Funnily enough i was tested with this just today. I dont really understand the test, nor can I find raised results from this test associated with hashimoto’s or graves disease.
the reason I put these test result is that I told doctor about auto immune and antibodies and she wrote me this test. I don’t know how it tells about auto immune.
I think I messed up my tests by not stopping my supplements so my test results mean nothing.
This may be relevant: when I was in the 2nd ER of the night the day i crashed (first ER thought I was just another guy who couldn’t get it up) my white blood cell count was up. 12.2 where 5-10 is normal.
I can directly relate to this topic… I have been feeling random muscle pain and had blood tests that revealed that I am low in Vitamin D and low in Testosterone along elevated levels of CPK(711) and Aldolase.
My doctor is telling me that its indicative of myositis an autoimune disease. I work out often so I was really hoping that the CPK and Aldolase levels were from that. Very nervous…
I am suffering from continual muscle loss since stopping finasteride. I actually got my Creatine Kinase checked and it was normal (89, 38-201). This is actually the standard test for autoimmune myopathies which i really do think is causing my muscle loss at the moment.
Its possible CK will be normal with autoimmune muscle loss see; ncbi.nlm.nih.gov/pmc/articles/PMC170091/pdf/020001.pdf
Dont know if im grabbing at straws though, or even if im pinpointing the cause. Ill push for more tests in this area. Muscle biopsy, urine test?
my CRP has been very high and doctor called me to the office to tell that I am at high risk of heart attack. Is CRP and CPK are related?
I think it is all because of low androgen level or non effectiveness of androgens.
I am having low grade fever with chills at night time to time, once or twice a week (temperature 101 +)
this is not the sign of auto immune?
C-reactive protein and ESR are normal in most patients with an inflammatory myopathy.
AR (androgen receptor (dihydrotestosterone receptor; testicular feminization; spinal and bulbar muscular atrophy; Kennedy disease)) Antibody (against the N terminal of AR) (50ug) from Aviva Systems Biology
does this mean that anti androgen anti bodies will cause these symptoms? if present?
I am sure if these companies can look at our problem, if not cured, can easily be diagnosed at least.
if you click on the link and read under " disease" you will see the list of all of our problems like
Disease Product Link Publications Link Androgen insensitivity syndrome Androgen insensitivity syndrome Products Publications with AR AND Androgen insensitivity syndrome Prostate cancer Prostate cancer Products Publications with AR AND Prostate cancer Prostate tumor Prostate tumor Products Publications with AR AND Prostate tumor Partial androgen insensitivity syndrome Partial androgen insensitivity syndrome Products Publications with AR AND Partial androgen insensitivity syndrome Kennedy disease Kennedy disease Products Publications with AR AND Kennedy disease Hormone-refractory prostate cancer Hormone-refractory prostate cancer Products Publications with AR AND Hormone-refractory prostate cancer Atrophy muscle Atrophy muscle Products Publications with AR AND Atrophy muscle Infertility male Infertility male Products Publications with AR AND Infertility male Prostate cancer recurrent Prostate cancer recurrent
guys I just spoke with a technical person from an antibodies producer lab. First time very nice guy, who listened to me and took our website address and while I was talking to him, he even opened the website. He has asked me to what kind of tests we are looking for and he will help us and will guide us to right direction. He has given me his email address.
Oscar and other biology experts please let me know what do you think and how should I use this opportunity. I will send him email.
Ask how to test for Testosterone, dihydrotestosterone or 5ar2 antibodies. Dont mention your experiments on hamsters.
As I said, my Creatine Kinase was normal so i checked my Myoglobin (29.9, 28 - 72) it is normal too. Both of these tests are markers of damaged muscle tissue.
I had assumed that an autoimmune attack against an enzme would have a by-product of attacking the enzyme in muscles and lead to muscle loss. To my laypersons mind this now doesnt seem to be the case otherwise my CK or myoglobin would be raised. The fact they are not must only mean something is ‘lacking’ which is needed for muscles (ie T), not that something is being destroyed.
I think it is also true that you might expect damaged/raised liver enzymes, and you wouldnt expect the mental side effects (loss of libido, initiative, energy etc) to exactly correlate with testosterone deficiency if it was just an enzyme being attacked. Also an autoimmune attack on genitals might have more severe effects.
As an autoimmune attack is still more likely than awor’s idea I think this narrows it down to a hormone allergy or a reaction against ARs.
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Are you taking any vitamins or supplements?
My CRP was very high and I was having very painful muscles cramps After I started my vitamin D my testosterone went up and all my muscle atrophy stopped. I took again CRP tests and came back normal.
Further proof that drugs that bind to an enzyme can trigger an autoimmune attack against that enzyme;
Anti-cytochrome P450 autoantibodies in drug-induced disease ncbi.nlm.nih.gov/pubmed/8987248
Of course an ‘attack’ against 5a-reductase doesnt seem to be enough. Finasteride must now trigger an autoimmune response against 5a-reduced metabolites, DHT/neurosteroids and/or their respective hormone receptors. And there must be some evidence that this can happen with other enzymes too else this theory thread is little better than hot air.
Its worth noting that as a 4-Azasteroid analogue Finasteride is almost chemically identical to Testosterone and similarly Dihydrofinasteride (5a-Fin) is almost identical to DHT.
Based on the principles of molecular mimicry, autoimmunity can be triggered by the immune system attacking part of the self that is similar to a foreign antigen (in this DHT and 5a-Fin). As posted before an autoimmune attack can be triggered against a metabolite of a xenobiotic. In this way anti-DHT/ant-5a-Fin antibodies (Ab) can be produced.
As posted earlier in this thread anti-Test Ab have been noted before which cause hypogonadism by blocking Test from working. Maybe anti-DHT Ab simply blocking DHT would explain some peoples symptoms. But not everyones, you cant expect muscle loss and hairloss and normal/low LH to exist at the same time.
Maybe anti-DHT Ab create a partial agonist effect by competing with the DHT for Androgen Receptor occupancy. This in itself could theoretically be enough cause a host of downstream results such as inverse agonism. Or maybe ant-DHT Ab simply effect the dissociation rate of DHT from the Androgen Receptor. A slow dissociation rate may lead to receptor downregulation, this is how GnRH agonists like Leuprorelin work.
Inverse, protean, and ligand-selective agonism: matters of receptor conformation
ncbi.nlm.nih.gov/pubmed/11259378
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you repeated my theory viewtopic.php?f=27&t=5589&p=52351&hilit=mimicry#p52351
I kept asking and researching for Accutan to further strengthen this theory. Accutan looks different from Betasitosterol, finasteride etc. Maybe during its metabolism at some point it changes and looks like testosterone/DHT etc.
I also posted about autoimmune disease treatment by drshrader drshrader.com/autoimmune_diseases.htm
I sent all of our information and webiste and just got his email yesterday
It’s possible I can help, but there is just no way to tell. First, you’d have to make an appointment to talk to me about all the details. If you want to do this, just contact Deneice at my office.
having said this and Looking at his expenses+travelling+ stay in the hotel I don’t think I can make it near future as currently I have no job or insurance.
If any body plans to go there please do your own search, I have no idea about him I just picked him through google.
Spstriken I dont care about what travel plans you dont have.
Seriously though, its actually the last paragraph and the study I posted which bring something new to explain why LH is normal with muscle loss. Ligand effects on the AR can have a multitude of effects its not just as simple as ‘on - off’ there can be agonist/antagonist effects at the same time and even different effects on different tissue. A change in dissocation rate could cause downregulation in all AR sites effected. This could start whilst using Fin and get worse after stopping when theres more DHT floating about.
As it stands I can only find obscure evidence that ligand antibodies can effect the receptor too (although this might be because Im not a PhD biologist).
Using molecular mimicry to produce anti-receptor antibodies
onlinelibrary.wiley.com/doi/10.1002/bies.950030507/abstract
are you doing any more research why you have higher than normal anti bodies? or you just gave up?
One thing is sure at present current medical treatment can never treat us.