Any research about SARMs antagonism?

[alehman]

Hi all, this is my first post here but I've been following for a while. Have enjoyed this resource a lot so far.

I'm running 2.5 mg lgd with a 250mg/wk test-e base to counteract the significant shutdown of the lgd. That way I can be a little into the supraphysiological range of test with the further anabolic boost from the lgd. Will titrate up to 5mg daily lgd.

It's clearly understood that SARMs are agonists in skeletal/muscular tissue, but I'm wondering if anyone knows of studies out there (not speculation) about SARMs antagonizing tissues in which they're not agonists, or at least occupying the androgenic receptor sites--- much like how SERMs can be agonistic in certain tissues and antagonistic in others. I'm wondering if my lgd will compete with or block testosterone in non-skeletomuscular tissue, effectively reducing the desirable androgenic effects of the test.

Thanks for your help.

 

[hambone2493]

You may just wanna hit up Google scholar.

 

[user567]

Hi all, this is my first post here but I've been following for a while. Have enjoyed this resource a lot so far.

I'm running 2.5 mg lgd with a 250mg/wk test-e base to counteract the significant shutdown of the lgd. That way I can be a little into the supraphysiological range of test with the further anabolic boost from the lgd. Will titrate up to 5mg daily lgd.

It's clearly understood that SARMs are agonists in skeletal/muscular tissue, but I'm wondering if anyone knows of studies out there (not speculation) about SARMs antagonizing tissues in which they're not agonists, or at least occupying the androgenic receptor sites--- much like how SERMs can be agonistic in certain tissues and antagonistic in others. I'm wondering if my lgd will compete with or block testosterone in non-skeletomuscular tissue, effectively reducing the desirable androgenic effects of the test.

Thanks for your help.

This has been brought up before with no definitive answer. Great question though. Testosterone has many roles in the body and even plays a role in the brain/ emotions/thoughts

 

[bigdavid]

Hi all, this is my first post here but I've been following for a while. Have enjoyed this resource a lot so far.

I'm running 2.5 mg lgd with a 250mg/wk test-e base to counteract the significant shutdown of the lgd. That way I can be a little into the supraphysiological range of test with the further anabolic boost from the lgd. Will titrate up to 5mg daily lgd.

It's clearly understood that SARMs are agonists in skeletal/muscular tissue, but I'm wondering if anyone knows of studies out there (not speculation) about SARMs antagonizing tissues in which they're not agonists, or at least occupying the androgenic receptor sites--- much like how SERMs can be agonistic in certain tissues and antagonistic in others. I'm wondering if my lgd will compete with or block testosterone in non-skeletomuscular tissue, effectively reducing the desirable androgenic effects of the test.

Thanks for your help.

I’m not aware of data on LGD regarding this.
Rad140 is antagonistic in prostate tissue, though that may not help you much since you aren’t taking it lol

Regarding neurological effects. When I took LGD for about a month it definitely exacerbated depressive symptoms. Even when I was on a normal dose of test. I have a hx of depression though so that probably won’t happen with everyone. I had a similar reaction to ostarine. Feel great on rad140.

 

[bigdavid]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4018048/

If you find any studies you want to read on the topic but don’t have full access just send the link my way or post it here. I have university access to almost every journal/publication out there.

 

[alehman]

I am familiar with the antagonistic properties of sarms in the prostate but clearly theres not much out there about their effects in other tissues. I feel like this is where we would benefit greatly from more studies into sarms. If sarms are antagonistic in a variety of other tissues, then they are effectively testosterone blockers in those areas in addition to being suppressive to test production. This could be further concerning in how it may affect regulation of those receptor sites (possible upregulation), which there also doesnt seem to be a lot of studies about.

If this were the case then sarms could potentially wreak havoc in unexpected ways. As an example, for all the sarms advocates who say they dont affect hair, if androgenic receptors in scalp tissue are upregulated from sarms use then after a cycle one could experience heightened androgenic activity and potential hair loss. This would be compounded by possible PCT SERMs use, clomid and tamox both antagonizing estrogen activity at the scalp which can notably cause hair loss.

 

[alehman]

Also thanks for the link bigdavid. Ill check it out.

 

[bigdavid]

I am familiar with the antagonistic properties of sarms in the prostate but clearly theres not much out there about their effects in other tissues. I feel like this is where we would benefit greatly from more studies into sarms. If sarms are antagonistic in a variety of other tissues, then they are effectively testosterone blockers in those areas in addition to being suppressive to test production. This could be further concerning in how it may affect regulation of those receptor sites (possible upregulation), which there also doesnt seem to be a lot of studies about.

If this were the case then sarms could potentially wreak havoc in unexpected ways. As an example, for all the sarms advocates who say they dont affect hair, if androgenic receptors in scalp tissue are upregulated from sarms use then after a cycle one could experience heightened androgenic activity and potential hair loss. This would be compounded by possible PCT SERMs use, clomid and tamox both antagonizing estrogen activity at the scalp which can notably cause hair loss.

Your thoughts on high dose sarm use having some of the same side effects as traditional AAS have been discussed in great length on this forum to my recollection. The consensus seemed to be that high dose usage would decrease their selective nature and if something agonizes the AR, just as AAS do, then you will get a similar side effect profile.

Regarding further studies, any future ones that are conducted will surely be on the elderly, muscle wasting conditions, post menopause osteoproetic patients, etc. and the doses used will be in most cases lower than what we would use. Also, any biochemical assays done would likely be focused on those same dosing parameters (ie lower range), as it looks bad (for future marketing and other reasons) to test higher doses and expose the fact that it can have similar sides to AAS. The whole marketing scheme is based on the selling point that they are indeed selective and different from traditional steroids. Though in all likelihood lower doses of previously banned orals could have a similar selective nature just due to pharmacokinetic considerations.

 

[netflixNchill]

I know it's irrelevant to the question but 2.5-5mg of LGD isn't gonna do much. Maybe 2-3lbs in a 4-5week run

 

[alehman]

Bigdavid--- the loss of selectivity makes sense. Im assuming high doses means any amount that will cause appreciable muscle gain?

Netflix--- from what Ive read i would agree. Im trying to cut right now and dont care that much to gain muscle... just want to hold onto what i have. Figured a modest dose of lgd with 250mg/wk test would help me avoid sides of both and synergize well. Plus this is my first AAS cycle (only ever run ostarine by itself) so i expect i will be pretty responsive to test w/ lgd. We will see.