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 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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... 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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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.
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...
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
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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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.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.
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)