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Cycle critique please

Don't take my word for it, I'm not a medical doctor but check out some of the medical literature available.
Would be great hear some of the more knowledgeable promuscl take on all of this too..
 
i think i read somewhere that without ELEVATED e2 there will be no prostate issues, even with high DHT levels...
high dht + high estrogen seems to be the killer combo here
im not saying ONE of both high CANT cause trouble. it probably can, but having them both high seems to be the worst...

im not stewie though so no idea about the scientific explanation.

i for once ALWAYS use an AI and never in my life did i have any issues with my prostate, not even on cycles with huge amounts of androgens (test, tren, mast, sdrol / adrol etc) in multiple grams...and i always keep my estrogen lowish with letro or adex. im still young though, but i have buddies who have trouble urinating on mast etc even in their young years...
same with hair loss or acne... i never get any "typical dht sides"...however if i use dbol or when i use too little AI i IMMEDIATELY notice a few painful zits forming on my back. my facial skin also gets much worse when im on highly aromatizing compounds (=dbol)...

i believe most sides are caused by high estrogen. not dht.
 
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Sides yes. I just had a slightly enlarged prostate and slightly elevated psa last time i had a checkup. Well i can only attribute that to gear, trt, or a combination of both. And the first thing they put me on to lower that, is a dht blocker..

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But yeah, estrogen is what typically causes by acne too.

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DHT blockers are horrendous for any man

id much rather try to fix it via the estrogen route first if you like your dick functioning :cool:
 
Hey gentlemen, i need some help. I am running a moderate cycle and am 3 weeks in with gyno rearing its ugly head. I can't seem to get it under control. Been doing a lot reading, again, but thought id just see if anyone had run into similar.

Stats: 33yrs 6'3 211 pounds 6.3% bf
Bench 315X3 squat 405X3 DL 385. Lifted for 15+ years
Many cycles under the belt from years ago, but this is the first one in >3 years.

Running a popular tren blend of
100mg tren enanth/75mg tren hex/25mg tren ace.
Twice weekly Sunday and Thursday

500 mg test e twice weekly

50mg tbol/day

25mg aromasin/day
.60 prami/day
5mg dutasteride/day
250iu hcg q3d


Have letro on hand, but hesitant to pull that gun out just yet. I could up my prami but i need to do it slowly cause it messes with my gastro system bad. Im consisting dropping the aromasin and switching to nolva, but i like the less bloat i get from aromasin.

What do you guys feel i should do?

I'd drop that dutasteride down to .1mg/day, I'm serious. 5mg is INSANE. That is more insane than 5mg of finasteride/day. FYI, .2mg of finasteride works 90% as well as 5mg. There are diminiishing returns with increased doses of 5ARIs.

This is a chart from a study on dutasteride:

Placebo -32.3 hairs
Finasteride 5mg 75.6 hairs
Dutasteride 0.1 mg 78.5 hairs
Dutasteride 0.5 mg 94.6 hairs
Dutasteride 2.5 mg 109.6 hairs

I mean, in theory i understand the concept. But i guess both have to bind to a limited amount of receptors on cell surface before they can even get to point of synergy.

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Androgen receptors aren't on the surface of the cell they just float around in the cytoplasm.

... Yes. And is more helpful information in short than I've read at length. Which brings more questions.

Is there a point to which saturation occurs? If so, is it defendant upon the how many receptors the body has... A while back I read an article describing a test that can be performed to determine the amount of receptors in the body, describing a ratio from 6-36 as it's scale. The writer suggests the lower the number, the greater a probability of being a "high responder" to AAS and could account for greater "sides" as opposed to someone with with more receptors whom could absorb more (thus the need for a higher dose to effect the same as the next who does less with equal response). I think it was called a GAC profile I've looked and googled for this. Can't find it, though I remember it was posted on Meso-RX (thinksteroids.com if that helps).

Or do dimers continue to be created as needed when more anabolic is introduced? And could this effect be responsible for the OP's gyno...




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"Saturation" if it does occur, doesn't have to do with a limited number of AR, but rather a limited number of co-binding factors, so it's not really saturation.

Cut tren, add masteron problem solved.
Masteron is very effective in addition to test for bulking and cutting.
Tren is not necessary and does more harm than good... Gives me bad gyno even after a single shot. Bad sleep, bad mood, depression, bad sex long term, I'll feeling....

Most think masteron is only for cutting and only see results at low bodyfat, but this is just not true.
Moderate test + moderate masteron = fantastic gains with enough calories. The gains are solid, and you won't be a bloated mess. If you really want to see amazing things add in 3-4iu of good gh.
To lean out same thing but lower test dose by half or more, keep masteron on the moderate to high side and calories balanced properly using higher protein, moderate to low carbs mostly complex, and fats moderate and you'll see amazing things as well.

If your masteron doesn't provide the results I mention, its not real masteron period.

Masteron would be a poor choice if hairloss is a concern.

What you are referring to is CAG repeat, not GAC. Easy to confuse nonetheless. It's one of the 4 domains of the androgen receptor gene. It's located in the DNA segment. It's not determined by a ratio, rather it's the total amount of CAG repeats one has. Which some research states 10 to 36 repeats, as others claim 6 to 37 on the chromosomes. Testing for total CAG repeats has been used for a number of years in research and treatment for different diseased states. As far as anabolic response, I'm sure there's some interplay with one's total amount of CAG repeats. There's other genes involved that differentiate anabolic response. I've posted on this a few times.

Dimers are in constant replication, unless there's some mutations or DNA damage.

As for saturation. I'm sorry to say, I'm a bit burned out on the whole upregulation/downregulation and saturation of the androgen receptor. There's much more to it than a claiming these three things. It gets boring reading people trying to put a new spin on anabolics.

I totally agree, I think co-binding factors are the main players, but there may be up/down regulation in those...
 
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Hairloss is not the concern, im not prone, but long term prostate health is. Cause i have a slight case of bph and an elevated psa
 
I totally agree, I think co-binding factors are the main players, but there may be up/down regulation in those...

Without saying, that was my point.

If people understood that there's rate limiting steps involved with activation/deactivation of the androgen receptor, it becomes more complex than simply saying "upregulation/downregulation". Saying this is very vague and basically a blanket statement.

Many, many things are involved just to initiate the complexity such as heat shock protiens, NH2-terminal transactivation, DNA-Binding, ligand-dependent activation function, receptor dimerization, zinc fingers, ect, ect. That's just a few, without mentioning repressors, copressors, coactivators, ect.

Improper sequencing or miscommunication (dysfunctional) between cross-talk of the androgen receptor with any of the complexities would cause "downregulation".

Nice to see you posting again, Kaladryn :)
 
Without saying, that was my point.

If people understood that there's rate limiting steps involved with activation/deactivation of the androgen receptor, it becomes more complex than simply saying "upregulation/downregulation". Saying this is very vague and basically a blanket statement.

Many, many things are involved just to initiate the complexity such as heat shock protiens, NH2-terminal transactivation, DNA-Binding, ligand-dependent activation function, receptor dimerization, zinc fingers, ect, ect. That's just a few, without mentioning repressors, copressors, coactivators, ect.

Improper sequencing or miscommunication (dysfunctional) between cross-talk of the androgen receptor with any of the complexities would cause "downregulation".

Nice to see you posting again, Kaladryn :)

Thanks, I try to visit now and then. I really like this topic, it's important for people to know how much more complex this stuff is than the simple dogma that has been tossed around, and how we don't even understand how every mechanism works.

I've always wondered if there may even be more truth to Duchaines theories about the anti-catabolic action of androgens being more of a player than is commonly thought...
 
So i got my caber and tamox in. What do you guys suggest starting for caber based on my tren amount

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So i got my caber and tamox in. What do you guys suggest starting for caber based on my tren amount

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Have you checked your prolactin levels to even warrant the use of a D2 agonist?

The whole elevated prolactin levels on Tren has been shot down many-a-times by Patrick Arnold and Bill Roberts.

I think people stress out over-thinking, worry their prolactin is going to be elevated, therefore inducing prolactin to transiently rise.

Control your estradiol levels (and stress), that in itself mediates prolactin response.
 
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Have you checked your prolactin levels to even warrant the use of a D2 agonist?

The whole elevated prolactin levels on Tren has been shot down many-a-times by Patrick Arnold and Bill Roberts.

I think people stress out over-thinking, worry their prolactin is going to be elevated, therefore inducing prolactin to transiently rise.

Control your estradiol levels (and stress), that in itself mediates prolactin response.
I haven't this time, but im leaking fluid, and i can run a gram of test without gyno. Ive just used tren enough times in my life to recognize it. Happens every time. Im going to run .25 q3d i think to start.

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FYI, there is an interesting study that showed that blocking BOTH E2 and DHT causes MASSIVE prostate hyperplasia. I have posted the study before, it's floating around. There is more to the BPH story that just sex hormones.

(it wasn't in humans, rats or dogs I believe)
 
Wow. Now that would be interesting. Ill try and look for it. Thanks Kaladryn

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FYI, there is an interesting study that showed that blocking BOTH E2 and DHT causes MASSIVE prostate hyperplasia. I have posted the study before, it's floating around. There is more to the BPH story that just sex hormones.

(it wasn't in humans, rats or dogs I believe)

do you mean CAUSES or does not prevent?

agree on the sex hormone part. there are literally thousands of people who have BPH issues from ephedrine for example.
i also find peeing harder on ECA. and not just while its in the system (terminal half life), but all the time when i use it, so these are no direct effects.
 
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See everything i am reading talks about prevention, but nothing related to causes except the presence of(e2 and dht), not the absence. Ill post some studies that i was reading later on today

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**broken link removed**

There was some investigations into Dr.Jonathan Wright's practice a few years ago. Nevertheless, I do believe he has some fascinating insight on prostate cancer.
 
This particular study shows that E2, 3-dol, and dht all contributed to the proteins manufactured in the prostate thereby leading to an elevated psa and resulting bph.

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