Arimidex is too low. 0.5mg eod.
Also use an AI during PCT as estro will be pretty high.

1-12 Testosterone Enthanate 600mg
1-4 Dianabol 30mg
2-14 HCG 600IU
1-12 Arimidex .25mg twice a week (will adjust if needed)
15-18 Nolvadex 40/20/20/20
15-18 Clomid 100/50/50/50

Thanks for the responses guys.
Heavy, should I just run the Adex straight through from weeks 1 to 18 then you think?
Depending on what Im taking, I run it 1-12 0.5mg
Inzer Advanced
(Pump till you Puke).


Estro is only blocked in certain tissues with SERM's. High circulating estro causes bloat which leads to high BP and female pattern fat distribution not to mention low libido.
Take your AI's guys. Aromasin is preferred as there will be less chance for estro rebound when it is discontinued.


Yup, low or High estradiol can cause libido issues especially if free T is not in a proper ratio to Estradiol. 10-25pg/ml Estradiol usually will maintain libido IF free T is high.
Aromasin is a suicidal aromatase inhibitor so once it attaches to the aromatase enzyme it permanentaly deactivates it therefore estro rebound is unlikely. Arimidex only attaches to the enzyme while the drug is in your system. Once you stop taking Arimidex it detaches from the aromatase enzyme potentially flooding your body with estro so some guys taper when using Arimidex. With Aromasin you don't have to sweat it. Aromasin reduces circulating estro about 62% in MALE applications and Arimidex about 50%. Aromasin is obviously superior but not too strong.
The following studies clearly show estradiol increases with either SERM;
Hormonal changes in tamoxifen treated men with idiopathic oligozoospermia.
Hampl R, Heresová J, Lachman M, Sulcová J, Stárka L.
Research Institute of Endocrinology, Prague/Czechoslovakia.
Three months of tamoxifen treatment of 43 men with idiopathic oligozoospermia, out of which 20 completed the study, resulted in a significant enhancement of sperm motility, but the improvement of sperm parameters was in no relation to the FSH response to short time tamoxifen treatment. There was a significant increase of testosterone, estradiol, LH, FSH, SHBG, 17 alpha-hydroxy-progesterone and also of 11 beta-hydroxyandrostenedione, an androgen of exclusively adrenal origin, during the treatment and (with the exception of the latter), on the first week after discontinuation of the therapy. Significantly elevated testosterone and SHBG concentrations were retained still 9 weeks after finishing of the therapy. The results confirm that tamoxifen treatment provides conditions more favourable for conception and demonstrate that also adrenal steroidogenesis is positively influenced by this antiestrogen.
PMID: 3243340 [PubMed - indexed for MEDLINE]
Recovery of persistent hypogonadism by clomiphene in males with prolactinomas under dopamine agonist treatment.
Ribeiro RS, Abucham J.
Division of Endocrinology, Department of Medicine, Escola Paulista de Medicina, Universidade Federal de São Paulo, Rua Pedro de Toledo, 910. São Paulo 04039-002, Brasil.
CONTEXT: Persistence of hypogonadism is common in male patients with prolactinomas under dopamine agonist (DA) treatment. Conventional therapy with testosterone causes undesirable fluctuations in serum testosterone levels and inhibition of spermatogenesis.
OBJECTIVE: To evaluate the use of clomiphene as a treatment for persistent hypogonadism in males with prolactinomas. DESIGN: Open label, single-arm, prospective trial.
PATIENTS: Fourteen adult hypogonadal males (testosterone <300 ng/dl and low/normal LH) with prolactinomas on DA, including seven with high prolactin (range: 29-1255 microg/l; median: 101 microg/l) despite maximal doses of DA. INTERVENTION: Clomiphene (50 mg/day orally) for 12 weeks. MEASURES: Testosterone, estradiol, LH, FSH, and prolactin were measured before and 10 days, 4, 8, and 12 weeks after clomiphene. Erectile function, sperm analysis, body composition, and metabolic profiles were evaluated before and after clomiphene.
RESULTS: Ten patients (71%), five hyperprolactinemic and two normoprolactinemic, responded to clomiphene (testosterone >300 ng/dl). Testosterone levels increased from 201+/-22 to 457+/-37 ng/dl, 436+/-52, and 440+/-47 ng/dl at 4, 8, and 12 weeks respectively (0.001<P<0.01). Estradiol increased significantly and peaked at 12 weeks. LH increased from 1.7+/-0.4 to 6.2+/-2.0 IU/l, 4.5+/-0.7, and 4.6+/-0.7 IU/l at 4, 8, and 12 weeks respectively (0.001<P<0.05). FSH levels increased in a similar fashion. Prolactin levels remained unchanged. Erectile function improved (P<0.05) and sperm motility increased (P<0.05) in all six patients with asthenospermia before clomiphene.
CONCLUSIONS: Clomiphene restores normal testosterone levels and improves sperm motility in most male patients with prolactinomas and persistent hypogonadism under DA therapy. Recovery of gonadal function by clomiphene is independent of prolactin levels.
PMID: 19359408 [PubMed - indexed for MEDLINE]

I heard this from a MIT proffessor so I believe it, and ive used this method and my blood work from my endo showed it to be effective.
During PCT the circulating Estro actually benifits for the rebound of test. The body wants to maintain homostasis, if test levels are high then estro raises, and if estro levels are high then test raises ( in males). The serm blocks the negative effects from the estro, while its blocked the HPTA still knows its there, so in theory ( or personnel experimentation) the body will react by raising test levels to compete with the estro.
BUT!!!!!!! AI's should be used during pct bridging the end of pct, after the excess estro has aided in rebounding test levels around about week 3 the AI should be added. The AI should be tapered down during a 3 weeks period, to reduce estrogen to accepted normal levels. Aromasin is prefferable since its milder than adex and letro hence not causing a rebound effect unless used in extreme doses.


A SERM attaches to the estrogen receptor which makes the body think it has high Estro which it does NOT. Then more T is produced. In other words SERM's do not directly raise Estro. The problem is a SERM raises T and then that T aromatizes to Estro. The higher the SERM raises T the more aromatase activity to Estro. That Estro then causes problems in the male body EXCEPT where the SERM blocks its action. These problems include bloat/high BP/libido isssues/fat deposits etc. Remember a SERM is selective in which tissues estrogen is blocked. If an AI is employed alongside a SERM you will eliminate the aromatase activity which means T stays high and estro controlled within normal ranges for a male. Some men have more or less aromatase activity than others so some men may not need much AI during SERM treatment.
Aromasin is about 12% stronger than Arimidex at controlling aromatase activity.
I have seen a number of labs durning SERM treatment and Estro is above normal limits for males. Next time you run a SERM get labs and see for yourself. Keep in mind Estro above normal ranges for men is not good.


I never heard or read that. Are you saying the fraction that would be bound is now unbound or are you talking compensatory aromatization of androgens to estrogens.. or something else?
Edit: Ok I see your above post. I don't know if the whole situation is that dramatic.


Yes, the rise in testosterone from the serm causes a significant rise in estradiol. I posted a few abstracts above that prove that. Also HCG will aromatize and can cause significant rises in estradiol. If you read the op's first post he is running both Serms and HCG. Perfect combo for huge rises in estradiol which means he needs an AI preferrably a suicidal inhibitor.

I wasnt saying that aromasin was weaker, but its milder on the lipids, and increases IGF which will help maintain gains. And it doesnt seem to have the blacklash effects that letro or adex does.
Also Test levels are not fully recovered after pct, it just brings you back up to base line. Im not arguing against you Heavy Iron, just kinda relaying the point from a average joe perspective. But i dont believe that AI's should be run at the very begining of pct, since your coming off of the hormones test levels are bottomed out, which is one of the reasons that we use SERMS to block the Estro from specific tissues which cause adverse effects, But the high estro levels that were caused by the excess hormone levels do help the body jump start test production along with the SERM. I think that the excess estro levels out live there purpose after the second week, thats when ive added the AI or during the 3rd week just depends on the serm im using. This is mearly from my experience after reading the Proffesors post, ive used this method with great success and minimal adverse effects, i also dont use HCG because i dont seem to get testicular shrinkage, im not saying that it wouldnt benifit me to use HCG i just dont seem to need it. I get my blood work done every other month from my endo, most of the time it comes back good, unless she feels the need to agrue my AAS use.
I agree the OP needs an AI during his pct though, he might wanna watch out for leaky nips too, ive heard a few HCG horror storys.
Once again not arguing against you, just at a different angle.


Yeah, I hear you I just am not a fan of excessive estradiol in mens body's.
btw, testicle size has very little to do with determining intratesticular testosterone levels. The leydig cells (the cells that produce testosterone) only make up about 10% of total testes size. Theoretically your balls could be completely incapable of making T and only be shrunk 10%.


Yeah, like heavy said...Adex is too low.
Also, I wouldn't run the dbol at the tail, up front like you said. I'd also bump the HCG up just a bit, closer to 800-1000 iu per week.
And lastly your clomid, I always take 300mg the first day and taper off both the clomid and nolva (if I'm using it). Last week of nolva, take 10mg ed. IMHO. Good luck.
/V

Great info as always guys.
I'm thinking I'm going to go with Aromasin instead. Dosing reccomendations?
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