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mirena iud side effects auto immune disorder

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sp2000 Views: 2,598
Published: 9 years ago

mirena iud side effects auto immune disorder

I have been here for few months but never posted.
After reading how marina IUD can cause auto-immune disorder I did some research.I was shocked by finding the fact that people who used finasteride /dutestride/ saw palmetto extract (for their hair loss)are suffering from the same sides,and for many these side effects got worse after stopping the medicine. Many have the same auto immune disorders.I am not going into detail of these sides any body can google, they are exactly the same with obvious difference
1- women became pre-menopausal : boys became pre-Andropausal
both have very low sexua| hormones.
the rest of the story is the same.

So what is in common here?
women got injected artificial progesterone into their body, boys got finestaride/dutasteride / betasitosterole(the active ingredient in the sawpalmetto extract).These chemicals act to replace natural progesterone, testosterone in our body. Body's immune system launches antibodies against these chemicals and we started feeling side effects. When we stop these chemicals for many of us side effects stop too but for some unlucky ones the immune system never stops firing anti bodies because it can not differentiate between artificial and natural hormones. Not only that there are some non-target specific anti bodies as well and these antibodies target each hormone that looks like actual targets. For this reason women not only have low progesterone but their other hormones will drop too like testosterone, free testosterone etc.
Just google and see the chemical structure of progesterone, testosterone, finasteride, dutasteride etc they all look the same. If you think I am bringing far fetch ideas here then please read the following

Molecular Mimicry - An exogenous antigen may share structural similarities with certain host antigens; thus, any antibody produced against this antigen (which mimics the self-antigens) can also, in theory, bind to the host antigens, and amplify the immune response. The idea of molecular mimicry arose in the context of Rheumatic Fever, which follows infection with Group A beta-haemolytic streptococci. Although rheumatic fever has been attributed to molecular mimicry for half a century no antigen has been formally identified (if anything too many have been proposed). Moreover, the complex tissue distribution of the disease (heart, joint, skin, basal ganglia) argues against a cardiac specific antigen. It remains entirely possible that the disease is due to e.g. an unusual interaction between immune complexes, complement components and endothelium.
there are many many articles on autoimmune caused by mocular mimicry.
for example

this is very good article and highly recommend to read .

what is Molecular mimicry ?

Molecular mimicry is generally interpreted as the sharing of molecular structures (or their protein products) by portions of dissimilar genetic material (i.e. "resemblance" or cross-reactivity, most often between different organisms). This produces an "error in identification" by the host. The mimicking material is usually foreign ("non-self" e.g. bacteria) but the material contains components similar enough to certain host cells that the host then mounts an attack on "self." In other words, a bacteria can trick the body into attacking normal cells that have a few characteristics of the bacteria. When you think a great deal about this, the prospect is frightening.

If a peptide bound by HLA-B27 were the result of molecular mimicry between host and organism, the receptor site would be considered by the host to be "foreign". This could easily explain autoimmunity, or the breaking of self-tolerance, since autoreactive cytotoxic CD8 cells could then continue to attack the HLA-peptide reaction site and persist, despite the absence of any initial triggering agent, such as bacteria, virus, etc.

Molecular mimicry--hypothesis or reality?
A number of observations support molecular mimicry as a possible pathogenetic mechanism in diseases such as acute rheumatic fever, reactive Arthritis after enteric infection or associated with Reiter's syndrome, myasthenia gravis, or even in Rheumatoid Arthritis . Molecular mimicry can be defined as a sharing of epitopes in linear or 3-dimensional presentation on disparate proteins from entirely different sources--for instance, group A streptococcal membranes and human cardiac myosin. How exposure to or infection with organisms sharing molecular similarity with antigens of the human host can evade tolerance and actually induce a self-reacting humoral or cellular immune response is still not clear; however, a large body of evidence has now been accumulated that documents apparent molecular mimicry mechanisms in these disorders

Now doctor shrader claims to cure many of auto immune disorders we have.
I have no experience of doctor Shrader. I was googling for auto immnue disorder and he showed up.
look at what he treats


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