Cycle Regimen Critiques

[pharmbiak]

Okay guys, I'm looking to start a cycle fairly soon here and I need some critiquing from everyone.

Just to get this out of the way first: No, this isn't my first cycle. Yes, to a certain extent I am very familiar with, and know exactly what I am doing. Please don't post about how only diet and exercise is necessary to obtain goals and that anyone considering supraphysiological alternatives is an imbecile. Supraphysiological is the goal; the very root of the word implies obtaining a level beyond that which is physiologically possible under unenhanced conditions. Therefore, no; a clean diet and exercise are not all that's necessary to get to a supraphysiological level.
Getting off my soapbox now...

Liver support and things of the like are a given.
I do have some IGF-1 LR3, but I haven't found a place for it in my cycle... I'm thinking of saving it for post cycle. What do you all think?

Current Stats:

Height: 6'2"
Weight: 100 kg/ 220 lbs
BF %: 13.6 (measured using DEXA)

The regimen is as follows:

Oxandrolone:
Week 1: 50 mg ED
Week 2: 80 mg ED
Week 3-8: 100 mg ED

Testosterone:
Week 1: 300 mg
Week 2: 500 mg
Week 3-10: 750 mg
Week 11: 500 mg
Week 12: 250 mg

Tamoxifen Citrate:
Week 1-16: 40 mg ED

Anastrozole:
Week 1-16: 0.5 mg ED

GHRP-2:
Week 1-infinite: 100 mcg 3xday

Mod GRF 1-29
Week 1-infinite: 100 mcg 3xday

2,4-Dinitrophenol
Week 14-16: 500 mg ED (possibly with the exception of weekends)
*** Please do not post your philosophy on DNP use and how dangerous it is. I'm a molecular neurobiologist and have had extensive coursework in molecular and cellular biology and biochemistry - I'm well aware that this uncouples oxidative phosphorylation and as such results in an inhibition of ATP production.


Should be able to start within a couple of weeks... let me know where I can make some tweaks.

Cheers!

 

[nolys]

Why are you staggering your test dosages

 

[blazR]

I do have some IGF-1 LR3, but I haven't found a place for it in my cycle... I'm thinking of saving it for post cycle. What do you all think?

I'm thinking; is the IGF-1 LR3 recombinant..? AFAIK and according to datbtrue, most IGF- LR3 isn't.

 

[Genetic Freak]

GHRP-2: Week 1-infinite: 100 mcg 3xday

Mod GRF 1-29 Week 1-infinite: 100 mcg 3xday

Your choice of hormone and dosing schedule is optimal, you've obviously done your homework...

Oxandrolone:
Week 1: 50 mg ED
Week 2: 80 mg ED
Week 3-8: 100 mg ED

Testosterone:
Week 1: 300 mg
Week 2: 500 mg
Week 3-10: 750 mg
Week 11: 500 mg
Week 12: 250 mg

Tamoxifen Citrate: Week 1-16: 40 mg ED

I can see logic to your introduction of Anavar, and the testosterone taper (on-off protocol)

Please explain your reasoning for nolvadex 1-16 40mg/day it seems a high dose, and use on cycle is not the norm'... Are you estrogen sensitive or have a history of gyno whilst on cycle..?

I'm a molecular neurobiologist and have had extensive coursework in molecular and cellular biology and biochemistry

We are indebted to have someone of your calibre here in SD....

 

[CFC]

In addition to GF regarding the Tamoxifen, I wouldn't do the DNP in weeks 14-16. Why don't you use it weeks 10-12, or else a separate cycle altogether?

 

[pharmbiak]

Why are you staggering your test dosages

I'm tapering the testosterone dosages at the end of the cycle to help combat any estrogen rebound side-effects that might arise after I drop the testosterone. I know that the tamoxifen will essentially eliminate this, but I wanted to err on the side of caution. As for the beginning of the cycle I'm increasing the dose to maintenance level over the course of three weeks as this is just what I've always done. I'm not sure if it's necessary but I've read that gradual induction can be better for acclimation than full dose upon first injection. You guys may have more wisdom about this than I do.

 

[pharmbiak]

Your choice of hormone and dosing schedule is optimal, you've obviously done your homework...



I can see logic to your introduction of Anavar, and the testosterone taper (on-off protocol)

Please explain your reasoning for nolvadex 1-16 40mg/day it seems a high dose, and use on cycle is not the norm'... Are you estrogen sensitive or have a history of gyno whilst on cycle..?



We are indebted to have someone of your calibre here in SD....

I wasn't sure exactly how much nolvadex I would need; I know that 20-40mg is typical dosage. I don't have a huge estrogen sensitivity currently, however, when I was younger during puberty I had major issues with gyno from high testosterone levels. In all of my previous cycles (even my first cycle where I did a testosterone trenbolone stack and didn't use any tamoxifen until the very end) I have had very little, if any, problems with gyno. I think that just having the issues I did when I was much younger kind of scares me away from using tamoxifen until the very end of my cycle. I recently came into a near endless supply of tamoxifen for literally pennies, so I figured it couldn't hurt too much to take it the entire cycle. My only concern is, as you all well know, estrogen is necessary for growth, so limiting my estrogen levels may hinder my gains. How substantially? I'm not sure.

Thanks; that wasn't meant to sound obnoxious or anything, but every time I bring up anything questionable such as DNP, there's always someone that tries to educate me on it's effects and how dangerous of a substance it is. After awhile, you just get tired of hearing it. ha

 

[pharmbiak]

In addition to GF regarding the Tamoxifen, I wouldn't do the DNP in weeks 14-16. Why don't you use it weeks 10-12, or else a separate cycle altogether?

The DNP was sort of an add-on and I wasn't sure exactly where to place it so I just stuck it at the end of the cycle. I was thinking that if I had some anabolics in my system, I would lose less muscle mass on a DNP cycle than if I were to take it alone (even though DNP burns mostly fat, catabolic is still catabolic).

I can see the logic of taking it in a separate cycle altogether, but why do you recommend taking it in weeks 10-12?
Do you think this will make a substantial difference in the amount of fat lost?

 

[pharmbiak]

I'm thinking; is the IGF-1 LR3 recombinant..? AFAIK and according to datbtrue, most IGF- LR3 isn't.

Thanks for the great question!

I did a little bit of research from my supplier and this is what they have said about their IGF-1 LR3: "This is a human recombinant, single, non-glycosylated, polypeptide chain containing 83 amino acids and having a molecular mass of 9200 Daltons. IGF1 mediates many of the growth-promoting effects of growth hormone (GH; MIM 139250). The LR3 is a long-term analog of human IGF-1, specifically designed and manufactured for mammalian cell culture to support large-scale manufacturing of recombinant biopharmaceuticals. Early studies showed that growth hormone did not directly stimulate the incorporation of sulfate into cartilage, but rather acted through a serum factor, termed 'sulfation factor,' which later became known as 'somatomedin'. The polypeptide Long R3 Insulin-like Growth Factor-I (IGF1 LR3) is an 83 amino acid analog of IGF-I actually comprising the complete IGF-1 sequence but with the substitution of an Arginine (Arg) for the Glutamic Acid (Glu) at position 3, as well as a 13 amino acid extension peptide. This sequence change causes IGF-1 LR3 to avoid binding to proteins and allow it to have a much longer half life, around 20-30 hours. This analog of IGF-1 has been produced with the purpose of increasing the biological activity of the IGF peptide.” IGF stands for insulin-like growth factor. Among the effects the most positive are increased amino acid transport to cells, increased glucose transport, increased protein synthesis, and decreased protein degradation. When IGF is active it behaves differently in different types of tissues. In muscle cells proteins and associated cell components are stimulated. Protein synthesis is increased along with amino acid absorption. As a source of energy, IGF-1 LR3 mobilizes fat for use as energy in adipose tissue. In lean tissue, IGF-1 LR3 prevents insulin from transporting glucose across cell membranes. As a result the cells have to switch to burning off fat as a source of energy.IGF-1 LR3 builds new muscle tissue by promoting nitrogen retention and protein synthesis. This causes the growth of muscles through both hyperplasia (which is an increase in number of muscle cells) and mitogenesis (which is the actual growth of new muscle fibers). Thus IGF-1 LR3 not only makes muscle fibers bigger, it makes more of them as well. Therefore, IGF can actually change the genetic capabilities in terms of muscle tissue and cell count. IGF increases and differentiates the number and types of cells present.
IGF-1 LR3 is a synthetic analog of the naturally existing insulin growth factor (IGF) which is a 93 amino acid residue. Modifications of the natural form occurred with the substitution of the Arg with Glu at the position 3, giving a code R3, and also an extension of a 13 amino acid at the B-terminus. Just like IGF-1, R3 has been shown to induce the development and growth of cells.
The studies on transgenic and knockout mice have shown that it can control its development and growth. It plays an important role as regulator in the G1 to S phase of the cell cycle. When applied to cardiomyocyte cultures, R3 have shown a large increase in proliferating cell nuclear antigen expression and in several cyclins involved in cell progression as well as in bromodeoxyuridien (BrdU) labeling (Kajstura et al. 1994). Other effects it has on cell lines are increased cell survival, inhibition of the apoptotic pathways, culture longevity and increased recombination of protein production (Fang et al. 1997). In another study, the application of the LR3 IGF-1 has led to an increase in the myocyte bromodeoxyuridine uptake by three to fivefold. But it has also shown that IGF-1 LR3 actions have been blocked by the ERK and P13K labeling which completely abolished the BrdU uptake. Furthermore, ut has been shown that in mycocytes, IGF-1 R3 stimulates the cardiomyocyte division in vivo (Sundgren et al. 2003). It has also been suggested that IGF-1-Long 3R is more potent than the IGF-1 because of its low binding capacity with all known IGF binding proteins (Tomas et al. 1995). In another investigation, feeding of LR3-IGF-1 in different amounts to investigate the effects on somatotropic axis (plasma levels of IGF-1 and 2, IGFBPs) was done. They have reported that plasma Long-R3 increased when administered subcutaneously but with no such behavior when administered orally. Furthermore, LR3 lowered the levels of native IGF-1 in rbGH-injected in calves, but L-R3 increased the amounts of IGF-II concentrations when administered with L-R3 subcutaneously. The parenteral administration of the Long R3 IGF-1 decreased the growth hormone concentration but did not affect the secretory system. It was also reported that the somatotrophic acis is basically functioning in neonatal calves and can be influenced by nutrition, growth hormone and Long-R3-IGF-1 (IGF1-LR3). (Hammon and Blum 1997). "

What I can tell you, is that I verify all my peptides using a nano-drop 2000 ( this is a UV-Vis spectrophotometer) as well as HPLC (high performance liquid chromatography). After analysis, this one checked out and matched their HPLC datasheet on their website. They say it is a human recombinant polypeptide and I absolutely trust my source.

However, could you please educate me a bit on this topic?
Are you insinuating that most providers simply stick regular IGF-1 in a bottle and sell it as LR3?
I guess I could see this being the case, wherein the half-life of IGF-1 non-recombinant is very short. I think that when using HPLC and a UV-Vis spectrophotometer, the difference would be obvious due to the modifications in the amino acid sequence... Maybe I'm wrong here?
I'm a member at datbtrue as well so I'll see if there's some more information on there about this topic. Anyway, thanks for the heads-up!

 

[Serotonin101]

Everything looks alright to me (I personally won't use dnp but as I say, your body your decision. Might want to use it while on gear to minimize muscle loss). I'd personally hold off on tamoxifen dosing til week 3-4 somewhere around there when the test has built up sufficiently. With adex being used you may not even need it since you're using ai while tapering up to prevent large fluctuations in e2. Start low with tamoxifen too as it reduces IGF in the body.

 

[pharmbiak]

Could someone also elaborate on whether or not Anastrozole needs to be taken at .5 mg every day, or if it should be taken at .5 mg every other day? The half-life is approximately 50 hours and I've read various reasons for each side of the argument.

 

[CFC]

I wouldn't recommend using Tamoxifen or Anastrazole prophylactically during the cycle unless you genuinely have need for it. Don't just take them because you have them. Tamoxifen is not without issues (eg liver) and oestrogen has numerous positive sides (especially lipids and elevated joint HA). If you do need to lower your oestrogen a bit due to noticing some puffiness/itchiness, Anastrazole at 0.5mg E3D would probably be sufficient.

I suggested either not doing the DNP or doing it when you still have enough circulating androgens because what you're proposing is fairly counterproductive: sticking it at the end of PCT, when you're already in a pretty catabolic state, you're likely to wash away some of your hard-won gains.

 

[Genetic Freak]

I can see logic to your introduction of Anavar, and the testosterone taper (on-off protocol)

Please explain your reasoning for nolvadex 1-16 40mg/day it seems a high dose, and use on cycle is not the norm'... Are you estrogen sensitive or have a history of gyno whilst on cycle..?

I wasn't sure exactly how much nolvadex I would need; I know that 20-40mg is typical dosage. I don't have a huge estrogen sensitivity currently, however, when I was younger during puberty I had major issues with gyno from high testosterone levels. In all of my previous cycles (even my first cycle where I did a testosterone trenbolone stack and didn't use any tamoxifen until the very end) I have had very little, if any, problems with gyno. I think that just having the issues I did when I was much younger kind of scares me away from using tamoxifen until the very end of my cycle. I recently came into a near endless supply of tamoxifen for literally pennies, so I figured it couldn't hurt too much to take it the entire cycle. My only concern is, as you all well know, estrogen is necessary for growth, so limiting my estrogen levels may hinder my gains. How substantially? I'm not sure.

Thanks; that wasn't meant to sound obnoxious or anything, but every time I bring up anything questionable such as DNP, there's always someone that tries to educate me on it's effects and how dangerous of a substance it is. After awhile, you just get tired of hearing it. ha

The reason Tamoxifen is not advised on cycle is due in part to its negative effects on IGF-1, Raloxifene is now advised if experiencing symptoms of gyno, or prostate issues...

As you (and CFC) have already stated estrogen if managed correctly can be beneficial to skeletal muscle hypertrophy, SERM's are not advised on cycle unless there is evidence of gyno, or prostate problems... Only use an AI if blood tests show E2 to be excessively elevated.... Or you are experiencing symptoms of high E2...

I know of advanced bodybuilders with many years experience that have used DNP with success, we try not to promote its use here as we are predominately a harm reduction web-site... Most people are not responsible enough to use it safely..!! Very few people have your experience and knowledge in SD...

I'm thinking DNP might best be employed whilst you have sufficient androgens in your body rather than end of cycle, to avoid any excessive catabolism....

Effect of tamoxifen on GH and IGF-1 serum level in stage I-II breast cancer patients.
Mandalà M1, Moro C, Ferretti G, Calabro MG, Nolè F, Rocca A, Munzone E, Castro A, Curigliano G.
Author information
Abstract
OBJECTIVE:
Tamoxifen suppresses insulin-like growth factor-1 (IGF-1) plasma levels in early and advanced breast cancer patients. Relationships between tamoxifen (GH) and IGF-1 are complex and not completely described yet. The present investigation was performed to evaluate the effect of acute and chronic tamoxifen administration on GH response to growth hormone-releasing hormone (GHRH), as well as on IGF-1 serum levels.
MATERIALS AND METHODS:
Evaluation of GH after administration of GHRH was performed (a) at baseline, (b) 3 hours after 20 mg oral administration of tamoxifen and (c) after 12 weeks of 20 mg a day oral tamoxifen treatment, in fifteen postmenopausal stage I-II breast cancer patients. IGF-I was measured at baseline and after chronic tamoxifen administration.
RESULTS:
The GH response to GHRH was significantly reduced after 12 weeks of tamoxifen 10 mg administered twice a day orally (mean peak 3.2 +/- 0.2 micrograms/l, mean AUC 261.3 +/- 18.2 micrograms/minute p < 0.01 versus basal AUC). A concomitant significant reduction of IGF-1 was observed after 3 months of tamoxifen treatment. Basal pretreatment levels of 113.2 +/- 15.5 micrograms/l were suppressed to 70 +/- 7.9 micrograms/l (p < 0.01).
CONCLUSION:
Our study confirm the inhibitory effect of tamoxifen on IGF-I and suggested, as shown in previous in vitro data, that its suppression could be directly related to GH reduction in response to GHRH stimulation.

http://www.ncbi.nlm.nih.gov/pubmed/11299809

 

[Genetic Freak]

Could someone also elaborate on whether or not Anastrozole needs to be taken at .5 mg every day, or if it should be taken at .5 mg every other day? The half-life is approximately 50 hours and I've read various reasons for each side of the argument.

AS previously stated E3rd day 0.5mg, but only if you really have to..!! if your test numbers are supra physiologic its ok to have elevated estro....

 

[pharmbiak]

Hi guys,

I wanted to take a little time to give an update. So first things first, I wasn't able to start my cycle as planned... In short, soon after I posted a few things came up that prevented me from doing so at that time - we made a breakthrough in the lab doing some research and as such we started pumping out data and getting ready to submit our publication. Because of this, I've been working 60 hour weeks to try and get all of our data put together so that we can publish in a very prestigious journal - good for grant money and my career but unfortunately very bad for my training and gains... Regardless, I figured it'd be smarter to wait until I had the time to do the cycle right instead of just half-assed whenever I could find time.

Just this week I started running my DNP cycle because I gained a bit of body fat that I want to get rid of before I start running my cycle - no point in cycling if you can't appreciate the gains that you make. As for that, I'm on day 5 of the DNP cycle running 400mg/day, 5 days on and 2 days (the weekend) off to help lower the plasma level of DNP as it has a half life of "5-30" hours (inconsistent as enough research hasn't been done narrow the range down to an exact time - however, common knowledge says it's closer to 30 hours). So far so good, minimal side effects (slightly hotter of course, and slight constipation) - I've lowered my calorie intake to 2000 kcal/day and kept it very high protein, (a common misnomer is that you have to eat a diet high in carbs for DNP to work, or that doing this makes it work better. This is simply incorrect, and if you understand the basics of oxidative phosphorylation you know this) and I'm down about 10 lbs from my previous weight. I tend to store fat more in my thighs and butt and I can already tell a fairly drastic difference in appearance, but my abdominal area is a little more distended than usual - this is typical due to high water retention on DNP.

Anyway, I plan on running the DNP for one more week, taking a week off and then starting my blast. I've made a few adjustments to the cycle and wanted to get a final critique from those that know what they're talking about, just to tidy up any loose ends. Let me know what you guys think.

The NEW regimen is as follows:

Oxandrolone:
Week 1: 50 mg ED
Week 2: 80 mg ED
Week 3-8: 100 mg ED

Testosterone:
Week 1: 300 mg
Week 2: 500 mg
Week 3-9: 750 mg
Week 10: 500 mg
Week 11: 250 mg
Week 12: 125 mg

Trenbolone Acetate:
Week 1-4: 100 mg
Week 5-8: 150 mg
Week 9: 100 mg
Week 10: 50 mg
Week 11-12: 25 mg

GHRP-2:
Week 1-infinite: 100 mcg 3xday

Mod GRF 1-29
Week 1-infinite: 100 mcg 3xday

Anastrozole:
Week 1-16: 0.5 mg EOD/As needed *** will be taking ED for sure last few days of cycle at 0.5mg

Dutasteride/Finasteride:
Week 1-16: As needed for DHT related side effects, mainly male pattern baldness (I'd like to preserve my hairline)

PCT: *** Stolen from GF (Thanks btw)

GHRP-2:
Week 1-infinite: 100 mcg 3xday

Mod GRF 1-29
Week 1-infinite: 100 mcg 3xday

Clomiphene:
Week 1: 50 mg ED
Week 2: 50 mg ED
Week 3: 25 mg ED
Week 4: 25 mg ED

Tamoxifen Citrate:
Week 4: 20 mg ED
Week 5: 20 mg ED
Week 6: 10 mg ED
Week 7: 10 mg ED

Anastrozole:
Week 8: 0.5 mg ED

 

[CFC]

Looks fine. Not quite sure on the rationale for the taper-off at the end. I taper up and off all the time, however I do it differently and not because of oestrogen rebound, which the Anastrazole you should have at the end of the cycle proper will take care of before you head into PCT.

 

[Serotonin101]

If you'd like you can add the anavar back in for the two weeks after your last test injection up until you begin pct. It's short half life wouldn't change anything pct wise.

 

[pharmbiak]

Looks fine. Not quite sure on the rationale for the taper-off at the end. I taper up and off all the time, however I do it differently and not because of oestrogen rebound, which the Anastrazole you should have at the end of the cycle proper will take care of before you head into PCT.

The taper off at the end is just to prevent rebound but, as you said, the anastrozole at the end of the cycle should help with that. I just prefer to be extra cautious because I'm estrogen sensitive.

 

[pharmbiak]

If you'd like you can add the anavar back in for the two weeks after your last test injection up until you begin pct. It's short half life wouldn't change anything pct wise.

Do you think there'll be a noticeable benefit to adding the anavar in during the two weeks before I start my PCT? I had planned originally to go directly into PCT without waiting for the test levels in my system to dwindle, hence the taper at the end. I've read conflicting accounts on this as to whether or not it's beneficial to wait to start PCT, what's your opinion on this?

 

[Serotonin101]

Lol, my stance on pct is that it's pointless to do if you plan on using gear for a long period of your life. If you're just dabbling then by all means pct is OK. If you want to push the envelope and see what your body can really do, then pct isn't going to allow that.

Now then, as for waiting for the circulating compounds to dwindle in the blood is for a good reason. The body won't start producing test again, even when coerced with a serm, unless circulating androgen levels are below normal. Otherwise the negative feed back loop is active in the sense: high androgens, no more test is needed, nuts still shut down. Once levels get low enough then the body recognizes it needs to start production again. The time before pct begins is all based on the active life of the drugs in the body. Dropping longer esters like cyp and enanthate a couple weeks out allows blood levels to drop, but also means progress will stall out, gains may begin being lost although minimally. So the idea is to substitute in short life drugs during the time the longer active drugs are leaving the body. This can be done with injectable like test prop/ace/pp or with orals. This allows you to bridge that time so that the amount of time spent with low hormones is minimal.