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 âlackingâ 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 aworâs 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 âattackâ 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
Itâs possible I can help, but there is just no way to tell. First, youâd 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 donât 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 âon - offâ 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.
Oscar i have talked about this in other threads and there is a little proof to back it, as in the amounts of hormones people are pissing out compared to blood tests.
I thought that when finasteride was removed, the pregnane x receptor started to sense testosterone as finasteride or Dht as an exogenous substance.
When i went on a broccoli sprouts diet (they are rich in sulforaphane, the only ânaturalâ pregnane x receptor antagonist) my penis went really large and healthy looking for a couple of days.
Sulforaphane is also a strong HDAC inhibitor and a promoter of de-methylizationâŚ
Summary of ideas In this Thread: That an autoimmune reaction against DHT/5aR is causing the symptoms.
I thought I would summarise for easy-reading. This idea has problems and is highly based upon my own personal symptoms but this is basically it;
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Drugs that are metabolised by CYP450 enzymes can trigger an autoimmune reaction against that enzyme (and its substrate).[1]
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DHT is almost chemically identical to DH-Finasteride (5alpha reduced metabolite of Finasteride) and, following the theory of molecular mimicary, maybe a trigger for an autoimmune attack against it.
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Scientists specialising in AIS have theorised that both pre- & post-receptor problems may cause androgen insensitivity, as well as AR mutations.[2]
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The only documented case of post-receptor androgen insensitivity was by anti-testosterone antibodies.[3]
Good
It is a convenient idea because autoimmune attacks can cause numbness (not low T). Also, symptoms could start whilst on the drug and perhaps get worse after stopping when more DHT created.
Bad
Hairloss is still a problem, would have to be explained by the ligand now having altered occupany at the receptor or some other effect (not just blocking) (see [4]). Or possibly by anti-Testosterone (not anti-DHT) antibodies only being produced in 5aR2 areas.
[1] ncbi.nlm.nih.gov/pubmed/8987248
[2] bioscience.org/1996/v1/a/lee1/htmls/lee.pdf
[3] jcem.endojournals.org/content/83/1/14.long
[4] ncbi.nlm.nih.gov/pubmed/11259378
Should read:
- The only documented case of pre-receptor androgen insensitivity was by anti-testosterone antibodies.
The other good point about this idea is that it explains the rarity of symptoms. No case of androgen insensitivity has ever been recorded as a result of androgen deprevation - despite billions of $$$ spent on studying androgen receptors.
I am not sure if it is related but looks like anti bodies can affect ARs.
neuromuscular.wustl.edu/antibody/motpn2.htm
CASE 3: A 55 year old man was referred for possible immunosuppression to treat a lower motor neuron syndrome with anti-GM1 antibodies. He had noted increasing difficulty climbing stairs and arising from a chair for 10 to 15 years. In recent years his speech had become slurred and he needed more time to eat. On general examination there was mild gynecomastia. Neurological testing showed weakness and fasciculations of the tongue and face. The tongue showed severe atrophy. Moderate symmetric, proximal weakness was present. Tendon reflexes were difficult to elicit. Sensation was reduced to all modalities distally in the feet. Electrodiagnostic testing showed chronic denervation, most prominent in the face, tongue, and proximal muscles. Repeat anti-GM1 antibody testing showed a pattern of polyreactive serum IgM binding to GM1 ganglioside and to histone H3 at titers of about 1,500.
COMMENT: The patients weakness was proximal and symmetric, more typical of inherited motor neuron disorders than of acquired motor neuropathies. Although the patient had high titers of anti-GM1 antibodies, the pattern of binding was polyreactive. Polyreactive antibodies are not specific for immune motor syndromes, and are also found in 3% to 5% patients with ALS and adult-onset spinal muscular atrophies. Further testing revealed an excessive number of trinucleotide repeats in the androgen receptor, a finding consistent with X-linked hereditary bulbo-spinal muscular atrophy. This case emphasizes that determination of the specificity of anti-GM1 antibodies helps to determine their clinical relevance. The polyreactive antibodies in a patient with features atypical of a motor neuropathy were not, of themselves, an indication for immunosuppressive therapy.
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These things arent a secret. The reason this is a good idea is that it takes KNOWN disease states and applies them to T/DHT/5aR/ARs. There is no point discussing anything else.
FACT⢠Medical texts describe dozens of autoimmune endocrine diseases that involve antibody reactions against Hormones, Enzymes and Hormone Receptors. Which can also be triggered by using drugs.
IDEA ⢠Maybe Finasteride has triggered an autoimmune reaction towards 5aR and/or DHT?
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FACT⢠Autoimmune reactions are a cause of loss of sensation (paraesthesia).
IDEA⢠Maybe an autoimmune reaction against 5aR/DHT is the cause of this in the genitals (and scalp!)
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FACT⢠Adverse reactions to Finasteride are v. uncommon (or v.rare). Autoimmune reactions are a rare side effect of common drug use.
IDEA⢠Some (or all) of the side effects are the result of an autoimmune reaction triggered by Fin. (Rather than DHT inhibition.)
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FACT⢠Autoimmune endocrine diseases often involve antibodies which block the activities of hormones. In fact this is the only known cause of pre-receptor androgen insentivity.
IDEA⢠Many of the symptoms are similar to an incorrect response to T/DHT, maybe this is due to blocking antibodies.
~
FACT⢠Adverse reactions usually only last for the duration of the drug use - but many men get worse after stopping Finasteride.
IDEA⢠Since DHT increases (by 300%) after drug use, it must be an adverse reaction to DHT/5aR triggered by Finasteride. However, for others this may only be a transient reaction to 5aR (and the lower DHT) whilst using the drug - or the autoimmune reaction is not as severe.
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FACT⢠Increasing T/DHT has transient, zero or negative effects. It is also true that antibodies can have competitive, antagonist effects at hormone receptors.
IDEA⢠Increasing the level of receptor agonists (T & DHT), also increases the antigen (DHT & 5aR) which increases these antibodies.
~
erm, thats all i can think of for now.
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