Hypotheses: Autoimmune Cross-targeting, Co-carcinogenesis, and Quorum complications : September 2016

Wednesday, September 28, 2016

Does the virus that triggers scleroderma also trigger the associated cancers specifically small cell lung cancer? Is it Epstein-barr?

Does the virus that triggers the scleroderma also trigger the associated cancers?

Cancers with Scleroderma: lung, breast, non-melanoma skin, lymphoma
http://www.medscape.com/viewarticle/846109

EBV associated cancers
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3887666/
https://www.ncbi.nlm.nih.gov/pubmed/15129648 (lymphomas)

Scleroderma and EBV
https://www.ncbi.nlm.nih.gov/pubmed/8299265

scleroderma: EBV virus and Cryptococcus (autoimmune cross-targeting hypothesis)
http://angelabiggs.blogspot.com/2014/02/is-scleroderma-autoimmune-disease.html

CMV and EBV in breast cancer
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4344231/

lung and breast cancer in scleroderma
https://www.ncbi.nlm.nih.gov/pubmed/8457221

adenocarcinoma and ebv
https://www.ncbi.nlm.nih.gov/pubmed/21654679

gastro/ esophogeal cancer nd EBV
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4374449/

scleroderma and small cell lung cancer!!!
http://onlinelibrary.wiley.com/doi/10.1002/jso.2930290109/abstract
https://www.ncbi.nlm.nih.gov/pubmed/2841907
https://www.ncbi.nlm.nih.gov/pubmed/15897643

small lung cancer and gastric cancer
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4316115/

Scleroderma and breast cancer
https://www.ncbi.nlm.nih.gov/pubmed/15801071
https://www.ncbi.nlm.nih.gov/pubmed/24103404

Alpha-herpes viruses: Herpes simplex 1, herpes simplex 2, herpes zoster : Estrogen-beta receptors (nerves and uterine tissue)...these beta receptors cycle to the mitochondria and won't cause cancer?

Beta-herpes viruses: CMV, HHV6, HHV7 : Estrogen-related receptors (CMV binding confirmed)

Gamma-herpes viruses: EBV, HHV8 : Estrogen-alpha receptors (lymphocytes, breast involved)

estrogen-alpha receptor up regulated in scleroderma ( EBV? )
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3825457/

antibodies to estrogen alpha receptors in scleroderma
https://www.ncbi.nlm.nih.gov/pubmed/24058548

estrogen-alpha receptor and non small cell lung cancer
https://www.ncbi.nlm.nih.gov/pubmed/16033821

Estrogen alpha receptor and breast cancer
http://www.ncbi.nlm.nih.gov/pubmed/14973389

EBV infects epithelial cells
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4246291/

EBV in nasopharyngeal carcinoma
https://www.ncbi.nlm.nih.gov/pubmed/9624611

EBV, nasopharyngeal, and burkitt's lymphoma
http://www.pnas.org/content/70/11/3265.full.pdf

Sclerodermas and nasopharyngeal carcinoma
https://www.ncbi.nlm.nih.gov/pubmed/11085820

scleroderma, EBV and lymphoma
https://www.ncbi.nlm.nih.gov/pubmed/10227462

pulmonary lung fibrosis and EBV
http://www.atsjournals.org/doi/full/10.1164/ajrccm.159.4.9807077#.V-xVp5MrKL8

Fibrosis of the lung is common with scleroderma
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340472/

NOTE that other viruses could trigger the autoimmune cross-targeting with cryptococcus

Tuesday, September 27, 2016

The sixteen medical hypotheses which will change our lives

1. Allergy hypothesis: Allergies reveal the infections we have. Severe allergies and infections can be matched up: peanut and Staph, bee and T.gondii, daisy and Clostridium, poison ivy and spirochetes. If an infection can be killed by a compound or inhibited by the compound our immune system sees the interaction and we associate all the compounds present with the infection. If an infection makes a pigment from a compound we will react to that too. For example aflatoxin with peanuts could cause staph to counter respond. Our immune system would identify everything there at the scene of the crime as part of the infection.

2. Quorum hypothesis: Infections talk using quorums. These quorums interfere with our body's pathways. ( for example mycobacteria's cGMP causes such things as type 2 diabetes, high cholesterol, and synuclein bodies)

3.. Autoimmune cross-targeting hypothesis: The Cross-targeting of simultaneous infections on one tissue, one infection inside and one infections outside, triggers autoimmunity. Antibodies or chemicals/drugs can replace one of the infections. By antibodies I mean even those triggered by vaccines.

4. Co-carcinogenesis: a virus and a carcinogen together cause cancer. The carcinogen is a polymerase inhibitor which binds the viral polymerase with higher affinity. Cancers wear the receptors that the virus that triggered it used to enter and the characteristics of the cancer will be from the receptor's pathways.

5. Barrier crossing infections, ones that can cross the intestine or the blood brain barrier, cause gluten sensitivity and allow other infections across with the hole they leave behind.

6. Viral families use receptor families. Influenzas use dopamine receptors. HPVs use Cannabinoid receptors. Herpes viruses use estrogen and estrogen-like receptors. Flaviviruses use melanocortin receptors. Polyomaviruses use serotonin receptors.

7. Aflatoxin like compounds cause tau bodies. ALS and picks disease are caused by different infections but both have tau. Both infections secrete an aflatoxin like compound. Vitamin D is protective against it because aflatoxin uses the vit D receptor.

8. Pituitary tumors are caused by an infection releasing butyrolactones which interfere with normal GABA signals and cause the immune system to confuse nerves with the infection. (or someone taking too many GHB sleeping pills)

9. The receptors used by a virus when triggering autoimmunity cause pathways to be activated which makes the various types of one autoimmune disease. There are 3 types of schizophrenia which match up with the 3 receptors use by the 3 herpes viruses. (sort of a continuation of 6)

The receptor pathway triggered by a virus involved in an autoimmune disease can cause symptoms of the disease that will be distinct. Example: The 3 types of schizophrenia has all 3 herpes virus families....each receptor activated can be matched to symptoms. Estrogen-related receptor and disorganized symptoms for example. 3 receptors used equals 3 types of schizophrenia

10. Alzheimer's disease is caused by damage to the mitochondria: alpha-herpes family, diacetyl, inherited and linked to down syndrome, or radiation damaged mitochondria.

11. Postural orthostatic tachycardia could be caused by reoviruses and the adrenergic receptors they bind.

12. The HLAs are mailboxes for T cells from different areas of the cell. HLA-A is the nuclear mailbox. HLA-B is the mitochondria's mailbox. HLA-C is the endoplasmic reticulum's mailbox. HLA-DR is the cytosol's mailbox for RNA viruses. HLA-DQ is the cytosol's mailbox for non encapsulated viruses there. HLA-DP is the endocytosis mailbox.

13. Carcinogens use certain receptors to get into cells which matches them up with specific cancers.

14. TLRs, toll like receptors, are the innane immune system of nets catching conserved molecules in a non specific way but identifying the region as well as general type of infection. Like HLAs they exist in the different areas of the cell. When the internal viral seeking TLRs are activated the IFN matches the region they are in thus the appropriate HLA is produced helping to find the exact culprit.

15. TLRs send IFNs which tells infected cells to express the corresponding HLAs and macrophages to wear the corresponding TAMs (hands to grab infected cells)

Cytosol TLR3 IFNbeta HLA-D Tyro3
Nucleus/ Mito TLR7/9 IFNalpha HLA-A HLA-B Mer
Endoplasmic R TLR 8 IFNgamma HLA-C Axl

(because an ER infected means little gets to the surface of a cell Natural killer cells step in here and secrete IFNgamma)

16. Nuclear viruses awaken embryonic Hervs. They do so by methylating or demethylating DNA. If the virus family demethylates the cancer will be aggressive while the methylating viruses are slow growing. (Cancer occurs when a carcinogen inhibits the viral polymerase..so the virus opens the DNA up but can't use it)

Atherosclerotic plaques are caused by a herpes virus like CMV methylating the DNA when a carcinogen is not around and the virus infects.

Monday, September 26, 2016

Myelodysplastic syndromes and idopathic thrombocytopenia have an overlap because they share viral infections

Myelodysplastic syndromes and idopathic thrombocytopenia have an overlap because they share viral infections: the EBV virus and flaviviruses.

Co-carcinogenesis : Rous' hypothesis requires a virus and a carcinogen together to start cancer.
Autoimmune cross-targeting has a virus marking the inside of cells for immune attack.

Older post:
Benzene, leukemia, and these same viruses: EBV or flaviruses
http://angelabiggs.blogspot.com/2016/04/leukemia-and-co-carcinogenesis.html

Note that benzene alone, with no the virus there, would inhibit polymerases causing stunted cell division thus anemia.

benzene inhibits polymerases
http://www.ncbi.nlm.nih.gov/pubmed/3381009
http://www.ncbi.nlm.nih.gov/pubmed/2926830

Myelodysplastic syndromes

EBV and myeloma
http://www.ncbi.nlm.nih.gov/pubmed/22234097

Hepatitis C and myeloma (hepatitis C is a flavivirus)
http://www.ncbi.nlm.nih.gov/pubmed/16610042
http://news.cancerconnect.com/hepatitis-c-infection-increases-risk-of-lymphoma-and-multiple-myeloma/

HLA-dr15 connected to Flaviviruses (Added dec 2016)

HLA-dr2/ HLA-dr15 and myelodysplastic syndrome (added dec 2016)
http://www.bloodjournal.org/content/100/5/1570?sso-checked=true

Autoimmune cross-targeting hypothesis: the layering of 2 different infections on one target triggers autoimmune disease. A viral infection marking the inside of the target then a bacterial, or fungal, or mycobacteria, spirochete infection marking the outside.

Schizophrenia and autoimmune cross-targeting of the amygdala with herpes virus....breaking up the 3 types of schizophrenia?

Autoimmune cross-targeting hypothesis: the layering of 2 different infections on one target cell type triggers autoimmune disease. A viral infection marking the inside of the target then a bacterial, or fungal, or mycobacteria, spirochete infection marking the outside.

Schizophrenia and autoimmune cross-targeting of the amygdala. Different infections on the amygdala will trigger schizophrenia as long as one infects the inside and one infects the outside.

we know the amydala is involved in schizophrenia and it's hallucinations
http://www.ncbi.nlm.nih.gov/pubmed/24619536
http://www.ncbi.nlm.nih.gov/pubmed/20071145

Schizophrenia and t.gondii has long been suspected
http://wwwnc.cdc.gov/eid/article/9/11/03-0143_article
http://www.medicalnewstoday.com/articles/284681.php

Other infections at the amygdala could cause it...but t.gondii has the most evidence so far.
(at the bottom of the page I will look at mycobacterias as another culprit. )

(Also note that the T.gondii group I suspect may have bee allergies where as the mycobacteria group are more likely to have shellfish allergies)

So what virus is infecting the inside? Several have been looked at:

herpes and t.gondii
http://www.ncbi.nlm.nih.gov/pubmed/21991754

mother's antibodies to HSV-2 and a child with schizophrenia
https://www.ncbi.nlm.nih.gov/pubmed/15319094

resent onset schizophrenia antibodies: CMV and HHV6
https://www.ncbi.nlm.nih.gov/pubmed/14991372

Earlier post about hearing loss, schizophrenia, and newborns
http://angelabiggs.blogspot.com/2014/12/tgondii-and-cytomegalovirus-both.html

So which herpes virus causes Schizophrenia by cross-targeting with t.gondii?

All 3 receptors are there at the amygdala and I believe they each cause a different type of schizophrenia based on the receptor they use....thus the 3 major types of schizophrenia.

(these receptor virus match ups are another hypothesis that is not proven but they help describe what we are seeing and since LYSINE has been shown to slow replication of all herpes viruses this simple amino acid could help....IF....these hypotheses are correct)

Alpha-herpes viruses: Herpes simplex 1, herpes simplex 2, herpes zoster : Estrogen-beta receptors (nerves and uterine tissue )

Beta-herpes viruses: CMV, HHV6, HHV7 : Estrogen-related receptors (CMV binding confirmed)

Gamma-herpes viruses: EBV, HHV8 : Estrogen-alpha receptors (lymphocytes, breast involved)

the amygdala has estrogen alpha receptors and beta receptors
http://languagelog.ldc.upenn.edu/myl/ldc/llog/Brizendine/Jasnow2006.pdf
and estrogen-related receptor-gammas.

Can we divide these into different types of schizophrenia: disorganized, catatonic, paranoid?

DISORGANIZED : HLA-A2 and HLA-A11 : beta-herpes (CMV)

The estrogen related receptors have been connected to spatial learning.
https://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-47134/
http://www.omim.org/entry/602969

Some schizophrenia has spatial learning issues
http://www.sciencedirect.com/science/article/pii/S2213158212000253
http://www.ncbi.nlm.nih.gov/pubmed/16048451

Could this be the "disorganized schizophrenia" group be similar to spatial issues and linked to the Estrogen Related Receptors and CMV?

CMV and estrogen related receptors link
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4284536/

CMV, hearing loss, schizophrenia, and t.gondii in young children
http://angelabiggs.blogspot.com/2014/12/tgondii-and-cytomegalovirus-both.html

CMV and HLA-A11
http://www.bloodjournal.org/content/98/2/500?sso-checked=true

CATATONIC : HLA-B16 : Alpha-herpes (zoster, simplex)

Could the catatonic group be linked to the estrogen-beta receptor?

catatonic and herpes simplex 1 which uses beta
http://www.ncbi.nlm.nih.gov/pubmed/21364369
http://www.ncbi.nlm.nih.gov/pubmed/6487432
http://www.ncbi.nlm.nih.gov/pubmed/6722708
http://www.ncbi.nlm.nih.gov/pubmed/4370982

"spice" has been shown to trigger catatonic schizophrenia
http://www.schizophrenic.com/news/schizophrenia-research/studies-link-spice-drug-catatonic-psychosis
http://guilfordjournals.com/doi/abs/10.1521/psyc.2014.77.2.206

studies of this drug cold help elucidate if the beta receptor is used in catatonic schizophrenia

The beta-estrogen receptor cycles to the mitochondria of cells. The mitochondria is the "ATP power generator" for the cell allowing for movement. Catatonic is by definition the lack of movement. How does this all fit together?

HLA-B16 and schizo
https://www.researchgate.net/publication/14045457_HLA_antigens_in_schizophrenia_and_mood_disorders

PARANOID: HLA-A9 and HLA-A3 : Gamma Herpes (EBV)

Does paranoid schizophrenia use the alpha-estrogen receptor?

When just paranoid schizophrenia was looked at only EBV antibodies were found. Which would imply the alpha receptor.
http://www.sciencedirect.com/science/article/pii/S0920996411001605

Looking at the estrogen receptor genes they found that alpha receptor and beta receptor differences in schizophrenia
http://www.ncbi.nlm.nih.gov/pubmed/22001950

For paranoid schizophrenia an alpha estrogen gene mutation has been linked!
https://www.ncbi.nlm.nih.gov/pubmed/23497414

HLA-A9 and HLA-Cw4 (HLA-A is the nuclear mailbox) with paranoid schizo
https://www.cambridge.org/core/journals/psychological-medicine/article/is-schizophrenia-an-hla-associated-disease/2D67B606AE25A4C05A087DA7F9E31887

estrogen appears to be protective for woman against schizophrenia
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860106/

alpha-receptors are strongly correlated with social behaviors
http://www.ncbi.nlm.nih.gov/pubmed/12488114
http://www.ncbi.nlm.nih.gov/pubmed/9213137

schizophrenia and social behaviors
http://www.ncbi.nlm.nih.gov/pubmed/20417974

We have known that during hormonal fluxes estrogen psychosis can result
http://psychcentral.com/news/2010/01/21/estrogen-may-prevent-psychosis/10886.html

Mycobacterias might replace T.gondii as the large outer infection

Previously on this blog I connected Mycobacterias to type 2 diabetes and high cholesterol through the use of it's quorum cGMP

http://angelabiggs.blogspot.com/2015/12/mycobacterias-possible-connection-to.html

Schizophrenia and metabolic disorder
http://www.ncbi.nlm.nih.gov/pubmed/17685741

Schizophrenia and type 2 diabetes
http://www.mdedge.com/currentpsychiatry/article/64865/schizophrenia-other-psychotic-disorders/link-between-schizophrenia
http://www.ncbi.nlm.nih.gov/pubmed/16280338
http://www.ncbi.nlm.nih.gov/pubmed/15538314

Schizophrenia and high cholesterol
http://www.sciencedirect.com/science/article/pii/S0165032705002995

psoriasis and schizophrenia
https://www.ncbi.nlm.nih.gov/pubmed/21985649
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4928455/ (and mood disorders)
file:///Users/angelabiggs/Downloads/fulltext-schizophrenia-v2-id1006%20(2).pdf

note that those with both schizophrenia and bipolar are at the highest risk for metabolic syndrome
http://www.healthyplace.com/diabetes/mental-health/metabolic-syndrome/

Bipolar is cross-targeting of the Anterior cingulate

Bipolar 1 : T.gondii and CMV
(more common in children?)

Bipolar 2: mycobacteria and CMV
(overlaps with high cholesterol and type 2 diabetes)

Hyperthyroid caused Bipolar-like...connected to graves and RA?

Hoarding and depression: spirochetes secreting high cortisone...not autoimmune either no cycles

HLA-A2 group (the nuclear mailbox)
https://www.researchgate.net/publication/14045457_HLA_antigens_in_schizophrenia_and_mood_disorders

Alzheimer's and schizophrenia should exist only in the catatonic type
Alzheimer's I had hypothesized caused by damaged mitochondrias.

In the case of Schizophrenia only one herpes virus type damages the mitochondria the Alpha herpes family including herpes zoster, HSV1, and HSV2 which uses the beta estrogen receptors. Beta-estrogen receptors cycle to the nerves mitochondria.

Alzheimer's and schizophrenia ....catatonic?
http://onlinelibrary.wiley.com/doi/10.1111/j.1479-8301.2007.00218.x/abstract
https://www.ncbi.nlm.nih.gov/pubmed/8732586
https://www.ncbi.nlm.nih.gov/pubmed/19748376
https://www.ncbi.nlm.nih.gov/pubmed/12788685
http://www.techtimes.com/articles/20929/20141125/the-surprising-link-between-alzheimers-and-schizophrenia.htm

HLA-B16 group (mitochondrial mailbox)

Parkinson's, Lewy bodies, bipolar, and schizophrenia
This overlap can only be caused by the shared mycobacterias

Lewy bodies are caused by mycobacteria's quorum, cGMP, in the brain

Parkinson's is the autoimmune cross-targeting of mycobacteria with a virus (flavivirus or flu) at the substantia nigra.

Bipolar 2 is mycobateria and cmv at the anterior singulate.

Schizophrenia is the mycobacteria with a herpes virus at the amygdala.

Thus if you are unlucky and catch a mycobacteria you are vulnerable to these autoimmune reactions if it gets into your brain. (and then you catch viral infections hence these autoimmune diseases can appear in different orders)

HLA-B27 I had linked to mitochondrial issues from bacterial proteins

HLA-B27 appears with schizophrenia...is this from the mycobacterias or t.gondii?
https://www.researchgate.net/publication/16252641_HLA_antigens_and_schizophrenia_A_pool_of_two_studies

Thursday, September 22, 2016

Acute Disseminated Encephalomyelitis (ADEM): are there multiple types? Autoimmune cross-targeting hypothesis suggests there should be because not all nerves have the same receptors.

Autoimmune cross-targeting hypothesis: the layering of 2 different infections on one target cell type triggers autoimmune disease. A viral infection marking the inside of the target then a bacterial, or fungal, or mycobacteria, spirochete infection marking the outside.

Different viral infections can trigger ADEM and it seems logical that since these virus families use different receptors to enter the nerves....there should be different types of ADEM.

Zika and ADEM
http://www.medscape.com/viewarticle/861811

Zika could be using the ACTH receptor

ADEM and autism (measles vaccine in common?)
http://www.huffingtonpost.com/robert-f-kennedy-jr-and-david-kirby/vaccine-court-autism-deba_b_169673.htm

ADEM after vaccination for / or infection with measles, mumps, or rubella
http://www.ncbi.nlm.nih.gov/pubmed/19179725

Paramyxoviridae (measles family viruses) bind Muscarinic receptors

ADEM has been PROVEN to be triggered by the rabies vaccine

ADEM has also been linked to Enteroviruses which bind Nicotinic acetylcholine receptors

ADEM and enteroviruses
http://www.ncbi.nlm.nih.gov/pubmed/20677593
http://www.ncbi.nlm.nih.gov/pubmed/25576193
http://www.ncbi.nlm.nih.gov/pubmed/17106158
http://www.ncbi.nlm.nih.gov/pubmed/11419405

Multiple sclerosis has associations with herpes zoster which by using the beta estrogen receptor hides in the mitochondria of the nerves. Thus this form of autoimmune disease could possibly wax and wane with the herpes zoster virus.

Pervious blog posts about MS connect the mycobacteria of psoriasis with the herpes zoster virus as the possible triggers of MS.

It is possible that some cases of ADEM are mycobacterias crossed with other viruses that do not wax and wane. (I had connected high cholesterol and type 2 diabetes to the quorum of mycobacterias : cGMP so this might be the vulnerable group)

The paralysis caused by enteroviruses like polio and D68 are very likely to be autoimmune in nature because not everyone who catches these viruses develop paralysis. An autoimmune cross-targeting of the spinal region instead of the brain?

Any thoughts?

Wednesday, September 21, 2016

What is the relationship of Chamomile (tea oil), urease secretion, H.pylori, C.sordellii, ulcerative colitis, and Takasyasu? Can enterotoxins explain lactose intolerance?

Chamomile inhibited the production of urease by H.pylori
http://www.ncbi.nlm.nih.gov/pubmed/17724768

C. Sordellii is urease positive
http://jb.asm.org/content/86/3/605.1.full.pdf

Chamomile and ulcerative colitis (improves the condition)
http://onlinelibrary.wiley.com/doi/10.1111/apt.12397/full

H.pylori causes stomach ulcers through the urease

It is my contention that C. sorderllii causes ulcerative colitis. Chamomile could help the condition by inhibiting the urease production of C. Sordellii

note that C.diff has been linked to antibiotic triggered pseudomembranous colitis
http://www.ncbi.nlm.nih.gov/pubmed/700321
http://www.ncbi.nlm.nih.gov/pubmed/549188

Aortic aneurysm and c. diff
http://www.jiac-j.com/article/S1341-321X(16)30141-6/abstract
http://www.ncbi.nlm.nih.gov/pubmed/22306098

Takasyasu (chronic inflammation the aorta of unknown etiology) and C. ulcerative colitis
http://www.ncbi.nlm.nih.gov/pubmed/25931203
http://www.ncbi.nlm.nih.gov/pubmed/25948351
http://www.ncbi.nlm.nih.gov/pubmed/21709638
http://www.japi.org/february2006/CR-151.pdf
http://www.medpagetoday.com/rheumatology/arthritis/52967
http://onlinelibrary.wiley.com/store/10.1002/art.39157/asset/art39157.pdf?v=1&t=itczssyy&s=63dfcd7cb7b58274d612a04683a2f1edf5306a81
http://www.govaresh.org/index.php/dd/article/view/833
http://content.onlinejacc.org/article.aspx?articleid=1361678
http://gut.bmj.com/content/31/7/831.full.pdf

Vasculitis in patients with ulcerative colitis
http://www.ncbi.nlm.nih.gov/pubmed/26315859

Could Takasyasu be connected to a C.sordellii infection?

Note that I have an unproven association of ulcerative colitis and daisy/mum allergies. The chamomile flower is in the same flower family as daisies and mums.

c.diff and lactose intolerance are known to be linked
https://cdifffoundation.org/2013/07/05/suggested-foods-to-avoid-during-a-c-diff-infection/

Are the toxins of C. diff and C. sordellii the reason for the diarrhea?

ToxinA ( an enterotoxin) and C.diff's diarrhea
https://en.wikipedia.org/wiki/Clostridium_difficile_toxin_A

Note that Lactose is a natural ligand of the toxin ricin and cholera
http://pubs.acs.org/doi/abs/10.1021/am900846r
https://www.ncbi.nlm.nih.gov/pubmed/20369893
https://www.ncbi.nlm.nih.gov/pubmed/12000304
https://www.ncbi.nlm.nih.gov/pubmed/7766178

Lactose is able to bind enterotoxins!!!!
http://www.nature.com/nature/journal/v355/n6360/abs/355561a0.html

Lactose intolerance and IBS (irritable bowel syndrome)
https://www.ncbi.nlm.nih.gov/pubmed/12439117
https://www.ncbi.nlm.nih.gov/pubmed/12591050
https://www.ncbi.nlm.nih.gov/pubmed/11407668
https://www.ncbi.nlm.nih.gov/pubmed/15380888
https://www.ncbi.nlm.nih.gov/pubmed/20522486

Summary: It is possible that the reactions of ulcerative colitis to dairy involve C.sordellii. C.sordellii has an endotoxin that causes diarrhea and a urease that causes ulcers. Lactose would bind both of these causing the bacteria to ramp up production. Takasyasu could be when so much damage has occurred at the intestine S.sordellii has crossed over into the bloodstream's vessels?

Any thoughts?

Tuesday, September 13, 2016

Do Paramyxoviridae (measles family viruses) bind Muscarinic receptors?

Enteroviruses (coxsackie, polio etc) may bind nicotine receptors
http://angelabiggs.blogspot.com/2016/08/enteroviruses-and-nicotine.html

Nectin-like interactions of polio virus binding
http://www.ncbi.nlm.nih.gov/pubmed/25631086

Measles virus binds nectin-4
http://www.ncbi.nlm.nih.gov/pubmed/27483301

since polio virus binds nectins and measles binds nectin 4 is it possible that paramyxoviridae viruses bind muscarinic receptors?

do measles bind muscarinic receptors? Muscarinic receptors are found on smooth muscles.

eye and bladder have muscarinic receptors

neurogenic bladder after measles
http://www.ncbi.nlm.nih.gov/pubmed/2087429

bladder and muscarinic receptors
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1751864/

Measles is the leading cause of childhood blindness !!!

Measles issues: croupy cough, loss of voice, swelling eyes, uncontrolled salivation

M1 receptors and eye development
https://www.ncbi.nlm.nih.gov/pubmed/20964868

joints and muscarinic receptors?
http://www.sciencedirect.com/science/article/pii/036192309190296V

measles and smooth muscle antibodies in joint of RA
http://ard.bmj.com/content/36/4/302.full.pdf+html
http://www.ncbi.nlm.nih.gov/pubmed/901028

muscarinic receptors and the cerebellum
http://www.ncbi.nlm.nih.gov/pubmed/23776234

M3 and cerebellum?
http://www.ncbi.nlm.nih.gov/pubmed/26823384

cerebellum type 2 and 3 muscarinic receptors
http://www.ncbi.nlm.nih.gov/pubmed/18358697

measles and cerebellum
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC375852/

parainfluenza viruses
https://en.wikipedia.org/wiki/Human_parainfluenza_viruses

HPIV 1 and 2 cause CROUP

M2 receptors and croup?
https://www.ncbi.nlm.nih.gov/pubmed?term=9649578

HPIV 3 Bronchiolitis ( inflammation of the bronchioles)

Bronchioles have M3 receptors
https://en.wikipedia.org/wiki/Bronchoconstriction

Can't clearly match up viruses and muscarinic receptors: measles virus could bind more than one type?

Kids who had RSV can later have asthmatic reactions to viral infections...why?

eosinphils express muscarini receptors (M2)
http://digitalcommons.ohsu.edu/etd/540/

RSV and eosinphils: eosinphils as targets of infection
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2741084/

eosinphils and measles (eosinphils increased)
http://jid.oxfordjournals.org/content/180/4/950.full

Are they increased to counter the numbers of eosinphils infected by the virus?

increased eosinphils in bronchial asthma
http://www.ncbi.nlm.nih.gov/pubmed/2215562

has the immune system adapted because of the RSV and started making more eosinphils each time?

Note that eosinphils are required for the development of plasma cells
http://www.ncbi.nlm.nih.gov/pubmed/21217761

Could doses of measles destroy eosinphil populations?

A woman was cured of plasma cell cell cancer (Myeloma) by measles virus treatments
http://www.medicalnewstoday.com/articles/276966.php

How did they "engineer" these cancer treatment measle viruses? could they infect cells but not replicate?

Sunday, September 11, 2016

Looking at Charles Richet's life, T.gondii, and hallucinations

Looking at Charles Richet's 1930 discovery of anaphylaxis and then his obsessions with the "sixth sense".

I can't help wonder these things:

France in general has a high infection rate of T.gondii. This parasite which prefers the host of cats can also infect other mammals including cows, people, and dogs.

T. gondii has strong associations with Schizophrenia which involves hallucinations. I have been suggesting that schizophrenia could be a cross-targeting autoimmune reaction of T.gondii and another infection in the brain.

During Charles Richet's lifetime the drink Absinthe was popular among the poor. This worm wood green fairy drink was known to cause hallucinations in a percent of the population.

Richet was trying to explain the ability, the spiritual energy, as real not hallucinations. (was he himself infected?)

What if....this is a huge assumption and leap....what if the percent of the population that had hallucinations to Absinthe had t.gondii infections.

What if the Absinthe goes to the same area of the brain as the t.gondii thus causes the hallucinations similar to schizophrenia ?

Bee sting reactions and schizophrenia patients
http://www.ncbi.nlm.nih.gov/pubmed/5239954

What if the dogs that had fatal bee reactions in Richet's experiment had t.gondii infections too?

a toxin from sea anemone blocks potassium channels like honey bee toxin does.

T.gondii and T. cruzii have potassium channels
http://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0032264

T.gondii and t.cruzii infections and bee venom
http://www.ncbi.nlm.nih.gov/pubmed/23562368
https://www.researchgate.net/publication/277891898_14_In_vitro_Effects_of_Some_Bee_Products_on_T_gondii_Tachyzoites

I doubt that dogs are exposed to bees as much as bee keepers which currently seem to be the favored bee anaphylaxis allergy explanation now.

Does thujone play are role? Thujone is a compound in absinthe that acts on GABA receptors. (not a high concentration) But if the number of receptors are increased in a person.

Schizophrenia patients have increased GABA receptors.
http://www.ncbi.nlm.nih.gov/pubmed/16362364?dopt=Abstract

T.gondii and GABA receptors
http://mbio.asm.org/content/6/6/e01428-15.full
http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1003051

Thursday, September 8, 2016

Hypothesis: Our allergies reveal unhealthy infections within us

The Roman philosophy of Janus states that to figure out what is in front of us now it helps to look back. How did we discover allergies and how can that change our view of allergies now?

Clemens von Pirquet and Bela Schick in the 1890s noticed a serum sickness with 10% of their dipertheria antitoxin vaccines. Since the reaction was not serum dose dependent they concluded that it must be a difference in the immune system. Clemens coined the term "allergy" in order to explain the new concept that one's own immune system can cause sickness.

What was not answered back then and remains unanswered now is why do some people develop allergies? What was different about the immune system in the 10%? What causes the immune system to malfunction? A genetic flaw?

For years without genetic evidence for this belief it has been said that allergies must be genetic because of the observed clustering and inheriting of allergies in families. Reality is that a person can go through most of their life allergy free then suddenly develop a severe one. If allergies were only genetically based, a genetic flaw, allergies couldn't spontaneously develop later in life. An infection on the other hand could easily be shared between family members or caught out in the environment.

When an infection occurs the immune system marks as much foreign infection material as it can with antibodies. Then memory B cells circulate with these infection crime scene antibodies for future identification. Perhaps the 10% who had the serum sickness reaction had seen the material before?

In 1913 Charles Richet received the Nobel prize for recognizing that the most severe allergic reactions, he coined "anaphylaxis", were due to a second exposure. Ten to twelve days after dogs were given a first octopus toxin exposure if a second toxin exposure was given to the dogs they had severe and sometimes fatal reactions.

Looking at the known plant based allergies: trees, grass, poison ivy, daisies, and lilies which a person could see daily and all of which are not considered toxic it does not make sense to apply the second exposure notion of Richet unless you add pathogenic infections. why? because the immune system needs a reason to be making antibodies and memories.

Let us take this even one step further: why this allergen? With all the substances we are exposed to why does an allergen get selected? Perhaps the allergen is something the infection doesn't like.

Allergy Hypothesis: An allergen has an antimicrobial effect against an infection within us.

Imagine a spirochete infection like lyme disease or h.pylori. Often the infected person has no idea they are infected. Spirochetes can be killed by a compound found in poison oak and poison ivy. Now imagine that a person infected with spirochetes is exposed to poison ivy. Instead of a typical reaction of rash and itchiness the person has a severe reaction boarding on anaphylactic.

Now, imagine a person infected with T.gondii or T.cruzii. These parasites can be killed with the venom of bees. Now imagine the possibility that people with anaphylactic bee allergies are the people with these T.gondii or T.cruzii infections. This would not be the people working with bees who are constantly stung thus becoming allergic rather people who are allergic because of the T.gondii parasite.

Which brings us to the notorious peanut allergy which is strongly associated with eczema. The peanut protein itself is not an antimicrobial but the aflatoxin so commonly contaminating peanut butter is. Aflatoxin has been found to be antimicrobial against the antibiotic sensitive strains of staph and e.coli. The more susceptible to traditional antibiotics the more susceptible to aflatoxin the bacteria is. (http://www.ncbi.nlm.nih.gov/pubmed/3091837)

The association of staph and eczema has been sketchy. Staph has, but not always, been isolated from skin scrapings. The anaphylactic peanut allergy is a bit convoluted but it could be that peanut is seen with aflatoxin by the immune system and it is guilt by association. The peanut is not harming the infection the aflatoxin is but our immune system remembers everything there. The aflatoxin acts as an antimicrobial against staph which fits our allergy hypothesis. Do antibodies to aflatoxin exist in children with peanut anaphylaxis?

Tuesday, September 6, 2016

Postural orthostatic tachycardia, Reoviruses, and adrenergic receptors...is there a connection?

Postural orthostatic tachycardia, Reoviruses, and adrenergic receptors...is there a connection?

This blog has been looking at autoimmune diseases. It is unclear if hyperadrenic POTS is an autoimmune disease. This is the pattern so far with reoviruses looking like culprits of the disease not so much as triggers of an autoimmune reaction.

Disease cluster : POTS, Ehler-danlos syndrome, mast cell activation
http://www.jacionline.org/article/S0091-6749(14)02927-3/abstract

(hyperadrenic POTS)

reoviruses are found in mast cell tumors in dogs
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0073555

mast cell syndrome in people..90% is cutaneous (reovirus involved here too?)
http://www.medscape.com/viewarticle/450039_2

Autoimmune diseases with POTS

http://www.ncbi.nlm.nih.gov/pubmed/26038344

1 in 4 ( 25% ) of POTS patients had ANA (antinuclear antibodies)

1 in 9 POTS patients had Hashimoto's

Reoviruses create ANA

http://www.jstor.org/stable/1590868?seq=1#page_scan_tab_contents

http://onlinelibrary.wiley.com/doi/10.1002/ana.410190606/abstract

http://www.tandfonline.com/doi/pdf/10.1080/03079459008418691

Fungal infections can have reoviruses in them

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4517262/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC368758/

Hashimoto's, I had hypothesized, as connected to fungal infections

Gardasil and POTS connection
http://www.ncbi.nlm.nih.gov/pubmed/25882168

detection of reovirus in bird flu vaccine
http://www.ncbi.nlm.nih.gov/pubmed/15620400

POTS after chicken pox infection (zoster)....and anti-virals?
https://www.researchgate.net/publication/290480129_P-B34_Postural_tachycardia_syndrome_POTS_after_Varicella_Zoster_virus_infection_chicken_pox

Any thoughts?

celiac and rotavirus
http://www.ncbi.nlm.nih.gov/pubmed/17032199

I had hypothesized celiac as autoimmune cross-targeting of e.coli or sutterella like infections marking the outside and a virus like rotavirus marking the inside of the intestinal cells.

autonomic dysfunction and celiac
http://www.ncbi.nlm.nih.gov/pubmed/25554987
http://www.ncbi.nlm.nih.gov/pubmed/25962148
http://www.ncbi.nlm.nih.gov/pubmed/20940666

Is this the celiac group that was triggered by rotaviruses?

raynaud's and scleroderma
http://www.medscape.com/viewarticle/493381

aspergillus and scleroderma
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116216/

remember aspergillus can have reovirus infections

ANA is in 12% of scleroderma patients
http://www.ncbi.nlm.nih.gov/pubmed/25580285

older post of aspergillus, scleroderma, raynauds,
http://angelabiggs.blogspot.com/2016/07/pernio-chilbain-raynoids-sle.html

norepinephrine and collagen???
http://www.ncbi.nlm.nih.gov/pubmed/19575289

scleroderma is the build up of collagen in skin cells (collagen was also the issue in EDS)

not exactly sure what this means yet

the norepinephrine transporter gene is the suspect for "panic disorder"
http://www.ncbi.nlm.nih.gov/pubmed/21416264
http://www.ncbi.nlm.nih.gov/pubmed/15722184

anxiety and panic in lupus
http://www.ncbi.nlm.nih.gov/pubmed/26748551
http://www.ncbi.nlm.nih.gov/pubmed/21078764
http://www.ncbi.nlm.nih.gov/pubmed/19500858

Panic disorder vs anxiety and EDS
http://www.edhs.info/about1-cs05

joint pain and ANA: to determine SLE in children:
http://www.ncbi.nlm.nih.gov/pubmed/26114367
http://www.ncbi.nlm.nih.gov/pubmed/15245579

Mycophenolic acid inhibits reovirus replication
http://www.ncbi.nlm.nih.gov/pubmed/15163710
http://www.ncbi.nlm.nih.gov/pubmed/15451179

Note that it also inhibits B and T cells and is currently used in immunosuppression
https://en.wikipedia.org/wiki/Mycophenolic_acid
and Mycophenolate mofetil is being used in some lupus and scleroderma cases

How does the immune system normally fight reoviruses? with NO

Nitric oxide increases during rotavirus infections
http://www.ncbi.nlm.nih.gov/pubmed/16721855
http://www.ncbi.nlm.nih.gov/pubmed/16004984 NO inhibits reoviruses too!!!

what a strange thought: could laughing gas stop panic attacks?

Hypotheses: Autoimmune Cross-targeting, Co-carcinogenesis, and Quorum complications