Based on my experienced, megadosing fish oils does nothing except perhaps make it easier to exercise. I have both megadosed fish oil (i.e., EPA/DHA combo, about 45 g of fish oil in total), and tried separately megadosing DHA.
I have tried DHA (210 mg twice a day) in the last 7 days and I can tell that I ve some improvements so far. My main problem is brain fog but also I have sexual sides. But for me the most important thing right now is brain fog (I have all the sides that most of you report). I have had severe problems to concentrate or to think and other problems for the last 4 or 5 years (that is when I stoped using finasteride).
I certainly support the idea that is been promoted in this thread about the demyelinization.
At the moment with DHA I have had 2 improvements:
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I can concentrate much better and I am able to think a little better. This was a great problem to me in the last years.
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It is very curious but the first 3 nights that I started to take DHA I had dreams during the night, even more I woke up at the middle of the night because I had nightmares. THIS HASN´T HAPPENED [Size=4]IN YEARS[/size](I couldn´t dream or at least I didn´t remembered what I could have dreamt during the night FOR YEARS. I don´t remember having had nightmares in the last 5 years and in the first 3 nights after starting using DHA I had 3 nights with dreams. For me it is incredible and curious.
In the following 4 days I only remember I have dreamt another additional night.
I am reluctant to start taking magnesium sulfate (which is another of the products recommended for myelinization) because I´ve been reading it could be somehow dangerous to take.
May be I should start trying some anti-oxidants (also with DHA). Do you know which anti-oxidants would be beneficial to us (people with brain fog)?.
Why don´t those that have brain fog give a try to DHA (200 mg or more) and tell us your experiences?. Mew have you tried DHA?. Why don´t you give it a try?.
Here you can find some:
Greetings.
Kazman has posted that DHA down regulate androgen receptors. I think this is one of those items that might have pluses and minuses (like zinc) for us. Might not want to take too much if your having sexual sides.
young genius named Alex Miller seems to have found out the reason and cause for propecia problems!!!
totally debunked anyone who thought otherwise…very convincing!!
heres the link- http://www.hairlosshelp.com/forums/messageview.cfm?catid=10&threadid=85335
This entire thread is a copy of the one you just posted.
After reading this thread I have been experimenting with taking magnesium pills. I know it isn’t the same as the Epsom salts or other types of magnesium, but for me it makes an unbelievable difference even 30 minutes after I take it. I can think, I can laugh, I can dream, my imagination can run wild, emotional flatness goes away, libido returns, energy is better, memory is better, even my eyes feel better. It feels like it’s the only thing I have ever tried that puts a dent in these horrible symptoms. I have spoken to 2 other forum members and one has had no results taking magnesium and one has had half the results I have had. I wish I understood why or how magnesium has this effect on me. After several hours the finasteride symptoms come back and I fall flat again until I take my next morning dose. I have to take it easy because in higher doses the magnesium pills really upset my stomach.
Anyway, this works great for me, if anyone wants to try and see, I think it can give you a taste of what recovery feels like, even if it is only for a few hours.
Interesting that you experience improvement and 2 others reported none or only some. What dosages have you and the others been taking?
At first I was taking 2 250 mg pills but that was too much for my stomach to handle and I started to get diarrhea. I have been taking one lately and that’s enough for a nice boost.
BTW - I’m the one that this approach did nothing for. Took 500mg magnesium for at least a week, and it didn’t do anything for my mood or dull emotions.
I also tried Magnesium/Calcium pills at the US RDA dose while I was on Fin. Had an AMAZING reaction for 2 days, the same as being reported here, then it dropped off to nothing.
unfortunately magnesium doesn’t help me. i tried taking up to 700mg a day, plus using magnesium oil on my skin with no improvements. I think i read somewhere that people with changes in DNA/gene-expression need more minerals and vitamins to get the same effect before their genes were altered. I’ll see if i can find the link
Would 7 months of Finasteride usage at 1 mg per day qualify as long enough to cause significant damage?
unfortunately tom, yes.
You sure?
Alex talks about years of use for damage.
Alex is a kid. Not a doctor. Some people on here used the pill less then a week
True, but there’s a difference between long term changes and damage.
I was on it for 9 weeks…
8 years later im not the same.
Hey, this is me, initiator of the “finasteride and neurological damage” thread over at hairlosshelp.com.
I have been following the new discussion there regarding neurosteroid inibition ( hairlosshelp.com/forums/mess … adid=85335).
Before presenting the information, I want you to know that a lot of debate is going on recently in the academic world regarding the use of finasteride for hair loss and funnily enough, no matter what the doctors say, the general consensus of people that understand the real mechanisms behind the drug (regarding neurological issues) is that Merck created a real mess when introducing it. What I have been saying in the other thread almost a year ago is starting to get validated with the newest research.
Now, the following information that I am going to present should anyone who is using finasteride for hair loss make this decision reconsider again. And this time I am NOT coming with rodent studies but with real studies carried out on humans. I don’t know why they are still discussing rodent studies over at hairlosshelp (e. g. in the new thread there, and then they are yelling "humans are different blabla I want to keep my hair) when there are much better studies around.
The first study is not really new but contains some really valuable information. For anyone disbelieving that finasteride can have a serious effect on neurosteroid formation in humans look at the study “Finasteride Treatment and Neuroactive Steroid Formation”. 20 men have been given 5 mg of finasteride (the difference between 1 mg and 5 mg is negligible). The concentration of 5a-reduced and 5b-reduced neurosteroid metabolites have been measured. The results are shown in the following picture:
See attached image below, from: img23.imageshack.us/img23/4656/32114410.jpg
As you can see, the biggest change in the concentration of 5a-reduced metabolites has occured for the neurosteroid allopregnanolone. After 4 months of finasteride use, there has been a median reduction of 300% (!) in the concentration of allopregnanolone. Now, one can safely say that finasteride does not only “reduce” allopregnanolone - it literally eradicates it. (The concentration of another 5-beta neurosteroid, Epietiocholanolone increased by 600% - there is not much information about this particular steroid. Still, its impressing…).
With this study, the general misunderstanding that in humans 5a-reductase II is only responsible for T->DHT conversion and 5a-reductase I is only responsible for neurosteroid production in the brain has been disproved. Both types of 5AR do both tasks and type II that is inhibited by finasteride does most of it.
I recommend you read the whole study at lf1.cuni.cz/Data/Files/Pragu … 9a0025.pdf .
Now a new study that has been published just a few days ago (source: May 17, 2010)).
Quote:
Allopregnanolone Levels are Reduced in Temporal Cortex in Patients with Alzheimer’s Disease Compared to Cognitively Intact Control Subjects:
Abstract:
BACKGROUND: The neurosteroid allopregnanolone has pronounced neuroprotective actions, increases myelination, and enhances neurogenesis. Evidence suggests that [b]allopregnanolone dysregulation may play a role in the pathophysiology of Alzheimer’s disease (AD) and other neurodegenerative disorders[b]. Our prior data demonstrate that allopregnanolone is reduced in prefrontal cortex in male patients with AD compared to male cognitively intact control subjects, and inversely correlated with neuropathological disease stage (Braak and Braak). We therefore determined if allopregnanolone levels are also reduced in AD patients compared to control subjects in temporal cortex, utilizing a larger set of samples from both male and female patients. In addition, we investigated if neurosteroids are altered in subjects who are APOE4 allele carriers. METHODS: Allopregnanolone, dehydroepiandrosterone (DHEA), and pregnenolone levels were determined in temporal cortex postmortem samples by gas chromatography/mass spectrometry, preceded by high performance liquid chromatography (40 subjects with AD/41 cognitively intact control subjects). RESULTS: Allopregnanolone levels are reduced in temporal cortex in patients with AD (median 2.68ng/g, n=40) compared to control subjects (median 5.64ng/g, n=41), Mann-Whitney p=0.0002, and inversely correlated with Braak and Braak neuropathological disease stage (Spearman r=-0.38, p=0.0004). DHEA and pregnenolone are increased in patients with AD compared to control subjects. Patients carrying an APOE4 allele demonstrate reduced allopregnanolone levels in temporal cortex (Mann-Whitney p=0.04). CONCLUSIONS: Neurosteroids are altered in temporal cortex in patients with AD and related to neuropathological disease stage. The APOE4 allele is associated with reduced allopregnanolone levels. Neurosteroids may be relevant to the neurobiology and therapeutics of AD. Copyright © 2010. Published by Elsevier B.V.
As you can see, the neuroprotective actions and myelination function of allopregnanolone have been mentioned. The AD patients who have been studied were carriers of the APOE4 allele which causes early AD - (probably) by a reduction of allopregnanolone. Finasteride users who are not even carriers of this allele can themselves cause neurodegenerative deseases like AD since they also experience a similarly sharp reduction in allopregnanolone concentration and do so for years or even decades. Research that was known to be true for mice (see “Allopregnenolone (synthesized from 5AR) may prevent neurodegeneration”) is starting to become true for humans.
One could argue now that 5AR type II is not expressed in the brain but only type I is. But when you look at the allopregnanolone reduction which is almost an eradication, I do not think it matters anymore since, as written before in the original thread, the neurosteroids which are created by the peripheral 5AR type II also carry out their function in the brain as they enter it. Regarding other areas in the nervous system like the spinal cord where mostly 5AR type II is expressed the chance of neurological damage (demyelination) due to the eradication of allopregnanolone is even higher (this is what the whole thread was about). With the newest research, I think it does not even matter whether one selectively inhibits 5ARII or uses a dual inhibitor like dutasteride. An allopregnanolone eradication can cause damage in the long run. The damage takes some time to manifest but eventually will. Be it 10, 20 or 30 years.
To the sufferers: New research on this is coming out right now and also in the near future. The big picture is starting to form - you don’t need to wait much longer and the medical world will wake up. The academic world is waking up already that’s why they are doing these studies. There are more studies - if I find the time I’ll post them here.
Cheers,
Alex
PS: It would be cool if someone posted the above info in the new thread at hairlosshelp, as some users still have not grown a brain. They probably still have the outdated believe that pseudohermaphrodites are good models for finasteride lol.
Welcome to the forum Alex, thanks for joining us.
The studies you quoted are certainly interesting, one of which I had read before: lf1.cuni.cz/Data/Files/Pragu … 9a0025.pdf
It certainly does provide further insights into the drug’s effects on neurosteroid metabolism – which is of particular importance considering this study involved human subjects, not rodents.
We hope you will check back frequently to answer questions, share research, and provide additional thoughts. Thanks again for joining the site.