T Nation

Bridging Between Cycles


#1

Anyone ever heard of anyone doing this ?

1st time i've ever read it to be honest ...


#2

Well, a problem with that is that one still needs to deal with the matter of alkylated androgens, even if low dose, properly being used for only limited periods of time with reasonable off periods.

As a different thing but on the same subject, a while back I was actually thinking of writing an article (!) on something I think could be quite promising. But, I wouldn’t do that unless it were supported with some measured data and certainly more than just one subject.

Actually went to the trouble of beginning to line up some that might be willing to put up with the blood tests involved. (Just beginning to.) And of drafting an e-mail to TC outlining the costs that would be involved, as I wouldn’t be able to do it on my own dime.

However, I didn’t wind up doing so as I considered it better to document in my own case first with blood tests, and I didn’t get around to doing that.

So, what is it already?

There is limited data that ongoing substantial Primobolan use off-cycle can still allow good T production.

Primobolan is generally very expensive in the US. I had a hope which I thought reasonable that Masteron might do the same.

So I thought perhaps the following factors could be employed:

  1. E2 maintained at low normal, which is known to enhance T production quite considerably relative to mid-normal E2, as a positive factor.

  2. Ongoing Masteron at some moderate dose, as a moderate negative factor through androgenic inhibition. But androgenic inhibition is not very much at for example even the top end of the normal range of free T, else that could not be generated naturally.

  3. Optionally some HCG to increase natural T production. The main part of the inhibitory effect of HCG is I think from aromatization of resulting T, though some certainly is from the androgenic effect of T.

  4. Optionally a low-dose SERM, for example 10 mg/day Nolvadex or 25 mg/day Clomid, if this gave better results than simply keeping E2 low-normal, as I expect it would. Part of the effort would be establishing and quantitating how much.

Ideally the protocol would be adjusted to have as much free T and as high a Masteron dose as possible while still keeping LH not much below midnormal.

Anyhow, personally I used 15 mg/day Masteron along with I think 100 IU/day HCG and about 0.36 mg/day letrozole and this was really nice. I did not take any test to establish that LH was still being produced in the normal range. I tend to expect it was but have no proof.

The dosage was sufficient, surprisingly to me, to fully have the added weight increase that I attributed to added glycogen storage and glycogen associated water that supraphysiological doses of androgen allow. Which for me is 9 lb extra weight for same bodyfat.


#3

[quote]Bill Roberts wrote:

Anyhow, personally I used 15 mg/day Masteron along with I think 100 IU/day HCG and about 0.36 mg/day letrozole and this was really nice. I did not take any test to establish that LH was still being produced in the normal range. I tend to expect it was but have no proof.
[/quote]

I have seen you mention this several times and it is intriguing. What made you tend to expect that LH was in the normal range?

If you could put together a small experiment with TC that would be awesome.


#4

I was also very interested in this when you posted about it in the past, Bill. I would very much like to see more about it. Could one also use this in a recovery context, or would this only work for someone with normal LH levels when starting?


#5

Only because of estimation that there wasn’t enough androgen and not enough estrogen to be likely to drive it below normal.

Impossible to tell for a fact without testing for LH.

A beauty part of such protocols that don’t include or generate testosterone is that’s all that’s needed to verify decent LH product is measuring testosterone. But of course when HCG is elevating that, or testosterone is being injected, then LH needs to be actually measured.

Again, the thing to do really is to do it on myself first. I’ve always preferred a proof of concept that way before involving others.

Though sometimes that can be a bad thing, if one happens to be an unusually poor responder to something and thus ditches it on the n=1 example. I doubt that would be the case here though.

At the moment I don’t have any Masteron and wasn’t planning on having an extended “off” period for a while, but that doesn’t mean I ought not to get to it reasonably soon.


#6

How would the addition of a SERM result in better results? Better in terms of lipid profile? Or better for endogenous test production?

These answers are probably staring me right in the face. Apologies for the ignorance.


#7

[quote]Bill Roberts wrote:
I think 100 IU/day HCG and about 0.36 mg/day letrozole and this was really nice. I did not take any test to establish that LH was still being produced in the normal range. I tend to expect it was but have no proof.

[/quote]

I am curious about your opinion of chronic HcG use and its subsequent effect on LH receptor down-regulation. Also, I believe HcG stimulation also leads to an uncoupling of adenylate cyclase from the LH-R (or perhaps it was,or even in addition to, a lesion between the Gs and LHR) leading to lowered levels of cyclic-AMP formation, decreasing the activity of 17a-hydroxylase.

Now, it seems intravenous administration is popular on this site, and I certainly imagine that HcG administration IM or IV would alter the half life, perhaps leading to a more “pulsatile” secretion, which would in part, prevent the aforementioned? Or do you believe the lowered cyclic AMP formation and down-reg is overstated in this amount?


#8

What is your evidence that the things you are concerned about occur at dosages such as I mentioned?

Also btw, it would not be correct that IV administration is popular on this site for HCG or fpr any performance enhancing drug. It has been advocated as advantageous for GH by one experienced user who is an excellent source of information, but even he has stated that most will not do this, and in fact most don’t. And by most I mean probably 99% plus.

Additionally, HCG, unlike GH, is long-lasting once in the bloodstream, so any sub-Q/IM/IV differences in speed with which it gets there would be IMO of no particular importance.


#9

[quote]downintucson wrote:
How would the addition of a SERM result in better results? Better in terms of lipid profile? Or better for endogenous test production?

These answers are probably staring me right in the face. Apologies for the ignorance.[/quote]

I wasn’t clear. My principal meaning was possibly higher LH. This could occur because of net inhibitory estrogenic effect being even less due to ER antagonism; and oddly enough (by this time I forget exactly how) there also seems a mechanism where SERMs via an estrogenic effect enhance LH production.

They are capable of acting both as estrogens and anti-estrogens. Very nicely, the pharmaceutical SERMs are quite well matched to being anti-estrogenic where that is a good thing, and estrogenic where that is a good thing. Exceptions being that some are bothered by estrogenic effect of Clomid on mood, and for women, uterine estrogenicity of tamoxifen and clomiphene is undesirable in terms of cancer risk. As a complete side note, raloxifene does not have that problem, being anti-estrogenic there as well.

I don’t know for a fact that there would be an advantage in LH production in the exact situation I was describing. That would have to be tested. I just see it as a possibility worth exploring.

There wouldn’t necessarily be much higher T from a resulting improvement in LH. The testes are only going to produce so much. For example there isn’t necessarily much more produced from increasing daily dosage of HCG past that figure, though on average there is probably a little bit more yet to be gained.

As to why, if it were the case that without the SERM, LH was say just barely normal, at the very low end, if with the SERM this improved to midnormal or near it, why one would want to bother, it seems to me there’s a chance that if the protocol were used for really extended periods, staying at midnormal LH over all that time might be more favorable, if discontinuing the protocol, than if one had at all that time just barely been scraping the bottom end of the normal range. Maybe not, maybe there would be no difference. I don’t know, but not knowing, personally I’d rather take the more conservative approach, which I see as trying to keep the LH production pretty good the entire time.

Additionally, though, as you point out there would be an expected advantage in blood lipid profile.

Just as an n=1 example, I do know an individual who found Masteron, used alone, to improve his blood lipid profile, a thing he is always (or at least often, it seems) worried about. I don’t know if that would happen with T also being elevated by concurrent low-dose HCG use, or whether it would happen with other people generally. It’s an interesting result he had.\

I would be including blood lipid profiles in any such testing.


#10

http://books.google.com/books?id=KQstnA8Bb58C&pg=PA171&lpg=PA171&dq=LH+receptors+down+regulated&source=bl&ots=QlX-Srmc1r&sig=GXGUo_3mlqodGYxUph3pHygF5Qs&hl=en&ei=aQ5yStPfM5O8MMnqkbEM&sa=X&oi=book_result&ct=result&resnum=7

Massicotte J, Borgus JP, Lachance R, Labrie F.

PMID: 6261040

http://www.jbc.org/cgi/content/abstract/266/2/780

I obviously know that steroids were not being recommended to be injected intravenously. Sorry if that offended you, Bill, it was not my intent. I also inferred from previous knowledge on GPCR as their is some similarity between the different receptors of the same class. I could quote some of that information too, if need be.

Thanks for your time = )


#11

You did not offend me, but above you do move towards doing 2 things that bug me.

First, I never like when people snap out references as if they prove what they are saying (as many readers will, sadly, assume that they do) that don’t do any such thing.

I asked you specifically what evidence you had that this occurred at the doses I was referring to.

Neither of your references addresses this at all except that the first specifically refers to high-dose.

Second, you come up with this “Sorry if I offended you” by insisting that you didn’t mean what I supposedly said you did, when in fact nowhere did I say that you had stated steroids were injected IV.

I really don’t need for you to “quote some of that information too, if need be.”

You can go away. You are a fool.

Learn to understand what is written first before you waste my time further. Don’t read things that make no mention of dose, and where dose medically has in the past typically been at levels 50 times higher than I am referring to, and EVEN AFTER it’s pointed out to you that dose is relevant and what is your evidence at the dose in question, go spouting references that don’t address dose except to make clear that they are talking about high dose.

And do not read replies and write bullshit apologies for supposedly being misinterpreted when you are not.

For all I know and can tell, you are a 13 year old trying to play pharmacologist. You have failed. Sit back and read what is already available and what becomes available as it appears in various places from various sources. Don’t waste my time. I usually don’t announce people being on my Ignore list – they just get there – but just to be clear, there you are. So I am assured of your not wasting my time with more crap such as every single word you have written in this thread.


#12

Wow, I really don’t know what to say. I was asking YOU, because I didn’t know. I even said I was inferring from other knowledge that I knew to be true, that is why I was ASKING YOU. I have NEVER ONCE since I started posting here pretended to be some authority. I don’t even take fucking steroids, I just find the stuff you guys talk about interesting. I won’t ever post in here again, thanks for being a big jackass.

Also you know damn well as I do, that they JUST DON’T DO an abundant amount of studies on these topics, especially in human males, so don’t fucking pretend like they do. Half the shit on HcG is in fucking female rat tissue and has no relation to what you are even talking about.


#13

[quote]Bill Roberts wrote:
Well, a problem with that is that one still needs to deal with the matter of alkylated androgens, even if low dose, properly being used for only limited periods of time with reasonable off periods.

As a different thing but on the same subject, a while back I was actually thinking of writing an article (!) on something I think could be quite promising. But, I wouldn’t do that unless it were supported with some measured data and certainly more than just one subject.

Actually went to the trouble of beginning to line up some that might be willing to put up with the blood tests involved. (Just beginning to.) And of drafting an e-mail to TC outlining the costs that would be involved, as I wouldn’t be able to do it on my own dime.

However, I didn’t wind up doing so as I considered it better to document in my own case first with blood tests, and I didn’t get around to doing that.

So, what is it already?

There is limited data that ongoing substantial Primobolan use off-cycle can still allow good T production.

Primobolan is generally very expensive in the US. I had a hope which I thought reasonable that Masteron might do the same.

So I thought perhaps the following factors could be employed:

  1. E2 maintained at low normal, which is known to enhance T production quite considerably relative to mid-normal E2, as a positive factor.

  2. Ongoing Masteron at some moderate dose, as a moderate negative factor through androgenic inhibition. But androgenic inhibition is not very much at for example even the top end of the normal range of free T, else that could not be generated naturally.

  3. Optionally some HCG to increase natural T production. The main part of the inhibitory effect of HCG is I think from aromatization of resulting T, though some certainly is from the androgenic effect of T.

  4. Optionally a low-dose SERM, for example 10 mg/day Nolvadex or 25 mg/day Clomid, if this gave better results than simply keeping E2 low-normal, as I expect it would. Part of the effort would be establishing and quantitating how much.

Ideally the protocol would be adjusted to have as much free T and as high a Masteron dose as possible while still keeping LH not much below midnormal.

Anyhow, personally I used 15 mg/day Masteron along with I think 100 IU/day HCG and about 0.36 mg/day letrozole and this was really nice. I did not take any test to establish that LH was still being produced in the normal range. I tend to expect it was but have no proof.

The dosage was sufficient, surprisingly to me, to fully have the added weight increase that I attributed to added glycogen storage and glycogen associated water that supraphysiological doses of androgen allow. Which for me is 9 lb extra weight for same bodyfat.[/quote]

For these kind of tests and experiments - where are the costs? Is the main cost the drugs… or the scientific testing methods?

If in detail you might want to email me… :wink:


#14

Thank you Mr. Roberts. Lots of great info in your response.


#15

[quote] Brook wrote:
For these kind of tests and experiments - where are the costs? Is the main cost the drugs… or the scientific testing methods?

If in detail you might want to email me… ;)[/quote]

The costs would be the blood tests. Those I was asking if they’d consider doing it would have been paying for their own drugs.

Really no fancy science, just standard blood tests for LH, free T, E2, and lipid profile.


#16

[quote]Bill Roberts wrote:
Well, a problem with that is that one still needs to deal with the matter of alkylated androgens, even if low dose, properly being used for only limited periods of time with reasonable off periods.

As a different thing but on the same subject, a while back I was actually thinking of writing an article (!) on something I think could be quite promising. But, I wouldn’t do that unless it were supported with some measured data and certainly more than just one subject.

Actually went to the trouble of beginning to line up some that might be willing to put up with the blood tests involved. (Just beginning to.) And of drafting an e-mail to TC outlining the costs that would be involved, as I wouldn’t be able to do it on my own dime.

However, I didn’t wind up doing so as I considered it better to document in my own case first with blood tests, and I didn’t get around to doing that.

So, what is it already?

There is limited data that ongoing substantial Primobolan use off-cycle can still allow good T production.

Primobolan is generally very expensive in the US. I had a hope which I thought reasonable that Masteron might do the same.

So I thought perhaps the following factors could be employed:

  1. E2 maintained at low normal, which is known to enhance T production quite considerably relative to mid-normal E2, as a positive factor.

  2. Ongoing Masteron at some moderate dose, as a moderate negative factor through androgenic inhibition. But androgenic inhibition is not very much at for example even the top end of the normal range of free T, else that could not be generated naturally.

  3. Optionally some HCG to increase natural T production. The main part of the inhibitory effect of HCG is I think from aromatization of resulting T, though some certainly is from the androgenic effect of T.

  4. Optionally a low-dose SERM, for example 10 mg/day Nolvadex or 25 mg/day Clomid, if this gave better results than simply keeping E2 low-normal, as I expect it would. Part of the effort would be establishing and quantitating how much.

Ideally the protocol would be adjusted to have as much free T and as high a Masteron dose as possible while still keeping LH not much below midnormal.

Anyhow, personally I used 15 mg/day Masteron along with I think 100 IU/day HCG and about 0.36 mg/day letrozole and this was really nice. I did not take any test to establish that LH was still being produced in the normal range. I tend to expect it was but have no proof.

The dosage was sufficient, surprisingly to me, to fully have the added weight increase that I attributed to added glycogen storage and glycogen associated water that supraphysiological doses of androgen allow. Which for me is 9 lb extra weight for same bodyfat.[/quote]

Expecting a few one line answers and get an essay excellent !

I suppose i “could” try this… i have more than enough time to purchase Masteron Nolva i already have… would HCG be needed ? I have the money recession has had zero effect on my job thank god but i’ve never tried it before not a fan of adding more than 1 compound i haven’t tried before in a “cycle”

I have “heard” of people using Nolva at low levels even when not on cycle to somewhat raise T, i have seen on other boards of reccomendations of 0.3 ( 2 sprays) EOD of Arimadex … but the other 2 parts are completely new to me.

If one was to try this, how many tests would one need to do ? If i can read between the lines Brook is maybe thinking of it. And if you have done it, then that is 3 peoples results… obviously not excellent but better than none.

Thank you once again for your time, every question i have asked via PM or on here you have answered fully. It’s appreciated.


#17

No, i was on a different page to that actually. Nothing i can write in public.

As per your post - i know it is directed primarily at BR but i would like to have a few shots too if you don’t mind?

I personally think that many AAS in low enough doses alongside SERM can be used as a bridge (or more accurately be used with little impact on the HPTA) - the only issue is finding a balance between low doses that are not suppressive (with SERM) and actually being worth the effort and money WRT results.

The drug would have to be Androstan based, rather than a Nortest or Estren, etc. as they are known to be more suppressive and rightly so. AFAIK any other drug is up for grabs, what depends is if it is going to be of any use in those low doses needed - however Var which is known as a particularly weak AAS is one of the most famous bridging AAS so… that makes most contenders i would imagine. (although it isn’t weak per se as in potency, just mild in effect)

I know that Test E with a SERM is around 15mg/day. Mast is Ok to use too according to Bill… and is ~15mg/day.
I would think that Stanazolol at 10-20mg/day would also be possible too. We know that Anavar has been used at 10-20mg as has Dbol at 5-10mg ED… i would imagine Tbol would be fine as would Eq… but i am speculating now of course…

I think that HCG could be used as a bridge in and of itself, just 50iu ED with a low dose Adex would surely bring the natural test level to high normal. I think this is more than viable. But as an ancillary to the bridge and an aid to recovery i would say it would definitely help.

Not to mention just an AI like adex at low dose between cycles to keep natty test as high as naturally possible.

In fact, the B+C protocol is an aggressive form of bridging, where recovery isn’t the goal but a break, a drop of activity at the receptor is - and that works too.

I would use any of the drugs given above with low dose HCG and SERM as a bridge, sure.

JMO :wink:


#18

On whether HCG is needed: No. I think its inclusion would optimize the program, but if wanting to do without it an absolutely reasonable Stage I, so to speak, is using simply Masteron at low dose and nothing but.

A beauty part of that is that now all it takes is testing for T to see if there’s an inhibition problem or not. A cheap salivary test would be reasonably good. Things to watch out for are that a very small invisible trace of blood (don’t brush the teeth for a good length of time, I’d say 24 hours but 12 may suffice, before the test) will give way-high readings, and potentially there’s some risk that the test could mistake dromostanolone for testosterone and give a falsely high reading for that reason. However, the test isn’t going to come out falsely low.

I’d recommend 15 mg/day as the initial dose.

A reasonable stage II would be, using the result from an estradiol value obtained at the same time as doing the test for T, deciding on an AI dose. Additionally, if the T value was quite good in the first test, the Masteron dose might be knocked up 30-50% depending on T values.

I’m glad I managed to answer all your questions! Unfortunately, on PM’s there’s a lot I’ve failed to get to :frowning:


#19

On Brook’s post, which I hadn’t seen when writing the above: I agree, HCG with an AI is fine for a bridge also (I have done that but it does not have near the effect that the Masteron-plus program I described had. Nor does just 15 mg/day TP and an AI.)


#20

Really? Mast is that good in that manner? wow - i am surprised and impressed.

I have been using it in a low dose alongside low dose test (100~200mg of each) for a cruise and it has served me very well… significantly better than test alone - i habe a new found fondness for drostanolone!