SARM’s the RAGE in Bodybuilding

SARM’s (selective androgen receptor modulators) thus far have been a relative disappointment in the bodybuilding world.  Primarily because just like anabolic steroids and prohormones, they seem to be suppressive in higher doses, and come at a high price.  I just recently explained why this occurs with the use of Ostarine – Ostarine in PCT.  Essentially they are only SARM’s when doses are low.  Even the mother of all hormones trenbolone has been studied for it’s SARM like properties in low doses [1].

Why Testosterone is not a SARM

Testosterone is anabolic in muscle tissue, which is great for the purpose of a SARM, but it’s also known to have anabolic action in the prostate.  Follistatin, however does not have anabolic action in the prostate.  You also know follistatin as a myostain inhibitor, and they have consistently shown an inverse relationship (myostatin bad, follistatin good).

In a new study scientists gave mice testosterone, or follistatin and measured prostate growth [1].  Of course only the testosterone treated mice experienced prostate growth.  They believed polyamine biosynthesis regulated the prostate growth.  They knew that in order for polyamine biosynthesis to occur in the prostate that Ornithine decarboxylase (an enzyme that converts ornithine to putrescine) expression was needed.  Ornithine decarboxylase is known to increase with androgen receptor activation [2].  Now this all sounds fucking complicated, and it is to some degree.  But their theory was as simple as this – Give mice testosterone, and an ornithine decarboxylase inhibitor, and it will act as a SARM.

Ornithine Decarboxylase and Heart Health

It’s worth pointing out that several drugs are known to up-regulate Ornithine decarboxylase, including beta-agonists like clenbuterol up-regulate Ornithine decarboxylase expression.  While I’m not aware of any human studies (it’s too dangerous and unethical to study such a thing), several studies have tied heart hypertrophy to an increase in Ornithine decarboxylase, and it’s exacerbated with beta-agonist use.  [3, 4, 5, etc].

“In addition to b-agonists, androgens, which increase skeletal mass and strength, have also been shown to stimulate polyamine accumulation in a number of tissues. In muscle, androgens act via the androgen receptor to regulate expression of polyamine biosynthetic enzyme genes, including Odc1 and Amd1, which may be one mechanism via which androgens promote muscle growth.” [6]

Perhaps this is a reason we see bodybuilders have heart attacks at a young age (the combination of years of tesoterone/anabolics, and beta-agonists).

Inhibiting Ornithine Decarboxylase Creates a SARM

Back to the original study.  In this study they gave mice testosterone and a drug called a-difluoromethylornithine (or the drug known as Eflornithine).  Which is notably also a topical drug used to inhibit excessive facial hair growth in women.  Nonetheless at the end of the study the mice that were given eflornithine still increased muscle mass (that’s important), but did not experience the prostate growth that the testosterone only group did.  Here’s a look at both the levator ani (muscle) weights, and prostate weight, post treatments:

Ornithine DecarboxylaseIntact – Not Castrated
Cx – Castrated
T – Testosterone Propionate
DFMO – Eflornithine

 The Next SARM Super Star?

So you might be thinking, should I stack my testosterone (or theoretically other anabolics) with an ornithine decarboxylase inhibitor?  Well it’s hard to say, since zero human research exists on this combination.  It’s possible, just like other SARM’s, high doses of anabolics will simply overcome the benefits of a SARM.  There are also potential side effects from ornithine decarboxylase inhibitors you might not want to experience.  Either way, it’s most interesting because it might be something to reduce heart hypertrophy, and subsequent early death from steroid use.  I’m not expecting we know for sure in this lifetime though.

– Travis DeGraff


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