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  1. #1
    Eminent is offline New Member
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    Second cycle advice plz deca/sust

    28 years old
    185
    5'11"
    12% BF
    First cycle was sust 250 once a week which didn't give me much of a gain I ran it low just to make sure I don't get any crazy side affects

    Starting second cycle sept 1st
    Deca 300/once a week and sust 250/twice a week. Can I expect good gains with this working out 6-7 days a week and putting in 4k-6k calories a day?
    Also what would you recommend for pct so I can order and have it ready now.
    Appreciate the advice

  2. #2
    TheClinch's Avatar
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    Quote Originally Posted by Eminent View Post
    28 years old
    185
    5'11"
    12% BF
    First cycle was sust 250 once a week which didn't give me much of a gain I ran it low just to make sure I don't get any crazy side affects

    Starting second cycle sept 1st
    Deca 300/once a week and sust 250/twice a week. Can I expect good gains how long are you running the compunds? with this working out 6-7 days a week and putting in 4k-6k calories a day? are you really getting 4-6k calories a day? doubtful bro. post up your intended diet.
    Also what would you recommend for pct so I can order and have it ready now. you should have nolvadex for controlling the estrogen during entire cycle, and you should have a prolactin agonist like dostinex incase you find you are succeptable to prolactin gyno even while using nolvadex.
    Appreciate the advice
    answers in bold.

    do you know what pct is?

  3. #3
    dec11's Avatar
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    Quote Originally Posted by TheClinch;5707***
    answers in bold.

    do you know what pct is?
    nolva wont 'control' estro, it stops it binding. what he wants is an AI which will control all on that cycle

  4. #4
    dec11's Avatar
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    Quote Originally Posted by Eminent View Post
    28 years old
    185
    5'11"
    12% BF
    First cycle was sust 250 once a week which didn't give me much of a gain I ran it low just to make sure I don't get any crazy side affects

    Starting second cycle sept 1st
    Deca 300/once a week and sust 250/twice a week. Can I expect good gains with this working out 6-7 days a week and putting in 4k-6k calories a day?
    Also what would you recommend for pct so I can order and have it ready now.
    Appreciate the advice
    i wouldnt go training 6-7 days pw, you'll over train and encourage injury, 3-4 days is plenty. rem you need good quality rest for CNS aswell as muscle

    pct:

    clomid 50/50/50/50/50
    nolva 20/20/20/20/20

    hcg 250iu's e3d while on cycle wouldnt hurt, deca can be a bitch to recover from

  5. #5
    TheClinch's Avatar
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    Quote Originally Posted by dec11 View Post
    nolva wont 'control' estro, it stops it binding. what he wants is an AI which will control all on that cycle
    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


    Originally written by D7M

    food for thought OP...

  6. #6
    ata1979's Avatar
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    You said in your first cycle you were worried about sides so you ran the sus at 250 week. Make sure you know what your getting into with the deca . Your 1st and 2nd cycle sound very similiar to mine except I also had Anavar in both of them. Your gonna love the deca, just saying make sure your ready for the sides cause they're alot heavier than Sus.

  7. #7
    Eminent is offline New Member
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    What kind of side affects did u get from deca 300 per week? An yes im aware of pct. So u prefer HCG and nolva durin my entire cycle?

  8. #8
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    Deca shut me down hard and also did a number on the hairline. But I must admit, I never felt better.
    Begin the PCT the last week or two of the cycle.

  9. #9
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    Quote Originally Posted by ata1979 View Post
    Deca shut me down hard and also did a number on the hairline. But I must admit, I never felt better.
    Begin the PCT the last week or two of the cycle.
    I didn't know deca was that harsh on hairline

  10. #10
    chuckt12345's Avatar
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    no do not start your pct the last wk or 2 or your cycle.

  11. #11
    TheClinch's Avatar
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    Deca is active in your system longer than Sustanon is... You could run the Sust two weeks longer than Deca then start pct two weeks after you stop the Sust. This would help to reduce the down time in pct recovery after using Deca.

  12. #12
    ata1979's Avatar
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    different roids effect diferent people in different ways. For me, deca was hard on the hair.

    @chuckt12345 I'm not the authority, but I would have started on my last week. please feel free to expand on when to start it and why.

  13. #13
    chuckt12345's Avatar
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    pct needs to be started when the test has cleared your system. With sust the acceptable time frame is like 18 days after last shot,, for me on cyp for example i wait about 3wks. If you start to early it really is not doing anything. Like thecinch said,, drop the deca a wk or 2 before the test also.

  14. #14
    TheClinch's Avatar
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    Quote Originally Posted by Eminent View Post
    What kind of side affects did u get from deca 300 per week? An yes im aware of pct. So u prefer HCG and nolva durin my entire cycle?
    Hcg will help to avoid testicular atrophy while on cycle. The thought behind this is that bigger bslls will help you bounce back with enough natural test to support the new mass sooner than atrophied testicles that also need to recover size as well as function.

    Refer to the article by D7M I posted above about gyno to understand why it is important to use Nolvadex the entire Deca cycle.

  15. #15
    Eminent is offline New Member
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    How much nolvadex /temoxifen should I run throughout my cycle? And did it shut u down completely? I don't think I can go 8-10 weeks without sex :/

  16. #16
    Eminent is offline New Member
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    Also the confusion I'm running into is if I'm doing hcg and nolva my entire cycle then what's left on my pct just add clomid 2 weeks after my last shot?

  17. #17
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    the artificial test will keep your sex drive through the roof,, if you run nolva during cycle i would go with 10mg a day.

  18. #18
    Eminent is offline New Member
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    Sorry if this is a dumb question but I was doing some shopping on ar-r and is "clomi" clomid on there? I alreadygot the tamoxifen (nolvadex )

  19. #19
    chuckt12345's Avatar
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    Quote Originally Posted by Eminent View Post
    Sorry if this is a dumb question but I was doing some shopping on ar-r and is "clomi" clomid on there? I alreadygot the tamoxifen (nolvadex)
    yes..

  20. #20
    Eminent is offline New Member
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    Alright appreciate the advice chuck

  21. #21
    dec11's Avatar
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    Quote Originally Posted by TheClinch View Post
    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


    Originally written by D7M

    food for thought OP...
    yep ive had tren induced gyno recently, adex cleared it right up, no need for that caber caper

  22. #22
    dec11's Avatar
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    Quote Originally Posted by TheClinch View Post
    Hcg will help to avoid testicular atrophy while on cycle. The thought behind this is that bigger bslls will help you bounce back with enough natural test to support the new mass sooner than atrophied testicles that also need to recover size as well as function.

    Refer to the article by D7M I posted above about gyno to understand why it is important to use Nolvadex the entire Deca cycle.
    clinch mate, you are barking up the wrong tree and would be best not advising unless you know what you're talking about, no offence intended.

    nolva stops it from binding and causing breast lumps, it will still be in the system causing shitty sides, im speaking from personal experience, i always used to use nolva for this reason, an AI is a much much better option as it controls and lowers estro.

    i had been using nolva on my last tren cycle for gyno symptoms, my gains stagnated around weeks 3-4, i had bloods done, my estro was sky high and once i went on adex i felt fantastic and gains exploded

  23. #23
    TheClinch's Avatar
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    Quote Originally Posted by dec11 View Post
    clinch mate, you are barking up the wrong tree and would be best not advising unless you know what you're talking about, no offence intended.

    nolva stops it from binding and causing breast lumps, it will still be in the system causing shitty sides, im speaking from personal experience, i always used to use nolva for this reason, an AI is a much much better option as it controls and lowers estro.

    i had been using nolva on my last tren cycle for gyno symptoms, my gains stagnated around weeks 3-4, i had bloods done, my estro was sky high and once i went on adex i felt fantastic and gains exploded
    Dec11 you are right that I do not advise from experience on this topic. I do take the advice from D7M as solid and undeniably reliable. My intention was to pass on D7M's knowledge about progesterone and prolactin related gyno to the OP.

    I agree with your point. Experience says a lot.

    Which AI are you using while on a 19nor cycle? At which dose?

    Thanks Dec

  24. #24
    dec11's Avatar
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    Quote Originally Posted by TheClinch View Post
    Dec11 you are right that I do not advise from experience on this topic. I do take the advice from D7M as solid and undeniably reliable. My intention was to pass on D7M's knowledge about progesterone and prolactin related gyno to the OP.

    I agree with your point. Experience says a lot.

    Which AI are you using while on a 19nor cycle? At which dose?

    Thanks Dec
    no probs mate. D7M put me onto the ai thing with 19nors (and indeed is a v knowledgeable chap) whereas before i thought caber etc was needed.

    after seeing my horrific blood report on estro, 630 when it shouldnt be higher than 150-160, (only was on 250mg test e and 350mg tren a) i went on adex at .5mgs eod and within 7 days lumps disappeared, no nipple itch and i felt x5 lighter on my feet, strength went through the roof and i started growing and putting on the lbs again. nolva should be used post adex as a rebound can occur on discontinuing it

    nolva only just barely kept things at bay for me on tren and deca cycles, adex was the biz and i wouldnt run them without it again. aromasin is an even better choice apparently, although i havent yet used it myself
    Last edited by dec11; 08-02-2011 at 09:27 PM.

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    Quote Originally Posted by dec11 View Post
    no probs mate. D7M put me onto the ai thing with 19nors (and indeed is a v knowledgeable chap) whereas before i thought caber etc was needed.

    after seeing my horrific blood report on estro, 630 when it shouldnt be higher than 150-160, (only was on 250mg test e and 350mg tren a) i went on adex at .5mgs eod and within 7 days lumps disappeared, no nipple itch and i felt x5 lighter on my feet, strength went through the roof and i started growing and putting on the lbs again. nolva should be used post adex as a rebound can occur on discontinuing it

    nolva only just barely kept things at bay for me on tren and deca cycles, adex was the biz and i wouldnt run them without it again. aromasin is an even better choice apparently, although i havent yet used it myself
    I appreciate your clarification on this Dec

  26. #26
    dec11's Avatar
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    Quote Originally Posted by TheClinch View Post
    I appreciate your clarification on this Dec
    no worries mate

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    Eminent is offline New Member
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    Dec11. Can I order adex from that ar-r site ?

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    Quote Originally Posted by Eminent View Post
    Dec11. Can I order adex from that ar-r site ?
    yeah, they have liquid form

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    What is it called on there bro? And also where can I get my hands on HCG ?

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