So if it is antibodies then how do we treat it to cure ourselves???
First thing is to get tested. Which is simple, quick and cheap to do. But is a non-standard blood test.
Because I would guess it probably cannot be treated without serious medical intervention. Treatment might include: high dose I.V. corticosteroids, powerful drugs like Rituximab or Azathioprine, dialysis/Plasmapheresis or intravenous immunoglobulin. (Possibly in combination with anti-androgens)
Has anyone had this tested? This is another thing I wanted to check. Does anyone know how/where we can do this?
Treatment of Type B Insulin Resistance: A Novel Approach to Reduce Insulin Receptor Autoantibodies ncbi.nlm.nih.gov/pmc/articles/PMC2913034
Immunological Insulin Resistance Due to Insulin Antibodies Developed After Cessation of Insulin Therapy in a Patient With Type 2 Diabetes care.diabetesjournals.org/content/31/11/e84.full
Beyond the hormone: insulin as an autoimmune target in type 1 diabetes. ncbi.nlm.nih.gov/pubmed/21700723
Severe insulin resistance due to anti-insulin antibodies: response to plasma exchange and immunosuppressive therapy. ncbi.nlm.nih.gov/pubmed/19125765
This is really interesting - sorry if I am asking an obvious question (and the answer was in an earlier post), but is this theory being tested? Is anyone having tests done? Iâd been keen to be involved and help out if possible, either getting tested myself if its possible, or helping to fundraise if thatâs needed.
To my knowledge this theory is not being tested.
I found the following website which lists 25 possible causes of 5-alpha-reductase deficiency:
evi.com/q/causes_of_5-alpha-reductase_deficiency
One possible cause, which may be relevant to this thread is âAutoimmune polyendocrine syndrome type 2â:
en.wikipedia.org/wiki/Autoimmune_polyendocrine_syndrome_type_2
Autoimmune polyendocrine syndrome, type 2 (also known as âSchmidtâs syndromeâ, or APS-II) is the most common form of the polyglandular failure syndromes. It is more heterogeneous and has not been linked to one gene. Rather, patients are at a higher risk when they carry a particular human leukocyte antigen genotype (DQ2, DQ8 and DRB1*0404).
Features of this syndrome are:
Addisonâs disease
hypothyroidism
diabetes mellitus (type 1)
hypogonadism
vitiligo
Thanks to Finasteride my brain is slowly being destroyedâŚand now i have the proof for all doctors to pay attention to what i say. I was diagnosed with an MRI scan as having signs of demyelination. I am 100% certain this was caused by Finasteride and the theory of this guy is correct :
hairlosshelp.com/forums/messageview.cfm?catid=10&threadid=85335
Probably i am one of the oldest ex-users of Finasteride in here. I took it back in 1998 (now i am 43) and this medication has ruined my life.
I am trying to put the pieces of the puzzle together. Hopefully you will find the information given below useful.
My crash with Finasteride was quite different. When i stopped the medication i developed gyno and then something happened which now seems to me as an inability to control inflammation. I had Urticaria, joint pains, dry skin and pigments in my skin, i could not swallow properly because my esophagus had spasms and every swallow was painful. The doctors back then had no idea on what was going on and believed it was some kind of autoimmune disease.
For some reason, the way that Finasteride affected me was different. I had what i call âattacksâ. I knew that i had an attack when i would hear a very brief tinnitus usually in my left ear. Then the problems of libido would start for about 3 days. Then, i would be fine - until the next attack.
I went to an endocrinologist and she said that libido problems and tinnitus were all because of stress. The blood tests have shown that i am hypothyroid,my Total testosterone was low normal and had high LDL.
One thing i noticed back then is that my attacks would be much more frequent when i was dieting. Then i realized that my attacks were more frequent when i would not eat foods with cholesterol.
When i was 30-35 i would have an attack once every two months. After 35 the attacks became progressively more frequent : once every month, then once a week then once every three days.
Right now i know that an attack is demyelination being progressing. I am not sure if i have Multiple Sclerosis and this is one thing i will find out over the next month or so. Only lately i have experienced on what other people say here as Brain Fog and Memory problems. However i have more problems apart from low libido including
Involuntary Spasms
Heart Arrhythmias
Brain Fog
Bad Memory
Sleep Problems (waking up early)
I decided to take things seriously about a year ago. That was before finding out about demyelinationâŚand what i did is that for every single day i wrote down how i felt , what i ate, whether i was stressed, how my erections were, whether i had brain fog, etc.
I also started educating myself about Neurosteroids, hormones, etc. i also use some statistical techniques to analyze all the data i have collected to see when i tend to have attacks and when not, when my erections are better, etc
I found out the following
-After an attack several neurological problems begin : arrhythmias, brain fog, memory problems, low libido etc
-I believe that this whole thing is reversible. More on this later
-I realized that due to Finasteride, my body could not convert cholesterol to neurosteroids and other hormones. So i found about P450scc and the role it has to cholesterol conversion.
-The analysis that i have done shows that some foods induce an attack (chicken breasts) and some other foods reduce the attacks such as red bell peppers. I have no idea why red bell peppers help but i have found that they do help.
-Vitamin D3 helps but in combination with Retinoic Acid (Vitamin A). This is because Vit. A helps the production of pregnenolone and progesterone which in turn helps in neuroprotection from demyelination. Here are the links :
ncbi.nlm.nih.gov/pubmed/19744992
jb.oxfordjournals.org/content/early/2012/07/03/jb.mvs074.abstract
These are the things that i am sure for. Now for the things that i am not sure :
It appears that Finasteride creates an autoimmune response to DHT. Last week i felt like i am 20 years old. My girlfriend and myself could not believe how horny i was and i also got a bonus of getting a pimple in my nose 
The reason was a combination of
-HCG (twice a week 450 IU)
Vitamin d3 5000 IU and Vitamin A
5 days of Creatine (helps convert Testosterone to DHT)
Note that i started HCG 3 weeks ago but with no good results. However the attack that i had this time with the regimen above was a really bad one (duration and intensity of tinnitus) which says to me that the theory of developing autoimmunity to DHT is a correct one. Again i am not sure for this but i will try again the same regimen to see what happens. It could be that Red Bell Peppers are a 5ar inhibitor and thus stop the conversion of testosterone to DHT (and as a consequence they stop attacks).
Hope that helps, let me know if you have any questions
I agree with you mariovitali 100%. We have some kind of autoimmunity developed against our own DHT or DHT receptors. I strongly believe this is because of molecular mimicry of finasteride to DHT. I have made a long post here as well.And so far Alex Millerâs theory is closest to reality. It looks like our body is constantly going through demyelination and remyelination.
I am having swellings up and down, especially in my legs (near ankles), wrists and forearms. Any simple physical work results in inflammation (after 24 hours to 48 hours).
whether we discover it today or ten years after, it is autoimmune related to our Androgens.
mariovitali where MRI showed demyelination? I mean brain or spinal cord?
I am sure as years go by some will show demyelination as is the case with many acutane users.
I found black seed or Nigella Sativa is useful and stops demylination fast.there are many experiments in pubmed with NSativa.
ncbi.nlm.nih.gov/pubmed?term=nigella%20demylination
I also read account by an MS patient who claims to reverse his MS after using black seed oil. I donât know how true he is in his claim though.
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Can you tell us about the process of being diagnosed with demyelination?
-What kind of doctor was responsible for the test?
-What kind and strength of MRI machine was used?
-Was the demyelination location specific or general throughout the body?
-When were you first diagnosed and if it wasnât recently has the demyelination shown progression since then?
Thanks
Mariovitali, thanks for reporting this info. How much did these vitamins help you?
-
Can you clarify this entire section? Are you saying that HCG helped increase DHT? And that HCG + Creatinine boosting DHT lead to improvements (horniness), that then subsided (and caused an âattackâ) because your body has an autoimmune reaction to the DHT?
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Does this relate to the pudendal neuropathies diagnosed in roughly 13 totaly PFSers so far? Hereâs one discussion of this: propeciahelp.com/forum/viewtopic.php?f=27&t=5661&hilit=pudendal+neuropathies
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What is the suggested treatment, then (anyone)? Anything that upregulates 5AR? The anti-finasteride? Proviron?
Thanks
This is not a thread about whatever.
Oscar
What you are referring to is a pituitary antibody test, which checks for inflammation in the pituitary.
According to wikipedia:
âa test does exist to detect antibodies to the pituitary without biopsy: autoantibodies to MÂŽ 49,000 pituitary cytosolic protein may represent markers for an immunological process affecting the pituitary glandâ.
More info on the pituitary antibodies test can be found here:
mdjunction.com/forums/hypopituitarism-discussions/general-support/2284688-pituitary-antibodies
Is it worth creating a separate thread for this??
I dont know. That was just one of my rants.
I was talking about why LH/T is sometimes low after stopping and why LH/T isnt higher due to a percieved lack of T.
I think antibodies that are interacting with the AR cause negative feedback and some downregulation of the Hypothalamicâpituitaryâgonadal axis.
Another antibody to consider is a âTestis Steroid Cell Antibodyâ.
This is an antibody against leydig and sperm cells as outlined here and is a cause of low testosterone.
drsaulmarcus.com/hormone/naturopathictestosterone.html
Here is an test which could detect it:
USA:
immcodiagnostics.com/products/product-display.aspx?ID=59
General info on types of antibody tests can be found here:
patient.co.uk/doctor/Plasma-Autoantibodies-(Disease-Associations.htm
An antibody against leydig cells may explain testicular pain and atrophy of testicles as described here:
wisegeek.com/what-is-testicular-atrophy.htm
Has anyone on the forum had this test??
THis is should be N/A for us as there are some chaps who have been on TRT for years before taking Fin, in other words theire testis were already shutdown any way.antibodies or no antibodies against leydig cells make no difference.
another thing
on fin
fin+5AR---->di hydrog finasteride
total T -------> Estrogen - DHT
after Fin
total T-----> estrogen + DHT
So technically we shoud have lower E and more free T after stopping Fin but results are opposite. Many had normal or close to normal T ,LH, FSH but as time goes by their LH, FSH and free T go to below normal or close to low normal, why?
When I stopped SP I had LH 4 but gradually LH and free kept declining until LH was 1 and free T was low out of normal range.
our body is making some thing which become more active as we make more DHT and cuase a down regulation.
I disagree SP.
If you develop a leydig cell antibody as a result of an auto immune disorder, then it may explain why your testosterone production declines and does not return to normal. Something to consider, thats all.
An adrenal antibody test may be worth considering too:
muschealth.com/lab/content.aspx?id=150344
I cannot find any lab that tests for a 5ar2 antibodyâŚ