SARMs during ADT

[PCaWarrior]

I thought that Rad-140/150 was safer than Ostarine or Ligandrol. The majority of the evidence now points me to Ostarine being the safest.

Risk Comparison Table

Parameter Ostarine Ligandrol RAD-140 Winner

AR Agonism Partial Full Full Ostarine

Prostate AR Activation Low Moderate High Ostarine

Hepatotoxicity Risk Moderate High Very High Ostarine

Clinical Data in ADT Phase II Limited None Ostarine

Anabolic:Androgenic Ratio 10:1 10:1 (preclin) 90:1 Irrelevant

Testosterone Suppression Mild Severe Severe Ostarine

Lipid Impact Mild HDL ↓ Severe HDL ↓ Severe HDL ↓ Ostarine

Muscle Selectivity High Moderate Low Ostarine

FDA Warnings Yes Yes Yes All risky

My experience with SARMs is that a few weeks of a combination of Rad-140 at doses of 15 mg/day and Ostarine at doses of 15 mg/day does not interfere with the PSA and T control of ADT (or the low phase of BAT). My HDL cholesterol decreased, but I didn’t notice other changes in my blood labs. Both SARMs are supposed to promote bone growth. They seem to do an excellent job of maintaining and even increasing muscle mass.

[Bhraen2]

They maintain or increase muscle mass in the low T phase of BAT even when you are on darolutamide

[PCaWarrior in reply to Bhraen2]

They do? How?

[Bhraen2 in reply to PCaWarrior]

It was a question. I forgot the question mark at the end.

[Bhraen2 in reply to PCaWarrior]

it was a question. I forgot the question mark at the end

[PCaWarrior in reply to Bhraen2]

Ok. SARMs need functional ARs to work. Daro blocks about 95% of the AR. High affinity.

Anyway, I am going to look into it more but first guess would be maybe 5% action? That isn't inconsequential. If you took 10 mg that would be like 0.5mg of SARM action. But I'm going to look into their binding affinity. Perhaps it's more than that, maybe less. Be worth an experiment.

[PCaWarrior in reply to Bhraen2]

So < 10%. More binding affinity but the daro in the system is 120x more than a 10mg dose of Ostarine. Maybe it'd do a bit though.

If we just are using ADT and not daro then Ostarine should work full strength. I've tried that and my subjective opinion is that it works for hypertrophy.

[PCaWarrior in reply to Bhraen2]

You might already know this.

Just in case though, ADT (GnRH drugs like Lupron or orgovyx) stops testosterone production in the body. But it does not prevent anything from binding to the ARs and doing their work - good or bad. So, ADT doesn't affect our testosterone shots and it doesn't affect SARMs. Zytiga is similar to ADT. It stops testosterone production in our body. It's a little more complicated and hasn't been characterized for this stuff. It has a couple of metabolites. Main one weakens SARMs and our T shots. The main one has another metabolite that acts on the ARs. Weird stuff. Which is stronger? Is everyone the same? Does the cancer stage matter (probably)? I don't think anyone has researched any of this stuff.

So, I use SARMs when I don't use daro or AA. I'm on the fence about using AA. Trying to figure that out now - neither here nor there.

And I'm on ADT continuously. I inject my T and measure and I have a boatload of T in my body. And I can tell just from the way my workouts go. Big gains and big muscles and lots of strength.

[PCaWarrior in reply to Bhraen2]

Interesting and exciting. If we can use Zytiga during BAT (not as part of an SOC therapy which inevitably leads to CRPC) then the androgen competition with Ostarine is reduced. So Ostarine very likely will be even more powerful than usual! And if we only use ADT for BAT the hypertrophy of Ostarine might be slightly reduced from the BAT/Zytiga therapy but still should be more powerful than normal.

If we go through a standard SOC therapy of long term CRPC inducing environment, the ARs will be upregulated but desensitized to Ostarine. And splice variants will emerge in the majority of cases. Ostarine will still be effective but at maybe 50%-75% of it's standalone power.

[Bhraen2]

Thanks for explaining. The high T phase when you are on Testosterone has the most impact on strength and muscle gains, that makes sense. And it is also bio identical to our own T so it’s works for resetting the cancer cells to the sensitive state they were in before we started taking ADT and ARSIs and killed the sensitive cells which makes resistant cells start to populate.

How long does the effects of the high T carry over into the ARSI phase in BAT. Do you start to feel the fatigue and lose strength right away or does it carry over through some of the low T phase?

SARMS especially the ones that kill prostate cancer cells (which we can’t get) seem like they would be a good medium between high T and low T.

[PCaWarrior in reply to Bhraen2]

I bulk a lot during the high T phase. I'm dieting, so I plan a refeed during high T.

The low T phase sucks but doesn't seem much worse than what I used to get before PCa. So, some carryover. And when I do SARMs during low T, I get a good hypertrophy environment.

It's not the ARSIs and ADT that are the culprit. It's the length of time doing them. SOC is to keep us in a low T environment until the inevitable CRPC emerges. That thinking just plain sucks. Denmeade has clinical trial data showing that BAT in CRPC men is non-inferior to Xtandi but has a much better QoL. And it resensitizes 75% of CRPC men to Xtandi! Not only that, but the therapy lasts longer! The FDA didn't like it because it wasn't a pre-planned objective. The FDA ruling makes sense, though, because without that hard and fast rule, we'd suffer from people data mining.

But in this case, they should get some medical researchers on board, and they would quickly realize that there is no data mining going on. It's science.

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