I'm glad we have another scientist looking into the post-fin syndrome - that can only be a good thing.
He isn't a scientist to my knowledge, he's a student studying biology with a specialization in neurology and neurological sciences (as he mentioned in his first post).
Here are some followup posts/replies he made in the original hairlosshelp.com thread:
-----------------Posted by Alex Miller:
The explanation to this is really easy: Real Multiple Sclerosis affects the brain and spinal chord. Most symptoms come from neurodegeneration in the brain then ED follows when the neurones of the spinal chord get demyelinated. Obviously, you see the effect of the brain damage first.
But: The brain has 5AR1 but the spinal chord has mainly 5AR2. Finasteride only inhibits 5AR2. I said the CONDITION at the spinal chord is the same. It's not a real case of MS though since the brain is not as strongly affected of 5AR2 inhibition as the spinal chord. But I personally still think the brain is somewhat affected from peripheral neurosteroid inhibition although not as much as the spinal chord neurons.
This also explains why these neurological effects appear years after finasteride usage. It takes a longer period of time of allopregnanolone depletion for neurodegeneration to occur.
The symptoms of "brain fog" are definitely the same as demyelination of spinal chord motor neurons, as written in my first post.
Hope this answers your question."
------------Posted by Alex Miller:
"lol, do you think the spinal chord is just like an electrical cable? It is a highly complex structure. Within the spinal chord, you have specific regions, each has its function. 5AR2 is expressed in ANDROGEN SPECIFIC parts of the spinal chord.
Maybe this ( http://pt.wkhealth.com/pt/re/jned/abstr ... 28!8091!-1
"Spinal cord motoneurones express high levels of androgen receptor. However, in responsive tissue, the effects of testosterone is often mediated by the more potent androgenic derivative 5-alpha-dihydrotestosterone (DHT). This compound is formed in androgen target cells by the enzyme 5-alpha-reductase. Two isoforms of the 5-alpha-reductase, with limited degree of homology, have been cloned, type 1 and type 2. The low affinity-constitutive type 1 isoenzyme is widely distributed in the body; the high affinity-androgen regulated 5-alpha-reductase type 2 is confined to androgen-dependent structures and shows a peculiar pH optimum at acidic values. We have previously shown that high levels of 5-alpha-reductase activity are detectable in rat spinal cord. Here, using reverse transcriptase-polymerase chain reaction, we show that both isoforms are expressed in the whole spinal cord of the rat. The enzymatic pH optimum measured in immortalized spinal cord motoneurones (NSC34) is typical of the type 2 isoenzyme. Using in situ hybridization technique, we found that 5-alpha-reductase type 2 is confined to the motoneuronal cells of the anterior horns of the rat spinal cord, the cells that also are known to express high levels of androgen receptor. Because of the close association of androgen receptor and 5-alpha alpha-reductase type 2, motoneuronal cells should be considered as target cells for androgens."
I understand this is a rat study. But from the study of polletti at al. 2003b I know that the human spinal chord has similar androgen dependent structures.
And again: The brain fog symtoms are the same as the ones of spinal chord motor neuron degeneration. Is that so hard to understand? It even makes sense as cognitive function / speech behaviour are regulated by androgens too, so there will be an effect when the androgen dependent part of the spinal chord undergoes neurosteroid inhibition. Obviously, the strongest effect will be on sexual function as without impulse propagation through the androgen dependent structures of the spinal chord it won't function properly. It's not like you inhibit neurosteroid production and then you can't walk anymore lol. I still think this theory is correct and people suffering these effects had demyelination going on in their (androgen dependent structures of the) spinal chord.
I hope this is clear now.
--------------Posted by Alex Miller:
This is brain fog: http://en.wikipedia.org/wiki/Cognitive_dysfunction
- Of course while taking finasteride, sexual dysfunction can occur but THEN its because of an hormonal imbalance (low androgen levels / high estrogen levels).
- Even when sexual dysfunction is not because of an hormonal imbalance but from demyelination, it CAN in fact be a selective symptom. See my last post.
People don't seem to understand that Multiple Sclerose is demyelination IN THE WHOLE BODY while finasteride inhibits 5AR2 IN A PART OF THE SPINAL CHORD (in the androgen dependent structure). Surely, the symptoms of myelination there are selective. Again: The spinal chord is not a cable! "
----------------Posted by Alex Miller:
Regarding the pseudohermaphrodites:
Smitty109 is right. It's because they were born with this condition.
Puberty is the key. Pseudohermaphrodites never had DHT in their bodies. During puberty, certain androgen dependent structures in the body are activated by DHT. It's the case with hair loss and also with other androgen dependent structures of the body such as parts of the spinal chord. A body of a pseudohermaphrodite works totally different since it never had its androgen dependent structures activated by dht. (And no: Testosterone can't do this task.)
Normal men after puberty have totally different androgen dependent structures in their body. So finasteride's effect is different too.
----------------Posted by Alex Miller:
"Some people really want to take propecia for their hair. Ok. They can do it. I just wanted to enrich your knowledge about what actually happens in your body when you take it. I just don't understand how you can use such a risky drug.
--------------Posted by Alex Miller:
"Alright. Regarding the pseudohermaphrodites: I tried to explain it before but I will try to make it clearer now:
First, look at a normal male. Before puberty everything looks different. The body isn't fully developed, the hormonal profile is different, the CNS is different too. During puberty, all of these things change and a lot of these changes are activated by androgens, especially by DHT
. As the body produces androgens, genitals develop, sexual function is starting to work, the CNS develops which is also necessary for sexual function and for thinking and behaving like a male. The CNS looks different before and after puberty
Now lets look at a pseudohermaphrodite. He goes through puberty too. But he is 5AR2 deficient so can't produce DHT
. He has less body hair, a different hormolal profile, and a different CNS since the androgen dependent part of the CNS which is activated by DHT hasn't fully developed
In the end, both went through puberty. But the normal male has another CNS, especially another spinal chord since it contains a lot of 5AR2 which the pseudohermaphrodite never had.
So a pseudohermaphrodite doesn't only look different, his CNS works different since it is not fully developed like the one of a real male. Point is: He is not only sexually different but also neurologically different
Now: A normal male goes on finasteride and artificially changes his hormonal profile to match that of a pseudohermaphrodite. THEN, demyelination of specific parts of the spinal chord who have been developed with the help of DHT produced by 5AR2 will occur because the body is now, after puberty dependent on that specific part. It can't function properly without it. A pseudohermaphrodite doesn't experience such a kind of demyelination because his spinal chord is a different, not a fully developed one. The part that experiences demyelination in a normal male after puberty taking finasteride isn't even present. His body can function without it because the spinal chord never underwent that change because he is 5AR2 deficient.
It does function differently though.
You see: you can only compare the two (a pseudohermaphrodite and a normal male) if the normal male starts using finasteride BEFORE PUBERTY. But then both of them are actually pseudohermaphrodites.
Hope this is clear now.
Another thing I wanted to tell you: I researched on the internet (I know, not very scientific, but it's still anecdotical evidence) in the hope to find other cases of multiple sclerose like symptoms induced by finasteride. And I came across these:
Quote from here: http://www.patientsville.com/medication ... ffects.htm
"Propecia Side Effects Report #5225179-3
Physician from GERMANY reported PROPECIA problem on Jan 26, 2007. Male patient, 39 years of age, was treated with PROPECIA. After drug was administered, patient experienced the following problems/side effects: multiple sclerosis PROPECIA dosage: unknown. Patient recovered."
And another quote from here: http://www.askapatient.com/viewrating.a ... e=propecia
"like many others, I began taking propecia shortly after it came out. I mainly wanted to keep the hair I had and wasn't too concerned with growing any back. I tried rogaine several years earlier and not only was it messy to deal with, I didn't see any results. Within a few months of taking propecia, I noticed my hairloss had significantly decreased and had actually seen some new growth in the front portion of my head. Everything seemed to be going along fine until a little over a year ago. I started having problems that included dizzyness or off-balance feeling, slurring words or speaking incoherently, tired, headaches, night sweats. I saw every specialist in the book and was misdiagonosed with having inner ear problems, migraines, possible early signs of MS & very high anxiety. I was put on all different kinds of medication but to no avail. All along I continued to take propecia since none of the many specialists (ent, GP, neurologist) didn't tell me to stop taking it."
And there is probably a lot more. I found these two cases within two minutes. And they have been posted before I said anything about my theory. The latter case is about a finasteride user who took the drug for 10 years. He had the same "side" effects as my friend who goes through hell right now because of this drug. There definitely is anecdotical evidence which suggests that neurodegeneration takes place in the long term.
Another point: Some people still don't understand that demyelination can be selective. I just tell you: finasteride is a selective 5AR2 inhibitor, so the depletion of allopregnanolone and therefore the demyelination will be selective too, namely in androgen dependent structures of the CNS.
Last point: I don't know why people scream at me when I post wikipedia articles. I just posted them about demyelination, multiple sclerosis, spinal chord injury and about some neurosteroids. I posted them so you can have a look at them and roughly understand what I am talking about. It's not like an experimental study on wikipedia which might be forged. These articles are about certain conditions and facts which I can assure you are true.
I hope some guys feel different today, when they put this drug into their body.
--------------Posted by Alex Miller:
Guys: I continued my research and I think I finally see the big picture and I think I know what is going on and why several symptoms of finasteride side effects are similar to a "partial" multiple sclerosis.
Let me explain it to you:
First, I'll quote from a study: http://www3.interscience.wiley.com/jour ... 5/abstract
"The complementary activities of 5-reductase (5-R) and 3-hydroxysteroid dehydrogenase (3-HSD) are crucial for the synthesis of neuroactive 5/3-reduced steroids, such as 3-androstanediol, allopregnanolone, and tetrahydrodeoxycorticosterone, which control several important neurophysiological mechanisms through allosteric modulation of -aminobutyric acid type A receptors. Immunocytochemical localization of 3-HSD in the central nervous system (CNS) has never been determined. The presence and activity of 5-R have been investigated in the CNS, but only the brain was considered; the spinal cord (SC) received little attention, although this structure is crucial for many sensorimotor activities. We have determined the first cellular distribution of 5-reductase type 1 (5-R1) and type 2 (5-R2) and 3-HSD immunoreactivities in adult rat SC. 5-R1 immunostaining was detected mainly in the white matter (Wm). In contrast, intense 5-Alpha-Reductase-2 labeling was observed in dorsal (DH) and ventral horns of gray matter (Gm). 3-HSD immunoreactivity was largely distributed in the Wm and Gm, but the highest density was found in sensory areas of the DH. Double-labeling experiments combined with confocal analysis revealed that, in the Wm, 5-R1 was localized in glial cells, whereas 35% of 5-R2 and 3-HSD immunoreactivities were found in neurons. In the DH, 60% of 5-R2 immunostaining colocalized with oligodendrocyte, 25% with neuron, and 15% with astrocyte markers. Similarly, 45% of 3-HSD immunoreactivity was found in oligodendrocytes, 35% in neurons, and 20% in astrocytes. These results are the first demonstrating that oligodendrocytes and neurons of the SC possess the key enzymatic complex for synthesizing potent neuroactive steroids that may control spinal sensorimotor processes.
J. Comp. Neurol. 477:286-299, 2004. © 2004 Wiley-Liss, Inc."
As you can see, grey matter is present in the dorsal horn (=posterior horn) and in the ventral horn (=anterior horn) of the grey matter in the spinal cord.
So it seems, that demyelination in grey matter regions in the spinal cord occurs. This is the exact same demyelination process of multiple sclerosis. The only difference is, that finasteride induces selective demyelination in these regions whereas in multiple sclerosis demyelination takes place everywhere
, including in the brain (people actually taking dutasteride undergo exactly this process...).
See link: http://jnnp.bmj.com/cgi/content/abstract/80/2/182
"Regional variations in the extent and pattern of grey matter demyelination in multiple sclerosis: a comparison between the cerebral cortex, cerebellar cortex, deep grey matter nuclei and the spinal cord."
As you can see, in multiple sclerosis the gray matter is affected and so is it from selective 5AR2 inhibition in these spinal cord grey matter regions. As I said: The underlying CONDITION is the same.
Now, even more interesting is to know, that this is exactly the part of the spinal cord which is responsible for proper sexual function. See http://www.ninds.nih.gov/disorders/sci/detail_sci.htm
about sexual dysfunction resulting from spinal cord injuries (MS = spinal cord injury and so is finasteride usage).
"Depending on the level of injury, men may have problems with erections and ejaculation, and most will have compromised fertility due to decreased motility of their sperm. Treatments for men include vibratory or electrical stimulation and drugs such as sildenafil (Viagra). Many couples may also need assisted fertility treatments to allow a spinal cord injured man to father children."
Many of the finasteride side effects symtoms who most people think come from low DHT levels are actually from the finasteride induced spinal cord injury, including things like erectile dysfunction, ejaculatory disorders, and compromised sperm fertility. Aren't these EXACTLY the finasteride induced side effects? People, wake up!
Another short insight about grey matter being responsible for multiple sclerosis from the Multiple Sclerosis Resource Center:
Quote from link: http://msrcsharing.yuku.com/topic/14096
"It has long been assumed that myelin is the most important target for the misdirected immune response. This white, fat-rich protective layer of specialized cells enshrouds the long extensions of neurons. However, the central nervous systems of MS patients also exhibit damage in the grey matter, where the nerve cell bodies are located. How the patient's disability develops depends greatly on the damage of the gray matter."
Furthermore, have a look at the attached screenshot.
... Interesting point: Cognitive loss ("brain fog"), depression is mentioned too, what many people experience during fin intake.
I hope people understand this "theory" now. For me it is already reality.