MESO-Rx Exclusive Peter Bond on how to prevent anabolic steroid-induced hair loss

[MESO-Rx Administrator]

@PeterBond examines the effectiveness of FDA-approved and popular treatments for AAS-induced hair loss (androgenetic alopecia) in his latest MESO-Rx original article.

How effective are oral 5a-reductase inhibitors like finasteride and dutasteride? What about topical treatments involving finasteride or minoxidil? And are there any new and promising experimental drugs on the horizon?

Treatment and Prevention of AAS-Induced Hair Loss, Part 1

In my previous article on male-pattern baldness, or androgenetic alopecia, I narrated how hair growth and this condition roughly work. In this article

thinksteroids.com

 

[MFAAS]

Questions for people...specifically maybe @PeterBond if you have some minutes to spare...no rush

1. They cause hair shedding to happen in a cyclical manner (maybe that is just the topical treatments and not the oral drugs). So your hair looks thicker for most of the month, but then at some point you shed a larger amount of hair all at once. Is that true?

2. They can cause long term erectile dysfunction...this was the biggest reason why I never touched them.

3. Would there be any detriment regarding gains when it comes to reducing DHT? DHT is also highly anabolic, so this has me curious.

4. With DHT helping to counteract estrogen, wouldn't systemically lowering DHT potentially cause issues for those who have "dialed in" their TRT and cycles?

5. Any other downsides to lowering DHT? DHT has mental benefits and such too. So many guys have Masteron in their "feel good" cycles.

 

[PeterBond]

Questions for people...specifically maybe @PeterBond if you have some minutes to spare...no rush

1. They cause hair shedding to happen in a cyclical manner (maybe that is just the topical treatments and not the oral drugs). So your hair looks thicker for most of the month, but then at some point you shed a larger amount of hair all at once. Is that true?

2. They can cause long term erectile dysfunction...this was the biggest reason why I never touched them.

3. Would there be any detriment regarding gains when it comes to reducing DHT? DHT is also highly anabolic, so this has me curious.

4. With DHT helping to counteract estrogen, wouldn't systemically lowering DHT potentially cause issues for those who have "dialed in" their TRT and cycles?

5. Any other downsides to lowering DHT? DHT has mental benefits and such too. So many guys have Masteron in their "feel good" cycles.

I'm not sure what you're refering to with they.

1. Hair indeed grows in cycles. A growth phase (anagen), a regression phase (catagen), and a resting phase (telogen). The anagen phase determines how long a hair strand will become and for the hairs on top of your head this phase lasts a couple of years. With androgenetic alopecia, this phase becomes progressively shorter, and the telogen phase becomes longer. Which hair follicle is in which phase varies quite randomly. It's not that all hair follicles are at the same stage at the same time. Either way, these drugs prolong the anagen phase, reduce the time of the telogen phase, and also counteract the shrinking of the hair follicle (and thereby of the hair strand). As a result, you'll have more hairs on top of your head at any point in time. You won't shed a larger amount of hair all at once; except sometimes when starting treatment with minoxidil. It's something called telogen effluvium. This is transient and is caused by a larger amount of hair follicle cycles entering the telogen phase before starting the hair follicle cycle again. After the start of treatment this doesn't occur anymore.

2. As far as I know, this has only been reported for 5a-reductase inhibitors such as finasteride. It's estimated that around 1 in 80 men experience erectile dysfunction from finasteride use. This is reversed after cessation of the drug, but there are some cases in which it seems persistent (post-finasteride syndrome). It's unclear what the incidence is, but it's relatively rare.

3. No, and for two reasons. One is that DHT is not produced in skeletal muscle to any appreciable extent. As such, it needs to solely rely on the low serum levels to diffuse into it. Second, DHT is actively broken down in skeletal muscle, further reducing any effect of it. A clinical trial also showed no difference between a placebo or dutasteride (a 5-reductase inhibitor) when combined with testosterone enanthate up to dosages of 600 mg weekly in fat free mass: Effect of testosterone supplementation with and without a dual 5α-reductase inhibitor on fat-free mass in men with suppressed testosterone production: a randomized controlled trial - PubMed

4. Yes, there's a slightly increased risk of gynecomastia with finasteride use. Also around 1 in 80 might get gynecomastia from its use compared to placebo.

5. Not much, finasteride in generaly is tolerated very well. Let me quote:

Overall, 5α-inhibitors are well-tolerated [14]. Nevertheless, sexual dysfunction and psychiatric side effects have been reported. While no causal link had been established, anecdotal evidence of mood changes and small studies reporting depressive symptoms relating to finasteride use have led to depression being added as an adverse reaction to the product labeling of the drug in 2011 [14]. Either way, this does suggest this side effect is quite rare. Erectile dysfunction seems to be more common. A 2010 meta-analysis suggests that, compared to a placebo, 1 in 80 will experience erectile dysfunction as a result of finasteride use [15]. However, no significant difference compared to a placebo was found in decreased libido or ejaculation dysfunction. A 2013 Similarly, around 1 in 80 also can get gynecomastia from its use compared to placebo [16]. Side effects usually resolve after discontinuation of the compound, although they are suggested to persist in some cases. This is also called the post-finasteride syndrome and is described as a “constellation of sexual, physical, and psychological symptoms that develop during and/or after finasteride exposure and persist after drug discontinuation” [17]. Considerable debate exists in the literature about whether or not post-finasteride syndrome even exists [17, 18, 19]. One paper went as far as suggesting it may represent a delusional disorder, stating: “We present the first case of PFS [post-finasteride syndrome] in our 20-year prescription practice of oral finasteride for treatment of male pattern baldness, with circumstantial evidence that PFS may represent a delusional disorder of the somatic type, possibly on a background of a histrionic personality disorder, and with the potential of a mass psychogenic illness due to its media coverage.” [19] Regardless, while it’s obviously hard to get solid evidence for a causal link, the lack of sufficient data to establish this doesn’t mean it’s not real. As such, it seems prudent to support further research in order to paint a clearer picture of its causal link with finasteride use, incidence and pathophysiology, while also maintaining a cautionary stance and informing the public of this rare possible side effect.

 

[PeterBond]

And I certainly wouldn't call DHT highly anabolic: Clinical evidence indicates that DHT's muscle-building potency is relatively low