Autoimmune Thyroid disease

I am trying to separate Graves and Hashimoto's.

Graves has TSH receptor antibodies.  Does the enterotoxin of things like Staph and E. coli which could bind the receptor involve this? Can we try to connect bacterial infections to graves as the trigger for the autoimmune graves disease? Bladder infections (e.coli) or eczema (staph) should be higher in graves patients.

Hashimoto's has anti-peroxidases. The thyroid makes peroxides which could be confused with fungal infections like aspergillus and candida because they secrete peroxidases.  Do patients with candida induced diabetes have Hashimoto's not Graves?  Do patients with aspergillus infections have bulb allergies along with Hashimoto's? (aspergillus niger grows on blubs like onions, garlic, tiger lilies)

Added 4/2
I am looking for the viruses that could be infecting and causing the cross-targeting of the immune system.

For Hashimoto's I found this reference http://www.ncbi.nlm.nih.gov/pubmed/22998463 where they see evidence of a virus that could cause the inflammation but it is unclear which one it is.

Any virus that would infect inflaming the thyroid could push the immune system into the autoimmune disease and they may be the same ones for both of these disease since all it needs to do is confirm the target of the immune system which is already looking because of the antibodies which as built up. (at least my hypothesis predicts this)

Further I want to know if the hepatitis viruses will infect the thyroid and replicate there...not just in the liver.  Can someone look even if it is in a pertri dish thyroid? Can these viruses be jumping to another organ?

Another virus under consideration is the Epstien-barr virus.  Does this virus infect the thyroid itself? This virus has been connected to skin cancer...could it cause thyroid cancer? Could it cause Hashimoto's until that point?

Added 8/3/13   High levels of TSH are associated with bipolar (see new posting) where as low TSH seems connected to tics and Obsessive compulsive disorder.

T3 levels when low in Hashimoto's effects the levels of serotonin.  Extremely low levels of serotonin are currently being investigated for suicide.  Hypothyroid disease is also under consideration through T3 as an instigator of suicide.

The thyroid levels of T, T4, and TSH should all be constantly checked in autoimmune thyroid patients.

I hope the CDC consider these ideas and test them. (these are theories not proven)

Hopeful,
Angela Biggs




 

Could colored letters help dyslexia?

This is not really an autoimmune topic...I just stumbled upon the idea reading up on Asperger's. 

I read an article in the new scientist where an Asperger's patient dealt with the sensory overload of emotion by projecting a color aura.  His mind simplified what he was seeing using color which is probably one of the first neural networks laid down in our minds.

I have heard of minds projecting color before: color-graphemic synesthesia.  Where children who learned their numbers using colored frig magnets had the colors forever automatically projected even on to black type numbers by their minds.  Imagine rainbow phone numbers...much easier to remember.

If one's brain can learn to use colors to overcome sensory overload could this be use this for Dyslexia?  If the shapes of letters are overwhelming could we assign colors to letters when they are learning and overcome the issue? Could their minds eventually project the color and aid them in reading?

It would be a simple program to write on the computer...each letter getting it's own color.  Could someone out there try it? Maybe it could help Dyslexia?

Hopeful
Angela Biggs

NOTE: I am considering that dyslexia maybe connected to ulcerative colitis which has daisy allergies (sometimes including latex which was made from dandelions)

Autoimmune Schizophrenia

Schizophrenia:

Here are the references and thoughts I have on Schizophrenia.

First schizophrenia can be autoimmune in that antibodies generated against the NMDA receptor of the brain can cause Hallucinations

ref: Antibody mediated encephalitis: a treatable cause of schizophrenia
British Journal of Psychiatry 2012
200:92-94

The bacteria infection T. gondii can be linked to the NMDA receptor through pan/apple domains.

 T. gonii has pan/apple on it. 

ref: A novel pan/apple domain containing protein for Toxoplasma gondii: characterization and receptor indentification 
PLoS

Schizophrenia has T. gondi antibodies

ref: Antibodies to Toxoplasma gondii in patients with Schizophrenia.
schizophrenia bulletin vol 33 no 3 pp 729-736

In our body when blood clots are degraded, plasminogen which has the PAN sequence in  it, is activated by tPA (tissue plasminogen activator)

t-PA binds not just plasminogen but the NMDA receptor.   Does this mean the NMDA receptor has a PAN/apple domain?

ref: t-PA is a new ligand of NMDA receptor
JBC papers Sept 23. 2004

If antibodies develop against T.gondii included the pan/apple domain does this mean the antibodies might also bind the NMDA receptor? 

Now I can apply my autoimmune hypothesis to it.  A dimorphic infection triggers an autoantibody precursor stage which then progresses into the the disease following a viral infection cross targeting event.

The strain ME49 of T.gondi contains more then one morphology. Both spherical vesicles and tubular elements are found.

The change in morphology might be just like e.coli using LON.  T.gondii apears to trigger a gluten response.

ref: Anti-gluten immune response following toxoplasma gondii infection in mice.
PLo S Nov 29 2012 , 7 (11)e50991

Schizophrenia has been associated with gluten and casein

ref. The gluten connection: the association between schizophrenia and celiac disease.
Acta Psychiatr Scand 2006 Feb: 113(2): 82-90

ref: Specific IgA antibody increases in Schizophrenia
1995 society of biological psychiatry 

So we have the bacteria creating the antibodies where the immune system is looking at the receptor but then we need the cross-targeting virus. The virus would infect the nerves bearing these receptors thus causing the immune system to have verification of the neuron, brain cell, as an issue...cross targeting would push one into attacking one's self. 

Retroviruses were linked to schizophrenia patients in 2001in Germany.  An example of a retroviruses is the Borna virus...a virus which infects the central nervous system. 

Only then would the autoimmune form of schizophrenia develop...but this is a hypothesis and this is just something to consider. It is not proven.

Multiple sclerosis and cross-targeting autoimmunity

Autoimmune hypothesis:

Stage one
A bacterial or mycobacterial infection creates  a hyper state of auto-antibodies through morphology changes or pigment changes. The infection appears to disappear and reappear to our immune system.

Stage two
A virus infection causes cross-targeting by infecting or creating antibodies that overlap the existing ones from stage one.

Multiple sclerosis

Stage one
Multiple sclerosis is associated with eczema. A meningitis type of bacteria like the staphylcoccus aureus has been associated with eczema.  (Staph produces yellow pigment when exposed to milk or egg which explains the eczema allergies)  It is possible this bacteria produces antibodies against the nervous system but not does not succeed in causing meningitis.  These antibodies are the first to target nerves.

Reference: Varicella, ephemeral breastfeeding and eczema as risk factors for multiple sclerosis in Mexicans.  Acta Neurol Scand 2002 105, 88-94 http://www.ncbi.nlm.nih.gov/pubmed/11903117

Donald Leung of National jewish has isolated staph from some eczema but has not claimed that it is the cause.

Staph and MS (specific type of staph is involved)
http://www.ncbi.nlm.nih.gov/pubmed/21212089


Bacterial toxins and MS
http://www.direct-ms.org/pdf/InfectiousMS/Bacterial%20toxins%20MS%2007.pdf

C. pneumoniae  is another possible culprit
http://www.medscape.com/viewarticle/574944_3

It can infect the CNS
http://www.medscape.com/viewarticle/574944_3 
http://www.ncbi.nlm.nih.gov/pubmed/10401775

NOTE: it is not the exact infection so much as the location of the infection marking the outside of the target nerve that is significant.

Mycobacteria and MS
 http://www.ncbi.nlm.nih.gov/pubmed/21409957
http://www.ncbi.nlm.nih.gov/pubmed/14616302
also
http://www.ncbi.nlm.nih.gov/pubmed/15150306 and http://rheumatology.oxfordjournals.org/content/39/8/930.full (which I think psoriatic athritis and psoriasis are mycobacterias)

note that the mycobacteria bind to the nerves : http://www.pnas.org/content/96/17/9857 
using the laminin which the myelin forms on http://www.ncbi.nlm.nih.gov/pubmed/10576890

Hypothesis: The cross-targeting of infections at the same tissue causes autoimmune disease.  One infection marks the outside while another marks the inside...only then does the immune system become confused and attack. A virus as infecting the inside of a cell marks the inside for immune system attack.

Stage 2
 A virus that infects the nerves such as Herpes Zoster, shingles, causes the immune system to cross target the nerves.

References:
 Increased risk of multiple sclerosis following herpers zoster: A nationwide, population based study.
http://www.ncbi.nlm.nih.gov/pubmed/21653524

Herpes Zoster and Multiple sclerosis
JID 2011:204, 177-178
http://www.ncbi.nlm.nih.gov/pubmed/23035074


I have also been considering that fact that HERVs could act as the virus causing cross-targeting but i do not have enough information. Cross-targeting or something else...i am not sure.
  http://www.ncbi.nlm.nih.gov/pubmed/15782388

Again this is not proven it is a hypothesis. Does anyone see the pattern I see?

Lupus: mycoplasmas were linked to RA in 1974. Could lupus be cross-targeting autoimmunity with mycoplasmas andepstein barr virus? (mono)

Lupus

30% have photo sensitivity
We know from genetic Heme disorders that excess porphyrins cause photosensitivity. So is something happening to the red blood cells?
 
81 % have fatigue with anemia
This would support the notion that somehow Lupus is a blood autoimmune disease. 

Epstein barr virus, aka mono, has been associated with Lupus. EBV infects the B cells of the immune system.  If you consider my cross targeting theory of autoimmunity we need to find the culprit that created the antibodies that started the immune system looking at the B cells.

B cells are not red blood cells but both of these are in the bloodstream.  I would think that we are looking at some kind of bacterial blood infection which is consuming the cells of the blood stream indiscriminately, red and white cells.

Lupus with antibodies against red blood cells
http://www.ncbi.nlm.nih.gov/pubmed/10723973

Could blood infections in Lupus be the initial instigator?  Which is then triggered by mono compromising the immune system by making it attack itself to a degree? Going everywhere blood goes.

Looking at mycoplasmas.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1006269/

Fibromyalgia tends to be nightshade sensitvie or triggered.  I have no evidence to substantiate this notion but I hope people look and make sure this is not what is happening. 

Xanthomonas is a bacteria that infects nightshade plants.  They use butyrolactones as signalling molecules between them.

In our bodies butyrolactones is converted to GHB which is then converted to GABA.  GABA is the neurotransmitter. How our nerves talk to each other. 

A form of Xanthomonas has been found to infect the respiratory tract of people and is considered a new bacterial genus: named Stenotrophomonas. 

My notion is actualLy a question: does the Stentorophomonas still make these signalling molecules when exposed to nightshades like a bell pepper when it infects us? Could this explain the painful reactions to nightshades that Fibromyalgia patients have? Are antibodies directed at the butyrolactones causing antibodies to GABA thus causing one's own immune system to attack our nerves?

Just a thought. Has anyone looked at this?