test cyp deca cycle

[HollywoodHam]

this is my first cycle and was curious as to what everyone thinks about 400 mg test cyp, and 400 mg of deca a week. Does anyone know if i will have loss of libido side effects, or if i should possibly take down the deca less. any ideas or thoughts would be appreciated. thanks

[Neoamerican]

Most will tell you to run T+D 2-1 ratio Like 400mgT 200mgDeca
But if you run caber .5mg 2X EW from first pin it illiminates the deca dik so you can run both the same dose
It is a strong misconception running T higher will keep labido up but the real ED prob is elevated progestin levels.
That will be a great cycle. Just stop the deca 3 wks before you stop the T.
Gods speed

[DetroitHammer]

Most will tell you to run T+D 2-1 ratio Like 400mgT 200mgDeca
But if you run caber .5mg 2X EW from first pin it illiminates the deca dik so you can run both the same dose
It is a strong misconception running T higher will keep labido up but the real ED prob is elevated progestin levels.
That will be a great cycle. Just stop the deca 3 wks before you stop the T.
Gods speed

Caber will not eliminate deca d ick. Prolactin is a problem with nandrolone decanoate, but it is not the main cause for a failed libido. Anyone who runs deca takes the risk of short or long term ed issues. There is absolutely nothing you can do to prevent deca d ick if you are sensitive to its sides. Running higher test will help with ed issues, but it's not the higher test as much as it is the lower dosage of deca. You'll get 50% of the board testifying how great deca is and that they never had any sides, while the other 50% will never use it again due to sides, mainly no libido for months afterwards. The only reason anyone could logically add deca to a cycle is to increase water to the joints. Its actually not a very potent AAS and carries with it bad sides. So it's a risk. If you feel lucky, go for it, but be prepared for zero sex life for a while if you experience ed issues. In my opinion, the two most over rated and worthless drugs to add to a cycle are nandrolone decanoate and equipoise.

[CrazyChemist]

For a first cycle the general dogma is to run test solo. The gains are great on test and you can titrate other compounds in once you know how you respond. That said, most ppl have already made their purchases by the time they post and aren't amenable to holding onto their extra supplement. I would personally run more test, like 600mg test cyp/300mg deca. or even 600/200..... hell even 750/250. This is why stacking on a first cycle is difficult. You'd be better off figuring out your optimal dosing for the test and then tossing in the deca later.

Anyway, check this out -->Unreal's Guide to Injectables

[burlyman]

Detroit, tell us how you really feel about Deca. Don't hold back. lol. You are absolutely right about one thing, though--people either love it or hate it. I'm a fan, but since I already have ED, losing libido isn't a concern for me.

Caber doesn't work for deca dick because there is a misconception that the nors (deca/tren) raise prolactin when they do not. They are progestins and progestins by nature cannot raise prolactin. I have an article on this, but I'm too new for the system to let me post links. At any rate, studies with bloodwork will confirm this.

They can however, affect E2 even though they do not aromatize, so having some potent anti-Es on hand is a good thing. An AI simply may not be up to the task. With the right ratio of E2 in the mix, you can keep your libido. Test/Deca at 400/400 will work well. Just keep your E2 in check.

[CrazyChemist]

Detroit, tell us how you really feel about Deca. Don't hold back. lol.

LOL

[burlyman]

For a first cycle the general dogma is to run test solo. The gains are great on test and you can titrate other compounds in once you know how you respond.

I didn't even notice the "my first cycle" part of the post. I'd agree that test solo is a great first cycle. It allows the user to learn how their body handles test, how much aromatization they get, what dosage works well, etc.

Nice resource guide, too. Reps for giving that link to a newbie.

[Neoamerican]

I too over looked the first cycle part. My B
But people swear running caber during deca to keep labido from dropping. And to avoid progestin gyno.
Deca raises progestin levels cause it is a progestin correct?
Sux boute the ED broly

[burlyman]

I too over looked the first cycle part. My B
But people swear running caber during deca to keep labido from dropping. And to avoid progestin gyno.
Deca raises progestin levels cause it is a progestin correct?
Sux boute the ED broly

Caber increases libido because it lowers prolactin, whether or not you are on a cycle. But you are mixing up prolactin with progestin. Caber DOES lower prolactin, but Deca is a progestin. Prolactin and progesterone are two entirely different hormones with different actions. The "caber for progestins" is brolore that goes against science, I'm afraid. You CAN use caber on a deca cycle, but if it does work, it works for the wrong reasons. It is better to attack the off balance hormones to solve the problem of libido AND gyno at the same time.

[DetroitHammer]

You CAN use caber on a deca cycle, but if it does work, it works for the wrong reasons.

Brilliantly stated!

[Trauma1]

Detroit, tell us how you really feel about Deca. Don't hold back. lol. You are absolutely right about one thing, though--people either love it or hate it. I'm a fan, but since I already have ED, losing libido isn't a concern for me.

Caber doesn't work for deca dick because there is a misconception that the nors (deca/tren) raise prolactin when they do not. They are progestins and progestins by nature cannot raise prolactin. I have an article on this, but I'm too new for the system to let me post links. At any rate, studies with bloodwork will confirm this.

They can however, affect E2 even though they do not aromatize, so having some potent anti-Es on hand is a good thing. An AI simply may not be up to the task. With the right ratio of E2 in the mix, you can keep your libido. Test/Deca at 400/400 will work well. Just keep your E2 in check.

It's good to see you over here, Burly.

You nailed it here as well. Prolactin and Progesterone cannot cause gyno unless there is a hormonal environment already present with an excessive imbalance of E2. There is plenty of evidence to support that. Progesterone and Prolactin are both cofactors in the equation and can add insult to injury, but the E2 is the dominant hormone needed for glandular growth and proliferation of actual ductal breast tissue. If you control/block E2, you will control your risk of developing it. I should mention that GH/IGF-1 also play a major cofactor role in gyno development as well.

I've said it for years and I'll say it again...Cabergoline/Dostinex is bad sh*t; and people should steer clear of it. Anytime you play around with a potent dopamine receptor agonist you need to fully understand the potential risks/side effects involved. Essentially, the guys that try to mitigate every potential side effect of a cycle are the ones that have major issues in the end. The hormonal milieu is so fragile that even minor mitigations can cause detrimental changes in the short/long term. Just a little bit can go a long way, and I would always advise when making changes or taking steps to mitigate issues to start small and titrate/adjust as needed. Control the estrogen, and all should be well.

I absolutely agree that 400/400 should work out just fine as long as he keeps the E2 in check; not destroy it or allow it to become excessive . If all else fails at that point your would introduce a SERM and hit the problem directly by blocking E2 receptors in the breast tissue.




Here's an interesting little read to peruse:



PROGESTERONE AND PROLACTIN INDUCED GYNECOMASTIA


Before delving into this subject, I’d like to say first and foremost, that in users of anabolic/androgenic steroids (AAS) the first step in combating the development of gynecomastia, or male breast enlargement, is to eliminate the causative agent: the anabolic steroid. Drug-induced gynecomastia almost invariably resolves on its own when a person quits taking the drugs responsible for it, if caught before permanent fibrosis develops. Unfortunately, most AAS users don’t want to employ this simple approach, for obvious reasons, so the foregoing will all be under the assumption that a person wants to prevent or treat gyno and still continue steroid use.

In the belief that certain anabolic steroids increase prolactin levels as well as act as agonists at the progesterone receptor, some have advocated the use of antiprolactin agents, like bromocriptine, or progesterone receptor blockers like RU-486 to treat AAS related gynecomastia, in lieu of more traditional drugs like tamoxifen.

In truth, the etiology of gynecomastia is unknown and a number of agents including estrogens, progestins, GH, IGF-1, and prolactin may be involved. However, most authorities believe that a decreased (T+DHT)/E ratio is central to the development of gyno, and that blocking the effects of estrogen, or increasing T + DHT levels, is central to ameliorating the problem.

Regarding prolactin, androgens decrease prolactin levels whereas estrogens increase prolactin. Non-aromatizing androgens have never been shown to elevate prolactin levels in humans, but testosterone has, due to its aromatization to estradiol (19). Prolactin secreting tumors, or prolactinomas, are often associated with gyno. But in these cases the prolactin is believed to induce gyno by suppressing testosterone production: “Prolactinomas that are sufficiently large to cause gynecomastia do so as a result of impairment of gonadotropin secretion and secondary hypogonadism”. (20). However, this is a moot issue in AAS users whose gonadotropin secretion is already blunted.

According to research cited in (20), prolactin may have a direct stimulatory effect on mammary tissue development, but only in the presence of high estrogen levels:


The presence of mild hyperprolactinaemia is therefore not uncommon in patients with estrogen excess. Significant primary hyperprolactinaemia, on the other hand, may directly stimulate epithelial cell proliferation in an estrogen-primed breast, causing epithelial cell proliferation and gynaecomastia.

So rather than focusing solely on lowering prolactin levels which may be elevated in users of aromatizing androgens, attacking estrogen should be the first line of action.

GH and IGF-1 are considered critical to the proliferation of mammary tissue. An excellent review of the role played by these hormones, as well as a general overview of gynecomastia can be found here:




Since elevated GH and IGF-1 are considered important to the anabolic effect of AAS, it would be impractical and counterproductive to attempt to prevent gynecomastia by blocking GH/IGF.

Progesterone acts in concert with estrogen to promote breast development, and at least part of any role played by synthetic progestins may be to stimulate IGF-1 production in the breast. But again, blocking the action of progesterone or synthetic progestins is not practical. Specific progesterone receptor antagonists like RU-486 block not only the progesterone receptor, but the androgen receptor as well, and have actually been associated with the development of gynecomastia (21). In any case, progesterone is thought to act on the breast to enhance the effects of estrogen (22) so once again, attacking estrogen is the easiest and most logical approach.

DHT gel (Andractim) or a generic knockoff might help as well. DHT is thought to act as an aromatase inhibitor (23) and perhaps compete directly with estrogen for binding at the estrogen receptor (24). DHT has been used in several case reports and controlled trials to successfully treat gynecomastia. So perhaps a viable strategy would be to combine DHT gel with tamoxifen. I would recommend tamoxifen rather than an aromatase inhibitor due to the simple fact that tamoxifen has been widely used in numerous controlled studies to succesfully treat gynecomastia, whereas the evidence to support the efficacy of aromatase inhibitors is scanty at best. -DZM

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(6) Mystkowski P, Seeley RJ, Hahn TM, Baskin DG, Havel PJ, Matsumoto AM, Wilkinson CW, Pea****-Kinzig K, Blake KA, Schwartz MW. J Neurosci 2000 Nov 15;20(22):8637-42

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(9) Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, Chua Teco GN J Clin Endocrinol Metab 1975 Jul;41(1):70-80

(10) Liva SM, Voskuhl RR J Immunol 2001 Aug 15;167(4):2060-7

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[Trauma1]

Caber increases libido because it lowers prolactin, whether or not you are on a cycle. But you are mixing up prolactin with progestin. Caber DOES lower prolactin, but Deca is a progestin. Prolactin and progesterone are two entirely different hormones with different actions. The "caber for progestins" is brolore that goes against science, I'm afraid. You CAN use caber on a deca cycle, but if it does work, it works for the wrong reasons. It is better to attack the off balance hormones to solve the problem of libido AND gyno at the same time.

Exactly!

Broscience has become so rampant on these boards over the years that the battle with actual scientific fact(s) was sadly over before it even began.

Hearsay is this generations "science"...



-T1

[HollywoodHam]

i want to thank everyone for the imformation. as a result, im going to just save the deca for another time and run test cyp and see how i do with that.

[burlyman]

i want to thank everyone for the imformation. as a result, im going to just save the deca for another time and run test cyp and see how i do with that.

You don't want it to go bad....send it my way

[HollywoodHam]

haha

You don't want it to go bad....send it my way

[Trauma1]

i want to thank everyone for the imformation. as a result, im going to just save the deca for another time and run test cyp and see how i do with that.

Good to hear. It's always best to discern how you react to one compound before adding in another to stack. You'll have plenty of great gains with the Test Cyp itself for a first cycle.

Good luck!



-T1