Cycle recommendation

[Bigwhite]

You want to have some AI's on hand and your PCT in hand when you start the cycle, but given the low dose of test you will be using, it is possible you will not get any sides and won't need the AI's at all. Prami and Caber are to counter the effects of Progesterone, which is a side effect of Tren or Deca or Nandrolone (all Nor-19's), so you don't need prami or caber if you are running test only. A good AI for test only is nolvadex (tamoxifen).

Arimidex……

 

[IronSoul]

Arimidex……

I would go with adex here too that's what I ran and use most of the timr

 

[dr jim]

I agree BW test is fine for a first cycle AND if you keep the dose at or below 500mg/week (which is actually only TWICE that used for TRT) PCT is also unlikely to be needed especially considering your age of TWENTY THREE. So again providing you cycle TT at a dose less than 500mg/week your "NO PCT" HTPA recovery, God forbid I even suggest such a thing, will be uneventful!

Finally although you would need to pin at least twice a week vs once a week if T-prop is chosen rather than T-c or T-e, HTPA recovery requires only half the time if T-p is selected because of their differing half lives (2-3 VS 6-8 DAYS)

I also agree although an Ai is unlikely to be needed, (but should available) IF your TT dose remains less than 500mg per week.

Finally since there is NO EVIDENCE progesterogenic AAS (Bolo, Tren or Deca) raise serum prolactin or progesterone levels (UNLESS your breast feeding pregnant or have a prolactin secreting tumor) the use of dopamine agonists such as Gabergoline or Bromocriptine is unwarranted.

Incidentally, I appreciate your questions but it's blatantly CLEAR you have A LOT more reading to do fella, in part since there is so much to know in this field of AAS yet also because there are MANY WAYS to run a cycle, prevent side AAS effects or use PCT and in part because your questions are rather fundamental but typical for someone whose cycling experience is limited.

Why is that? Because the evidence is sparse in certain areas and is often extrapolated from other indirect scientific studies.

For instance where does ALL the supportive PCT literature come from? I mean did some contemporary physician prescribe AAS to his BB patients and thereafter develop different means of weaning them off THUS restoring their HTPA? Was this data eventually published? Or how about these AI's people use for Estrogen side effects?

Of course the answer to the first question is NO since the prescribing of AAS as PED's is ILLEGAL and can cost a physician his license! So what then?

Well a considerable portion of existing PCT recommendations are extrapolated from males attempting to recover from "low T" for various reasons such as prostate cancer therapy, testicular failure, testicular tumors, infertility etc! So these patients actually USED "PCTherapy" as a means to recover the gonads or HTPA.

Now obviously some of the contrasts and comparisons may be INAPPROPRIATELY extrapolations and therefore NOT applicable to BB using PEDs.

For instance what is the data that supports the use of TWO SERMS? What studies was that therapy based on? Are their any one vs two SERM comparisons? (Nope) Needless to say I think the evidence approaches ZIPPO and some would disagree with my assertion.

However, I have my reasons and they have theirs, BUT those conflicting views should be EVIDENCE BASED, and that is the reason YOU need to read more. To develop YOUR OWN opinion based on the literature rather than parroting what I or someone else suggests as "the truth"!

Best
JIM

Oh most of the evidence on AI's AND SERMS is derived from females with BREAST CANCER! And we are using those studies for male BB on mega doses of AAS?

Yep! Why? Because it's the best we have, and one hell of an improvement over RATS,

 

[CBS]

Finally since there is NO EVIDENCE progesterogenic AAS (Bolo, Tren or Deca) raise serum prolactin or progesterone levels (UNLESS your breast feeding pregnant or have a prolactin secreting tumor) the use of dopamine agonists such as Gabergoline or Bromocriptine is unwarranted.

Not only is it unwarranted, it is the most persistent myth to ever come out of the bro lore. It simply will not go away despite the fact there is not a single shred of evidence showing trenbolone induces PRL or gynecomastia.

 

[dr jim]

Not only is it unwarranted, it is the most persistent myth to ever come out of the bro lore. It simply will not go away despite the fact there is not a single shred of evidence showing trenbolone induces PRL or gynecomastia.

But we keep trying,

 

[Bionixx]

I would go with adex here too that's what I ran and use most of the timr

I heard good things about adex but I always use letrozole it stronger works longer better and is cheaper. I use 5 drops at 2.5mg/ml (20drops/ml) ED to E3D depending on bloat.

 

[Get Some]

Not only is it unwarranted, it is the most persistent myth to ever come out of the bro lore. It simply will not go away despite the fact there is not a single shred of evidence showing trenbolone induces PRL or gynecomastia.

If people would read my write up in the cycle section they would understand that 19-Nors actually INHIBIT prolactin and the absence (coming off) of the 19-Nor is the only thing that can cause levels to rise (hence, why expectant mothers do not lactate until hormone levels are decreased following delivery.

The thing that people need to understand is that progesterone is not a worry without the presence of estradiol (estrogen or e2). If you take the proper amount of precaution by utilizing AI's correctly and in the correct dosages, you should not have any issues with gyno. But, 19-nors CAN aggravate gyno beyond normal means in the presence of high e2 levels. I have experienced this first hand and can tell you it sucks. But, it's not from the 19-nor alone, it's the test you are taking along with it. Any of you that have ever run tren solo should be able to attest to this! You should have had no gyno issues!

 

[IronSoul]

If people would read my write up in the cycle section they would understand that 19-Nors actually INHIBIT prolactin and the absence (coming off) of the 19-Nor is the only thing that can cause levels to rise (hence, why expectant mothers do not lactate until hormone levels are decreased following delivery.

The thing that people need to understand is that progesterone is not a worry without the presence of estradiol (estrogen or e2). If you take the proper amount of precaution by utilizing AI's correctly and in the correct dosages, you should not have any issues with gyno. But, 19-nors CAN aggravate gyno beyond normal means in the presence of high e2 levels. I have experienced this first hand and can tell you it sucks. But, it's not from the 19-nor alone, it's the test you are taking along with it. Any of you that have ever run tren solo should be able to attest to this! You should have had no gyno issues!

Bumping this for a good post. And his article in the cycle section is great.

 

[graniteman]

I know this is a lil off track and the OP will probably run it anyways. BUT.. at 23 with the base you're building off I would say hold off for a few more years and build on it natty. You've got a good head start just looks like you need to up your diet and grow

 

[schultz1]

I know this is a lil off track and the OP will probably run it anyways. BUT.. at 23 with the base you're building off I would say hold off for a few more years and build on it natty. You've got a good head start just looks like you need to up your diet and grow

This. I was going to say the same thing. Honestly surprised it wasnt already recommended in one of the first few posts. I say wait grasshopper.

 

[IronSoul]

This. I was going to say the same thing. Honestly surprised it wasnt already recommended in one of the first few posts. I say wait grasshopper.

I thought the same thing when I read Gmans post. I think a lot of us may have gotten used to just offering the best advice as if they are going to run it no matter what. But definitely left out this recommendation, I definitely agree. Still a lot of room for natty gains and maturation. I was a hard headed kid that started young though. Sometimes wish I would have waited a few years.

 

[CBS]

If people would read my write up in the cycle section they would understand that 19-Nors actually INHIBIT prolactin and the absence (coming off) of the 19-Nor is the only thing that can cause levels to rise (hence, why expectant mothers do not lactate until hormone levels are decreased following delivery.

The thing that people need to understand is that progesterone is not a worry without the presence of estradiol (estrogen or e2). If you take the proper amount of precaution by utilizing AI's correctly and in the correct dosages, you should not have any issues with gyno. But, 19-nors CAN aggravate gyno beyond normal means in the presence of high e2 levels. I have experienced this first hand and can tell you it sucks. But, it's not from the 19-nor alone, it's the test you are taking along with it. Any of you that have ever run tren solo should be able to attest to this! You should have had no gyno issues!

Are you referring to your article, The Estrogen Conundrum? Nice write up with a lot of useful information that I'm sure will benefit many members. And I agree with you that progesterone is not a worry without the presence of estradiol.

However, can you provide some clarification on this quote from your article: "19-nor compounds such as trenbolone and nandrolone will have a pronounced effect on progestenic activity and can stimulate prolactin over-production in breast tissue."

Specifically, what evidence do you have that 19-nors have a pronounced effect on progestogenic activity? This is not meant as a challenge but a genuine inquiry. I've searched the literature extensively in the past and have been unable to locate anything to suggest this is the case.

While it's true that the literature has shown trenbolone has a high affinity for the PR, it's also shown the ED50 needed to produce biologic activity is up to 100 times higher than that of progesterone - blood serum concentrations of roughly 300 - 400 nM are needed for 50% of maximal effect (McRobb et al). Even if used in high doses, serum levels will not get anywhere close to these levels.

Thanks

CBS


Environ Qual Saf Suppl. 1976;(5):253-64.Pharmacological and endocrinological studies on anabolic agents.
Neumann F.

Abstract

When used in connection with animal production the term "anabolic agents" covers a wide range. Ther steroidal male and female sex hormones are included in this list, as are the nonsteroidal estrogens. For the clinician and for the endocrinologist, anabolics are only steroids chemically related to testosterone and 19-nortestosterone. Estrogens, though possessing anabolic properties, too, do not belong to this class. This paper will deal with anabolic agents in in the stricter sense of which mainly trenbolone acetate combined with hexestrol has been recommended for bull and heifer fattening. To consider possible consumer injury from ingestion of meat from anabolic agent treated animals, it is necessary to know the pharmacological properties of the agents, the doses producing certain effects or might produce, and the levels of residues in the meat. Trenbolone acetate will be compared with the following anabolic agents: methenolone acetate, methandrostenolone, nandrone, androstanazole, and 19-nortestosterone. The activity spectrum of trenbolone acetate is similar to that of 19-nortestosterone or those anabolics that are derived from 19-nortestosterone. The compound has about three times stronger androgenic effect than testosterone propionate. Its index of dissociation between anabolic/androgenic activity is 2--3. This index is 3--10 for the other anabolic agents. As regards the virilizing potency, trenbolone acetate is also on the top of the list. It seems that androgenicity and degree of virilization run paralle. The antigonadotropic activity (inhibition of ovulation and testicular growth) of trenbolone acetate exceeds that of testosterone propionate by the factor 3. The compound is not estrogenic and seemingly not or only weakly progestationally active. In principle, the androgenic activity (symptoms of virilization) as well as the antigonadotropic effect (disturbances of the menstrual cycle in women, inhibition of spermiogenesis in men) of trenbolone acetate might be noted. This risk, however, can be excluded by mere calculation. In rats, 0.1 mg/kg trenbolone acetate have an antigonadotropic effect. This corresponds to a daily dose of 5--7 mg in humans. By the same extrapolation, a daily human dose of 100 mg can be calculated for androgenic activity. Such factors of conversion are, of course, not precise because rats are much less sensitive to androgens and anabolics than humans. Thus, testosterone propionate is active only in daily doses of 10--20 mg. If in humans trenbolone acetate also has three times the activity of testosterone propionate, effects in man had to be counted with not less than a daily intake of 3--5 mg trenbolone acetate. The dose which is recommended for livestock fattening is 300 mg. IT can, therefore, be excluded almost with certainty that the meat would contain such large amounts of hormone residues.





J Steroid Biochem Mol Biol. 2008 May;110(1-2):39-47. doi: 10.1016/j.jsbmb.2007.10.008. Epub 2008 Feb 12. Structure-activity relationships of synthetic progestins in a yeast-based in vitro androgen bioassay.

McRobb L[SUP]1[/SUP], Handelsman DJ, Kazlauskas R, Wilkinson S, McLeod MD, Heather AK.

Abstract

The recent identification of tetrahydrogestrinone (THG), a non-marketed designer androgen used for sports doping but previously undetectable by established mass spectrometry-based urine drug screens, and its production by a facile chemical modification of gestrinone has raised concerns about the risks of developing designer androgens from numerous marketed progestins. We therefore have used yeast-based in vitro androgen and progesterone bioassays to conduct a structure-activity study assessing the intrinsic androgenic potential of commercially available progestins and their derivatives, to identify those compounds or structures with the highest risk of forming a basis for such misapplication. Progestins had a wide range of androgenic bioactivity that was not reliably predicted for individual steroids by their progestin bioactivity. 17alpha-Hydroxyprogesterone and 19-norprogesterone derivatives with their bulky 17beta-substituents were strong progestins but generally weak androgens. 17alpha-Ethynylated derivatives of testosterone, 19-nortestosterone and 18-methyl-19-nortestosterone such as gestrinone, ethisterone, norethisterone and norgestrel had the most significant intrinsic androgenicity of all the commercially marketed progestins. Facile chemical modification of the 17alpha-ethynyl group of each of these progestins produces 17alpha-methyl, ethyl and allyl derivatives, including THG and norbolethone, which further enhanced androgenic bioactivity. Thus by using the rapid and sensitive yeast bioassay we have screened a comprehensive set of progestins and associated structures and identified the ethynylated testosterone, 19-nortestosterone and 18-methyl-19-nortestosterone derivatives as possessing the highest risk for abuse and potential for conversion to still more potent androgens. By contrast, modern progestins such as progesterone, 17alpha-hydroxyprogesterone and 19-norprogesterone derivatives had minimal androgenic bioactivity and pose low risk.