6th cycle comments/critiques

[drewbrezzy]

Hello all just seeing what you guys think about my 6th cycle and if you would change anything.
my stats 23 5'8" 205lbs 7% bf just doing lean gains mostly

Week 1-12: test cyp 750mg
Week 1-12: Deca 600mg, for gains and joints my shoulder is messed up
week 1-12: Eq 500 or 600mg haven't decided yet
Week 8-12: Tren Ace 50mg ed
Week 8-12: Winny 50mg ed

Standard pct of clomid, and I will be running HCG through out. Have nolva on hand for the first part of the cycle incase of gyno. I know not to mix it with the tren. I'm not prone to gyno but just incase.
Gonna be eating 4500 Cal's clean around 300-310g of protein ed.

Look solid? Any suggestions or comments would be great.

Thanks a bunch bros

[The Bear 79]

23 & 5 cycles under ur belt?!?!? WOW!! R u aware of the risk of permanent damage 2 ur undeveloped Endocrine & HPTA that comes with cycling under the age of 25? I will admit, ur stats r pretty impressive, but @ wut cost bro???!!! I'd stop now & go c an Endocrinologist.

[drewbrezzy]

Yes I am, I have been under the care of a doctor since the first cycle.

[The Bear 79]

Yes I am, I have been under the care of a doctor since the first cycle.

Wut kind of Doc?

[drewbrezzy]

My primary care physician and endrocinologist

[Exilus]

Im 21 and on my 7th cycle and i still recover perfectly, even tough i'm probably just lucky...


thats a big cycle bro, thats over 2000mg of gear per week.

[The Bear 79]

Im 21 and on my 7th cycle and i still recover perfectly, even tough i'm probably just lucky...


thats a big cycle bro, thats over 2000mg of gear per week.

Mor brilliant encouragement from another desperately, impatient tike.........

[yeahbuddy289]

Exilus mirin them lats bro. You gotta PM me your back routine.

[Exilus]

i was not encouraging him, far from it.....Anyway i think 23 is a good age, SOME people have not finished their endocrine developpement until 25 but the big majority is done by 21-22....that 25 number is just a rule of thumb to be extra safe.

[rippedfromabove]

Im 21 and on my 7th cycle and i still recover perfectly, even tough i'm probably just lucky...

thats a big cycle bro, thats over 2000mg of gear per week.

When did you start juicing? Im just curious

[xelnaga]

@ Drew are you going to front load?

[Knockout_Power]

I really dont see any benefit of adding in 350/wk of tren for 4 weeks. All its really doing is adding more oil, more possible sides without being used long enough for any reasonable gains.

The EQ is one most would stay away from as its mainly just filler, but if you like it, go for it.

[markdbg]

i think you should run the cycle 15 weeks as ur running eq, run the 750 test, 600 eq the 15 weeks, add the tren A in at week 8 and run it till week 15. if your joints and shoulders is bad id drop the winni, save the stress on your liver/or up the tren dose to 75ed if u can handle it.

for pct run the nolva with the clomid, as you can still get gyno during pct, esp with long esters.you will really wanna get amiridex or another ai for on cycle with those doses you will need.

[drewbrezzy]

Thanks for the input guys, I will drop the winny run the cycle for the 15 weeks like you suggested and just do the tren for the last 8 weeks at 75mg ed.
I like the Eq for the appetite mainly and vascularity.
I will leave the orals out of this cycle, only thing I might consider is var but its hard to get a hold of around me

[Exilus]

at 19, 3x 2month cycles a year.

[jimmyinkedup]

i was not encouraging him, far from it.....Anyway i think 23 is a good age, SOME people have not finished their endocrine developpement until 25 but the big majority is done by 21-22....that 25 number is just a rule of thumb to be extra safe.

Im not trying to be argumentative here but I do want to clarify 1 FACT. Peak test production in males is proven to be at age 25 - a sure fire sign that hpta has fully developed and is working at its peak. Not 21,22 or 23.
The choice is a personal one of course - but if people are going to make it they should do so based on medical fact.

[jimmyinkedup]

Hello all just seeing what you guys think about my 6th cycle and if you would change anything.
my stats 23 5'8" 205lbs 7% bf just doing lean gains mostly

Week 1-12: test cyp 750mg
Week 1-12: Deca 600mg, for gains and joints my shoulder is messed up
week 1-12: Eq 500 or 600mg haven't decided yet
Week 8-12: Tren Ace 50mg ed
Week 8-12: Winny 50mg ed

Standard pct of clomid, and I will be running HCG through out. Have nolva on hand for the first part of the cycle incase of gyno. I know not to mix it with the tren. I'm not prone to gyno but just incase.
Gonna be eating 4500 Cal's clean around 300-310g of protein ed.

Look solid? Any suggestions or comments would be great.

Thanks a bunch bros

Lets talk a liitle about your last couple cycles and your past experiences with these compounds. I see several things i would change (honestly i wouldnt be and wasnt cycling at your age ) - things that could lead to very bad effects.
Also have you paid any heed to the " time off=time on + pct " ?

[jimmyinkedup]

You should read this, then use what u learn to make some changes:

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.
References:

(1) Price TM, O'Brien SN, Welter BH, George R, Anandjiwala J, Kilgore M. Am J Obstet Gynecol 1998 Jan;178(1 Pt 1):101-7

(2) Bjorntorp P. Hum Reprod 1997 Oct;12 Suppl 1:21-5

(3) Ramirez ME, McMurry MP, Wiebke GA, Felten KJ, Ren K, Meikle AW, Iverius PH Metabolism 1997 Feb;46(2):179-85

(4) Zmuda JM, Fahrenbach MC, Younkin BT, Bausserman LL, Terry RB, Catlin DH, Thompson PD. Metabolism 1993 Apr;42(4):446-50

(5) Tomita T, Yonekura I, Okada T, Hayashi E
Horm Metab Res 1984 Oct;16(10):525-8

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

(7) Greer,M. N Engl J Med 244:385, 1951

(8) Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH. N Engl J Med 1975 Oct 2;293(14):681-4

(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

(11) Ulloa-Aguirre A, Blizzard RM, Garcia-Rubi E, Rogol AD, Link K, Christie CM, Johnson ML, Veldhuis J Clin Endocrinol Metab 1990 Oct;71(4):846-54

(12) Hochman IH, Laron Z Horm Metab Res 1970 Sep;2(5):260-4
.
(13) Steinetz BG, Giannina T, Butler M, Popick F
Endocrinology 1972 May;90(5):1396-8

(14) Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ.
Am J Physiol Endocrinol Metab 2002 Mar;282(3):E601-7

(15) Sheffield-Moore M, Urban RJ, Wolf SE, Jiang J, Catlin DH, Herndon DN, Wolfe RR,
Ferrando AA
J Clin Endocrinol Metab 1999 Aug;84(8):2705-11

(16) Doumit ME, Cook DR, Merkel RA..Endocrinology 1996 Apr;137(4):1385-94

(17) Bricout VA, Germain PS, Serrurier BD, Guezennec CY.Cell Mol Biol (Noisy-le-grand) 1994 May;40(3):291-4

(18) Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ.
Am J Physiol Endocrinol Metab 2002 Mar;282(3):E601-7

(19) Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F
Acta Endocrinol (Copenh) 1984 Feb;105(2):167-72

(20) Ismail AA, Barth JH.Ann Clin Biochem 2001 Nov;38(Pt 6):596-607

(21) Grunberg SM, Weiss MH, Spitz IM, Ahmadi J, Sadun A, Russell CA, Lucci L, Stevenson LL J Neurosurg 1991 Jun;74(6):861-6

(22) Nomura K, Suzuki H, Saji M, Horiba N, Ujihara M, Tsushima T, Demura H, Shizume K
J Clin Endocrinol Metab 1988 Jan;66(1):230-2

(23) Perel E, Stolee KH, Kharlip L, Blackstein ME, Killinger DW
J Clin Endocrinol Metab 1984 Mar;58(3):467-72

(24) Casey RW, Wilson JD.
J Clin Invest 1984 Dec;74(6):2272-8

[drewbrezzy]

Jimmy I have had ran a plain test cycle for my first 500mg a week 12 weeks
second cycle dbol 30mg ed week 1-4 and test 500mg weekly 1-12
third cycle test 500mg week 1-12 and Deca 400mg 1-12
Fourth cycle test 500mg week 1-12 Deca 400mg 1-12
Fifth cycle test 750mg week 1-12 Deca 400mg 1-12 and Eq 400mg 1-12 and tren 75mg ed 6-12

And like I said I have been under the care of doctors I respect your opinion very much and concern. I don't want to to come off as an ass or anything but I can't revert the cycles I've done so i would just like to see what you would change.

And Jimmy yes I do time off + time on and pct. I would like to know what you would change seeing as you have a lot of experience with cycling . Again I don't want to sound like an ass or condescending I really do value your opinion and input but seeing as I'm already cycling I would like the best advice for this.