Sust + Winny

[Yeah-Buddy]

Im currently into the 3rd week of my 2nd cycle.

Im running Sust @ 500mg a week and Dbol @ 25mg for the first 4 weeks. My original goal was for lean mass & strength gain while ensuring my current bodyfat (about 13-14%) didnt go any higher to make dieting for competition later this yr not a long drawn out affair. Currently after 3 weeks I am 3kg up and bodyfat is the same (waist is actually a couple cm smaller).

However I found out yesterday I need to be in fairly good lean condition for a photo shoot by mid April which has made me change my goal a bit. I want to continue to grow but need to get in decent condition also. I dont need to be super shredded/stage condition just looking sharp.

I have access to oral winny so was wondering if adding that in from weeks 6-12 would be a good move? so my cycle would look like this:

Sust: Weeks 1-12 500mg

Dbol: Weeks 1-4

Winny Weeks 6-12 (unsure on dosage?)

I have enough Sust to go to 14 weeks but the photo shoot would be at the 12 week mark.

I have Nolva sorted for PCT.. will this still be sufficient?

Cheers guys, hope i havnt forgotten anything important

[tomsammce]

its just ur diet bro, sus and winny can cut u up fine.

[Yeah-Buddy]

Yeah im definately keeping my diet very clean this time. Would keeping at just the sust be good enough you reckon or is adding the winny a good addition to help ensure things get to where i need them to be while still adding a bit of size?

[tomsammce]

yeah i suppose itd be better than just the sus y wouldnt it be.. but yeah up to u.. ru in howick area now? when we training?

[Yeah-Buddy]

My place I was moving to fell thru so Im still not out there yet. Im back to looking for somewhere so as soon as Im there Ill move gyms and get in touch.

[clash]

Unless you use some form of estrogen management you are likely to be holding to much fluid to be looking as sharp as you could be for the photo shoot. I would suggest possibly switching to Tren/Winny in place of the Sustanon for the last four weeks. This will certainly have you looking dry,and defined. If Sustanon is your preferred option, I would suggest adding Pronviron for estrogen management in the last four weeks. This will eliminate 90% of the fluid and add some added androgens to harden and dry you out before the photo shoot....Nolvadex alone is not sufficient for PCT. You are not running an aromatase inhibitor with your course so you will need look a lot closer into you PCT and what you have available to use, Nolvadex, Clomid, Femara, HCG. A combination of at least two of these will be required for an effective PCT phase :-)

[Daz69]

Unless you use some form of estrogen management you are likely to be holding to much fluid to be looking as sharp as you could be for the photo shoot. I would suggest possibly switching to Tren/Winny in place of the Sustanon for the last four weeks. This will certainly have you looking dry,and defined. If Sustanon is your preferred option, I would suggest adding Pronviron for estrogen management in the last four weeks. This will eliminate 90% of the fluid and add some added androgens to harden and dry you out before the photo shoot....Nolvadex alone is not sufficient for PCT. You are not running an aromatase inhibitor with your course so you will need look a lot closer into you PCT and what you have available to use, Nolvadex, Clomid, Femara, HCG. A combination of at least two of these will be required for an effective PCT phase :-)

Tren is a 19-nor, I had been led to believe you shouldn't use synthetic estrogens (Nolvadex, Clomid) with 19-nors, or a short time after you drop em'...

19-nors are progestins, therefore they increase PgR receptors in breast tissue, nolva being an estrogen binds to progesterone receptors, which raises posibility for a nipple tumor growth.... :?

[WANABJAKD]

Unless you use some form of estrogen management you are likely to be holding to much fluid to be looking as sharp as you could be for the photo shoot. I would suggest possibly switching to Tren/Winny in place of the Sustanon for the last four weeks. This will certainly have you looking dry,and defined. If Sustanon is your preferred option, I would suggest adding Pronviron for estrogen management in the last four weeks. This will eliminate 90% of the fluid and add some added androgens to harden and dry you out before the photo shoot....Nolvadex alone is not sufficient for PCT. You are not running an aromatase inhibitor with your course so you will need look a lot closer into you PCT and what you have available to use, Nolvadex, Clomid, Femara, HCG. A combination of at least two of these will be required for an effective PCT phase :-)

Tren is a 19-nor, I had been led to believe you shouldn't use synthetic estrogens (Nolvadex, Clomid) with 19-nors, or a short time after you drop em'...

19-nors are progestins, therefore they increase PgR receptors in breast tissue, nolva being an estrogen binds to progesterone receptors, which raises posibility for a nipple tumor growth.... :?

once the blood levels return to baseline for your pct it shouldnt be a problem. its more the issue of running nolva concurrently with 19nors steroids as it upregulates the progesterone receptor.

[musclenz]

Unless you use some form of estrogen management you are likely to be holding to much fluid to be looking as sharp as you could be for the photo shoot. I would suggest possibly switching to Tren/Winny in place of the Sustanon for the last four weeks. This will certainly have you looking dry,and defined. If Sustanon is your preferred option, I would suggest adding Pronviron for estrogen management in the last four weeks. This will eliminate 90% of the fluid and add some added androgens to harden and dry you out before the photo shoot....Nolvadex alone is not sufficient for PCT. You are not running an aromatase inhibitor with your course so you will need look a lot closer into you PCT and what you have available to use, Nolvadex, Clomid, Femara, HCG. A combination of at least two of these will be required for an effective PCT phase :-)

Tren is a 19-nor, I had been led to believe you shouldn't use synthetic estrogens (Nolvadex, Clomid) with 19-nors, or a short time after you drop em'...

19-nors are progestins, therefore they increase PgR receptors in breast tissue, nolva being an estrogen binds to progesterone receptors, which raises posibility for a nipple tumor growth.... :?

There is a wee bit of misinformation on this highlighted in this article but generally you are far better to run an AI over a SERM which are proven to reduce PgR expression in almost all cases when Progestins are involved. Obviuosly Nolva works differently in individuals but it does seem to work as an antagonist in breast tissueso in the end it is reasonably effective. But better be safe than sorry when it comes down to PgR Gyno.

"Effects of tamoxifen on endometrial estrogen and progesterone receptor concentrations in women with fibrocystic disease of the breast."

Published in Gynecological Endocrinology Magazine (See references).

At some point in time someone read this then came up with a false summation regarding Tamoxifen upregulatation of progesterone receptors. This falsity was then spread about and became a universal truth. Tamoxifen does in fact upregulate pregesterone receptors (PGR) in some individuals as I will explain later, however the Lopez-Comenge trial found that tamoxifen had no effect on progesterone receptors in endometrial tissue at all. That means no upregulation nor any down regulation.

This concept should have been apparent to many from the start as Nolvadex has a strong affinity to receptors in the pectoral region. Hence it's once famous usage tout regarding gynecomastia prevention. As a result of this affinity Nolvadex has very little effect on tissues outside of the pectoral region. I have provided the abstract as a reference point.

Most online medical journal sites have a copy of the entirety of the clinical trials, but for the purposes of this treatise we are concerned with end results thus a abstract proves a suitable alternative since most of you are not willing to pay a subscription fee to view medical trials (though I urge you to start).

I have taken the liberty of emphasizing the key point.

Quote:

Abstract

Endocrine changes were determined after a 3-week cycle of tamoxifen treatment in 11 regularly cycling women with clinical and radiological evidence of fibrocystic disease of the breast. Blood and endometrial samples were obtained during the luteal phase prior to and at the end of treatment. Tamoxifen treatment (20 mg/day orally for 3 weeks), produced a significant increase in plasma estradiol (p = 0.0018) without simultaneous changes in plasma luteinizing hormone, follicle stimulating hormone, prolactin or progesterone. Tamoxifen treatment significantly reduced endometrial estrogen receptor levels compared to the control cycle (p = 0.0018) while endometrial progesterone receptor levels remained unchanged. Endometrial histological studies showed secretory transformation in both the control cycle and after tamoxifen treatment. The reduction in endometrial estrogen receptor concentrations would suggest a tamoxifen-induced effect or a down-regulatory mechanism to protect target tissues from high estradiol levels. These changes were not associated with alterations in either plasma progesterone or endometrial progesterone receptor concentrations. The tamoxifen-induced changes did not produce any interference in the glandular secretory response of the endometrium.

So that is one myth dispelled. Tamoxifen has no effect on receptors other than those found in the pectoral region. So the endometrial progesterone receptor upregulation story is a myth.

Proceeding to the pectoral region of the body we do notice a different story. In the long run Tamoxifen down regulates both progesterone and estrogen receptors. I know this is contrary to popular belief but note I said in the long run meaning 3-4 weeks. A study was done by Dr. N Waseda, Dr. Y Kato, Dr. H Imura, and Dr. M Kurata. The title of the article was:

"Effects of tamoxifen on estrogen and progesterone receptors in human breast cancer."

Published in Cancer Research Magazine (See references)

The results showed that use of tamoxifen during the first two weeks actually did in fact upregulate both estrogen and progesterone receptors. This may seem counter-intuitive to some of you. Your probably thinking. "Wait, if tamoxifen actually upregulates estrogen receptors then why is it used for gynecomastia prevention?" The key element here is that tamoxifen is a SERM. Tamoxifen may upregulate estrogen receptor sites but, it also binds them.

Tamoxifen cannot bind to progesterone receptors though. So in the short run Tamoxifen can in fact aggravate progesterone related gynecomastia for some individuals. Note the study utilized twenty individuals and only 3 out of 5 (60%) had PGR upregulation. In the span of 3-4 weeks those same patients with increased PGR noticed a decrease in PGR levels.

So in summation, in the short run I.E. a span of 1-2 weeks approximately 60% of people will experience progesterone upregulation. In the long run however, EVERYONE will experience PGR downregulation.So what's my recommendation? Implement Tamoxifen use 4 weeks prior to a 19-nor cycle to down regulate PGR receptors. Of course this whole treatise is a moot point as the use of a prolactin inhibitors makes progesterone gynecomastia a thing of the past.

Once again I have provided the abstract and highlighted key points.

Quote:

Abstract

Twenty patients with primary breast cancer were treated with tamoxifen (10 mg p.o. twice a day) for 1 to 4 weeks. Before and after the tamoxifen administration, tumor specimens were obtained and assayed for estrogen receptors and progesterone receptors (PGR). Total cytosol estrogen receptor (ERC) and occupied nuclear estrogen receptor (ERN) were measured by hydroxylapatite assay, and unoccupied PGR was measured by the dextran-coated charcoal assay. ERC, ERN, and PGR were detectable in 11, 8, and 6 tumors, respectively, before tamoxifen administration. After tamoxifen treatment, ERC decreased in 10 of 11 ERC-positive tumors. Occupied ERN increased in three of five ERN-positive tumors treated with tamoxifen for a short period (1 to 2 weeks), but they decreased in all of three ERN-positive tumors after longer administration (3 to 4 weeks). PGR increased in three of five ERN-positive tumors after short-term tamoxifen treatment, but they decreased in all of three tumors treated by the drug for a longer period. Increased PGR responses were accompanied by an increase of ERN in two of three ERN-positive tumors. These results suggest that tamoxifen interacts with the estrogen receptor system in human breast cancer tissue and may be estrogenic during short treatment, while longer treatment results in an antiestrogenic response.

I of course have several more sources regarding this matter I put the two referenced and two others in my references. I have a total of 31 articles related to this though and I am too lazy to put them all in. If you have questions regarding certain topics I can point you towards an article that may clarify the topic for you.

References

1. Gynecol Endocrinol. 1993 Sep;7(3):185-9. Effects of tamoxifen on endometrial estrogen and progesterone receptor concentrations in women with fibrocystic disease of the breast. Pérez-López FR, Blasco Comenge C. Department of Obstetrics and Gynecology, Hospital Clínico, Zaragoza, Spain.

2. Cancer Res. 1981 May;41(5):1984-8.

Effects of tamoxifen on estrogen and progesterone receptors in human breast cancer. Waseda N, Kato Y, Imura H, Kurata M.

3. Br J Cancer. 1993 March; 67(3): 606***8211;611. PMCID: PMC1968274

Effect of tamoxifen on Ki67 labelling index in human breast tumours and its relationship to oestrogen and progesterone receptor status. R. B. Clarke, I. J. Laidlaw, L. J. Jones, A. Howell, and E. Anderson

Clinical Research Dept., Christie Hospital NHS Trust, Withington, Manchester.

4. Clinical Cancer Research. High Progesterone Receptor Expression Correlates to the Effect of Adjuvant Tamoxifen in Premenopausal Breast Cancer Patients. Maria Stendahl1,2, Lisa Rydén1, Bo Nordenskjöld3, Per Ebbe Jönsson4, Göran Landberg1 and Karin Jirström1

[clash]

Very good read that Musclenz :nod: I have also come across some information about Nolvadex interefereing with the IGF-1 pathways and therefore may not be the best estrogen management during a mass phase. When IGF-1 is release from the breakdown of CAA orals or HGH the subsequent growth is sought after to achieve maximum potential from a course. It is suggested that in fact Clomid is the better choice...? Comments..?

[WANABJAKD]

thats interesting mnz, i always considered it bro-talk and wasnt sure if there was any literature to dispel the myth. i figured there would be something out there.

do you have any abstracts that suggests why the estradiol and progesterone receptors become down-regulated after a short period of time following their up-regulation? i assume they are up-regulated as the receptor sites are starved of their hormones. it wouldnt make sense as to why the body would down regulate the receptors further on...is any literature in favour of the opposing idea?(being that the receptors stay up-regulated)

p.s did you interpret this yourself?

[Android]

WTF are you guys talking about

Just tell us what the answer is after reading all that...more or less juice?

[thatwaslight]

WTF are you guys talking about

Just tell us what the answer is after reading all that...more or less juice?

LOL! liked :pfft:

[Grover]

WTF are you guys talking about

Just tell us what the answer is after reading all that...more or less juice?

You would think there were more than a few doctors in the house!

[WANABJAKD]

first of all, you shouldnt use SERMS during cycle. an aromatase inhibitor like aromasin is far superior, having the ability to suppress E1 by 85% and E2 by 95%. personally i still think this is too strong if used incorrectly.

Effect on Estrogens: Multiple doses of exemestane ranging from 0.5 to 600 mg/day were administered to postmenopausal women with advanced breast cancer. Plasma estrogen (estradiol, estrone, and estrone sulfate) suppression was seen starting at a 5-mg daily dose of exemestane, with a maximum suppression of at least 85% to 95% achieved at a 25-mg dose. Exemestane 25 mg daily reduced whole body aromatization (as measured by injecting radiolabeled androstenedione) by 98% in postmenopausal women with breast cancer. After a single dose of exemestane 25 mg, the maximal suppression of circulating estrogens occurred 2 to 3 days after dosing and persisted for 4 to 5 days.

secondly, clomid isnt good for much besides stimulating LH/FSH and letting you shower your girl with a huge load. it comes with a handful of side effects and requires a larger dose for effectiveness.

Abstract

The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. A significant increase in sperm density was observed only in subjects with oligospermia below 20 X 10(6)/ml and normal basal FSH levels. When basal FSH levels were increased or oligospermia was moderate (greater than 20 X 10(6)/ml); no effect on sperm density was seen. As sperm density increased, FSH levels decreased, suggesting an inhibin effect. Sperm motility was not improved by tamoxifen treatment. In five boys with delayed puberty, tamoxifen treatment appeared to activate the pituitary-gonadal axis and pubertal development.

and lastly tamoxifen lowering IGF-1

The Journal of Clinical Endocrinology & Metabolism Vol. 95, No. 12 5443-5448

Copyright © 2010 by The Endocrine Society

Neuroendocrine Regulation of Growth Hormone and Androgen Axes by Selective Estrogen Receptor Modulators in Healthy Men

Vita Birzniece, Akira Sata, Surya Sutanto and Ken K. Y. Ho

Garvan Institute of Medical Research and Department of Endocrinology (V.B., A.S., S.S., K.K.Y.H.), St. Vincent’s Hospital, Sydney, New South Wales 2010, Australia; and The University of New South Wales (V.B., K.K.Y.H.), Sydney, New South Wales 2052, Australia

Address all correspondence and requests for reprints to: Prof. Ken K. Y. Ho, Pituitary Research Unit, Garvan Institute of Medical Research, Darlinghurst, New South Wales 2010, Australia.

Context: In men, the stimulation of GH and inhibition of LH secretion by testosterone requires aromatization to estradiol. Tamoxifen, a selective estrogen receptor modulator (SERM), possesses central estrogen antagonistic effect but peripheral hepatic agonist effect, lowering IGF-I. Thus, tamoxifen is likely to perturb the neuroendocrine regulation of GH and gonadal axes. Raloxifene, a SERM, is used for therapy of osteoporosis in both sexes. Its neuroendocrine effects in men are poorly understood.

Objective: The aim was to compare the impact of raloxifene and tamoxifen on GH-IGF-I and gonadal axes in healthy men.

Design: We conducted a randomized, open-label crossover study.

Patients and Intervention: Ten healthy men were randomized to 2-wk sequential treatment with tamoxifen (10 and 20 mg/d) and raloxifene (60 and 120 mg/d), with a 2-wk intervening washout period.

Main Outcome Measures: We measured the GH response to arginine and circulating levels of IGF-I, LH, FSH, testosterone, and SHBG.

Results: Tamoxifen, but not raloxifene, significantly reduced IGF-I levels by 25 ± 6% (P < 0.01) and increased SHBG levels by 20 ± 7% (P < 0.05) at the higher therapeutic dose. There was a nonstatistically significant trend toward a reduction in the GH response to arginine with both SERMs. Both drugs significantly increased LH, FSH, and testosterone concentrations. The mean increase in testosterone (40 vs. 25%; P < 0.05) and LH (70 vs. 30%; P < 0.01) was significantly greater with tamoxifen than with raloxifene treatment.

Conclusions: Tamoxifen, but not raloxifene, reduces IGF-I levels. Both SERMs stimulate the gonadal axis, with tamoxifen imparting a greater effect. We conclude that in therapeutic doses, raloxifene perturbs the GH and gonadal axes to a lesser degree than tamoxifen.

[Yeah-Buddy]

So with all this information :shock: what would be the best approach for me?

[train hard]

So with all this information :shock: what would be the best approach for me?

if you just got to look good for a photo shoot stick with the 500mg of sust and 40 to 50 mg per day of winny from 5 weeks out from shoot and with a good diet you could look really good you could also deplete for the photo shoot. A little bit of adex .5 mg eod 3 weeks out is an option too if you wanted too be a bit dryer

[clash]

So with all this information :shock: what would be the best approach for me?

A little information is a dangerous thing...Too much information is just confusing sometimes. Wile you are on a course and want to get the most growth potential, I would recommend taking 50mg of Masteron/day. It is a useful AAS in its own right and it has a the fantastic ability to amplify the effect of other gear you are taking while at the time it competes for the aromatase inhibitor making it a useful AI as well, this offers great estrogen management at a level that supports growth

[musclenz]

So with all this information :shock: what would be the best approach for me?

Haaaa! We got a bit side tracked YB. It will depend if you are going to use cutting drugs or diet, water/sodium manipulation, cardio etc to achieve a cut Yeah-Buddy by your photo shoot. Cetainly you will achieve a reasonable result using Sust, Winny & Nolva. As suggested in our discussions there are much better anti estrogens now than Tamoxifen & as Clash pointed out it does have a determental effect on natty Igf & Gh amongst other sides. If you could afford to switch to an AI like Arimidex or even Letrozole & add in Clenbuterol, Proviron or Masteron to your mix you may get better results. However, diet, training, cardio & day to day analyses of your body will still be paramount. It all comes down to money & motivation in the end

[WANABJAKD]

So with all this information :shock: what would be the best approach for me?

Haaaa! We got a bit side tracked YB. It will depend if you are going to use cutting drugs or diet, water/sodium manipulation, cardio etc to achieve a cut Yeah-Buddy by your photo shoot. Cetainly you will achieve a reasonable result using Sust, Winny & Nolva. As suggested in our discussions there are much better anti estrogens now than Tamoxifen & as Clash pointed out it does have a determental effect on natty Igf & Gh amongst other sides. If you could afford to switch to an AI like Arimidex or even Letrozole & add in Clenbuterol, Proviron or Masteron to your mix you may get better results. However, diet, training, cardio & day to day analyses of your body will still be paramount. It all comes down to money & motivation in the end

two words: f*ck that...stay away from that shit at all costs

[musclenz]

thats interesting mnz, i always considered it bro-talk and wasnt sure if there was any literature to dispel the myth. i figured there would be something out there.

do you have any abstracts that suggests why the estradiol and progesterone receptors become down-regulated after a short period of time following their up-regulation? i assume they are up-regulated as the receptor sites are starved of their hormones. it wouldnt make sense as to why the body would down regulate the receptors further on...is any literature in favour of the opposing idea?(being that the receptors stay up-regulated)

p.s did you interpret this yourself?

I will let you do our own research on this WB. I expect it may have something to do with individual base levels & the body over compensating for exogenous upregulation by progestins or androgens. Your theory on starvation at the PgR is interesting. Think your Degree is better than my Non Degree

[musclenz]

So with all this information :shock: what would be the best approach for me?

Haaaa! We got a bit side tracked YB. It will depend if you are going to use cutting drugs or diet, water/sodium manipulation, cardio etc to achieve a cut Yeah-Buddy by your photo shoot. Cetainly you will achieve a reasonable result using Sust, Winny & Nolva. As suggested in our discussions there are much better anti estrogens now than Tamoxifen & as Clash pointed out it does have a determental effect on natty Igf & Gh amongst other sides. If you could afford to switch to an AI like Arimidex or even Letrozole & add in Clenbuterol, Proviron or Masteron to your mix you may get better results. However, diet, training, cardio & day to day analyses of your body will still be paramount. It all comes down to money & motivation in the end

two words: f*ck that...stay away from that shit at all costs

Letrozole has got a bad rap. It is a competitive inhibitor & binds exactly the same way at the Aromatase Enzyme as Arimidex. It is just more effective & must be used at a much lower dose on cycle than in Gyno lump reduction. Around .25 - .5mg E3D

[WANABJAKD]

thats interesting mnz, i always considered it bro-talk and wasnt sure if there was any literature to dispel the myth. i figured there would be something out there.

do you have any abstracts that suggests why the estradiol and progesterone receptors become down-regulated after a short period of time following their up-regulation? i assume they are up-regulated as the receptor sites are starved of their hormones. it wouldnt make sense as to why the body would down regulate the receptors further on...is any literature in favour of the opposing idea?(being that the receptors stay up-regulated)

p.s did you interpret this yourself?

I will let you do our own research on this WB. I expect it may have something to do with individual base levels & the body over compensating for exogenous upregulation by progestins or androgens. Your theory on starvation at the PgR is interesting. Think your Degree is better than my Non Degree

degree? i graduated from the bro academy :pfft: only out of interest but i cant be bothered to look into this too carefully as i dont run nolva during.

one thing i am interested in that i cant seem to find anything on is trenbolone's effect on estrogenic activity within the body. lately ive had almost no activity. i stopped supplementing aromasin a week ago, its quite a remarkable thing and im finding a hard time finding anything on this.

[WANABJAKD]

Haaaa! We got a bit side tracked YB. It will depend if you are going to use cutting drugs or diet, water/sodium manipulation, cardio etc to achieve a cut Yeah-Buddy by your photo shoot. Cetainly you will achieve a reasonable result using Sust, Winny & Nolva. As suggested in our discussions there are much better anti estrogens now than Tamoxifen & as Clash pointed out it does have a determental effect on natty Igf & Gh amongst other sides. If you could afford to switch to an AI like Arimidex or even Letrozole & add in Clenbuterol, Proviron or Masteron to your mix you may get better results. However, diet, training, cardio & day to day analyses of your body will still be paramount. It all comes down to money & motivation in the end

two words: f*ck that...stay away from that shit at all costs

Letrozole has got a bad rap. It is a competitive inhibitor & binds exactly the same way at the Aromatase Enzyme as Arimidex. It is just more effective & must be used at a much lower dose on cycle than in Gyno lump reduction. Around .25 - .5mg E3D

after my experience with letro i dont even want to try it at low doses (.2-.5mg eod). mind you when i was on 2.5mg of letro and 100mg of var ED i was looking like a statue

[tomsammce]

yeah buddy, f*ck all that shit.. seriously.. just take your sus and stan eat clean and cardio if you want to stay leaner (yes u will get leaner and put on muscle mass with any steroid if diet is good) forgetting all this bro science and opinion thats what test pretty much does builds muscle and burns fat!

take a diuretic or two b4 the shoot, dont base your whole cycle around your photo shoot thats just popped up.