Everything has its place depending on the individual IMHO. If you respond horrible to something STAY AWAY, if you respond favorably, use it smartly. So many variables to consider.


Effects of Pharmacological Doses of Nandrolone Decanoate and Progressive Resistance Training in Immunodeficient Patients Infected with Human Immunodeficiency Virus

This nonplacebo-controlled, open label, randomized study was conducted to test the hypotheses that pharmacological doses of nandrolone decanoate would increase lean body tissue, muscle mass, and strength in immunodeficient human immunodeficiency virus-infected men, and that these effects would be enhanced with progressive resistance training (PRT). Thirty human immunodeficiency virus-positive men with fewer than 400 CD4 lymphocytes/mm3 were randomly assigned to receive weekly injections of nandrolone alone or in combination with supervised PRT at 80% of the one-repetition maximum three times weekly for 12 weeks. Total body weight increased significantly in both groups (3.2 ± 2.7 and 4.0 ± 2.0 kg, respectively; P < 0.001), with increases due primarily to augmentation of lean tissue. Lean body mass determined by dual energy x-ray absorptiometry increased significantly more in the PRT group (3.9 ± 2.3 vs. 5.2 ± 5.7 kg, respectively; P = 0.03). Body cell mass by bioelectrical impedance analysis increased significantly (P < 0.001) in both groups (2.6 ± 1.0 vs. 2.9 ± 0.8 kg), but to a similar magnitude (P = NS). Significant increases in cross-sectional area by magnetic resonance imaging of total thigh muscles (1538 ± 767 and 1480 ± 532 mm2), quadriceps (705 ± 365 and 717 ± 288 mm2), and hamstrings (842 ± 409 and 771 ± 295 mm2) occurred with both treatment strategies (P < 0.001 for the three muscle areas); these increases were similar in both groups (P = NS). By the one-repetition method, strength increased in both upper and lower body exercises, with gains ranging from 10.3–31% in the nandrolone group and from 14.4–53.0% in the PRT group (P < 0.006 with one exception). Gains in strength were of significantly greater magnitude in the PRT group (P ≤ 0.005 for all comparisons), even after correction for lean body mass. Thus, pharmacological doses of nandrolone decanoate yielded significant gains in total weight, lean body mass, body cell mass, muscle size, and strength. The increases in lean body mass and muscular strength were significantly augmented with PRT. - See more at: http://press.endocrine.org/doi/abs/10.1210/jcem.84.4.5610#sthash.RqmSGxuh.dpuf

Full text: http://press.endocrine.org/doi/abs/10.1210/jcem.84.4.5610
 
BeastFitness

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Subbed for knowledge. I like this thread already.
Awesome! Glad your enjoying the info man!

Very good read David Dunn. I find the logic behind omitting test from cycles very interesting. I wonder in what situations they would actually include test?
I'd be interested in trying out a more brief, short ester only AAS cycle just to see the results for myself. Maybe even without test
Remember the synergy between compounds as well as the comparison of esters. Again, everything has its place though haha

That WAS an interesting read. Currently (as of the 31st) running a tren ph. So that is a startig point for me. Have always been interested in tren though.
Anyone running a "tren ph" is likely running dienolone btw. Good stuff, but not tren. Never knew why that stuff was ever branded as a tren ph / trenavar etc.. Strange how marketing works
Agreed^^^^

Isn't trenavar the one that actually converts to trenbolone? I know trenazone, etc. convert to dienolone
It does convert to tren, but remember the nature of an oral PH...the effects are no where NEAR comparable to actual injected tren variants. Typically in order for trenavar to be efficacious, its gets to be pricey


Youre right. It isnt. I assumed it was. So OL tr3n is in fact dienolone?
That has Trendione in it right??

Remember that trendione also known as trenavar..the other difference hear between injectable tren is by a ketone at the 17th position.


In vitro and in vivo effects of 17beta-trenbolone: a feedlot effluent contaminant.

Concern has arisen regarding the presence and persistence of trenbolone in the environment. Trenbolone acetate is an anabolic steroid used to promote growth in beef cattle. It is hydrolyzed to the active compound, 17beta-trenbolone (TB), which is also one of the metabolites excreted by cattle. Reproductive alterations have been reported in fish living in waters receiving cattle feedlot effluent, and in vitro androgenic activity displayed by feedlot effluent samples has been related to these effects. In the current study, the androgenic potency of TB was examined both in vitro and in short-term in vivo assays. TB was a high affinity ligand for the androgen receptor (AR), with an IC(50) of about 4 nM in rat ventral prostate cytosol and about 33 nM in cells transfected with the human AR when competed with 1 nM [3H]R1881. TB induced AR-dependent gene expression in MDA-kb2 cells with a potency equal to or greater than dihydrotestosterone. In immunocytochemistry experiments with the human AR, concentrations as low as 1 pM significantly induced androgen-dependent translocation of the AR into the cell nucleus. TB also displayed antiglucocorticoid activity in vitro, inhibiting dexamethasone-induced transcriptional activity, and reduced adrenal gland size in vivo. In the Hershberger assay (in vivo), TB was as potent as testosterone propionate in tissues that lack 5alpha-reductase but less effective at increasing weight of tissues with this enzyme. Such tissue specificity was anticipated because other C-19 norsteroidal androgens display a similar profile in this assay. Subcutaneous TB treatment was about 50- to 100-fold more effective in stimulating growth of androgen-dependent tissues than was oral treatment. In our in utero screening assay, maternal TB administration increased AGD and attenuated the display of nipples in female offspring in a dose-related manner, similar to the published effects of testosterone propionate. Previous studies have documented that these types of malformations in newborn and infant rats are not only permanent effects but are also highly correlated with serious reproductive malformations as adults. In summary, TB is a potent environmental androgen both in vitro and in vivo and, in contrast to other reports, can induce developmental abnormalities in the fetus.

http://www.ncbi.nlm.nih.gov/pubmed/12441365





Another great study (animal) analysed trenbolone metabolites in the gall bladder of rats

Differences in the biotransformation of a 17 beta-hydroxylated steroid, trenbolone acetate, in rat and cow.

1. The metabolism of trenbolone acetate, 17 beta-acetoxyestra-4,9,11-trien-3-one (TBA), an anabolic compound used as a growth promoter, was compared in rat and cow. 2. [6,7-3H] TBA was injected i.v. into rats and a heifer, and bile was collected for 24 h. In both species, the bile was the major route of excretion. TBA undergoes an extensive hydrolysis to 17 beta-hydroxyestra-4,9,11-trien-3-one and the unchanged compound was not detected, but subsequent major metabolic pathways are different in the two species. 3. In the rat, oxidation of the 17 beta-hydroxyl to the 17-oxo group and hydroxylation in the 16 alpha-position are the major routes. The three major metabolites are 17 beta-hydroxyestra-4,9,11-trien-3-one, 16 alpha, 17 beta-dihydroxyestra-4,9,11-trien-3-one and 16 alpha-hydroxyestra-4,9,11-trien-3, 17-dione. 4. In the heifer, 17 alpha-epimerization is the major pathway and the main metabolite is the 17 alpha-hydroxyestra-4,9,11-trien-3-one. 5. In both species, estra-4,9,11-trien-3,17-dione and the other metabolites, resulting either from hydroxylation in 1, 2, 6 beta, 16 alpha or 16 beta positions, or from aromatization of the A ring, were minor products. 6. Overall, 60% of the 3-oxotriene structures identified in the rat bile were 17 beta-hydroxylated and the remainder were 17-keto metabolites, whereas in the heifer bile 90% were 17 alpha-hydroxylated compounds. 7. Thus, in bovine species, the major pathway is similar to those of testosterone or 17 beta-estradiol which are mainly excreted as their 17 alpha-epimers. The epimerization strongly decreases the biological potency, as with the natural 17 beta-hormones, and leads to detoxication of tissue residues.

http://www.ncbi.nlm.nih.gov/pubmed/7293236




Breaking down these studies, they pretty much "suggest" that rats neutralize trenbolone faster than humans do and that humans most likely need less trendione than you'd think (these user reports showed anabolic effects of 40 - 90 mg trendione per day and at higher doses, androgenic side effects appear.)
 
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Research says it contains one active ingrediant: Trendione.
 
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Any PH to trenbolone is not at all characteristic of real trenbolone.

Can we please disassociate PH products from this thread as they are not AAS. Thanks.
 
BeastFitness

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Research says it contains one active ingrediant: Trendione.
Below as well as read the study I posted above in post #39

Obviously an oral form of tren is not going to be as effective as an injectable form of tren

Any PH to trenbolone is not at all characteristic of real trenbolone.
This
 
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I had a question about dbol from a member on these forums and wanted to address dosages here, now, remember that dosages are going to vary from person to person and depends on the rest of the compounds in your cycle but MORE IS NOT ALWAYS BETTER. This research paper gave subjects 10 or 25 mgs of dbol per day and although the research is a little skewed on how the results were measured, both groups made the same amount of progress regardless of a higher or lower dosage.

Anabolic steroids in athelics: crossover double-blind trial on weightlifters.

Thirteen experienced male weightlifters taking high-protein diets and regular exercise took part in a double-blind crossover trial of methandienone 10 or 25 mg/day to seeif the drug improved athletic performance. Their improvemments were significantly greater on methandienone than on placebo; their body weights rose (though this seemed to be associated with water retention); and systolic blood pressure rose significantly. Methandienone caused many side effects, and three men had to withdraw because of them. All side effects disappeared after the drug was stopped. Anabolic steroids are effective only when given combination with exercise and high-protein diet.We deprecate their use in athletics but can suggest no way of stopping it.

Full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1673411/pdf/brmedj01449-0023.pdf
 
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BeastFitness is cycle support needed/recommend for orals such as dbol if ONLY used for up to 6 weeks?
 
BeastFitness

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BeastFitness is cycle support needed/recommend for orals such as dbol if ONLY used for up to 6 weeks?
To be honest, I am a fan of cycle support year round as both orals and injectables are a lot harsher on our bodies than many understand and it truly has a wide array of side effects that even via research, we cannot fully see all the potential side effects as long term studies haven't been done on newer compounds or even traditional ones (in most cases.) I'm a big proponent of a proper diet filled with micronutrient dense foods as well as some health based supplements.

Year Round I am a huge believer in utilizing these health based supplements (some of which provide some ergogenic effects as well):
NAC
Fish Oil
Basic Multi
Saw Palmeto
Vitamin D3
Milk Thistle
Green Tea Extract
CoQ10
Evening Primrose Oil
Garlic Extract
Melatonin
Alpha Lipoic Acid
Berberine
A proper liver care product

Obviously thats a long list to utilize year round but whenever any is going to blast, then I'd recommend you simply increase the dosages to the "AAS dosage" (for lack of a better work) compared to a "cruise dosage." I would also add in a few things like TUDCA while blasting but again, a lot of this depends on the person's bloodwork, genetic history, and current nutritional needs.

If you read that and think its overboard, read below...


Anabolic androgenic steroid-induced cardiomyopathy, stroke and peripheral vascular disease
Maged Y Z Youssef, Ahmed Alqallaf, Nabila Abdella


Summary
Acute stroke could be the presentation of unrecognised cardiomyopathy postanabolic androgenic steroid (AAS) abuse. A 39-year-old male patient displayed signs of acute stroke, which were associated with AAS abuse over the last 3 years. Despite the absence of symptoms and signs of congestive heart failure at presentation, AAS-induced cardiomyopathy with a thrombus in the left ventricle was discovered to be the aetiology of his stroke and peripheral vascular disease. Awareness of the complications of AAS led to the prompt treatment of the initially unrecognised dilated cardiomyopathy, and stroke.


Background
Acute presentation of stroke in a young patient with prolonged anabolic steroid use should alert us to underlying cardiomyopathy with thromboembolic events and peripheral vascular disease.


Case presentation
A 39-year-old male body builder presented with dizziness and expressive aphasia for the last 6 h.

Three months earlier, the patient presented to medical emergency with a transient ischaemic attack in the form of sudden loss of vision in left eye associated with weakness and numbness in the left upper and lower limbs lasting less than 1 h. The patient had intermittent claudication in the left lower limb. Neurological examination at the time, followed by CT of the head was completely normal. The patient refused admission to the hospital and was discharged on aspirin and follow-up which he did not pursue. [A rookie mistake which too many 'indestructable' bodybuilders repeat!]

The patient had no medical issues, 3 weeks prior to admission at the hospital. However, the patient admitted to have been abusing anabolic androgenic steroids (AAS) for the last 3 years, which were administered as intramuscular injections of nandrolone twice weekly [I think we can fairly assume that's not all he took! ]

On physical examination, he was alert and conscious with motor aphasia. Heart rate was 100/min, and blood pressure 140/100 mm Hg. Chest, heart and abdomen were normal. Jugular venous pressure was not elevated, and no peripheral oedema was noted. Peripheral pulsations were present on right side and absent dorsalis pedis pulsation on left side. Pupils were normal to exam. His fundi were normal with no visual field defects and no nystagmus. Right facial palsy, upper motor neuron lesion. No motor weakness was detected. Deep reflexes were normal in upper and lower limbs. Plantar reflexes were normal.


Investigations

Complete blood picture, erythrocyte sedimentation rate and C reactive protein were within normal range. Fasting blood sugar, liver function test, kidney profile and serum electrolytes were normal. Troponin, and coagulation profile were normal and his creatine kinase was 500 U/l (normal range 5–130 U/l).

Serum triglycerides 1.8 mmol/l (normal <2.20 mmol/l), total serum cholesterol 5.4 mmol/l (normal <5.2 mmol/l), high density lipoprotein-C 0.85 mmol/l (normal >0.9 mmol/l), low density lipoprotein-C (LDL-C) 4.19 mmol/l (normal < 3.37 mmol/l)[A typically poor lipid profile as regularly seen in AAS users - incidentally Deca doesn't appear to negatively affect lipids so we can assume it's whatever else he's taking], apolipoprotein B 1.29 mg/dl (normal range 0.60–1.33 mg/dl). Full thrombophilia screen, antiphospholipid antibodies, virology screen and immunology screen were negative. Urinalysis and microscopy was normal. Ankle brachial index: right side=1.2, 1eft side=0.69. Chest x-ray showed cardiomegaly [FYI: enlarged heart]. ECG showed sinus rhythm. Q waves were present in leads II, III and AVF. Poor R waves were observed in V1–V3. CT and MRI of brain showed left frontal infarction [Tissue death - due to the prior stroke]. Echocardiography showed dilated left ventricle (LV) with global hypokinaesia. Left ventricular cavity size was enlarged, end diastolic diameter was 6.9 cm and end systolic diameter was 5.7 cm. Left ventricular ejection fraction was 35% [very poor/inefficient] and there was an apical thrombus[A huge clot inside the left ventricle of the heart]. The left apical thrombus was mobile, measuring 1.6×1.5 cm. Left atrium diameter was 4.1cm. Carotid Doppler ultrasound showed no significant stenosis. Dipyridamol stress test of heart ruled out myocardial ischaemia. Magnetic resonance angiogram of left lower limb showed that there was an abrupt cut-off at the left superficial femoral artery at the beginning of the left popliteal artery, with total occlusion of left popliteal artery [piece of clot lodged in leg causing total aterial blockage].


Outcome and follow-up

Patient was managed with intravenous unfractionated heparin infusion, statins, angiotensin converting enzyme inhibitors and β-blockers. Repeat CT showed no evidence of haemorrhagic transformation with progressive improvement of motor aphasia. In addition to the previously mentioned medications, the patient was discharged on aspirin and warfarin as well.

Upon follow-up after 3 months, review echo showed resolution of thrombus with partial improvement of ejection fraction ( 40–45% ).

Upon follow-up after 6 months, ankle brachial index was improved, right side=1.20 and left side=0.82. The patient’s symptoms improved and he was able to resume work.


Discussion

Some athletes whether in competitive or non-competitive sports, abuse AAS to improve their performance or even their appearance as body builders.1

Abusers typically use 5–15 times the recommended medical doses of AAS. Athletes abusing AAS for years have high potential for arterial hypertension, cardiovascular, cerebrovascular disease and lipid metabolism disorder.2

We reported a 39-year-old man, who developed dilated cardiomyopathy, embolic stroke and peripheral vascular disease after self-administration of AAS for 3 years.

Several studies show that high doses of AAS such as nandrolone, may lead to growth-promoting effects on cardiac tissue, as seen in hypertrophic cardiomyopathy, followed by apoptotic cell death which is mediated by membrane-receptor second messenger cascades that increase intracellular Ca2+ influx [Hence the potential utility of Calcium Channel Blockers for AAS users] and mobilisation, leading to the release of apoptogenic factors.3 4

AAS abuse associated with sudden cardiac death, myocardial infarction, ventricular remodelling and cardiomyopathy is related to apoptosis.5 This relation may explain the clinical observations that AAS can lead to myocardial death without coronary thrombosis or atherosclerosis.6 7

Several studies in isolated human myocytes have shown that AAS bind to androgen receptors and may directly cause hypertrophy, via tissue upregulation of the renin-angiotensin system.8 [Hence part of the rationale for using Angiotensin Receptor Blockers EG: Losartan - other important reasons include inhibtion and reversal of AAS-induced scarring and fibrotic tissue accumulation in the heart and cardiovascular system]

AAS abuse causes decrease in high density lipoprotein cholesterol by 20% and increase in LDL cholesterol by 20% due to lipolytic degradation of lipoproteins and their removal by receptors through modification of apolipoprotein A-I and B synthesis.9 Apolipoprotein B has been experimentally linked to the development of atherosclerosis, mediating the interaction between LDL-C and the arterial wall.1

These lipoprotein abnormalities increase the risk for coronary artery disease by three to sixfold and may occur within 9 weeks of AAS self-administration.8 10 Fortunately, lipid effects seem to be reversible after discontinuation.1

AAS enhance platelet aggregation and thrombus formation by increasing platelet production of thromboxane A2, decreasing production of prostacyclin and increasing fibrinogen levels.1

Ischaemic stroke can occur as a result of atherothrombosis or embolisation either in the carotids or the heart as AAS has been associated with changes in vascular reactivity, lipid profile, haemostasis and platelet aggregation.1 Accordingly, peripheral vascular disease can occur through the same mechanism.1

Our case is unique as our patient developed an embolic stroke and peripheral vascular disease in the absence of any risk factors for either of the diseases, but rather as a complication of dilated cardiomyopathy with LV thrombus formation. These complications were deduced to be the result of AAS abuse after ruling out other aetiological factors.


References

Santamarina RD, Besocke AG, Romano LM, et al. Ischemic stroke related to anabolic abuse. Clin Neuropharmacol 2008;31:80–5.

Lane HA, Grace F, Smith JC, et al. Impaired vasoreactivity in bodybuilders using androgenic anabolic steroids. Eur J Clin Invest 2006;36:483–8.

D’Ascenzo S, Millimaggi D, Di Massimo C, et al. Detrimental effects of anabolic steroids on human endothelial cells. Toxicol Lett 2007;169:129–36.

Achar S, Rostamian A, Narayan SM. Cardiac and metabolic effects of anabolic-androgenic steroid abuse on lipids, blood pressure, left ventricular dimensions, and rhythm. Am J Cardiol 2010;106:893–901.

Zaugg M, Jamali NZ, Lucchinetti E, et al. Anabolic-androgenic steroids induce apoptotic cell death in adult rat ventricular myocytes. J Cell Physiol 2001;187:90–5.

Fineschi V, Baroldi G, Monciotti F, et al. Anabolic steroid abuse and cardiac sudden death: a pathologic study. Arch Pathol Lab Med 2001;125:253–5.

Wysoczanski M, Rachko M, Bergmann SR. Acute myocardial infarction in a young man using anabolic steroids. Angiology 2008;59:376–8.

Liu PY, Death AK, Handelsman DJ. Androgens and cardiovascular disease. Endocr Rev 2003;24:313–40.

Hartgens F, Rietjens G, Keizer HA, et al. Effects of androgenic-anabolic steroids on apolipoproteins and lipoprotein (a). Br J Sports Med 2004;38:253–9.

Maravelias C, Dona A, Stefanidou M, et al. Adverse effects of anabolic steroids in athletes. A constant threat. Toxicol Lett 2005;158:167–75.



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datsthat

datsthat

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How do you feel about NPP as a Kickstarter while running Deca entire time but adjust dose of each accordingly?
 
Toren

Toren

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How do you feel about NPP as a Kickstarter while running Deca entire time but adjust dose of each accordingly?
I'd also like to know his thoughts on also dropping the decanoate ester towards the end of the cycle and adding NPP back in. Thinking this mighht give the longer estered nandrolone more time to clear the system and allow for an easier transition into PCT for guys that get hit hard on the longer estered Nandrolone.
 

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