Planning on jumping on a cycle next month with
test c 500mg/wk
Tren e 200mg/wk
Dbol 30mg ed
Armidex .5mg eod
Been training for 8 years now, I am currently 180lbs trying to get to 200lbs.
Any device ?
If this is your first cycle drop tren and dbol.
They are both terrible choices for beginners due to sides and difficulty controlling said sides.
What is cycle length? If you are running an oral 4 or less weeks is best.
There is also conflicting views as to running Arimidex or Nolva during cycle. I have flipped on this and think Nolvadex is the better choice. With 500mg test you will probably only need 10mg EOD or so.
Not my first cycle, have taken Cycles before. So drop the armidex ? Cycle will be 12 weeks
@gethuge123
How tall are you? What’s your body fat percentage?
OK awesome then have fun!!!
Did you run Arimidex or Nolva in the past? If you ran Arimidex then imo definitely try Nolva. If you ran Nolva and liked it definitely stick to it. If you ran Nolva and hated it then try Arimidex.
I used to always run Adex or Aromasin and TONS of it on Tren to combat Gyno. Now I am running tren/test with Nolva and having 0 Gyno issues and think gains are better. In the end you will have to find what works for you but I really like the Nolva.
This is a lot of weight gain. This a bit of a “committed” bulk before a cut or?
That’s makes no sense. Tren doesn’t aromatize into E2 so adex or aromasin have no effect on your Tren dose. Its a progestin and the main way people combat progesterone side effects is with caber. If you are getting gyno from the Test that’s another story.
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Should I run hcg week 9-12?
Cabergoline is a dopamine agonists and as such the dopamine suppresses the synthesis/release/binding (I can’t remember) of prolactin, not progesterone.
Trenbolone doesn’t aromatize but the test/methandrostenolone type drugs most commonly used alongside trenbolone do, and the interplay of progestins, oestrogens and prolactin can result in lactation. If the E is allowed to rise in the presence of progesterone then sharply reduced (by taking an AI for instance) in the presence of increased prolactin while the progesterone levels aren’t too high, it’s the hormonal environment for lactation.
THATS often why users take bromocriptine/cabergoline (D-agonists)
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Thank you for the correction, I indeed misspoke.
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Need a good pct cycle, for my cycle. Would you be the best pct ?
I’m a 15 year aas user and 20 year bodybuilder, fitness professional and molecular biologist, chemist, medicinal biochemist graduate.
I specialise in performance enhancing pharmacology, advanced physiology and endocrinological advancements. So I feel safe recommending following my advice!
Boast much? 
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Need a pct cycle guide if you don’t mind
need some basic background info first additional to that which you’ve given.
BF%
Age.
Will you be taking bloods before/during/after?
How do you cycle, blast and cruise, cycles with proportionate/increased time off cycle, year round, yearly, etc?
You could try 10mg tamoxifen EOD and 0.25mg anastrazole 2x/w together, as tamoxifen has beneficial oestrogenic effects and anastrazole is necessary to reduce the actual level of E which has more harmful side effects than mere gynaecomastia. Benign prostatic hyperplasia for one.!
Rates of inhibition in females
SERD is a selective estrogen receptor down-regulator
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Not my first cycle. Planning to take it for 12wk cycle
test c 500mg/wk
Tren e 200mg/wk
Dbol 30mg ed
Armidex .5mg eod
So drop the armidex and take nov 10mg eod ?
Have you ever had a proper cardiac evaluation (Echocardiogram, cardiac MRI etc)? I’d be interested to see what you’re cardiac parameters/functioning is.
Do you model? Or compete in powerlifting/sports/stronogman style events or bodybuilding competitions
Just want to talk about this here, I don’t believe an AI is required in the absence of gynocomastia provided T->E ratio is appropriate, within realms of one another, provided the dosages being used aren’t absurd (my rule of thumb is generally say the equiv of 1g test in terms of aromatisation). Skewing said ratio impacts various parameters of ones health that are already under stress from AAS use. For one oestrogen is pivotal in regards to glucose and lipid management, endothelial functioning, vasodilation (in response to exercise, NO production etc)… all of which AAS impair
Literature demonstrates for example, supra dosages of test have relatively minimal impacts on cholesterol (say HDL drops 10-30 percent) but when combined with anastrozole the impact is far greater, as is to be expected when skewing androgen to oestrogen ratio. Tamox itself has very little affinity for the ER, the majority of it’s actions stem from the compounds it converts to (hepatically via cytochrome P450)… interestingly I’m a cyp2d6 ultrarapid metaboliser, thus tamox probably wouldn’t be particularly effective for me… codiene on the other hand is very effective… dangerously effective for me…
Interestingly norendoxifen (metabolite of tamox, however I wonder whether it’s actually present in any therapeutically significant concentration following oral ingestion) is a non steroidal aromatase inhibitor… so non suicidal in nature. Given that tamoox metabolites bind to receptors within tissues that have ER’s (breast tissue etc) it should be enough on it’s own to offset gyno absent of inducing lipid abnormalities, potentially deleterious effects on BMD (if oestrogen is crashed, however androgens independently have a positive effect on this… hence why stanozolol, oxandrolone, nandrolone etc are approved as adjunct aids to treat pain/low BMD associated with osteoporosis… largely phased out by newer and more selective medications now though.)
Just wondering, why recommend the AI + SERM and not just the SERM?
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