T Nation

Non-Test Cycle


#1

So I read up on SARMS-as both steroid-like, and T-replacement. could I run a short (12 week or less) cycle with a SARM (or 2 :wink:), and not have to use test? I'm really trying to wait till I'm 20 to use any test. any suggestions would be great!


#2

“Could” is a very broad word.

Is it a good idea? Probably not, but there’s not a complete amount of information posted about your situation. Is it the best idea in terms of effectiveness and health? Almost certainly not.

Using a SARM alone at effective doses can cause estradiol to drop too low, which can cause depression, joint pain, and loss of libido (as well as, over the long term increase risk of cardiovascular disease, but that probably has little relevance short term.) So running it alone at a dose high enough to have good muscle-building effect has a fair bit to be said against it.

For practical purposes and so far as the body is concerned, the fact that technically the atoms aren’t arranged in the steroid pattern makes no difference. The SARMs work like anabolic steroids except for in some cases giving adverse side effects to vision. Little or no safety advantage compared to non-aromatizing injectable steroids. (For example Masteron or Primobolan.)

As for combining with testosterone, little or no safety advantage to stacking a SARM with testosterone compared to stacking a non-aromatizing injectable steroid. Or compared to using testosterone alone at a dose giving equal effect, if combined with estrogen control.

Basically, it would be attempting to shortcut and not safer than various anabolic steroid cycles of equal or better efficacy.


#3

i dunno… i’ve heard of several instances where guys got gyno while using SARMs, so i presume E didn’t drop too low…

i’ve seen some bloodwork on some other forums, where one user’s test went from 565 to 140, but the E only went from 18 to 11.8…

^that was an Ostarine cycle, but i’ve seen similar results with LGD-4033.

normally, i think tossing DHEA into a cycle/PCT is pretty dumb, but i wonder if it might be beneficial with the SARMs (if one’s estrogen dropped too low)??


#4

^one of the explanations i read for the SARM-induced gyno, was that since the SARM was binding to the AR, the un-used circulating testosterone ended up aromatizing at a higher rate…


#5

To me the question really is why: it’s not as if there isn’t a much better body of knowledge and set of choices.

I have to admit having little interest in the SARMs, for that above reason. To me they’re neither here nor there: they’re neither best choices if wanting to use drugs, or legal nutritional supplements. (They are legal to possess however, I mean legal for a nutritional supplement company to sell.)

For others reading your post and not familiar with normal values, the second sentence might be read as support of the first though I’m not supposing you meant it that way. The blood test figures in the second test, if pg/mL, provide an example of estradiol dropping lower than desired from the SARM use.

I’ve never looked into how much DHEA can support estradiol level. I don’t think it’s very much but it would be something, but just how much is unknown to me.


#6

the only real advantage I could see of SARMs would be if they weren’t suppressive, but they are.

Renders them prettty much pointless, IMO.


#7

[quote]cycobushmaster wrote:
^one of the explanations i read for the SARM-induced gyno, was that since the SARM was binding to the AR, the un-used circulating testosterone ended up aromatizing at a higher rate…

[/quote]
I would have to disagree with that theory, as the percentage of testosterone that’s bound to AR’s at any given moment is nearly infinitesimal. It’s something such as one molecule in a trillion is bound to an AR (this is not the exact value: I calculated it once for an article but don’t recall the figure, but whether it’s one in a billion or trillion doesn’t change thngs.) The percent bound to AR’s is so exceedingly small that freeing it up doesn’t change concentration remotely significantly.

Another theory could be actual manifestation of the claimed “selective androgen receptor modulator” effect, in other words, acting differently at androgen receptors in differing tissues, analogous to the SERMs.

For example, tamoxifen activates the estrogen receptors in the uterus, but antagonizes the receptors in breast tissue.

What if (I am not saying it’s true) a given SARM activated androgen receptors in muscle, but antagonized or was only a weak agonist in breast tissue? Bad news if so. Not saying it is.

Another theory could be that some oral androgens are cheaper per dose than SARMs and so. I don’t know if substitution is ever the case though.


#8

[quote]Bill Roberts wrote:
the percentage of testosterone that’s bound to AR’s at any given moment is nearly infinitesimal. It’s something such as one molecule in a trillion is bound to an AR (this is not the exact value: I calculated it once for an article but don’t recall the figure, but whether it’s one in a billion or trillion doesn’t change thngs.) The percent bound to AR’s is so exceedingly small that freeing it up doesn’t change concentration remotely significantly.[/quote]

woah now, can I just jump in here a second:

If that’s true (and I’m sure it is, Bill, knowing your background) then doesn’t the whole idea that you need to let your receptors “de-sensitize,” as is popularly recommended as a reason to take time off, total bullshit?


#9

Yes, you’ve summed up that concept eloquently.

There are other reasons to take time off, but not that.

It could at least be a novel excuse for losing the Olympia: “I forgot to take time off so my receptors got desensitized.”


#10

[quote]Bill Roberts wrote:
Yes, you’ve summed up that concept eloquently.

There are other reasons to take time off, but not that.

It could at least be a novel excuse for losing the Olympia: “I forgot to take time off so my receptors got desensitized.”[/quote]

my eloquence is surpassed only by my loquacity!

I feel a little better about only taking 8 weeks off between cycles now.


#11

[quote]Bill Roberts wrote:

[quote]cycobushmaster wrote:
^one of the explanations i read for the SARM-induced gyno, was that since the SARM was binding to the AR, the un-used circulating testosterone ended up aromatizing at a higher rate…

[/quote]
I would have to disagree with that theory, as the percentage of testosterone that’s bound to AR’s at any given moment is nearly infinitesimal. It’s something such as one molecule in a trillion is bound to an AR (this is not the exact value: I calculated it once for an article but don’t recall the figure, but whether it’s one in a billion or trillion doesn’t change thngs.) The percent bound to AR’s is so exceedingly small that freeing it up doesn’t change concentration remotely significantly.

Another theory could be actual manifestation of the claimed “selective androgen receptor modulator” effect, in other words, acting differently at androgen receptors in differing tissues, analogous to the SERMs.

For example, tamoxifen activates the estrogen receptors in the uterus, but antagonizes the receptors in breast tissue.

What if (I am not saying it’s true) a given SARM activated androgen receptors in muscle, but antagonized or was only a weak agonist in breast tissue? Bad news if so. Not saying it is.

Another theory could be that some oral androgens are cheaper per dose than SARMs and so. I don’t know if substitution is ever the case though.[/quote]

interesting.

from what i understand, the SARMs (Ostarine and LGD-4033) are being tested in both prostate cancer and some other cancer treatments.

here’s a study on that topic: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2907129/


#12

i found this study, that seems to suggest that SARMs are able to reduce tumor size/weight in breast cancer. i’m not sure how that applies to gyno, however: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0103202


#13

Great find! I had not read that one.

I find it hard to come to a conclusion from it, but it could be worthy of note that ostarine (GTx-024) required about 77 times the concentration that DHT did to have the same effect on inhibiting cell growth. That doesn’t seem much potency in breast tissue. But that’s not a conclusion, I absolutely would have to put much more time into it, as again I really haven’t concerned myself with the SARMs much.


#14

[quote]cycobushmaster wrote:
i dunno… i’ve heard of several instances where guys got gyno while using SARMs, so i presume E didn’t drop too low…[/quote]

Are we talking Phase III clinical trials or RC SARMs?


#15

[quote]Apoklyps wrote:

[quote]cycobushmaster wrote:
i dunno… i’ve heard of several instances where guys got gyno while using SARMs, so i presume E didn’t drop too low…[/quote]

Are we talking Phase III clinical trials or RC SARMs?[/quote]

oh, just guys taking research SARMs on various forums…

one of those clinical trials was used to treat breast cancer tumors, interestingly enough