M-drol/E-stane/Anabeta/Erase 12 wks

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    I'm going to be running this in the next few weeks once my serm arrives. Here's the breakdown if you have any advice feel free to post.

    Preload Hawthorne berries for 2wks
    Wk 1-8
    Cycle assist
    Tudca
    Fish oil

    Wk1-5
    Mdrol-20/20/20/20/0
    E-stane 0/30/30/30/30
    Dermacrine
    Inhibit-p

    Wk6-9
    Torem 120/90/90/60/30
    Anabeta 4 caps
    Erase 3 caps
    Inhibit-p

    Wks10-13
    Anabeta 6 caps
    Erase 3 caps
    Forskolin
    Inhibit-p ( whatever's left of it)

    This is my fourth cycle, previous cycles were not impressive due to my lack of nutrition and diet. I got my nutrion in order and have made some good gains naturally. I'm ready to finish these bottles of DS and make some nice gains.
    My biggest concern here is gyno and rebound. I'm hoping the e-stane will be enough to keep me dry on cycle and the erase to keep rebound away. I have letro on hand and was debating on doing .5 mg e3d depending on how my nips are looking. If rather sacrifice a little gain lowering estrogen then get gyno flared up.
    I usually run nolva or clomid but I didn't like how I reacted to them so I'm hoping torem treats me better.
    Diet is key here and as I'm currently cutting at 2800 ill slowly bring cals up as I start the cycle.
    3500 wk1 3800 wk2 4000 wk3 and ill see how fat gain is from here and determine if I should increase cals.


    Training is 5/3/1 with high volume isolation work.
    Cardio on days off 3 days a week.
    Any advice regarding gyno prevention and rebound is much appreciated. I may turn this into a log. Not sure yet.

    Stats:
    6'4 214
    Legs: 24.5
    Arm: 16
    Waist: 36.5
    Chest:42.5
    Neck:16


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    gyno will be prolactin on this type of cycle, not estrogen. and you might wanna consider a sd epi bridge instead of a straight stack. its a little less harsh on the liver, and is better for keeping the sd gains. maybe

    mdrol 20/20/20/20
    epi 0/0/30/30/30/30

    then pct and post pct run
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    Quote Originally Posted by OnionKnight View Post
    gyno will be prolactin on this type of cycle, not estrogen. and you might wanna consider a sd epi bridge instead of a straight stack. its a little less harsh on the liver, and is better for keeping the sd gains. maybe

    mdrol 20/20/20/20
    epi 0/0/30/30/30/30

    then pct and post pct run
    I have about 2 wks worth of inhibit p left. And a month of endosurge. Will those be enough or should I buy more/something else.
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    I ordered some more inhibit-p and will run that for 10wks. Also changed the plan to a bridge as suggested.
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    Quote Originally Posted by beastybean
    I ordered some more inhibit-p and will run that for 10wks. Also changed the plan to a bridge as suggested.
    you gonn log it? i wanna do that cycle in the future lol
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    Quote Originally Posted by OnionKnight View Post

    you gonn log it? i wanna do that cycle in the future lol
    Ill be pretty busy with school/ work and gym, but ill post before and after pics as well as update if I anything out if the usual happens. Other than that we'll see if my schedule allows me to log.
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    Quote Originally Posted by beastybean

    Ill be pretty busy with school/ work and gym, but ill post before and after pics as well as update if I anything out if the usual happens. Other than that we'll see if my schedule allows me to log.
    hey ill take that. before and after stats/pics is the important part of a log
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    Good read


    Beastdrol/Superdrol and prolactin FAQ!!! Anyone who knows anything about chemical structures will see that superdrol is not a progestin, and shouldnt cause prolactin like side effects. The problem is everyone is different and eveyone has different amounts of progestin receptors, wich can cause worse sides in some users than others, one guy can use deca and get no bloat, another with the same dose will get bloat and gyno, because of this one reason alone. Now Beastsrol or superdrol is in itself not that androgenic, and as its structure suggests its not that different to other dht based steroids, now an action takes place that explains how it works... its doesnt act like a typical androgenic, but acts a little like oxymetholone, in that it doesnt show any real affinity for the 5AR enzyme, so you get weaker affinty for the androgen receptor than dht, but you get stronger androgenic effects as the enzyme 3beta hydroxysteroid dehydrogenase has little effect on the androgen affinity of superdrol. The problem is this same enzyme 3beta hydroxysteroid dehydrogenase, is used in the conversion of many metaobiles in the body, Superdrol produces a lot of metabolites that dont get bound by the androgen receptor like we just saw, it cant aromatize, so it doesnt bind to the estrogen receptor, but it circulates, as its also a di methyl, it is very biovailable so a lot of the product circulates in the blood, and these extra metabolites dont bind specificly...not in the way they should.. so i will explain in a detailed way then make it much easier to understand. Prolactin is normaly caused by progestins, but can also be caused by dht, how? For example, it is currently understood that when testosterone enters the cell cytoplasm it is subsequently converted to the more "active" androgen, dihydrotestosterone, DHT, by reduction at the 5alpha position, This is normal. Dihydrotestosterone is then either bound to a cytoplasmic "receptor" protein Rc, or is further metabolized to either 5alpha-androstane-3alpha,17beta-diol or 5alpha-androstane-3beta,17beta-diol ,DIOL. The binding of DHT to its cytoplasmic receptor protein results in translocation of the steroid-receptor complex into the nucleus where presumably the complex dissociates and DHT exerts its androgenic effects. The transport of DHT to the nucleus can also result from the conversion of testosterone to DHT by nuclear membrane-bound 5alpha-reductase. Prolactin augmentation of DHT effects is envisioned as resulting from interaction of prolactin with its receptor, which due to the large size of the prolactin molecule is probably located in or on the plasma membrane. Because superdrol is androgenic, but lacks the ability to show affinity via 5ar, it circulates, and this causes the large amounts of androgens to look for a transporter, so that it can bind to the androgen recptor, so it uses prolactin wich has a high affinity to cytoplasmic receptor protein, allowing the androgens, testosterone, to be carried and allowing them to convert to dht, only problem is prolactin hormone or luteotropic hormone is synthesised and secreted by sex binding lactotrope cells in the adenohypophysis (anterior pituitary gland, And this gland now produces more prolactin to help deal with the large amount of testosterone circulating that hasnt bound to the estrogen of androgen receptor, Part of the reason why superdol is so anabolic, So instead of binding to the androgen receptors in the scalp and the prostrate it converts to dht through this unique process, using prolactin to enter the cytoplasmic receptror protein, and allowing it to convert to dht and then bind to the androgen receptors in the muscle, causing its distinct hardening effects, it still cant bind to the scalp or prostrate via 5ar as the form of dht it has converted too doesnt allow for that affinity. So more prolactin is produced to allow for the superdol to find a receptor ,this excess prolactin triggers a process that fills the breast with milk via a process called lactogenesis, in men however it causes a distinct enlargment of the mammary gland and can even cause a man to lactate. If superdrol had better binding to the androgen receptor via 5AR then this problem would be prevented, the other thing is that prolactin production can remain elevated for months after a cycle has finished, and once the androgen has been removed, ( the cycle is over) the cytoplasmic receptor proteins have nothing to do other than to allow the prolactin to proceed with its hormonal action within the body, causing the male mammary gland to enlarge ready to produce milk... Hence the REBOUND gyno, this is why proper PCT is needed for superdrol, and the use of something to prevent prolactin. R.S
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    Started today, mdrol at 10 for three days then hold at 20 for the rest of the run. I also took ..25 mgs of letro just to be safe. Might keep it at .25 weekly.
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    Starting to feel the superdrol. Good pumps. Libidos still good. Eating around 4k cals daily. All clean no shakes. I'm up 3lbs. Probably just water and carb weight.

    Example meal: 12oz tilapia. 6oz carrots, 8oz sweet potato.


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    Weight this morning is 225. Strength is up. Lethargy is kicked in. Mild back pumps, nothing crazy. Oh and I decided to save the epi. So it's just a solo SD run.
  

  
 

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