Nandrolone for Hair Loss? (Science Explained)

Is Nandrolone worse for your hair loss than Testosterone?

Hey guys, in this post I am going to explain how some steroids can be relatively more safe for your hair and others not.

It basically ties into a concept called called ‘myotropic - androgenic’ dissociation. What is this guy talking about you might be thinking?

Basically this means; how aggressive is the split between how much an anabolic compound can grow your MUSCLES (myotropic) vs. how much it can grow ANDROGENIC tissues like the skin, hair follicles, prostate gland and your kidneys.

The Studies into Nandrolone and Hair Loss:

Now it’s pretty well established as I’ve spoken about in many of my previous posts that dihydrotestosterone (DHT) is the main androgen that is going to cause hair loss or balding. The skin is an androgenic tissue that has a high prevalence of the 5-alpha reductase enzyme that converts Testosterone to DHT (the 5AR enzyme catalyses this reaction) and it is DHT that binds to androgen receptors in the skin and hair follicle that can then start to miniaturise them and cause cell death, basically accelerating balding.

However, in this study, researchers looked at Testosterone vs. Nandrolone (Deca), and the reason I wanted to do this post is to explore the following idea: is Nandrolone more safe for your hair than Testosterone?

The study looked at 4 compounds:

  1. Testosterone
  2. What testosterone is converted to by 5AR: DHT
  3. Nandrolone
  4. What Nandrolone is converted to by 5AR: DHN. Nandrolone does interact with the 5-alpha reductase enzyme and DHN (long name: 5 alpha dihydro 19 nortestosterone) is the metabolite that is produced.

And this study wanted to look at these 4: T, DHT, Nandrolone and DHN to see the relative binding affinities of each of these to the androgen receptor. Basically, how strong are each of these as androgens?

And what they found was interesting: the relative competition index (RCI) is as follows in androgenic tissues:

DHT > Nandrolone > Test > DHN

As you can see in this table (the values in brackets are the ones to look at), DHN is going to compete for the androgen receptor the least, at around 12% of what DHT does:

Now if I stopped the post here, you’d be slightly concerned - Nortestosterone (Nandrolone) has a higher affinity for the androgen receptor than testosterone, so it should be even worse for hair loss right?

Well, no, because in androgenic tissues, 5AR comes into play in a big way.

Because we know that Nandrolone interacts with the 5AR enzyme, even though it’s more androgenic than testosterone, it is reduced to DHN in the skin tissue by 5AR.

Now usually, once T is reduced to DHT, it goes from a binding value of around 0.1-0.2 all the way to 1.0, a very significant increase in potency. However, Nandrolone once reduced to DHN goes from 0.32 to 0.12, an almost 3x decrease in potency at the nuclear androgen receptor. So whereas the reduction of T to DHT increases androgenicity, the reduction of N to DHN reduces androgenicity by a lot.

So, despite Nandrolone being more competitive for the androgen receptor and worse for balding at face value, it may actually be safer for hair as it is not converted to DHT when it interacts with 5-alpha reductase but something 1/10th as potent, DHN. However, the irony is that taking Finasteride or Dutasteride with Nandrolone would actually be worse for your hair.

Why? How can the usual hair-loss drugs be worse for my hair on Nandrolone?

Well, because the conversion of Nandrolone to DHN favours hair safety (i.e. DHN is the least androgenic out of the 4), stopping this conversion with Finasteride or Dutasteride which bind into the 5AR enzyme and stop it functioning (as seen in the image below) would lead to more Nandrolone in your skin and less DHN being produced (you’re taking 5AR out of the equation). If this was Testosterone and DHT we were talking about, that would be perfect, I would just rewrite the exact same sentence above as:

Stopping this conversion with Finasteride or Dutasteride which bind into the 5AR enzyme and stop it functioning would lead to more Testosterone in your skin and less DHT.

In the case of T and DHT, this is perfect, this is what we want, less DHT means less of the primary hair follicle killer being able to exert damage to our hair follicles (miniaturisation).

Finasteride binds to 5-alpha reductase and stops the conversion of Testosterone (T) to Dihydrotestosterone (DHT).

However with Nandrolone, because DHN has such a lower binding affinity, if you are on Nandrolone, you don’t want to stop 5AR. You actually want the 5AR enzyme to convert Nandrolone to DHN, because then you’re going to have the least androgenic compound in your skin (DHN), exerting much less damage on your hair follicles than Nandrolone, T or DHT.

To back this up, in this study you can see that when a 5-AR inhibitor is introduced, Nandrolone becomes significantly more androgenic (4th bar from the left, below). This is precisely because blocking 5AR in the Nandrolone only group leaves a more androgenic compound in serum, as opposed to it being able to be reduced to a much less androgenic compound in DHN by 5AR. As expected, 5AR inhibition of Testosterone significantly reduced androgenic load as measured by ventral prostate stimulation (an androgenic tissue), because in terms of androgenicity: DHT is much greater than T.

So in conclusion, DHN is significantly less androgenic than T, DHT and Nandrolone. Stopping the conversion (reduction) of T to DHT is conventional wisdom for hair loss and will absolutely reduce androgenicity in your skin and near your hair follicles and will slow down your balding. The opposite is true for Nandrolone, you actually want the reduction of Nandrolone to DHN, as it converts Nandrolone into a relatively ‘safer’ compound for hair loss. DHN occupying the active binding site of the androgen receptors in and around your hair follicles is going to exert around 90% less androgenic activity than DHT, akin to how something like RU58841 ‘occupies’ the androgen receptor and stops more potent androgens binding and wreaking havoc on our hair follicles.

So, if you are worried about your hair loss on certain compounds, understanding the pharmacokinetics and how they interact with 5-alpha reductase is key. Is a certain compound a substrate for the 5AR enzyme and able to be reduced? What is the androgenicity of this compound and what is the androgenicity of its reduced form? These are some questions that can help you decide how much of an effect a compound will have on your hair.

I hope I’ve given you guys something to think about if saving your hair is important to you.

Thanks for reading as always.

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