prop/tren cycle questions

[JimmySidewalk]

Age:25
Height: 5.9
Weight: 220
Bf unknown but not very high because i tend to keep lean
Training for about 6 years
4 cycles under my belt

I want to try tren in a cycle. It would be the first time with tren.
1-8 100mg prop ED
1-6(or 7) 37.5mg tren a ED

Followed by PCT with clomid and nolva.
Diet is in check at least 300g protein/day.

Because i can only find Nolva and clomid where i currently am, i was thinking of takin a dose of nolva ED to keep the estrogen down and avoid progesterone gyno. What would that dose be ? 10mg ED ? 20mg ED ?

Another alternative would be 50mg prop ED and 50mg tren ED but i was thinkin since its my first time with tren a smaller dose would be better and to keep test dosage bigger than tren to avoid libido issues.
What do you guys think, which would be better ?

Also, are the sweats really that bad ? I was planning this as a summer cycle, and i usually sweat alot during summer.

If you have any advice to give, shoot away, i'm all ears.

[Lemonada8]

i would go 75 test 100 tren, assuming everything is good to go ( diet, etc)
If libido is bad up test, if tren sides are bad lower tren. You typically have more progesterone on ur body than test, and tren is a potent protestin. So run a good minimal dose of test to stack with tren and you should be good. Run the tren higher because it is a progestin, it somewhat acts like a progesterone. You are going to be suppressing those hormones anyways, might as well add in a progestin, but you need to add it in at correct ratios to make it maximal efective. those exact ratios are yet to be foudn but it is foudn that tren higher than test in moderation is better than test higher than tren.
use HCG during cyce 500 2x week. if you are having prolactin gyno, then ur lactating. Dont take nolva, take some supplement L-dopa and vit b6 along with lowering dose a touch Lower the hcg to 250iu 2x week. Easy to do with short esters. If that doesnt help, or u dont wanna lower it then look for some bromo/caber to control it, but continue with the L-dopa and vit b6.
if its regular gyno with no other estro issues, (bloat, acne) the go with Nolva. start at 20mg ed if its already there, 10mg ed preventive if ur prone. dont go higher than 40mg ED(20mg morn/20 night) of nolva if gyno doesnt change. Look for Tore or rolaxifen if it is workign but need a higher dose.
Look into a AI if u have uncontrollable acne, bloat, etc. But know tren has similar sides and some AI's dont mix well with tren.
Nolva/clomid is a good PCT
use 1000iu on first day of HCG
40/40/20/20 nolva
100/100/50/50 clomid

good luck play safe!

[JimmySidewalk]

I feel you, its just that 700mgs of tren per week sounds kinda big, beeing that i'm popping my tren cherry.
As i said, problem is i can only get nolva and clomid here, no hcg, no tore, caber, nothing. I can't wait for an online source because it takes too long and at the moment i'm kind of on the run from country to country with work.
That's why i'm trying to get around it with nolva and correct dosages.
Usually i dont have gyno, acnee or bloat problems from test. I could say i'm lucky. I get the atrofy but clomid kicks them right back, its very effective for me.


Thanks for the input !

[marcus300]

Your right keep the dosage down seeing that its your first run with tren, it can be very. harsh for some. I would go with 50mgs prop and 50mgs tren ED and see how things are. You can also fight gyno caused by progesterone by taking tamoxifen, progeterone is caused by response to the estrogen receptor and tamoxifen down regulates the estrogen receptor in the breast tissue, so to control progesterone related sides take tamoxifen. But if you already have issues with proesterone take caber etc to reduce these symptoms but prevention look at tamoxifen.

[marcus300]

Read this what was posted by D7M, it will explain it in detail for you:


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

[JimmySidewalk]

Thank you for the info marcus, i have already read the article you posted above in another topic. That's why i was asking in the first place dosage for nolva on cycle in order to keep estrogen down mainly for the tren, because i'm really not prone to gyno from test. In a just test cycle i wouldnt take nolva, but beeing that i'm introducing tren.. i want to be able to control possible gyno. So... what dosage ? How much nolva ED on cycle , 10mg or 20mg ? I'm looking to prevent because its next to impossible for me to find caber

[marcus300]

You could use either an AI or a SERM to control estrogen, but the author does recommend Nolva, try 10mgs and see how that goes.

[JimmySidewalk]

Would it be wrong if i would go 100mg prop and 50mg tren a ? I want to have more test because i want to avoid libido problems and also i get minimal sides(if any) from test.

If i do this, should i go with 20mg nolva ED throughout the cycle or should i start with 10mg then up only if needed ? I would want to prevent gyno rather than fight it on cycle with higher doses of nolva and God forbid its prolactin induced cause i have nothing for that type of gyno.

Opinions ?

[baseline_9]

Just run them at between 50 and 75mg ED (both)

Your lifting you test to a higher level than it is currently at and from what I have read you should not get any ED problems...

As for the Nolva 20 my sounds high.... Use 10mg and see how you get on...

If I was you I would seriously look into getting an AI and some caber or bromo before you begin this cycle....

Don't rush in and be un-prepared, have everything on hand so your ready for anything that may come up....

[JimmySidewalk]

Ok so i started the cycle. I wanted to come back with feedback using the theory that marcus posted about using nolva/tamo to keep estrogen under control as to avoid any kind of gyno. I started on 10mg per day but i started getting puffy nipps, more than usually normal, without any knots though. Because i have no anti-progesterone induced gyno medicine i upped the dose of nolva in order to avoid problems and it seems that the 20mg per day marker is best, at least for me.

I'll keep you posted on how it goes.

[songdog]

Running a high amount of test when running a 19nor doesnt guarantee you wont have ED.I run 300mg test 580 tren.NO ED.I just ran 300 npp 600 test.I got ED big time.Nothing is written in stone.Thats all myth.Good luck and get some Viagra just in case.