Hair today, gone tomorrow.
At least, that’s what it can seem like if you’re one of the many men with a genetic predisposition to male pattern baldness – particularly if that is expedited by recreational steroid use.
Traditional hair-loss solutions have focused on the effect of the body’s natural steroids, particularly testosterone and DHT. Testosterone is converted in the scalp by the enzyme 5alpha-reductase into dihydrotestosterone, or DHT. DHT is a much stronger androgen than testosterone, and in predisposed men it can cause follicles to shrink or “miniaturize”. In turn, this shortens their lifespan and prevents them from producing hair normally, eventually leading to a receding hairline and/or spreading bald spot.
It is important to recognise that when synthetic anabolic steroids are used it isn’t DHT that is causing this androgenic effect, but the steroids administered (or their metabolites), triggering the same effect through their actions at the androgen receptor.
The most common solution to MPB or androgenic alopecia involves preventing the conversion of testosterone to DHT, using a 5AR inhibitor like finasteride or dutasteride. These are steroids that are inactive as far as the androgen receptor is concerned, but they bind to the 5AR enzyme, thus preventing the enzyme from converting testosterone to DHT.
While this can be effective in preventing further hair loss by natural causes, these drugs are not without their own side effects (which can include impotence and gynecomastia), and they are ineffective at preventing hair loss caused by almost all modern prohormones and anabolic steroids.
The reason for this is due to steroid metabolism, and here’s where we start to get technical.
Many of today’s steroids are based on the (5a)DHT structure. This means that they cannot be 5a-reduced by 5AR, since they are already 5a-reduced steroids. So disabling the 5AR enzyme has no effect on their metabolism – they are still just as androgenic in the scalp.
Designer steroids in this (DHT-based, or 5a-reduced) class include superdrol, protodrol, methyl sten, furazadrol, epistane, phera, prostanozol, and many others. DHT-based traditional oral steroids include stanozolol, oxymetholone, and oxandrolone.
However, even those taking compounds that do contain a delta 4 double bond are not necessarily going to benefit from taking a 5a-reductase inhibitor.
Nandrolone, unlike testosterone, actually increases shedding/hairloss when you prevent 5a-reduction (by using finasteride, for example). In order to understand why, you have to understand that the 5a-reduced metabolite of nandrolone (19-nor-DHT) is actually less androgenic than nandrolone.
Since this means that nandrolone is made less androgenic in tissues that have high concentrations of 5AR, it means that nandrolone is generally fairly “hair-safe”.
As soon as you prevent that 5a-reduction (by administering finasteride), you remove the good things nandrolone has going for it (low relative androgenic properties) and increase androgenicity in areas with lots of 5AR (scalp, skin etc.). [1-3]
The bioreduction of the C-4, -5 double bond of testosterone by 5a-reductase occurs selectively from the alpha-face. The product of this reduction, 5a-DHT, assumes a chairlike conformation and has a higher AR affinity relative to testosterone.
Interestingly, the compound resulting from simultaneous 5a-reduction and removal of the 19-methyl group has a lower binding affinity than testosterone.
So a 5AR inhibitor is not a good idea with nandrolone. What about other 19-nors like dienolone or trenbolone?
Actually, like the DHT compounds, 5AR inhibitors are ineffective with trenbolone and dienolone because the conjugated double bond system prevents the C4-C5 bond being reduced by the 5AR enzyme. [4-8]
Ok, so 5AR inhibitors are useless with DHT-based compounds, trenbolone, dienolone, and will actually increase hair loss with nandrolone. What else is there?
Another class of hormones that deserve separate consideration are the 1,4-dienes. These have the C4-C5 double bond of testosterone, but also have the C1-C2 double bond of 1-testosterone. These compounds include boldenone, boldione, methandienone (dianabol), 17a-methyl-1,4-androstadiene-diol (M1,4ADD), oral turinabol, and halodrol.
In vivo reduction of the delta-4 double bond (to produce 1-dehydro metabolites) does occur, however crucially they selectively reduce to 5b-reduced compounds. 5b-reduced compounds are inactive, they bind poorly or not at all to the androgen receptor, and so do not exert any significant androgenic effects (so they are not a concern for hair loss).
Proposed metabolism scheme for steroids with androst-1,4-diene-3-one structure
M1 concerns the reduction of the C-4,5 double bond leading mainly to the 5b-H isomer. The simultaneous presence of a C-1,2 double bond, as occurs in methandienone and boldenone molecules, inhibits the 5a-reduction.
Since finasteride is an inhibitor of 5b-reductase as well as 5a-reductase, finasteride may again do more harm than good when it comes to hair loss, when used in conjunction with 1,4-diene compounds. 
While finasteride for naturally occurring hair loss is effective for many, it serves little to no purpose in conjunction with most synthetic anabolic steroid or prohormone cycles, and for some would actually increase the risk of hair loss. It may be of some use to those on a testosterone-only cycle, though anyone considering it should consider the risk of attendant side effects.