Dose any body know if it is 5 AR inhitor? I want to know how it affects 5 AR it it does not work like fin or Saw palmetto.
thanx
sps
so no body knows for sure if Accutane is 5 AR inhibitor. It looks like it is not but works some way same as propecia.
According to the research I have read Accutane does have also have an effect on 5AR2… and androgen receptor quantity.
Broken, do you remember where you saw the information about accutane being a 5AR2 inhibitor? I have only found information showing that it is an inhibitor of the type-1 enzyme except for this post on a BB forum. http://juicedmuscle.com/archive/index.php/t-227.html
Not a reliable source itself, but I would like to know where he learned this.
So no body can give and source that accutane is 5AR inhibitor?
Yes, Accutane (isotretinoin) is a potent inhibitor of 5AR1. That is why it is causing similar problems to Accutane users as finasteride is to us. Isotretinoin is NOT an 5AR2 inhibitor.
Boudou P, Soliman H, Chivot M, Villette JM, Vexiau P, Belanger A, Fiet J. Effect of oral isotretinoin treatment on skin androgen receptor levels in male acneic patients. J Clin Endocrinol Metab. Apr 80(4), 1995, pp. 1158-61 (ncbi.nlm.nih.gov/pubmed/7714084).
Boudou P, Chivot M, Vexiau P, Soliman H, Villette JM, Julien R, Belanger A, Fiet J. Evidence for decreased androgen 5 alpha-reduction in skin and liver of men with severe acne after 13-cis-retinoic acid treatment. J Clin Endocrinol Metab. May 78(5), 1994, pp. 1064-9 (ncbi.nlm.nih.gov/pubmed/8175961).
Lookingbill DP, Demers LM, Tigelaar RE, Shalita AR. Effect of isotretinoin on serum levels of precursor and peripherally derived androgens in patients with acne. Arch Dermatol. Apr 124(4), 1988, pp. 540-3 (ncbi.nlm.nih.gov/pubmed/2965551).
Palatsi R, Ruokonen A, Oikarinen A. Isotretinoin, tetracycline and circulating hormones in acne. Acta Derm Venereol. Sep 77(5), 1997, pp. 394-6 (ncbi.nlm.nih.gov/pubmed/9298137).
Rademaker M, Wallace M, Cunliffe W, Simpson NB. Isotretinoin treatment alters steroid metabolism in women with acne. Br J Dermatol. Apr 124(4), 1991, pp. 361-4 (ncbi.nlm.nih.gov/pubmed/1827343).
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I have still yet to see any reliable information stating that accutane either does or does not have an effect on 5AR type II. Maybe I’m missing something. Could you please elaborate awor?
There is no evidence that isotretinoin has an effect on 5AR2. The substance inhibits 5AR1, which is highly expressed in the skin, thereby reducing acne. If it would inhibit 5AR2, you wouldn’t have people on acne.org wondering if they should supplement finasteride to their diet because they are loosing hair.
The bottom line is that you don’t need to inhibit 5AR2 to get this problem. Anything that you can do to reduce androgen levels will cause this problem with the genetically predisposed. Our problem is not about 5AR2, it’s about a reaction of our body to androgen ablation.
I agree with awor. We would have got in the same mess by taking any “castrating” substance, i.e. any substance that reduces androgens (T or DHT). In fact, there is evidence of people who were on lupron and who never recovered although their T went back up upon cessation. (I know that Mew has provided a link about this, but I can’t find it)
m_81, I think this is the study on long term effects of GNRH agonists you said Mew had mentioned: http://www.propeciahelp.com/forum/viewtopic.php?f=9&t=1961&p=10240&hilit=potency#p10240
I’m confused by the fact that I got into this mess by inhibiting the type-I enzyme only… Why did the type-II enzyme not convert a sufficient amount of DHT to prevent this from happening?
Same for you guys who got screwed by taking finasteride. Why did the type-I enzyme not convert an adequate amount of DHT to spare you from PFS?
I can understand “post androgen ablation syndrome” happening to guys who used dutasteride (very little of either form of the enzyme to convert T -> DHT)
or the men who took lupron (very little substrate material (T) for 5AR to act upon = low DHT)
I’m not sure of the ratio of 5AR type-I/type-II, but assuming it is around 50/50 and inhibiting only one form of the enzyme = 50% DHT reduction at max.
How did lowering DHT by half somehow cause PFS?
Is a 50% reduction in DHT enough to cause such problems?
Does the ratio of 5AR type-I/type-II vary greatly among different men? (I read at least one member story here where a guy developed sexual and mental sides after using accutane, then went on finasteride a few years later which made his problems worse. I think I read a few other similar stories) Wouldn’t this most likely mean it doesn’t matter what the ratio is unless reducing DHT by any significant amount <50% can still cause issues?
None of this makes sense because finasteride inhibits DHT by about 70% in only 24h for most men by inhibiting 5AR type-II, and several studies state that isotretinoin lowers DHT significantly (can’t find the numbers right now) by inhibiting 5AR type-I.
What confuses me even more is that a lot of accutane sufferers have symptoms that would be consistent with a disruption in areas of the body where the type-II enzyme is found at a higher concentration than type-I (genital areas), and it seems as if many finasteride victims are suffering sides involving parts of the body where the type-I enzyme is dominant (brain, skin).
My basic question is, how does either one of these drugs inhibit DHT to such a great extent that it can destroy our lives (via androgen (DHT) ablation) if each only acts to reduce one specific form of the enzyme?
I would guess that the recently discussed type-III enzyme might somehow be inhibited by most 5ARIs? I swear I remember reading that it is highly concentrated in parts of the body that are dependent on androgens for proper function.
I have just baffled myself, sorry you had to read this… Its late, forgive me 
well said.
but there is exection in my opinion. Problem starts when Androgen level drops at inter cellular level not in the blood. Steride users can fix their problem by going on TRT. Whalen72 is a good example, got trouble after steride use (his balls had shutdown too), was doing well untill used fin. Also primary people respond well to TRT. Again problem starts when 5ARIs bind to adndrogen receptors thereby starving cells. I don’t know maybe mitochondrea is affected.
Metformin is causing the same issues. I read one post on messo, the user went on clomid after the sides but colmid lost effects after few months. I did not bring this case here just as not to make this forum a general sexual dysfunction forum (sorry for my English). Now interesting thing is fin, saw palmetto,accutane,metformin all cross blood brain barrier, I dont know if our brain is the main cause or a big contributor to this problem.
Now is Metformin a 5ARI?
awor,
One question for you. You said that
Not sure if this is so true actually. You have suffered from primary hypogonadism before propecia, which means that at some point you found out that you had low T because of a testicular problem. Then, you went on TRT and it worked!! In other words, you had already a reduction in androgen levels long before propecia, but it didn’t cause you any untreatable issue. Why didn’t this drop in T cause you pfs, whereas propecia did?
PS: Obviously, I might be missing something, since I don’t know your medical history etc…
I think my post is the answer, reduction at cellular level.
Interesting idea. I’d like to hear awor’s take on this.
Old post but any update on how to reverse the early effects of 5ar inhibitor? i know st. john’s wort is a 51r inducer? any other herb or supplements or easily accessible medications that also do the same?
I have been researching both these compounds a lot, given I have suffered from persistent sexual dysfunction for nearly 9 years now. I’m pretty sure Isotretinoin has been shown to be a type 1 5a reductase inhibitor. Where as propecia is an inhibitor of all three types of 5a reductase inhibitor. This may explain why although many sufferers of accutane reports sexual dysfunction, they do not seem experience as many severe symptoms as some propecia sufferers such as shrinking penis, inability to gain muscle mass etc.
Dubya, your suggestion that both could affect type 3 5a reductase inhibitors is an interesting suggestion, as this would explain the cross over in symptoms related to sexual dysfunction. Does anyone know of any current research being conducted on propecia?
If these drugs truly have caused epigenetic changes to androgen signalling, its hard to imagine any drug treatment being developed any time soon. Given that, I don’t think many if any drugs which target epigenetics on the market at the moment. Thus I feel we need to look further a field, at perhaps more invasive treatments. I can’t help but feel like something like deep brain stimulation may be our holy grail. Its been used for depression, OCD, parkinsons, anorexia, cluster headaches etc. why could it not be used for sexual dysfunction?
I tried something similar, electro-convulsive therapy (ECT), it made no changes whatsoever in PFS symptoms. It did give me temporary amnesia though, and made me feel like I was going insane for about a week.
Accutane sufferers do experience shrinkage, no muscle gain…
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I don’t know about that but I know it causes severe brain fog, panic/anxiety, and the most obvious to teenagers; facial scarring and thinning (paper-thin), dry, pale, wrinkle-prone skin.
I took acutane in high school for acne back in the 90s and didn’t really have much trouble…I quit running the drug early as my cystic acne stopped and just got dry skin so I quit…The effects of finasteride compared to accutane is like a grenade compared to a fire cracker…Mainly because finasteride effects the brain, neuro steriods and the hpa axis…Causing failure in some after stopping and disrupting hormone production…