Help with Test E, Deca, DBol cycle

[Hbaz2k]

I am planning my third cycle, I am 25 and have previously done 2 cycles, 1x bulking Sus + Deca and 1x cutting Test prop, Primo + Anavar and both cycles were fine with no sides.

For my third Cycle I plan to run
Test E 750mg wk 1-12
Deca 450mg wk 1-10
DBol 45mg ED wk 1-4

I have read as much as possible and from what I have read the cycle looks fine but what I need help with is the PCT etc as there is conflicting advice about this and what should be used. What PCT should be used for this cycle? Should I take an AI during the cycle such as Arimidex? Should I run HCG through the cycle or/and with the PCT? I have some clomid + nolva left from previous cycles and 30 tabs of Med-Tech P.C.T (these contain clomid 25mg, tamoxifen 30mg and mesterolone 25 mg) I would like to use these PCT tablets with my PCT if possible although I know I have read some places not to use either clomid or nolva with Deca.

[Matt]

What are your stats

Age
Weight
Height
Bf%
Years Training???

[Honkey_Kong]

What are your stats? And don't you think 750mg of test E is a little hefty for a 3rd cycle?

[Hbaz2k]

Age - 25
Weight - 210 LB
Height - 6 FT
Bf% - 15%
Years Training - 3 Years

What are your stats? And don't you think 750mg of test E is a little hefty for a 3rd cycle?

From what I have read on other sites people have said 750mg of test E should be fine and advised others to go for this amount while using deca due to deca sides and keping test in proportion to the amount of deca. My first cycle was 500mg sus 300mg Deca and I had no sides.

[Honkey_Kong]

For your pct, you should look in to caber. Reason is that deca is a 19nor steroid, and that will raise your prolactin levels.

[Matt]

For your pct, I wouldn't take nolva. Reason is that deca is a 19nor steroid, and that will raise your prolactin levels. You should look it to clomid and caber.

Would you mind showing me some sort of evidence to back this statement up????

[songdog]

Well I can agree with you about wat some other sites say they run.I seen it but I cant understand why.You dont need that much test 500mg will be fine.Deca is fine I would run the Dball at 30mg.You need nova and Clomid for your pct.Read the PCT section Swiftos 2nd to none on that.There is a lot of BS about cycles out there.But this is a NO FLY ZONE no BS here.We dont advise high dose cycles.

[Honkey_Kong]

Would you mind showing me some sort of evidence to back this statement up????

The profile on steroids.com for nandrolone does say it raises prolactin levels.

http://www.steroid.com/Nandrolone.php

Now as far as the effectiveness of tamoxifen goes:

Previous investigations of animal treated with a variety of classical antiestrogenic compounds such as tamoxifen and its derivatives have also shown little or no changes in the expression of estrogen and progesterone receptors in their mammary tissue after treatment [31].

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1940067/

And in a study about lowering prolactin levels.

In conclusion, the results of the present paper showed that tamoxifen reduced estrogen-stimulated prolactin levels in some, but not in other hormonal conditions and that these effects were not mediated by an inhibition of lactotroph cell growth.

http://www.ncbi.nlm.nih.gov/pubmed/8...?log$=activity

That's why I suggest a drug like cabergoline.

[lovbyts]

Age - 25
Weight - 210 LB
Height - 6 FT
Bf% - 15%
Years Training - 3 Years



From what I have read on other sites people have said 750mg of test E should be fine and advised others to go for this amount while using deca due to deca sides and keping test in proportion to the amount of deca. My first cycle was 500mg sus 300mg Deca and I had no sides.

Old school thinking that you need more test than deca, not true. Keep your test up to a normal or high level and you wont have the dreded Deca d*ck. Raising your test to much gives you more chance of more sides from the test but you wont know if it's due to test or deca or what is doing the work/building, the test or deca.

If you want to use deca then drop your test down to 500 and let the deca do the work and see how it goes.

[Matt]

The profile on steroids.com for nandrolone does say it raises prolactin levels.

http://www.steroid.com/Nandrolone.php

Now as far as the effectiveness of tamoxifen goes:



Previous investigations of animal treated with a variety of classical antiestrogenic compounds such as tamoxifen and its derivatives have also shown little or no changes in the expression of estrogen and progesterone receptors in their mammary tissue after treatment [31].

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1940067/

And in a study about lowering prolactin levels.

In conclusion, the results of the present paper showed that tamoxifen reduced estrogen-stimulated prolactin levels in some, but not in other hormonal conditions and that these effects were not mediated by an inhibition of lactotroph cell growth.

http://www.ncbi.nlm.nih.gov/pubmed/8...?log$=activity

That's why I suggest a drug like cabergoline.

Yes we know deca can raise prolactin levels, but as yet you havn't shown any evidence to say that the use of nolva in healthy males will also help raise or make worse prolactin induced gyno???

[Honkey_Kong]

Yes we know deca can raise prolactin levels, but as yet you havn't shown any evidence to say that the use of nolva in healthy males will also help raise or make worse prolactin induced gyno???

Upon further research, I was unable to find evidence that will raise or worsen prolactin induced gyno. However; I've found a few studies that found tamoxifen ineffective at reducing prolactin. So I would still stand behind my recommendation of caber, but I'll take back my anti-tamoxifen argument.



Comparison of tamoxifen and testosterone propionate in male rats: differential prevention of orchidectomy effects on sex organs, bone mass, growth, and the growth hormone-IGF-I axis.
Author(s): Fitts, James M; Klein, Robert M; Powers, C Andrew
Source: Journal of andrology Volume: 25 Issue: 4 Pages: 523-34 Published: 2004 Jul-Aug
[ PubMed Related Articles ]
Abstract: Testis dysfunction can weaken bone and reduce muscle mass as well as impair sexual function. Testosterone (T) therapy has useful effects on sex organs, bone, and muscle in T-deficient males, but prostate concerns can preclude T use in some men. Although estrogens or other drugs can protect bone in men, gynecomastia makes estrogens unappealing, and other drugs may also be undesirable in some cases. Selective estrogen receptor modulators (SERMs) inhibit estrogen-evoked sex organ growth but mimic estrogen effects on bone and cholesterol and are advantageous for some women. SERMs may also be useful in men who must avoid androgens. As a preclinical test of this idea, tamoxifen (a SERM) and testosterone propionate (TP, a classic androgen) were compared for their efficacy in preventing varied effects of orchidectomy (ORX) in adult male rats. ORX led to ventral prostate and seminal vesicle atrophy and decreases in somatic growth, proximal tibia bone mineral density (BMD), and serum growth hormone (GH) and insulin-like growth factor I (IGF-I). ORX also increased anterior pituitary glandular kallikrein, serum cholesterol, and body temperature. Pituitary prolactin (PRL) content was unaltered. ORX effects on sex organs, somatic growth, IGF-I, cholesterol, body temperature, and pituitary kallikrein were prevented by TP at 1 mg/kg (3 doses per week), but BMD and GH were unresponsive. ORX effects on BMD and GH were prevented by TP at 10 mg/kg, but this dose evoked supraphysiologic increases in sex organs and PRL, failed to restore somatic growth, and further reduced IGF-I. Tamoxifen (1 mg/kg daily) prevented ORX effects on BMD, GH, and cholesterol without altering basal or TP-induced sex organ growth and further reduced IGF-I and somatic growth. Tamoxifen did not alter basal PRL but blocked increases caused by TP at 10 mg/kg. In summary, tamoxifen prevented ORX effects on bone and cholesterol in male rats without affecting sex organs or PRL and might be useful for men who must avoid androgens. Unexpectedly, a TP dose that replicated testis effects on sex organs and other targets had no effect on BMD or GH, and a larger TP dose that restored BMD and GH was worse at replicating normal male physiology. In addition, correlation/regression results suggested that the GH-IGF-I axis contributes to changes in BMD.

[Matt]

How about giving this a read, thanks to D7M...


Progesterone and prolactin induced gynecomastia
More from Nandi....

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.

[jelly]

^^^ Good stuff.

Matt, i was going to us Arimidex only for use during my cycle. Do you think I should run both Adex AND Tamox?

[Matt]

Whats your cycle mate??^^

[jelly]

Dbol @30-50mg for first 4-6 weeks (havent decided amount or duration yet)
Clen first 2 weeks and 5th and 6th week.
T3 first 6 weeks
Test E @500mg for 12 weeks

[Matt]

^^ You will be fine with just armidex mate..

Nolva is very good at prevention and reversal however if you keep you estrogen in check from the start then you should have no issues...

[Hbaz2k]

Thanks for all the information/help I have now read the threads on PCT and HCG by swifty and they were very helpfull, I have decided to drop the test dose down as you guys have suggested. The only question I have now which may seem stupid/obvious but I cant find the answer anywhere and want to clarify before starting the cycle, is HCG injected into muscle? Also can HCG be mixed in the same syringe as the Test E and Deca? I understand it has to be pre mixed with bac water and then refrigerated first. Also when into my cycle do I start taking HCG? Do I take it from the first week? I will also be taking Arimidex at 0.5mg EOD when into the cycle do i start to take this?

[jelly]

200iu to 250iu twice a week. Many recommend 250iu twice a week, but I play it safe and use 200iu twice a week. i'm afraid of burning out my LD receptors. The time at which you start hcg depends on the compounds you are using and how fast they suppress or halt natural test production. I'm on dbol and test E right now and just started yesterday. I will probably start using hcg on my second injection of test (friday for me). If i was using test only id start on my third injection. If you are using something like deca durabolin at the beginning or throughout your cycle I would start using HCG the day of your first injection.

HCG is injected subcutaneously. This is in fat tissue, not muscle. There are plenty of videos on youtube of people injected HCG and tips from them. Some tips are better than others. I use insulin needles to do this and rotate from each side of my bellybutton. I usually inject HCG right after the test. I also try to keep them on the same side to keep things simple. An example of this is on Tuesday I inject test into my right ass cheek and inject HCG to the right of my bellybutton. Then on friday it will all be on the left side. Simple! Self injecting your ass is a pain in the ass, lol. But I'm used to it. It's a piece of cake to me now. You might get a slight burning sensation when injecting the hcg into fat tissue on your belly, this is normal.

Also, make sure you research the mixing protocol for HCG so you dont contaminate your stuff or screw up your concentrations. I usually mix 5000iu in 5ml of bacteriostatic water. That way I know that it is 1000iu/ml. The 100 mark on the insulin syringe is 1ml (also known as 1cc). So if I filled the syringe I would have 1000iu (at the 100 mark on an insulin syringe). So for 250iu i would fill the insulin syringe to the 25 mark or for 200iu the 20 mark.

Summary: Do NOT inject HCG into your muscle (you actually can, but I wont get into this). Do NOT mix it in a syringe with your test and deca. You don't have to refridgerate the HCG before using it. You STORE it in a refridgerator. When I first mix the HCG I inject it unrefridgerated then refridgerate it soon after. Since you are using deca (which will halt your natural test almost immediately) inject the HCG on day 1. Look up subcutaneous stomach injection proceedures on youtube to see how to do it visually.

Good luck!

[Hbaz2k]

I have started on the cycle above as planned
Test E 500mg
Deca 450mg
D-Bol 45mg ED
HCG 250IU twice a week
Arimidex .5mg EOD

I have now had 4 injections but have just been told that I have to work away for 2 weeks (this was completely un expected and I have only worked away once before with my job which was 3 years ago) I will be working Sat-Wed nights and stopping in a hotel, the hotel does have a gym. Am I right in thinking because of the life of Deca and Test E I will be fine injecting sat day and Thursday afternoon so that I do not have to take this away with me, can I do the same with HCG or does that need to be split more evenley for example the split I have been doing is injecting sat night and wednesday morning. I have a mini fridge that I probably will be taking with me due to the hotel having no fridge etc but if possible I would like to not inject away due to the possibility of the maids going in the fridge etc.

[iforged05]

Thats a hefty amount of test