Anabolic Steroids and Male Pattern Baldness


by Mike Arnold

Over the last 10+ years I have been consulting with prospective steroid users, there is one side effect which consistently seems to concern more would-be users than anything else. This is the fear of hair loss. While some individuals don’t seem to be bothered by this, the overwhelming majority view this side effect in an extremely negative light. For many, the belief that steroid use is synonymous with hair loss is the overriding, although largely ignorant factor influencing the decision to abstain. In truth, there are numerous factors which can potentially play a role in the hair loss process, some of which have nothing to do with drug use.

Fortunately, many of these factors can either be controlled or eliminated altogether. However, in order to understand how steroid use can affect one’s hair line, we will first need to look at the genetic component involved and how AAS can accelerate this inherited trait.

The most common form of baldness in men is Male Pattern Baldness; also known as androgenic alopecia. Men affected by this condition lose their hair in a well-defined pattern starting on the sides of the temples and gradually receding from the front of the forehead back towards the crown. While MPB is also associated with variations to this pattern, significant uniformity will still be present. In short, androgenic alopecia is an inherited sensitivity to the presence of androgens in the scalp, particularly the hair follicles. When these hair follicles are repeatedly subjected to the affects of androgens over time, they shrink, resulting in a thinning of the hair. Eventually, the hair follicle will close up completely, preventing any further growth.

MPB is partially determined by a genetic variant in the androgen receptor on the X chromosome. Males have one X chromosome and one Y chromosome, whereas females have two X chromosomes. Since males always inherit their X chromosomes from their mothers, the genetic variant found in the AR (androgen receptor) responsible for causing MPB, is inherited maternally. Still, this does not tell us the whole story, as science is now confirming that fathers are also capable of passing on genes associated with MPB, particularly a variant located on Chromosome 20. Regardless of paternal-maternal liability, it is clear that there is a strong genetic component involved in hair loss and AAS have the ability to substantially speed up this process.

Does this mean that anyone who is genetically predisposed to MPB cannot use steroids or else they must suffer the consequences or premature hair loss? NO, in most cases, it does not (although selection may be limited or ancillary drugs necessary). As mentioned previously, there are multiple factors which play a role in the hair loss process and if one wishes to minimize/avoid this side effect as much as possible, then applying a combination of scientific research, anecdotal evidence, and examining personal response will play key roles.

For those who carry the MPB trait, administering the hormone testosterone at supra-physiological levels (unless accompanied by a 5 alpha-reductase inhibitor, which we will get to in a minute) is an off-limits practice. The reason for this is simple. Testosterone converts into a metabolite in the body known as DHT (Dihydrotestosterone) through the 5 alpha-reductase enzyme and it is this metabolite which is responsible for attaching to the androgen receptor at the hair follicle and initiating hair loss. By administering excess testosterone, the user will only increase the amount of hormone this enzyme has to work with, increasing the rate of DHT conversion and hastening the hair loss process. There is significant variance in the rate of hair loss among those who administer supra-physiological doses of testosterone, while carrying the MPB gene. More importantly, the individual cannot always know whether he carries this gene or not (unless he begins to experience MPB), nor can he know how quickly he will lose his hair should he decide to use testosterone.

In those who are not sensitive to the effects of DHT on the hair line, testosterone use, even when used at extremely high dosages, will not cause hair loss. We see this demonstrated in the lives of professional BB’rs all the time. It is safe to say that all of today’s professional BB’rs use significant dosages of testosterone, with most relying on testosterone as their base drug. However, it is quite normal to see some pro BB’rs with a full head of hair after many years of high-dose testosterone use, while other pro BB’rs will be nearly completely bald by age 30 (or sooner).

There is hope for those who suffer from androgenic alopecia. A class of drugs known as 5-AR inhibitors can be used to block the conversion of testosterone to DHT, preventing DHT from attaching to the hair follicles in the scalp and staving off DHT-initiated hair loss. There are tw primary drigs used for this purpose. The more commonly known and forerunner of the two is called Finasteride, while the 2nd drug to be developed is called Dutasteride. While many will find partial to total relief from hair loss with the use of Finasteride, there is a significant percentage of users who continue to experience an unacceptable degree of hair loss. This is because Finasteride only works to inhibit type-1 5 alpha reductase, while Dutasteride works to suppress DHT formation through both type-1 and type-2 5 alpha reductase. This makes Dutasteride the superior drug. As effective as these drugs can be, there are not without their own list of potential side effects (you didn’t think it would be that easy, did you?). Unfortunately, both Finasteride and Dutasteride can cause erectile dysfunction & suppressed libido in men. This is because DHT plays a critical role in achieving an erection and maintaining libido. Not all men experience these side effects, and while higher dosages of these 5 AR inhibitors are more likely to cause these side effects, there is no guarantee that administering lower dosages will prevent this problem from occurring.

For those men who consider hair maintenance a priority, but who still want to experience the benefits AAS have to offer, I recommend low-dose testosterone use while “on-cycle”. The reason I recommend low-dose use and not its complete elimination from one’s drug repertoire when running a “cycle” is because the body is reliant on testosterone for proper male functioning, including sexual function. By using steroids in the absence of testosterone, the body will eventually shut-down its own natural testosterone production, leading to a cascade of unpleasant side effects. By administering low-dose testosterone in conjunction with other steroids, DHT conversion will remain minimal, keeping hair loss at bay, while maintaining normal physiological functioning (Note: Certain steroids can cause sexual dysfunction even in the presence of testosterone, but that is another topic for another day).

DHT is not the only mechanism potentially responsible for steroid related hair loss. For example, some individuals may be able to get away with administering large dosages of testosterone, but as soon as they begin utilizing other non-DHT converting steroids, they run into problems. Clearly, in cases such as this, DHT is not the cause. Another potential contributor to hair loss is the androgenic potency of a steroid. While this factor is not always relevant, the majority of potent androgens are more likely to result in hair loss compared to steroids characterized by a weaker androgen component.

There is a myth being spread around both the net and the magazines today regarding which steroids are more likely to cause hair loss, but before we get to that, we must first gain an understanding of the subject of steroid “families”. Every AAS sold on the market today technically belongs to one of three classes (or families) of steroids. These are the testosterone-based, 19 nor-based, and DHT-based families of steroids. Each AAS is defined as belonging to one of these three classes of steroids, based on which of the three molecules it was originally derived from. For example, since the steroid Anavar is an alteration of the DHT molecule, it is classified as belonging o the DHT family of steroids. Since Dianabol is an alteration of the testosterone molecule, it is classified as belonging to the testosterone family of steroids. In reality, “all” steroids are derived from the testosterone molecule itself, but we utilize these 3 classes of AAS as basic sub-categories, in order to further categorize steroids into more specific groups.

With that said, it has often been claimed that those AAS which belong to the DHT family of steroids are more likely to cause hair loss simply because they were originally developed from the DHT molecule. This is blatantly untrue. There are many DHT-based steroids which have been heavily used by both BB’r and other athletes and have been anecdotally proven, through decades of user experience, to be much less likely to cause hair loss compared to numerous testosterone and 19-nor based steroids. As an example, the steroids Superdrol and Anavar both belong to the DHT class of AAS, yet these steroids have become well-known as some of the least likely to result in hair loss. This is one of the primary reasons why Anavar has long been considered the go-to steroid for 1st time women AAS users, as it is one of the least likely to initiate masculinizing side effects, including hair loss. In contrast, the 19-nor based drug, Trenbolone, and the testosterone-based drug, Halotestin, are both much more likely to cause hair loss in the average user, despite their non-DHT based status!

This brings me to an important point. When determining which steroids are generally more likely to cause hair loss, we should NEVER look to a steroid’s “family” as a causative factor. Rather, each steroid must be evaluated on a case by case basis. We cannot clump steroids into groups in an attempt to accurately pinpoint which drugs are the prime offenders. It just doesn’t work that way. Class is completely irrelevant as proven through the collective experience of generations of BB’rs and anyone who is knowledgeable regarding how steroids work in the real-world knows better than to make such a sweeping generalization.
When it comes to evaluating each steroid on a case by case basis, real-world experience may have shown us which steroids are the most likely to bring about thinning of the hair, but there is one other important factor we cannot ignore when it comes to hair loss. This is called personal response. It is important to remember that as individuals, none of us respond identically to all the various BB’ing drugs. Steroids have many different effects on the human body and each steroid affects the body in its own unique way. There are some effects which we all experience when using certain steroids (although to what extent may vary), but there are other effects which only apply to the majority. Every now and then, an individual will break away from the norm and respond in a different manner than the majority. It is no different when it comes to hair loss. We may know which steroids are the most and least “likely” to cause hair loss based on the experience of generations of users, but this does NOT mean “everyone” will always have the same experience, as personal response can and does vary. For this reason, only recommendations can be given…not guarantees.

Below I list a few of the most commonly known steroids, which have been proven to be among the least friendly on the hair line in the majority of users:

Testosterone
Trenbolone
Halotestin
Proviron
Methyltestosterone
Anadrol
Dianabol
Masteron

Below I list a few of the most commonly known steroids, which have been proven to be among the most friendly on the hair line in the majority of users:

Anavar
Nandrolone
SD
Boldenone (low-moderate risk)
Turinabol
Epistane
Primobolan
Testosterone used with an appropriately dosed 5-AR inhibitor

While those who want to preserve their hair may not be able to indiscriminately run any cycle they want, even those who are extremely prone to MPB will be able to put together some pretty potent cycles. Below I list a few example cycles for people included in this category:

Mass-Builder
Weeks 1-12: Testosterone Cypionate @ 400 mg/week.
Weeks 1-12: NPP @ 1,000 mg/week.
Weeks 1-4/ 9-12: SD @ 20 mg/day.
Weeks 1-12: Dutasteride @ 2.0 mg/day.
Weeks 1-12: Aromasin @ 5 mg/day.
Weeks 1-12: Nolvadex @ 10 mg/day, as needed (if gyno presents itself).
Weeks 1-12: Cabergoline @ .5 mg EOD, as needed (if sexual dysfunction becomes an issue)

*** Testosterone cypionate is preferable to faster esters of testosterone, as faster esters result in less estrogen conversion and greater DHT conversion.

*** NPP is used in place of Deca, as it is less likely to cause sexual dysfunction on a mg to mg basis compared to Deca. The use of NPP is even more preferable when the ratio of Nandrolone exceeds testosterone by 2.5:1

*** Aromasin is used at lower dosages, due to an A.I.’s ability to increase DHT conversion. However, allowing excess estrogen to flood the system, especially when nandrolone is being administered concurrently, can cause a variety of side effects. A better alternative in those seeking to minimize hair loss is to take a lower dose of an A.I. in combination with Nolvadex, if needed to prevent gyno. This will help manage estrogen levels moderately, while keeping DHT conversion from rising too high.

*** Dutasteride is administered in higher dosages than what it typically administered in non-steroid using men, as those using supraphysiological doses of testosterone will experience an increase in DHT production beyond that of their non-steroid using peers. If a user still has problems running this dose of testosterone, one can lower the dose as low as 150-200 mg/week, which should eliminate all issues in even the most sensitive, but keep in mind that decreasing the testosterone dose down to TRT levels increases the possibility of sexual dysfunction when used with Nandrolone (it will also reduce growth potential).

Cutter:
Weeks 1-12: Testosterone Propionate @ 200 mg/week.
Weeks 1-12: Primobolan @ 800 mg/week.
Weeks 1-12: EQ @ 600 mg/week.
Weeks 1-12: Anavar @ 50 mg/day.
Weeks 1-12: Dutasteride @ 1 mg/day.

*** Test prop, although resulting in a greater degree of DHT conversion than longer esters, is not an issue when used at only 200 mg weekly and in combination with a 5-AR inhibitor. Test prop results in a drier and harder look, making it more ideal for a cutter.

*** Anavar can easily be run for 12 weeks at 50 mg/day, according to all scientific, medical, and anecdotal research. If one is concerned with their cholesterol levels while running Anavar for 12 weeks, adding some cholesterol support supps will help normalize cholesterol levels.*** When running such low doses of testosterone propionate, especially in combination with the anti-estrogenic Primobolan & Anavar, an A.I. will not be needed to prevent gyno.

  

 

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