ending Dbol, Cyp, eq cyle

[Metal1877]

Just curious on a little feedback on a current cycle i have been doing. 1st 4 weeks dbol at 30 mg, 750 cyp a week, 500 eq for 10 weeks. Then i am finishing another 8 weeks at 1000mg cyp. I know this may not seem conventional to most. Just curious what some more experienced members input would be on this.

[songdog]

Not the best cycle I have seen.But not the worst either.How many cycles have you ran?

[Metal1877]

I have ran quite a few i would say 7 or 8 over the years. I understand it's not the best by any means. Just looking for as much bulk over the next 8 weeks i can get. i opted for eq because deca was scarce as that would have been my choice. Eq i am not a fan of at all. Instead of adding something else at the end, i have always responded great to test alone. So i wanted to see what i could achieve at 1000 mg the last 8 weeks, Also i am considering the last 4 weeks tossing in some inject dbol at probably 75 to 100 mg every 2 or 3 days. As the half life if i am correct is about 48 to 72 hours with inject rather than pill

[MickeyKnox]

Your EQ is a waste at that amount and too short a duration. And then Cyp @ 1 gram for last 8 wks?

This is poorly planned out. Bulking is about your diet, not a convoluted cycle with a shopping cart of gear.

What's your PCT look like? Diet? AI? hCG?

[Metal1877]

I agree with the nature of the cycle and i completely agree with bulking being about diet as i have been a personal trainer running weight loss programs around the country for the past few years. Diet is the number one key... once i learned that i took my 6ft 170 lb frame to 195 very lean naturally. i had a misconception about eq and have no use for something that is a waste at 5 and 600 mg. Deca was my first choice but things fell through and i listened to someone that swore deca and eq were very similar. As far as a gram of test a week. Test has always worked wonders for me and i have yet to have any negative sides or need for AI. Pct is just 500 hcg eod for 2 weeks and 4 weeks nolva. Im sure this isn't the best and may be well flawed. That's why i am asking for some input.

[MickeyKnox]

Start with this..

Why It's Important To Run An AI

http://forums.steroid.com/showthread...o#.UMPClazX_ft

Then this..

Why HCG is So Important

http://forums.steroid.com/showthread....#.UIlhVWfX_ft

[Metal1877]

Thanks Mickey, i will check it out soon as i get in from work, heading out now. I appreciate the knowledge

[MickeyKnox]

And here's some light reading on PCT....Originally posted by JimmyInk'd


"The following explains why it is prudent to use BOTH nolvadex and clomid together in your PCT . It is by Dr Scally - probably the foremost expert in the United States on this topic."

Med Hypotheses. 2009 Jun;72(6):723-8. Epub 2009 Feb 23.

Anabolic steroid -induced hypogonadism--towards a unified hypothesis of anabolic steroid action.

Tan RS, Scally MC.

Source
HPT/Axis Inc., 1660 Beaconshire Road, Houston, TX 77077, USA.

Abstract

Anabolic steroid-induced hypogonadism (ASIH) is the functional incompetence of the testes with subnormal or impaired production of testosterone and/or spermatozoa due to administration of androgens or anabolic steroids . Anabolic-androgenic steroid (AAS), both prescription and nonprescription, use is a cause of ASIH. Current AAS use includes prescribing for wasting associated conditions. Nonprescription AAS use is also believed to lead to AAS dependency or addiction. Together these two uses account for more than four million males taking AAS in one form or another for a limited duration. While both of these uses deal with the effects of AAS administration they do not account for the period after AAS cessation. The signs and symptoms of ASIH directly impact the observation of an increase in muscle mass and muscle strength from AAS administration and also reflect what is believed to demonstrate AAS dependency. More significantly, AAS prescribing after cessation adds the comorbid condition of hypogonadism to their already existing chronic illness. ASIH is critical towards any future planned use of AAS or similar compound to effect positive changes in muscle mass and muscle strength as well as an understanding for what has been termed anabolic steroid dependency. The further understanding and treatments that mitigate or prevent ASIH could contribute to androgen therapies for wasting associated diseases and stopping nonprescription AAS use. This paper proposes a unified hypothesis that the net effects for anabolic steroid administration must necessarily include the period after their cessation or ASIH.

PMID: 19231088 [PubMed - indexed for MEDLINE]

Future treatments:
A treatment goal of HPTA restoration will have its basis in the regulation and control of testosterone production. The HPTA has two components, both spermatogenesis and testosterone production.
In males, luteinizing hormone (LH) secretion by the pituitary positively stimulates testicular testosterone (T) production; follicle-stimulating hormone (FSH) stimulates testicular spermatozoa production. The pulsatile secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus stimulates LH and FSH secretion. In general, absent FSH, there is no spermatozoa production; absent LH, there is no testosterone production. Regulation of the secretion of GnRH, FSH, and LH occurs partially by the negative
feedback of testosterone and estradiol at the level of the hypothalamo-pituitary. Estradiol has a much larger, inhibitory effect than testosterone, being 200-fold more effective in suppressing LHsecretion [57–61].

In the case of ASIH, where the individual suffers from functional hypogonadism and the belief for eventual return of function, treatment is directed at HPTA restoration. A medical quandary for physicians presented with hypogonadal patients secondary to AAS administration is there is currently no FDA approved drug to restore
HPTA function. Standard treatment to this point has been testosterone replacement therapy (TRT), human chorionic gonadotropin (hCG ), conservative therapy (‘‘watchful waiting” or ‘‘do nothing”), or off-label prescribing of aromatase inhibitors or selective estrogen receptor modulators (SERM).

The primary drawback of testosterone replacement and hCG administration is that this therapy is infinite in nature. These treatments will remedy the signs and symptoms associated with hypogonadism, but do not alleviate the need for a life-long commitmentto therapy. Further, administration serves to further HPTA suppression.

Conservative therapy (‘‘watchful waiting” or ‘‘do nothing”) is the probably worst case option as this does nothing to treat the patient with ASIH. Also, conservative therapy will have the undesirable result of the nonprescription AAS user to return to AAS use as a means to avoid ASIH signs and symptoms.

The aromatase inhibitors demonstrate the ability to cause an elevation of the gonadotropins and secondarily serum testosterone [62]. The administration of SERMs is a common treatment in attempts to restore the HPTA because they increase LH secretion from the pituitary that leads to increased local testosterone production
[63–67].

Guay has used clomiphene citrate as therapy for erection dysfunction and secondary hypogonadism. Patients received clomiphene citrate 50 mg per day for 4 months in an attempt to raise their testosterone level [68]. Clomiphene has been reported in a case study to reverse andropause secondary to anabolic–androgenic steroid use [69]. The patient received clomiphene citrate 50 mg twice per day in an attempt to raise his testosterone level. The patient when followed up after two months had a relapse,
tiredness and loss of libido, after discontinuing clomiphene citrate. There are case study reports demonstrating the effectiveness of the combination of clomiphene and tamoxifen in HPTA restoration after stopping AAS administration [70–73].
Clomiphene is a mixture of the trans (enclomiphene) and is (zuclomiphene) enantiomers, which have opposite effects upon the estradiol receptor [74]. Enclomiphene is an estradiol antagonist, while zuclomiphene is an estradiol agonist. The addition of tamoxifen to clomiphene might be expected to increase the overall antagonism of the estradiol receptor.

This excerpt from an interview with Dr Scally probably explains it better - makes a lot of sense.

"Clomiphene is an antiestrogen, which decreases the estrogen effect in the body. It has a dual effect by stimulating the hypothalamic pituitary area and it has an antiestrogenic effect, so that it decreases the effect of estrogen in the body. Tamoxifen is more of a strict antiestrogen, it decreases the effect of estrogen in the body, and potentiates the action of clomiphene. Tamoxifen and clomiphene citrate compete with estrogen for estrogen receptor bind¬ing sites, thus eliminating excess estrogen circulation at the level of the hypothalamus and pituitary, allowing gonadotropin production to resume. Administering them together produces an elevation of LH and secondar¬ily gonadal sex hormones." Dr Michael Scally

[stpete]

Just curious on a little feedback on a current cycle i have been doing. 1st 4 weeks dbol at 30 mg, 750 cyp a week, 500 eq for 10 weeks. Then i am finishing another 8 weeks at 1000mg cyp. I know this may not seem conventional to most. Just curious what some more experienced members input would be on this.

I would just run the 1,000 from the get go. That's too much dbol at the end. 40-50 will be fine w/the test. I wouldn't be able to workout if i took that much dbol. The back pumps would kill me.

Forget the EQ and run a proper PCT like mentioned. I too get great gains from test alone.

Good Luck!!

[Metal1877]

Thanks guys for the info also thanks again Mickey because i learned a cpl things i had no clue about until i read what you sent. My question now is this, if eq is virtually useless at 5 to 600 mg a week then why is it so frowned upon to be running 1000 test? As its not really a shopping cart full of gear, especially when i see some using 4 and 5 different compounds on here the equal 2 grams or more?

[MickeyKnox]

There are a few compounds that require larger than average doses to produce desired results, and EQ is certainly one of them. Ideally, a small amount of test and approx 750mg EQ seems to work well in most cases.

But the argument is that if you require that much EQ, then youre better off choosing another compound and using less. Id be lying if i didn't agree with this.